First memorize all the single digit base 10 logs. Don't worry, it's not as painful as it sounds. I even made the chart for you:
|Log Base 10 of...||Is equal to...|
Remember this rule from high school?
log(a*b) = log a + log b
And what about this one, you remember it too?
log(10n) = n
Example #1: base 10 log of 400That's the same thing as log(4*100) which equals log 4 + log 100. log of 4 you know from the table above. Log of 100 is log of 102 and therefore is equal to 2. So the log of 400 is 2 + log 4 which is 2.602. It might sound like a tedious method but try a few examples first and you will see it's actually pretty quick.
Now you may ask, what if it isn't just a number with a bunch of 0's after it?
Example #2: base 10 log of 35Suppose you wanted to find the logarithm of 35. This is the same thing as log(3.5 * 10). The log of 3.5 is somewhere between the log of 3 and 4, but somewhat above the midpoint (since the log scale gets smaller as you go up). Log of 3 is .477 and log of 4 is .602 so we'll make a rough guess around .54 or .55 ish. Log of 10 is obviously 1, so our guesstimate for the log of 35 will be 1 + 0.545.
Our guess: 1.545
Calculator says: 1.544068...
Now you can convince all your friends and teachers that you are a robot.
Example #3: base 10 log of 290438572:This is fairly close to log(2.9 * 100000000) = log 2.9 + log 108
2.9 is close to 3. Log(3) = .477, so we'll guess something slightly below that like .45
Our Guess: 8 + .45 = 8.45
Calculated Answer: 8.46305...
Now run off and scare some people with your new powers.


CVE and CVSS: Explained
Although many IT managers are familiar with these terms, CVE and CVSS are some of the most commonly misunderstood aspects of patching today. These two different terminologies are synonymous with operating system, software vulnerabilities, and patching.
What is CVE?
The CVE (Common Vulnerabilities and Exposures) number is a unique identifier used by vendors such as Microsoft, RedHat, and Adobe to catalog individual vulnerabilities where patches are provided as a resolution. For example, every page of a book has a unique number. This solves the problem of finding the information on the page quickly.
Usually all CVE numbers look like this: CVE-nnnn-nnnn. You can see there is scope for millions of vulnerabilities.
“Our clients should feel confident that the CVE number is not owned by any specific software vendor,” said Robert Brown, Director of Services for Verismic Software. “Therefore, it is an unbiased and independent database for all vendors to publish their vulnerabilities.”
This also means that vendors must publish transparent content to these databases. At the very least, this provides some assurance to the accuracy of the data. Each company that wishes to publish its vulnerability announcements must become a CNA (CVE Numbering Authority) before its participation is considered reliable.
Vendors will include as much information as possible within each CVE record. For example:
- CVE number
- Description of vulnerability
- References to other CVE records (also known as supersession)
- Change History
- Publish Date
What is a CVSS Score?
The CVSS (Common Vulnerability Scoring System) is an independently assigned score (out of 10) which is based on a large number of factors to determine the importance of a vulnerability. To compare CVSS scores, let’s look at how Microsoft scores their vulnerabilities.
Microsoft’s rating system is relatively simple:
- Critical – A vulnerability that could allow remote code execution without user interaction or where code executes without warnings or prompts.
- Important – Vulnerabilities where the client is compromised with warnings or prompts and whose exploitation could result in compromise of data.
- Moderate – The impact is mitigated by numerous factors such as authentication or non-default applications being affected.
- Low – The impact is comprehensively mitigated by the characteristics of the mitigated component.
- NA – Not Available
However, Microsoft’s approach self-certifies vulnerabilities in its products.
Generating the CVSS score is highly complex, but it takes into consideration the following important questions:
- How easy is the vulnerability to be exploited? Do you need network or physical access and do you need elevated privileges?
- Can you exploit over the internet or do you need physical access?
- Is specific software or configuration of software needed? Does it impact everything?
- How much end-user interaction is needed?
Each of the above (and much more) are arranged in a sub score that is calculated together. The CVSS score is then calculated out of 10. Industry experts believe this offers the most accurate way to determine the priority of how quickly you must take action if any of these vulnerabilities exist within your environment.
||0.1 – 3.9
||4.0 – 6.9
||7.0 – 8.9
||9.0 – 10.0
Are CVSS scores necessary? Prove it!
Let’s take a couple updates from the August 2019 Patch Tuesday, and a few others to compare:
||High – 8.8
||High – 7.8
||Critical – 9.8
||Critical – 9.8
|The Document Foundation
||Critical – 9.8
As you can see from the sample above, vendor severity and CVSS scores are not always aligned. If you take Microsoft’s severity rating at face value, you can potentially waste two of the most precious assets you have—time and resources. Rolling out many patches across a massive distributed IT environment takes time.
The longer a known vulnerability is left unpatched, the greater the risk of having it exploited by an attacker. Evidence suggests that attacks against known vulnerabilities spike in the hours and days after the patches are released—this is why it’s important to know how urgent a vulnerability is.
What’s the solution?
Take any vulnerability ratings with a respectful pinch of salt and start looking at independently assessed scores, such as the Common Vulnerability Scoring System (CVSS). Each month US-CERT / NIST uses CVSS to rate most patch updates the same day they are released. This gives a better idea of the risk level for a particular vulnerability to your business.
Downtime for businesses can also be extremely costly. The best approach to patching is to have a dedicated window of downtime each month to update systems. If there is a compatibility issue with a patch and systems need to be rolled back, this extends the downtime and can impact the bottom line of a business.However, this is a service we provide to clients. We analyze the binary code for each patch update and begin testing and piloting the updates before deploying them through Syxsense. This allows us to discover any problems with patch updates before they’re implemented.
Patching is all about improving your security posture. By taking a measured approach and using independently assessed scores, you can confidently prioritize which patches need to roll out.


WHAT? Synthetic death
Currently, targeted therapies for malignant tumors are often directed at "oncogene addiction." The most typical example is that about 90% of patients with chronic myeloid leukemia (CML) have a BCR/ABL fusion gene, and tumor cells rely on the protein produced by this gene to survive. For normal cells, they are not dependent on it. gene. Therefore, imatinib targeting BCR/ABL can significantly prolong the survival of patients with CML, while being less toxic to normal cells.
[Noun explanation "oncogene addiction" refers to the survival of tumor cells depending on an activated oncogene]
Another therapeutic concept of tumors is synthetic lethality, which is expected to achieve the goal of killing only tumor cells without significant effects on normal cells. This concept has been successfully used in the treatment of BRCA 1/2 mutant ovarian cancer with PARP inhibitors.
[The term "synthesis-killing" refers to the cell-dependent gene B survival when the function of gene A is absent, that is, the inhibition of gene B and the loss of function of gene A lead to cell death, but only the loss of gene A function or the inhibition of gene B alone. In no case does it affect cell survival. ]
▲ Oncogene addiction and synthesis lethal
Synthetic lethality in DDR: familial hereditary BRCA mutations and PARP inhibitors
Various endogenous and exogenous factors can cause DNA damage in cells, and cells recognize DNA damage through a series of molecular pathways: DNA damage response (DDR) >>> Prevent cell cycle >>> Mediate DNA repair >>> Keep The integrity and stability of the cellular genome. Among them, poly(ADP-ribose) polymerase (abbreviated as PARP, mainly PARP1 and PARP2) is one of the key proteins in DDR. PARP1 recognizes DNA single-strand break (SSB), and when it binds to a single-strand break site, it activates its catalytic function, synthesizes poly ADP ribose chain (PAR) and assembles it on some proteins (PARylation) to recruit DNA. Damage repair proteins to the injury site to repair damaged DNA. Ultimately, PARP itself will also assemble PAR to dissociate from the repaired DNA.
After understanding the function of PARP, PARP inhibitors were gradually developed. Scientists initially developed PARP inhibitors in the hope that they would be able to sensitize traditional DNA damage therapies, including multiple chemotherapy drugs and radiation therapy. This is another synthetic lethal mode of PARP inhibitors, called “PARP trapping”, which will be done later. Detailed introduction. Until 2005, two research groups reported the combined lethality of PARP inhibitors and BRCA1/2 loss-of-function mutations, demonstrating a new therapeutic concept for tumors carrying BRCA mutations.
▲PARP binds to damaged parts of DNA
People with a family of hereditary BRCA1 or BRCA2 mutations have a significantly increased risk of malignancy, especially breast and ovarian cancer. Both BRCA1 and BRCA2 are key proteins in DNA double-strand break (DSB) homologous recombination repair (HRR). For family hereditary breast cancer patients, it is usually because of the loss of function on a homologous chromosome in the BRCA1 or BRCA2 gene. Mutation (heterozygous mutation, BRCA+/-), during life, some cells lose the function of BRCA1 or BRCA2 on another homologous chromosome, becoming a homozygous mutation (BRCA-/-), and the loss of BRCA function leads to HRR Loss of function, DNA double-strand break repair is blocked, causing genomic instability, which leads to tumors. However, other BRCA heterozygous mutations (BRCA+/-) still produce BRCA protein normally, which is involved in DNA double-strand break repair.
There are about 104 SSBs produced every day in tumor cells. These damages require PARP-mediated repair process. When PARP activity is inhibited, SSB continues to accumulate. During DNA replication, DNA single-strand breaks are converted into DNA double strands. The break, while the DSB produced during the replication process is mainly dependent on HR repair. For tumor patients with BRCA1/2 mutation, tumor cell HRR function is missing, DSB repair cannot be completed, and a large number of DSB accumulation causes DNA replication to collapse and cell death. Compared with BRCA-functioning tumor cells, tumor cells with BRCA function loss are about 1000 times more sensitive to PARP inhibitors than the former. For normal cells of these patients, functional BR BR proteins can be produced by carrying only heterozygous BRCA mutations, and therefore, PARP inhibitors have less effect on them. This is the initial understanding of the scientists' death from the synthesis of PARP inhibitors.
In subsequent studies, the scientists found that Talazoparib and Olaparib have comparable inhibition rates on PARP catalytic activity, but Talazoparib is significantly more cytotoxic to BRA mutant tumor cells than Olaparib. In addition, in a cell line with normal BRCA function, a combination of a cytotoxic DNA damaging agent methyl methanesulfonate (MMS) and a PARP inhibitor was also used to produce synthetic lethality. Later studies have found that PARP inhibitors can not only inhibit the catalytic activity of PARP, but also stabilize the complex of PARP protein and DNA, called "PARP trapping". When a DNA single-strand break occurs, the PARP protein binds to the cleavage site. At this time, the PARP inhibitor binds to PARP, which causes the loss of the catalytic function of PARP, affecting the PARP itself's PARylation, and the PARP protein cannot be dissociated from the DNA. Here, PARP is like a lock hanging on DNA, and the PARP inhibitor is like a key broken in the lock cylinder. It is firmly integrated in the lock cylinder, but it can't unlock, and it also prevents other keys from unlocking. Thus, PARP inhibitors form a stable complex of PARP and DNA, while the PARP-DNA complex has strong cytotoxicity and ultimately causes cell death. As mentioned earlier, MMS is a DNA damage reagent that increases the number of DNA single-strand breaks, so that PARP inhibitors can cause more "PARP trapping" and therefore have a synthetic lethal effect on cells with normal BRCA function. Although Talazoparib, Niraparib, Olaparib, and Niraparib have comparable PARP catalytic inhibitory activities, the ability to "PARP trapping" varies greatly. Talazoparib has the strongest "PARP trapping" ability, about 100 times that of Olaparib, followed by Niraparib, and Veliparib. The weakest. This also partly explains why PARP inhibitors with comparable PARP inhibitory activity have different cytotoxic effects on BRCA-mutated tumor cells.
▲The mechanism of action of PARP inhibitors
Clinical status of PARP inhibitors
The main function of PARP is to catalyze the synthesis of PAR, to make a variety of DNA repair proteins PARylation, involved in DNA repair, its substrate for coenzyme I (NAD+), the classic PARP inhibitor is bound to the substrate binding domain of PARP, therefore PARP inhibitors are all substrate analogs. Almost all PARP inhibitors have an aramid moiety to mimic nicotinamide in NAD+, thereby competitively blocking the catalytic activity of PARP. PARP inhibitors initially entered the clinical trial as a combination therapy with the chemotherapy drug temozolimide. Following the study of PARP inhibitor and BRCA mutant tumor synthesis lethal, PARP inhibitors are clinically used to treat BRCA1/2 mutant mammary glands. Cancer and ovarian cancer patients. At present, three PARP inhibitors have been approved by the FDA, and dozens of PARP inhibitors have been clinically tested at various stages, which are described below.
Olaparib is a PARP inhibitor developed by AstraZeneca. On December 19, 2014, the FDA approved its use in the treatment of advanced ovarian cancer patients who have received more than two treatments and have germline BRCA mutations. The concept of lethality is FDA-approved anti-tumor drugs. In 2015, the Nobel Prize in Chemistry was awarded to scientists who studied DNA damage repair and was also affirmed by this concept of treatment. Clinical studies have found that Olaparib is equally effective for patients with ovarian cancer who are able to benefit from platinum-based chemotherapy drugs, while platinum-insensitive ovarian cancer patients usually do not respond to Olaparib, suggesting that both therapies may be based on the same Mechanism. In a recent large phase III clinical trial, patients with recurrent ovarian cancer with germline BRCA mutations and sensitivity to platinum-based chemotherapy were treated with Olaparib (300 mg tablets twice daily) with no median progression. Survival was as high as 30.2 months, compared with 5.5 months in the placebo group. Common side effects were dizziness, fatigue, vomiting, anemia, neutropenia, and thrombocytopenia, which were consistent with previously reported side effects, indicating Olaparib. As a maintenance therapy, it has the potential to treat recurrent ovarian cancer with BRCA mutations. Currently, Olaparib has several clinical trials for different tumors ongoing.
Clovisarib, the PARP inhibitor of Clovis, was the first PARP inhibitor to be introduced into clinical trials. On December 19, 2016, Rucaparib was approved by the FDA for the treatment of advanced ovarian cancer with a germline or somatic BRCA mutation and at least two treatment regimens. The market was approved based on a phase III of 106 patients. In clinical trials, patients received 600 mg of oral daily treatment with an objective response rate (ORR) of 54%, complete remission (CR) of 9%, and a median duration of remission of 9.2 months. The sensitivity of these ovarian cancer patients to platinum-based chemotherapy drugs and the sensitivity to Rucaparib are highly consistent. Platinum-sensitive patients have an ORR of 66%, platinum-resistant patients with 25%, and platinum-refractory patients with 0%. Common side effects are nausea, fatigue, anemia, and the like. However, Rucaparib may have potential therapeutic risks, including myelodysplastic syndrome, acute myeloid leukemia, and fetal abnormalities. In previous studies, it was found that high concentrations of Rucaparib produced off-target cytotoxic effects compared to Olaparib and Talazoparib, but it is not clear whether these off-target effects are the main cause of toxic side effects.
Tesaro's PARP inhibitor Niraparib has been completed in Phase III clinical trials for platinum-sensitive advanced ovarian cancer and was approved by the FDA on March 27, 2017 for complete or partial response but relapse after platinum-based therapy Adult ovarian epithelial cancer, fallopian tube cancer, and primary peritoneal cancer are maintained without the need to detect the BRCA genotype. In a phase III clinical trial, 203 patients who had previously received at least 2 platinum-based therapies and who carried the BRCA mutation received 300 mg of Niraparib daily, with a median progression-free survival compared with the placebo group. Prolonged (21.0 months in the Niraparib group vs 5.5 months in the placebo group). Unlike Olaparib and Rucaparib, Niraparib's clinical trials included not only BRCA-mutated ovarian cancer patients, but also 350 patients who did not carry BRCA mutations. The study found that this group had a median progression-free survival of 9.3. At 3.9 months in the placebo group, patients who did not carry the BRCA mutation but had HRR deficiency had a median progression-free survival of 12.9 months in the Niraparib group, a significant improvement over the placebo group of 3.8 months. This indicates that Niraparib not only has a synthetic lethal effect on BRCA-mutated tumors, but also forms a synthetic lethality with other DNA double-strand repair defects. Common grade 3-4 adverse events are thrombocytopenia, anemia, and neutropenia.
Several clinical trials of Talazoparib are underway, including Phase III clinical trials for advanced breast cancer with BRCA mutations. In a previous clinical trial, 13 breast cancer patients with BRCA1/2 mutations received neoadjuvant therapy with Talazoparib. After two months, all patients had tumor shrinkage, and the treatment is currently under 4-6 months. Clinical trials of neoadjuvant therapy. In preclinical studies, Talazoparib has excellent PARP trapping ability, which is 100 times more toxic to BRCA mutant tumor cells than Niraparib. Therefore, in clinical trials, the clinical dose of Talazoparib is very low, only 1 mg per day.
▲Talazoparib's structural formula is undergoing several clinical tests
Iniparib was once considered a PARP inhibitor and has a different mechanism of action than traditional PARP inhibitors. In Phase II clinical trials, the combination of Iniparib with gemcitabine and carboplatin for the treatment of triple-negative breast cancer has achieved remarkable results, increasing progression-free survival and overall survival without increasing toxicity. However, Phase III clinical trials of non-small cell lung cancer and platinum-resistant ovarian cancer have failed. Moreover, this molecule does not selectively kill tumor cells that are BRCA-mutated. After detailed research, it was finally found that Iniparib is not a true PARP inhibitor, and its anti-tumor activity is not caused by inhibition of PARP. Iniparib and Olaparib's failure of several large phase III clinical trials reduced the enthusiasm of pharmaceutical companies for PARP inhibitors at the time, AstraZeneca terminated the PARP program, and other large pharmaceutical companies also sold their PARP products at a discount. Later, AstraZeneca found from previous clinical data that PARP inhibitors have excellent efficacy for BRCA-mutated tumors, and restarted Olaparib to treat phase III clinical trials of BRCA-mutant ovarian cancer, bringing people back to these drugs. interest. Iniparib has also become a typical counterexample in drug development.
▲Iniparib was confirmed not to be a PARP inhibitor
? PARP inhibitors for the treatment of BRCA mutant tumors successfully applied the concept of synthetic lethality to the treatment of tumors, but currently PARP inhibition
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No one knows where the city of Akkad was located, how it rose to prominence, or how, precisely, it fell; yet once it was the seat of the Akkadian Empire which ruled over a vast expanse of the region of ancient Mesopotamia. It is known that Akkad (also given as Agade) was a city located along the western bank of the Euphrates River possibly between the cities of Sippar and Kish (or, perhaps, between Mari and Babylon or, even, elsewhere along the Euphrates). According to legend, it was built by the king Sargon the Great (who ruled 2334-2279 BCE) who unified Mesopotamia under the rule of his Akkadian Empire and set the standard for future forms of government in Mesopotamia. Sargon (or his scribes) claimed that the Akkadian Empire stretched from the Persian Gulf through modern-day Kuwait, Iraq, Jordan, Syria (possibly Lebanon) through the lower part of Asia Minor to the Mediterranean Sea and Cyprus (there is also a claim it stretched as far as Crete in the Aegean). While the size and scope of the empire based in Akkad is disputed, there is no doubt that Sargon the Great created the first multi-national empire in the world.
The King of Uruk & the Rise of Sargon
The language of the city, Akkadian, was already in use before the rise of the Akkadian Empire (notably in the wealthy city of Mari where vast cuneiform tablets have helped to define events for later historians) and it is possible that Sargon restored Akkad, rather than built it. It should also be noted that Sargon was not the first ruler to unite the disparate cities and tribes under one rule. The King of Uruk, Lugalzagesi, had already accomplished this, though on a much smaller scale, under his own rule. He was defeated by Sargon who, improving on the model given him by Uruk, made his own dynasty larger and stronger. The historian Gwendolyn Leick writes, "According to his own inscriptions, he [Sargon] campaigned widely beyond Mesopotamia and secured access to all the major trade routes, by sea and by land" (The A-Z of Mesopotamia, 8). While Lugalzagesi had succeeded in subjugating the cities of Sumer, Sargon was intent on conquering the known world. The historian Durant writes, "East and west, north and south, the mighty warrior marched, conquering Elam, washing his weapons in symbolic triumph in the Persian Gulf, crossing western Asia, reaching the Mediterranean, and establishing the first great empire in history" (121-122). This empire stabilized the region of Mesopotamia and allowed for the development of art, literature, science, agricultural advances, and religion.
According to the Sumerian King List, there were five rulers of Akkad: Sargon, Rimush, Manishtusu, Naram-Sin (also known as Naram-Suen) and Shar-Kali-Sharri who maintained the dynasty for 142 years before it collapsed. In this time Akkadian came to replace Sumerian as the lingua franca except in sacred services and Akkadian dress, writing, and religious practices infiltrated the customs of the conquered in the region. A thorough understanding of the rise and fall of Akkad (relatively speaking) is best gained through an examination of the rulers of the city and the empire they maintained.
Sargon the Great either founded or restored the city of Akkad and ruled from 2334-2279 BCE. He conquered what he called "the four corners of the universe" and maintained order in his empire through repeated military campaigns. The stability provided by this empire gave rise to the construction of roads, improved irrigation, a wider sphere of influence in trade, as well as the above mentioned developments in arts and sciences. The Akkadian Empire created the first postal system where clay tablets inscribed in cuneiform Akkadian script were wrapped in outer clay envelopes marked with the name and address of the recipient and the seal of the sender. These letters could not be opened except by the person they were intended for because there was no way to open the clay envelope save by breaking it.
In order to maintain his presence throughout his empire, Sargon strategically placed his best and most trusted men in positions of power in the various cities. The "Citizens of Akkad", as a later Babylonian text calls them, were the governors and administrators in over 65 different cities. Sargon also cleverly placed his daughter, Enheduanna, as High Priestess of Inanna at Ur and, through her, seems to have able to manipulate religious/cultural affairs from afar. Enheduanna is recognized today as the world's first writer known by name and, from what is known of her life, she seems to have been a very able and powerful priestess in addition to creating her impressive Hymns to Inanna.
Sargon's Successors: Rimush & Manishtusu
Sargon reigned for fifty-six years and after his death was succeeded by his son Rimush (reigned 2279-2271 BCE) who maintained his father's policies closely. The cities rebelled after Sargon's death and Rimush spent the early years of his reign restoring order. He campaigned against Elam, whom he defeated, and claimed in an inscription to bring great wealth back to Akkad. He ruled for only nine years before he died and was succeeded by his brother Manishtusu (reigned 2271-2261 BCE). There is some speculation that Manishtusu brought about his brother's death to gain the throne.
History repeated itself after the death of Rimush and Manishtusu had to quell widespread revolts across the empire before engaging in the business of governing his lands. He increased trade and, according to his inscriptions, engaged in long-distance trade with Magan and Meluhha (thought to be upper Egypt and the Sudan). He also undertook great projects in construction throughout the empire and is thought to have ordered the construction of the Ishtar Temple at Nineveh which was considered a very impressive piece of architecture. Further, he undertook land reform and, from what is known, improved upon the empire of his father and brother. Manishtusu's obelisk, describing the distribution of parcels of land, may be viewed today in the Louvre Museum, Paris. His death is somewhat of a mystery but, according to some scholars, Leick among them, "Manishtusu was killed by his courtiers with their cylinder seals" though no definite motive has been offered for the killing( The A-Z of Mesopotamia, 111).
Naram-Sin: Greatest of the Akkadian Kings
Manishtusu was succeeded by his son Naram-Sin (also Naram-Suen) who reigned from 2261-2224 BCE. Like his father and uncle before him, Naram-Sin had to suppress rebellions across the empire before he could begin to govern but, once he began, the empire flourished under his reign. In the thirty-six years he ruled, he expanded the boundaries of the empire, kept order within, increased trade, and personally campaigned with his army beyond the Persian Gulf and, possibly, even to Egypt. The Victory Stele of Naram-Sin (presently housed in the Louvre) celebrates the victory of the Akkadian monarch over Satuni, king of the Lullubi (a tribe in the Zagros Mountains) and depicts Naram-Sin ascending the mountain, trampling on the bodies of his enemies, in the image of a god. Like his grandfather, he claimed himself "king of the four quarters of the universe" but, in a bolder move, began writing his name with a sign designating himself a god on equal footing with any in the Mesopotamian pantheon.
In spite of his spectacular reign, considered the height of the Akkadian Empire, later generations would associate him with The Curse of Agade, a literary text ascribed to the Third Dynasty of Ur but which could have been written earlier. It tells the fascinating story of one man's attempt to wrest an answer from the gods by force; and that man is Naram-Sin. According to the text, the great Sumerian god Enlil withdrew his pleasure from the city of Akkad and, in so doing, prohibited the other gods from entering the city and blessing it any longer with their presence. Naram-Sin does not know what he could have done to incur this displeasure and so prays, asks for signs and omens, and falls into a seven-year depression as he waits for an answer from the god. Finally, tired of waiting, he draws up his army and marches on Enlil's temple at the Ekur in the city of Nippur which he destroys. He "sets his spades against its roots, his axes against the foundations until the temple, like a dead soldier, falls prostrate" (Leick, The Invention of the City, 106). This attack, of course, provokes the wrath not only of Enlil but of the other gods who send the Gutium "a people who know no inhibition, with human instincts but canine intelligence and with monkey features" (106) to invade Akkad and lay it waste. There is widespread famine after the invasion of the Gutians, the dead remain rotting in the streets and houses, and the city is in ruin and so, according to the tale, ends the city of Akkad and the Akkadian Empire, a victim of one king's arrogance in the face of the gods.
There is, however, no historical record of Naram-Sin ever reducing the Ekur at Nippur by force nor destroying the temple of Enlil and it is thought that "The Curse of Agade" was a much later piece written to express "an ideological concern for the right relationship between the gods and the absolute monarch" (Leick, 107) whose author chose Akkad and Naram-Sin as subjects because of their, by then, legendary status. According to historical record, Naram-Sin honored the gods, had his own image placed beside theirs in the temples, and was succeeded by his son, Shar-Kali-Sharri who reigned from 2223-2198 BCE.
The Decline of Akkad
Shar-Kali-Sharri's reign was difficult from the beginning in that he, too, had to expend a great deal of effort in putting down revolts after his father's death but, unlike his predecessors, seemed to lack the ability to maintain order and was unable to prevent further attacks on the empire from without. Leick writes, "Despite his efforts and successful military campaigns, he was not able to protect his state from disintegration and, after his death, written sources dried up in a time of increased anarchy and confusion" (The A-Z of Mesopotamia, 159). Interestingly, it is known that "his most important building project was the reconstruction of the Temple of Enlil at Nippur" and perhaps this event, coupled with the invasion of the Gutians and a widespread famine, gave rise to the later legend which grew into The Curse of Agade. Shar-Kali-Sarri waged almost continual war against the Elamites, the Ammorites and the invading Gutians but it is the Gutian Invasion which has been most commonly credited with the collapse of the Akkadian Empire and the Mesopotamian dark age which ensued. Recent studies, however, claim that it was most likely climate change which caused a famine and, perhaps, disruption in trade, weakening the empire to the point where the type of invasions and rebellions which, in the past, were crushed, could no longer be dealt with so easily. The last two kings of Akkad following the death of Shar-Kali-Sharri, Dudu and his son Shu-Turul, ruled only the area around the city and are rarely mentioned in association with the empire. As with the rise of the city of Akkad, its fall is a mystery and all that is known today is that, once, such a city existed whose kings ruled a vast empire, the first empire in the world, and then passed on into memory and legend.
About the Author
- Obelisk | Louvre Museum | Paris
- Two examples of abrupt climate change
- Victory Stele of Naram-Sin | Louvre Museum | Paris
- Durant, W, Our Oriental Heritage (Simon & Schuster, 1954).
- Kramer, S. N, The Sumerians (University of Chicago Press, 1971).
- Leick, G, Mesopotamia / Mesopotamia/ The Invention of the City (Origenes/ Origins) (Paidos Iberica Ediciones S a, 2002).
CreateSpace Independent Publishing Platform (20 December 2015)Price: $6.14
HardPress Publishing (28 January 2013)Price: $15.95
Leopold Classic Library (04 July 2015)Price: $10.95
Vandenhoeck & Ruprecht (31 December 2011)Price: $219.00
Nabu Press (24 February 2014)Price: $17.75
2334 BCE - 2279 BCE
2261 BCE - 2224 BCEReign of Akkadian king Naram-Sin.
2218 BCE - 2047 BCEThe Gutian Period in Sumer.
c. 2150 BCEThe Akkadian Empire falls, Mari gains independence.
c. 2083 BCE - c. 2050 BCEThe Dark Age of Mesopotamia.
c. 2055 BCE - 2047 BCEUtu Hegel's reign over Sumerian and Akkadian cities.


Smoking used to be portrayed as being glamorous in advertisements and movies. In old films, actors constantly smoked cigarettes and a tough guy usually had one hanging out the side of his mouth. It’s debatable whether smoking still makes you look cool though, especially since there are fewer and fewer public places you’re even allowed to smoke. Plus we now better understand the health risks of tobacco products.
Tobacco use is the single largest preventable cause of disease and premature death in the United States, but nearly 44 million Americans still smoke cigarettes – 1 in every 5 adults. There are also 14 million cigar smokers and 2 million pipe smokers.
Tobacco use is not quite as widespread in California, where just over 1 in every 7 adults smokes cigarettes. In the past year, 61 percent of these smokers attempted to quit.
There are many good reasons to quit smoking, and health concerns usually top the list. Half of all smokers who keep smoking die from a smoking-related illness, including lung cancer, other types of cancer, heart attack, stroke, or lung disease. Women who smoke are also more likely to miscarry or have a baby with a low birth-weight.
There are both immediate and long-term health benefits when smokers quit. After quitting for:
- 20 minutes, your heart rate and blood pressure drop.
- 12 hours, the carbon monoxide level in your blood drops to normal.
- 2 weeks – 3 months, your circulation improves and lung function increases.
- 1 – 9 months, your coughing and shortness of breath decrease.
- 1 year, your risk of heart disease due to smoking cuts in half.
- 5 years, your risk of various cancers (mouth, throat, esophagus, and bladder) is cut in half.
- 15 years, your risk of heart disease is the same as a non-smoker.
Cigarettes are also expensive. You can use a savings calculator to see how much money you would save if you quit smoking. For example, a pack of cigarettes costs $6.77 on average in California. If you smoke a half pack (10 cigarettes) per day, this adds up $24 per week or $1220 per year.
Of course, the nicotine in tobacco is very addictive so quitting can be difficult, but the chance of success is increased with help. There are many treatment options used to help smokers quit and many of these treatments are covered by health insurance.
The most effective quitting method is a combination of counseling, social support and the use of cessation medication. The most common form of counseling is through telephone-quit lines, which provide free support and advice from an experienced cessation counselor. The counselor can provide a personalized quit plan, self-help materials, the latest information on cessation medications, and social support. For instance, 1-800-QUIT-NOW is a free national counseling service. Many clinics and hospitals also have counselors and support groups that you can meet with face-to-face. Counseling and support groups are also available online.
There are a variety of cessation medications that are available either over the counter or with a prescription. Nicotine replacement therapies deliver nicotine to help reduce the severity of nicotine withdrawal symptoms. The nicotine dose is gradually reduced over time. Nicotine gum, lozenges and patches can be purchased over the counter, whereas nicotine inhalers or nasal sprays require a doctor’s prescription.
Bupropioin SR (Wellbutrin or Zyban) is a non-nicotine prescription medication that acts on the chemicals in the brain that are related to nicotine craving. It can be used alone or with nicotine replacement products. Verenicline (Chantix) is a non-nicotine prescription medication that blocks the effects of nicotine, so it should not be used in combination with nicotine replacement products.
It is important for smokers to speak with their doctor and/or a cessation counselor to make a personalized quit plan that is right for them. And this week is a good time to get started, just in time to take part in the Great American Smokeout on November 21. Smokers across the nation will use this Thursday to make a quit plan, or plan in advance and quit smoking.
The Great American Smokeout happens every year on the third Thursday of November. It started in California back in 1976 when nearly 1 million smokers quit for the day, then the American Cancer Society expanded the program nationwide the following year. It has drawn attention to the deaths and chronic diseases caused by smoking, resulting in laws that ban smoking in restaurants and other public places.
The Great American Smokeout is celebrated with rallies, parades, stunts, quit programs, and “cold turkey” menu items. For instance, the community is invited to receive up-to-date cessation information, resources and giveaways at UCSF Medical Center’s Great American Smokeout event from 9-10 am and 12-1 pm on the Parnassus, Laurel Heights, Mission Bay and Mount Zion campuses. UC Berkeley is also celebrating the event with a “cold turkey” give-away – get a free cold turkey sandwich in exchange for a pack of cigarettes from 11 am – 2 pm at Sproul plaza.
This is a repost of my KQED Science blog.


This workshop gave both first-time and more experienced data users an insight into four of the UK’s internationally-renowned cohort studies run by the Centre for Longitudinal Studies (CLS).
Longitudinal data are a powerful resource for addressing a wide range of scientific questions in various social, health, political and geographical sciences.
For example, what determines health across life? How has social mobility changed? What determines voting preferences?
Led by CLS researchers – David Bann, Brian Dodgeon and Vanessa Moulton – this workshop gave delegates an insight into four of the UK’s internationally-renowned cohort studies run by the Centre for Longitudinal Studies (CLS):
- 1958 National Child Development Study;
- 1970 British Cohort Study;
- Millennium Cohort Study;
- Next Steps (previously known as the Longitudinal Study of Young People in England).
Delegates were given an introduction to each of the cohort studies and further information on how to access and use their data. There were also updates about recent developments in each of the studies, including upcoming new data releases.
The workshop was run by staff from CLS, which is based at the Department of Social Science, UCL Institute of Education and featured guest speakers, who discussed their use of the cohort data across a range of disciplines.
Visit the Centre for Longitudinal Studies website to access resources from this workshop.


Difference between revisions of "Almora"
Revision as of 11:48, 27 September 2008
Almora is a hill station in Uttarakhand State. Almora was the seat of power of the Chand Dynasty who ruled the land of Kumaon for almost one thousand years. An interesting fact about the discovery of Almora is that unlike other hill stations, it was not discovered and developed by the British. The Katyuri Dynasty ruled the region around Almora from the 9th century AD. Raja Balo Kalyan Chand made Almora as his new capital in 1568 AD, when he transferred his capital from Champawat to Almora. The Chands occupied Almora till the 19th century AD. The rivers Kosi and Suyal flow through Almora providing a natural barrier. There is an interesting local legend about the discovery of Almora. Raja Kalyan Chand, the ruler of the Chand Dynasty was riding on the horseshoe shaped spur in the pursuit of a prey. The hunted quarry protected its life by taking refuge behind the thick bushes of Kilgore, a local wild bush and revealed the place to the king. The story might not be corroborated by any literary or archaeological evidences but continues to be told by the locals. The Gorkhas captured Almora in 1798 AD and finally British took it over from the Gorkhas after the Gorkha wars of 1814-1815.
Almora, a town of about 30,000, is situated in the Kumaon mountains of the Himalayas in eastern Uttarakhand. Most of the town is situated on a crescent shaped mountain about 5 km long, and most of it is above 6,000 feet. Unlike Shimla, Ranikhet and Nainital which were developed by the English, Almora is a hill station totally developed by the Indians.
The town itself is your usual crowded hilltown in northern India, but the natural beauty around is astounding. Almora is also called a town of temples. Situated in the centre of the town is the temple of Goddess Nanda Devi. The mountain is visible from the nearby areas as well.
Almora is an agricultural base and also a trade centre.
By train The town is served by the Kathgodam station, which is located 35 km away from the town. Taxis charge Rs 600 to Almora. You can also share a cab at Rs 125 per person. Most hotels will arrange for a pick up on prior request, Rs 700-1000. The station handles 46 express trains per week.
BAGH EXP (daily) - Dep. Howrah 2145 Arr. 0935 - 2 nights SAMPARK KRANTI EXP (daily) - Dep. Delhi Jn 1600 Arr. 2245 - 7 hours RANIKHET EXP (daily) - Dep. Delhi Jn 2245 Arr. 0500 - 1 night DEHRADUN KATHGODAM EXP (Wed, Sun) - Dep. 2230 Arr. 0725 - 1 night
There are daily bus services from Delhi. The buses leave from ISBT Anand Vihar and are run by Uttarakhand Roadways. Driving to Almora takes 10 to 12 hours. From Delhi, it's highway driving throughout. NH 24 connects Delhi to Rampur via Hapur. At Rampur, turn and head north on NH 87 all the way upto Almora. En-route halts include the Wonderland, Rwy crossing, Moradabad and The Kaichi temple, Kaichi.
Contrary to popular belief, flying into Almora is the fastest way to reach the hill station. Almora is served by PantNagar Airport, located about 4 hours away. It is served only by Jagson airlines. It is one of the least busy airports in the country, handling only 6 scheduled flights a week.
JA 101 - Dep. Delhi 1315 Arr. PantNagar 1415 (Mon, Wed, Fri) JA 102 - Dep. Delhi 1445 Arr. PantNagar 1545 (Mon, Wed, Fri) FARE - Rs 2250/$ 90 for adults, Rs 1400/$ 55 for children. Taxi fare is around Rs 1200-1500.
Chitai Temple just 8 km from city, Kasar Devi to have a great look of city.
Walk the famous bazaar - still with glimpses of the old Kumaouni culture
Woolen garments. Copperware
Bal Mithai, a famous sweet of Almora.
Lots of tea - the popular local drink - to welcome guests & also to keep warm.
Hotels include the upscale Club Mahindra and the relatively down-to-earth KMVN (which has no electricity)
are all around Almora and attract nature lovers


Making A Difference On Invasive Plants Problems
The challenges associated with the prevention and management of invasive plants are here to stay. Complex issues such as the effectiveness of international agreements on minimizing plant introductions, the limited scientific understanding of invasive plant ecology and long-term management, and the degradation of undeveloped lands, are just some of the challenges.
Nevertheless, thanks to laws and policies, scientific research, and the hard work of agencies, organizations, and individuals, some invasive plant problems are being solved. Continued success will require steadfast commitment, creative thinking, cooperation, and collaboration at the local, regional, national, and global levels.
SUCCESS STORIES—MAKING HEADWAY
In spite of the challenges land managers face, many have made headway on their invasive plant problems in one way or another. At the annual National Invasive Weeds Awareness Week in Washington DC, people across the United States gather to brainstorm on how to more effectively meet the challenges associated with invasive plants. Thanks to their combination of commitment, creative thinking, cooperation, and collaboration, success stories can be told.
PUBLIC-PRIVATE PARTNERSHIP HUNTS HOUNDSTONGUE IN COLORADO
The US Fish and Wildlife Service and its coalition partners have been successful in reducing houndstongue (Cynoglossum officinale) infestations using an integrated management approach (hand-pulling, prescribed fire, and herbicides).
RECOVERY OF LEAST BELL’S VIREO AFTER SUPPRESSION OF GIANT REED IN CALIFORNIA
A partnership of several agencies in California helped restore a native plant community by suppressing giant reed (Arundo donax), making the ecosystem more habitable for an endangered bird.
OUSTING ORANGE HAWKWEED IN KODIAK NATIONAL WILDLIFE REFUGE
Through continuous efforts a pretty, invasive plant is kept under control in Alaska, improving habitat for bears.
MAINE OFFICIALS WORK TO CONTROL THE FIRST HYDRILLA OCCURRENCE IN STATE
Maine officials curb the spread of Hydrilla before it becomes a problem.
PROTECTING A RARE BEAUTY
Controlling leafy spurge (Euphorbia esula) in North Dakota improves habitat for a rare orchid.
PULLING TOGETHER RESOURCES TO HELP NESTING SEA TURTLES SUCCEED
In an effort to improve the nesting habitat of a threatened sea turtle species in South Carolina, collaborators are finding success in removing beach vitex (Vitex rotundifolia) from sand dunes.


Disclosure: This article may contain affiliate links. If you decide to make a purchase, I may make a small commission at no extra cost to you.
Since the 1980s, researchers have been conducting an experiment on rhesus monkeys by restricting their calories to see if a calorie restriction diet is beneficial for improving their health and longevity, as it does in other species such as yeast, worms, flies, spiders, rats, mice, dogs, cows, etc.
Rhesus monkeys live around 27 years on average and are thought to be the most similar physiologically to humans — so it’s believed the results would be translatable to humans. Pending the final results, I’ll go into what the current findings are and what they could mean for whether or not the work is likely to be translatable to people practicing calorie restriction.
Wisconsin calorie restriction study in rhesus monkeys
The study began in 1989 where they introduced 30 male rhesus monkeys into the study and then a further 30 females and 16 males in 1994. The animals were randomized and then put into either the control group or the calorie restricted group.
Reduction of calories was done in three stages, where food was cut by 10% at a time until they were restricted by 30%. The baseline was determined from monitoring the ad libitum food intake of each rhesus monkey.
The rhesus monkeys also received very good care, where any condition that developed during the study would be treated.
In 2009 we got a glimpse that calorie restriction in rhesus monkeys seemed to work and extended both healthspan and lifespan (1). Age-related mortality was slashed and control fed monkeys were 3-times more likely to die of age-associated diseases than the restricted monkeys. Although at this point, all-cause mortality between groups did not reach statistical significance.
The median survival for rhesus monkeys in captivity is about 26-27 years and a maximum lifespan of 40 years, with 10% reaching 35 years of age.
In this study, the calorie-restricted monkeys were far healthier and enjoyed complete protection from diabetes. They also had less heart disease, fewer rates of cancer, less muscle loss with age, less brain atrophy, among other benefits. It has been reported that calorie restriction monkeys also look a lot younger than their well-fed counterparts.
As you can see above in the survival curves, monkeys on a CR diet showed improved all-cause mortality and age-related mortality.
Age-related mortality includes deaths from cardiovascular disease, cancer, diabetes, arthritis, etc.
All-cause mortality takes into account deaths from accidents, anesthesia, gastric bloat (accidentally caused by overcooked batches of food), and endometriosis (a non-fatal human disease).
Some of the deaths in the study could have been prevented and were not caused by intrinsic aging. So a separate analysis for just age-related mortality was created to look at the effect of CR on deaths caused by aging.
So far, 63% (24/38) of the control monkeys have died from age-related causes compared to only 26% (10/38) of the calorie restricted group. This indicates that simply reducing calories can have a dramatic impact on the incidence of diseases caused by aging.
For all-cause mortality, the control group had 1.8 times the risk of death from any cause compared to the CR group. Right now there are currently 12 CR monkeys and 6 Control fed monkeys still alive.
CR ‘anti-aging’ protocol
Although calorie restriction has improved average lifespan in the study at Wisconsin, the effects of the diet on the monkeys metabolic, lipid and hormonal profile has been inconsistent with the changes that are observed in mice, rats, and humans that are subjected to CR.
Reasons for this could be that the reduction in calorie intake was not sufficient to signal low energy availability to activate the pathways and responses that are involved in retarding aging in this species.
However, even with the inconsistent results, the monkeys still benefited from a reduction in calories and stayed lean throughout their life, as well as being much healthier and younger for longer.
A sweet disaster
To understand why there might have been a longevity advantage in the CR group relative to the control group, even though the CR monkeys did not display the CR-phenotype, we have to take a look at the diet used in the study.
The monkeys in the Wisconsin study were fed a semi-purified diet which comprised of 65% carbohydrates with 28.5% coming from sucrose, and the remainder from cornstarch. In the NIA study, the monkey chow comprised of 56% carbohydrates with only 3.9% coming from sucrose (3).
The high level of sucrose in the diet that the Wisconsin monkeys received could explain why there were more cases of diabetes in the control group compared to the NIA controls.
Although, interestingly, there were two cases of diabetes in the young-onset monkeys in the NIA study whereas the WNPRC study reported complete protection from diabetes in the CR monkeys.
Blood glucose levels were also lower in the Wisconsin monkeys, but they had higher levels of insulin in the control group. The CR diet brought it down to healthier levels. This is in contrast with the NIA monkeys, which had lower levels of insulin but slightly higher levels of glucose.
As mentioned earlier, before the monkeys were placed on the diet, they were monitored for a 3-6 month period to assess their caloric intake when they had free access to food, so that the researchers could establish an individual baseline from which to reduce the calories from.
Researchers found that the difference between the calorie restricted group and the control group dwindled to only 18% difference because the monkeys in the control group voluntarily reduced their calorie intake.
Monkeys normally do this with age, but this was fairly early in the study, so the researchers lowered the intake of the CR group further to establish a 30% difference once again.
However, there were some exceptions, where not all monkeys had their intakes reduced further because of the appearance of the animal, and it was deemed too risky to the animal’s health.
No further reductions in calorie intake in the CR group are being performed at this stage of the study, even if control animals still continue to decrease their intake in old age.
It was reported that 5 of the 38 monkeys of the Wisconsin control group developed full-blown diabetes, whereas only 5 out of 64 in the NIA control group (11% vs 8%). This indicates that the diet in the Wisconsin study may have been poorly selected. The NIA monkeys also weighed less at all ages than the WNPRC monkeys (2).
Compare this with humans: the prevalence of diabetes (diagnosed) in the UK is as high as 5.8% in England, with the national average at 4.6% in 2013 (4).
A lot of research has gone into the biology of aging in recent years and it’s clear is that there is a specific phenotype that is common among long-lived individuals and families. Typically, they will have low levels of glucose and insulin.
Studies have shown a decreased functioning of the IGF-1 receptor and/or decreased levels of IGF-1 levels — which could be achieved by lowering protein intake to 10% of total calorie intake — leads to protection from diabetes, cancer and extends lifespan (5-8, 17).
Lower levels of thyroid hormones have also been found in people with exceptional longevity. Lower free T3, T4, and high-normal TSH can be exceptionally long-lived (9,10).
Higher HDL is protective, as well as low levels of LDL cholesterol and triglycerides (11).
in table 1 and 2, it shows the Wisconsin and NIA monkeys failed to display the changes that are typical with CR!
In the Baltimore Longitudinal Study of Aging, men with lower insulin, lower body temperature, and high DHEA were found to be longer lived.
Humans who voluntarily do CR, display these changes with the exception of changes in T4 and TSH thyroid hormones, which is mixed in humans.
Overall, humans seem to be responding more favorably to calorie restriction and more closely matches the phenotype displayed mice and rats that have a dramatically extended lifespan.
Extra weight is not good for you
Several reports have come out in the last few years suggesting that being overweight decreases mortality, where they either show a J-curve or a U-curve for BMI,
They show that if you are thin, you have a greater risk of death, although being obese is even worse. Shockingly, the results suggested that being slightly overweight was actually good for you! (12).
Researchers came to this conclusion by looking at a large number of people and excluding all obvious causes of being thin such as smoking, alcohol abuse, and pre-existing diseases.
Unfortunately, these studies have many methodological flaws and the inability to control for leanness that is caused by a huge number of factors. Being thin does not equate to being on CR, and being on CR does not equate to eating healthily. Some condition might cause thinness even 10 years or more prior to death.
A healthy diet which is associated with leanness is good for you
Healthy individuals eating a diet that is rich in vegetables, fruits, nuts, seeds, and fish are likely to represent a very small fraction of lean individuals.
One study that was conducted by Cardiff University found that only 15 men out of 2,235 men ate more than 5 fruits and vegetables a day.
Less than 1% followed all 5 healthy behaviors. It’s clear that following a ‘healthy lifestyle’ is not common in the UK and US (13).
This study indicates that being thin in the general population is more likely to be a result of poor lifestyle choices or underlying diseases than to a healthy lifestyle.
In fact, just recently it was reported that eating 7 more fruits and vegetables a day is associated with a 42% reduction in mortality. And the more fruits and vegetables consumed, the lower a persons BMI! (14).
Back to the rhesus monkeys… Both Wisconsin and the NIA primate studies’ show that lowering body weight is very important to health and lifespan.
While there is a question to whether or not there is diminishing returns in the effect CR has on lifespan as body weight is, there should be no doubt that excess body weight is bad news when it comes to diseases of aging such as diabetes, cardiovascular disease, and cancer. And it’s important to remember that these are some of the biggest killers in western countries today.
These studies’ show that changing dietary habits can have a dramatic impact on your disease risk and that you have more control than you might think.
NIA RHESUS MONKEY CALORIE RESTRICTION STUDY
In the NIA study, they had two groups on the diet to establish what effects CR has on health in young animals and old animals.
The study conducted at NIA was more in-line with rodent experiments where the control group was restricted by 10% to avoid the effects of obesity, and the CR group are restricted by 30%.
Energy intakes were calculated from tables of energy intake requirements for the rhesus monkeys by age, weight, and gender.
Both groups received a relatively healthy diet that was also supplemented with 40% extra vitamins and minerals to ensure that the calorie restriction group met the recommended daily intake for all nutrients.
However, as the control group also received the same diet, this meant they were super-supplemented.
The diet given to the monkeys a more natural diet and contains many phytochemicals and other micronutrients that are beneficial to health. These could also act synergistically with CR to improve health.
During the course of the study, many measurements were made to see what effects CR had on the monkey’s health.
In the CR’d male monkeys, there was no effect on glucose levels compared with the controls, while in females, there was only a very slight reduction.
Triglycerides tended to increase with age across all groups. Interestingly, young-onset CR’d females experienced a significant increase in triglyceride levels compared to the control female group (15), which is bizarre, because, in humans, there are no differences by gender in the response to CR when it comes to the dramatic lowering of triglycerides.
The monkeys also failed to exhibit several other distinct changes that usually occur with CR.
There was no reduction in testosterone or estrogen as we see in rodents and humans. And no increase in the stress hormone cortisol (CR usually acts as a mild stressor.)
Serum triiodothyronine (T3) was reduced by 14% in the young and old CR’d female monkeys but there was very little effect in males.
In humans practicing vigorous CR, there is a major reduction in T, but this was not observed when overweight people who had lost weight to get within the healthy BMI range, like those in the CALERIE study (more on that later.)
In males, there was a significant decrease in cholesterol in the CR’d group. Glucose was also reduced significantly, while there was only a modest effect was seen in CR’d females.
Triglycerides were significantly reduced in CR males and modestly reduced in CR females (15).
Blood pressure was not affected in the monkeys, which is inconsistent with the data in humans, as we see a dramatic decrease in blood pressure from average values for their respective ages to levels that of a child: approx 100/60 (16).
These results are indicating once again that humans respond better than monkeys to CR.
CR has a dramatic effect on cancer if started young
So far none of the calorie-restricted monkeys have developed cancer (CR 0/40 vs 6/64 AL). Calorie restriction initiated early in life is powerful in protecting against cancer in rhesus monkeys and possibly humans.
This is one effect that is consistent with what we see in rodents. Unlike old-onset rhesus monkeys, the young-onset do see reductions in IGF-1 levels, which may partly explain this effect (although not entirely).
In humans practicing vigorous CR with protein restriction (10% of calories), both young and old see significant reductions in IGF-1. (17).
Longest lived rhesus monkeys on record
Although survival was the same for both groups in the old-onset group (35.4 years), this was significantly longer than previously reported median lifespan of just 27 years for a rhesus monkey in captivity (15).
Not only that, of the 20 male monkeys in the old-onset group, 4 monkeys in the calorie-restricted group have lived beyond 40 years compared with only 1 control monkey.
To put this in perspective, 40 years is considered the maximum lifespan for a rhesus monkey.
Researchers analyzed data on the lifespan of 3264 rhesus monkeys, and only two 40-year old monkeys have ever been documented!
According to researchers, one year for a monkey is roughly equivalent to 3 human years (1).
Does this mean that 35.4 years for a rhesus monkey would correspond to about 106 human years?
Rhesus monkeys in this study in both old-onset groups gained 8-years of extra life (equivalent to 24 human years.)
Waiting for the final results
As the study is still about 10 years away from being completed, I would expect that we could see a few more 40-year old monkeys in the young-onset group.
The NIA group had a fairly significant survival advantage over all groups in the Wisconsin study. With a 10% restricted healthy diet, the NIA cohort broke longevity records.
Is it possible that the 10% reduction in calories with a very healthy diet that was rich in vitamins, minerals, phytochemicals, omega-3 fatty acids was additive in its effects with CR? And that the 10% CR group effectively got the same benefit as the 30% restricted group? Possibly.
As these monkeys have lived far beyond what is typical for a rhesus monkey, it’s clear that the quality of diet matters a lot and that being lean is very beneficial for health and longevity.
It’s worth noting that studies on rodents show that 10% CR can effectively extend lifespan as much as 30% for certain strains. However, in most, the lifespan gained is in proportion to the degree of restriction and the length of time the animal has been restricted.
Translation of ‘monkey years’ to ‘humans years’ might not be exact; it’s just a rough estimate.
What does this mean for CR working in humans?
At least 18 people practicing calorie restriction with optimal nutrition have been studied by Dr. Luigi Fontana at Washington University in St Louis.
In a study published in 2004, medical records were collected of the participant’s previous health data which included things such as body weight, blood pressure, glucose, cholesterol, etc, to see what effect years of calorie restriction has had on health.
Those doing calorie restriction were very lean: BMI of 19.6 ± 1.9 vs 25. ± 3.2 kg/m2. Average time on CR was 6 years ± 3 (range 3 to 15 years).
CR induces a younger gene expression profile in humans
Just recently participants from the CR society had their muscle biopsied and analyzed to look at gene expression profiles compared to that of 30-year-old controls and age-matched controls (58 years), and also they compared the molecular changes in rats on 40% CR.
They hypothesized that CR in humans would have induced a down-regulation of the Insulin/IGF-1/FOXO pathway which has been linked with longevity in animals and humans (20-22).
What they found was a very significant down-regulation of the Insulin/IGF-1/FOXO pathway at the transcriptional and post-transcriptional level. The key changes in skeletal muscle gene expression profile that are observed in long-lived rats are also observed in humans.
So not only are humans responding at a physiological level to CR as animals do, but the molecular adaptations seem to mirror that of mice and rats.
They also looked at SIRT 1 and AMPK: these two energy-sensing pathways were significantly up-regulated in people on CR.
FOXO3A and FOXO-4 were significantly up-regulated as well. These are known to modify many ‘longevity genes’ in animals and increase activities such as DNA repair, antioxidant defenses, immunity, protein turn over, and cell death genes (22).
Autophagy, which helps remove dysfunctional cell components, was also significantly up-regulated by CR.
Looking at (Figure 1b (23)), it looks as if people on CR had more similar gene expression profiles to the younger individuals in the study.
The ‘gene expression’ of people on CR is more like that of a 30-year-old than the age-matched 58-year old control group.
CR significantly improves cardiovascular health in humans
The average total cholesterol and LDL-C concentration for the CR group were in the lowest 10% for people in their age group (50 years).
Even more dramatic, the levels of triglycerides in the CR group were lower than 95% of Americans who are in their 20s. And their HDL (good cholesterol) was higher than 85-90% of people in middle age.
Fasting insulin was 65% lower than the western diet group and glucose was also significantly lower too. People on CR have also been found to have lower body temperature, lower thyroid hormone T3 as well, but people who exercise vigorously and maintained a similar BMI did not see these reductions (29, 31).
Participants of the study also had extremely low blood pressure, equivalent to that of a 10-year old. They had almost non-detectable or very low levels of inflammation measured by c-reactive protein.
IMT carotid artery thickness was measured and found to be 40% less in the CR group compared with the controls: 0.5 ± 0.1 mm in the CR and 0.8 ± 0.1 mm for controls.
None of those eating a CR diet had any evidence of atherosclerotic plaque.
To show the powerful effect that CR had on their health, the researchers were able to gather medical records from 12 of the individuals in the CR group and show that just like the western diet group, values for the CR group were average (50th percentile) before embarking on the diet.
Possibly even more impressive results showing that CR in humans might be slowing down the rate of aging of the heart.
They looked at the diastolic function of the heart and its ability to relax and fill the left ventricle and found that people on CR had hearts that were similar to those who were 15-years younger (17).
And those on the diet also had heart rate variability of a person 20 years younger (18).
Will calorie restriction work in humans?
Looking at the data we have thus far from mice, rats, rhesus monkeys, and humans, we are able to make comparisons to see the differences between each species in how they react at a molecular level and at the physiological level to CR.
It’s clear that people on a calorie restriction diet display a more CR-like state than either the NIA or Wisconsin rhesus monkey studies. This is promising for people that have been on a CR diet for many years in the hopes that it will extend their life.
People in the CALERIE study who were overweight and merely reduced their body weight to a ‘healthy’ weight from a BMI of 27 to 24 with 25% CR, never exhibited several CR signatures, nor did they have as significant reductions or changes in total cholesterol, LDL-cholesterol, triglycerides, inflammation, thyroid hormone levels, testosterone, estrogen, IGF-1 and cortisol.(26-28).
All of these are strongly influenced in people studied at WUSTL. These people are from the CR Society and practice moderate-severe CR. (16-19, 23).
Many of these signatures that were not observed in the CALERIE study were also either not observed in the CR primate studies, were very inconsistent, or modest in their change or effect (25-28).
This indicates that the level of CR in the primate studies, as well as the CALERIE human study, were insufficient to elicit the key changes that are responsible for the age-retarding effect of CR.
Aside from the level of CR being insufficient to elicit these changes, another possibility could be that the declining difference between energy intakes of the NIA rhesus monkeys (20% less than ad lib for males and only 12% for females) could be the reason why little differences were seen.
It was reported also that the calorie-restricted monkeys did not exhibit much sign of hunger during the study either. Yet another argument pointing to the fact that the CR group needed to be restricted further.
Before embarking on this very long study, it may have been wise to restrict monkeys to various degrees to see if there is a ‘cut-off point’ to where CR does not improve their health further.
If they display the CR-phenotype in a more consistent and powerful way, then establish this level of restriction for the CR group for a lifespan study, as long as the level of restriction was not inhumane and the animals did not display poor health from it.
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2. Ricki J. Colman, T. Mark Beasley, Joseph W. Kemnitz, Sterling C. Johnson, Richard Weindruch & Rozalyn M. Anderson. Caloric restriction reduces age-related and all-cause mortality in rhesus monkeys
Nature Communications 5, Article number: 3557 doi:10.1038/ncomms4557
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Dietary restriction of adult male rhesus monkeys: design, methodology, and preliminary findings from the first year of study.
4. Diabetes prevelence in the UK (2013).
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6. Levine ME, Suarez JA, Brandhorst S, Balasubramanian P, Cheng CW, Madia F, Fontana L, Mirisola MG, Guevara-Aguirre J, Wan J, Passarino G, Kennedy BK, Wei M, Cohen P, Crimmins EM, Longo VD
Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population. Cell Metab. 2014 Mar 4;19(3):407-17. doi: 10.1016/j.cmet.2014.02.006.
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The thyroid gland and the process of aging; what is new?
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de Craen AJ, Westendorp RG, van Heemst D. J Clin Endocrinol Metab. 2010 Nov;95(11):4979-84. doi: 10.1210/jc.2010-0875. Epub 2010 Aug 25 Familial longevity is associated with decreased thyroid function. PMID: 20739380
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Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and meta-analysis. JAMA. 2013 Jan 2;309(1):71-82. doi: 10.1001/jama.2012.113905.
13. John Gallacher, Peter Elwood, Julieta Galante, Janet Pickering, Stephen Palmer, Antony Bayer, Yoav Ben-Shlomo, Marcus Longley, Healthy Lifestyles Reduce the Incidence of Chronic Diseases and Dementia: Evidence from the Caerphilly Cohort Study Published: December 09, 2013
14. Oyinlola Oyebode, Vanessa Gordon-Dseagu, Alice Walker, Jennifer S Mindell
Fruit and vegetable consumption and all-cause, cancer and CVD mortality J Epidemiol Community Health doi:10.1136/jech-2013-203500
15. Julie A. Mattison, George S. Roth, T. Mark Beasley, Edward M. Tilmont, April M. Handy, Richard L. Herbert, Dan L. Longo, David B. Allison, Jennifer E. Young, Mark Bryant, Dennis Barnard, Walter F. Ward, Wenbo Qi, Donald K. Ingram & Rafael de Cabo. Impact of caloric restriction on health and survival in rhesus monkeys from the NIA study. Nature 489, 318–321 (13 September 2012) doi:10.1038/nature11432
16.. Fontana L, Meyer TE, Klein S, Holloszy JO. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6659-63. Epub 2004 Apr 19. PMID: 15096581
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18. Meyer TE, Kovács SJ, Ehsani AA, Klein S, Holloszy JO, Fontana L. Long-term caloric restriction ameliorates the decline in diastolic function in humans. J Am Coll Cardiol. 2006 Jan 17;47(2):398-402. PMID: 16412867.
19. Stein PK, Soare A, Meyer TE, Cangemi R, Holloszy JO, Fontana L. Caloric restriction may reverse age-related autonomic decline in humans. Aging Cell. 2012 Aug;11(4):644-650. doi: 10.1111/j.1474-9726.2012.00825.x. Epub 2012 May 21. PMID: 22510429
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21. Bradley J. Willcox*, Timothy A. Donlon*, Qimei He*, Randi Chen*, John S. Grove*, Katsuhiko Yano*, Kamal H. Masaki*, D. Craig Willcox, Beatriz Rodriguez*,and J. David Curb*,
FOXO3A genotype is strongly associated with human longevity. http://www.pnas.org/content/105/37/13987.long
22. Cynthia J. Kenyon. Insulin/IGF-1 and FOXO signalling affects mouse and human lifespan.
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23. Mercken EM1, Crosby SD, Lamming DW, JeBailey L, Krzysik-Walker S, Villareal DT, Capri M, Franceschi C, Zhang Y, Becker K, Sabatini DM, de Cabo R, Fontana. Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile. Aging Cell. 2013 Aug;12(4):645-51. doi: 10.1111/acel.12088. Epub 2013 Jun 5.
24. Luigi Fontana, Samuel Klein, John O. Holloszy, and Bhartur N. Premachandra
Effect of Long-Term Calorie Restriction with Adequate Protein and Micronutrients on Thyroid Hormones
25. Roth GS1, Handy AM, Mattison JA, Tilmont EM, Ingram DK, Lane MA.
Effects of dietary caloric restriction and aging on thyroid hormones of rhesus monkeys. Horm Metab Res. 2002 Jul;34(7):378-82 PMID: 12189585
26 . Leanne M. Redman, Johannes D. Veldhuis, The effect of caloric restriction interventions on growth hormone secretion in non-obese men and women
27. 1 Tam CS1, Frost EA2, Xie W2, Rood J2, Ravussin E2, Redman LM3; Pennington CALERIE No effect of caloric restriction on salivary cortisol levels in overweight men and women. am. Metabolism. 2014 Feb;63(2):194-8. doi: 10.1016/j.metabol.2013.10.007. Epub 2013 Oct 24. PMID 24268369
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The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake PMID: 3958810
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Article reviewed and updated: July 2019.


If you want to live the experience of seeing the Nazca lines, check this: Nazca Lines Experience
The mysterious Nazca Lines are found in the middle of the desert of southern Peru, located just outside the city of Nazca. To date, these lines remain a mystery to scientists. No one seems to know why they were made and what they were for. Fortunately, the only thing that experts can agree on is how the Nazca Lines were made. Live the experience of knowing the Nazca Lines thanks to our Peru travel packages. As usual, knowing exactly about real things from the past is almost impossible. Scientists and archaeologists can only guess the origin of some archaeological complexes and ancient objects. Even when they do their best, they only have similar opinions and research on how the Nazca Lines were made. Therefore, together with the experts from Machu Travel Peru, we have prepared a small article about how the Nazca lines were made.
How the Nazca lines were made and everything about this mysterious site
- What are the Nazca Lines?
- How were they drawn? Some theories
- Where are the Nazca lines?
- How to see them?
- The discovery of the Nazca Lines and other historical facts
- Theories surrounding the Nazca Lines
WHAT ARE THE NAZCA LINES?
The Nazca Lines are a series of geoglyphs, located in an arid coastal area of Peru. The region covers an area of approximately 170 square miles. The lines are etched into the ground and there are literally thousands of different designs depicting creatures from both the natural world and the imagination. These designs feature animals such as the spider, the Nazca lines hummingbird, the monkey, the lizard, the pelican, and a whale. You can also find plant designs like trees, flowers, and geometric shapes like wavy lines, triangles, spirals, and rectangles.
The geoglyphs were made in the middle of the desert canvas of the Nazca region. These were made by removing rocks and dirt from the ground and thus creating different images. The desert floor has had natural weathering that has occurred for thousands of years. So when the upper rocks are removed, they reveal a sand color much lighter than the surface. The same color that distinguishes this series of geoglyphs. And thanks to the dry climate, the lines have been preserved for approximately 500 to 2000 years. Some scientists claim that the Nazca lines were built by the Nazca culture around AD 10 – 700.
HOW WERE THEY DRAWN? SOME THEORIES
But the real question that everyone asks when visiting this site is, how the Nazca lines were made? The different lines are geoglyphs on the ground that are made by removing rocks and dirt to create a specific image. The desert floor has worn away for thousands of years, so when the upper rocks were removed, they revealed a light sand-colored rock. This light-colored rock is how we see lines.
Due to the dry climate, the lines have been preserved for a period of 500 to 2000 years. The Nazca lines were created by the Nazca culture, although there are also theories that state that other later cultures continued the work. Given the precision of the shapes of the Nazca lines and their enormous proportions, it is believed that the Nazca people used grids made of ropes and stakes to represent the scale drawings. The prestigious archaeologist Maria Reiche formulated some theories as to how the lines were made.
- Lines: The Nazca used wooden stakes attached by a rope. They set the stakes as a guide in a straight line. This technique allowed them to repeat the process and draw very long lines and shapes.
- Spirals: The inhabitants of the Nazca culture tied a rope to two or three posts in triangular patterns. They then rotate to draw a growing spiral.
- Figures: The Nazca geoglyphs were designed and even painted, to scale on canvas. To create them, the Nazca tied ropes to stakes and drew in different proportions.
- Conservation: The lines have endured for centuries thanks to two phenomena. After absorbing the heat of the day, the contour stones generate a cushion of hot air that protects them from the wind. Besides, the soil contains plaster which, when cooled by the morning mist, creates a protective layer. Thanks to these two phenomena, the lines were able to survive for so many years.
WHERE ARE THE NAZCA LINES?
The lines are located about 200 miles south of Lima, the Peruvian capital. The area has 800 straight lines, 300 geometric figures, and 70 designs of animals and plants. Some of the lines are around 30 miles long and some are 1,200 feet long. The Panamericana Sur traverses the entire Nazca plain in a straight line, usually as a guide to appreciate different figures and designs. On the left side of Panamericana are figures such as the llama, the hummingbird, the fish, the monkey, the dog, the vulture, and the spider. On the right side of Panamericana, you will find figures such as lizards, flamingos, and parrots. There are other figures near the Maria Reiche Neuman Airport, such as looms and needles.
The region where the Nazca lines were drawn is an area of the Peruvian desert called Pampa Colorada (also called Red Plain). The space has an area of about 15 miles wide and runs about 37 miles parallel to the Pacific Ocean and the Andes. The desert is not sandy per se, but it is composed of shallow stones with a dark red color. In addition, the subsoil has a lighter color below this stony surface. Shaping the contrast that these wonderful lines and geoglyphs have. If you were wondering how the Nazca lines were made, then you will find that these were created by picking the top layer of the soil. This is a darker layer, which when removed reveals a much lighter subfloor.
HOW TO SEE THEM?
To answer the question of how the Nazca lines were made, you should see them on your own. The flight over the lines can be taken from the Nazca airport or from the Paracas airport, which is located in the north of Nazca. In some tours in Paracas, you will have this destination included and you can also visit the fascinating Ballestas Islands and see the thousands of varieties of birds. Also, see the sea lions lazing around in the sun.
- Two ways to see them: Whether you want a luxury Nazca Lines tour or are on a travel budget, you will find something for yourself at this incredible location. The mysterious Nazca Lines await you to discover them. You can choose to take the adventurous plan of the trip on a plane or see the lines from the observation tower located on the outskirts of the city of Nazca. The best way to see the Nazca lines is by plane, this way you will see the lines clearly. Besides, you can go to the observation tower located on the outskirts of the city of Nazca, from the tower you will see some figures and it will cost you a few soles. This way is much cheaper but you will not be able to fully appreciate all the lines
- The real tour: The Nazca Lines tour allows you to witness the impressive feats of ancient Peruvian men throughout time. Also, it allows you to explore the colossal sand dunes of Paracas, ideal for a buggy or sandboard ride. You can continue to Ica to visit the beautiful natural oasis Huacachina. As you do so, you can end with a short tour of a winery. There, delight yourself with the best and delicious Peruvian Pisco. The different tours in Peru will give you so many alternatives and options to complement your trip, that you will be pleased with the result.
ALTERNATIVE WAYS TO SEE THEM
Another option available is to visit the Nazca Lines from Lima. Take into account that from the same capital there are flights available on the lines. Although these options are usually more expensive than those from the town of Nazca. Despite the price, it is still one of the options that many people choose. There are also flights available from the nearby town of Pisco. Pisco is only about four hours by car from Lima. These are great options if you don’t have that much time to travel from one destination to another. But if you have time, it is better to go to Nazca and see the lines in the original region where they are. Since the city also has some attractions that are worth visiting. Discover the mysterious Nazca Lines for yourself, and include Nazca as part of your adventure through Peru.
Come to know the Nazca Lines in the desert of southern Peru. The great mystery of the Nazca Lines is to know the purpose of this series of geoglyphs. Many theories have tried to prove the purpose, but the mystery remains largely intact. Something that should be on your wishlist no matter what. Don’t forget to see the rest of Peru and the incredible history that the country offers.
THE DISCOVERY OF THE NAZCA LINES AND OTHER HISTORICAL FACTS
Since its discovery, many have tried to delve into the question of how the Nazca lines were made. The Nazca lines are said to date back from 200 BC to 500 AD. This was the time when the Nazca people lived in the region. The ancient Nazca people, in their prehistoric culture, used engineering techniques to bring water to the surface for irrigation purposes. The purpose of the Nazca lines still remains a mystery. Still, there are a large number of theories that seem to come close to the main purpose. Some of the most interesting facts are the following:
- It is mentioned that the Peruvian archaeologist Toribio Mejía Xesspe was the first to study and report the Nazca Lines after discovering the lines on foot in 1927. Then, with the increase in air travel in the 1930s, these lines became more known and today attract multiple tourists each year. Thanks to him you can enjoy the Nazca lines map and all its wealth.
- In the 1940s, American professor Paul Kosok investigated the lines when the sun set. He noticed that the sunset was in direct alignment with the lines, which is why he called the lines the largest astronomy book in the world.
- Maria Reiche was another renowned student of the Nazca lines. Reiche studied the Nazca lines images for 40 years and fought tirelessly for the acceptance of her theories. She claimed that the Nazca lines were made for a clear astronomical purpose. Reiche believed that the geoglyphs functioned as a type of calendar.
- Mr. Proulx and Mr. David Johnson had been working on the Nazca Lines since 1996 and found the connection between the lines and the water system. Johnson mapped the location of wells and faults that were sources of fresh watermarked by geoglyphs.
- Johnson and Proulx stated the following: “Trapezoids were found directly above the tracks where the width of the tracks defined the width of the fault zone capable of transmitting groundwater.” The comments and observations led them to a new hypothesis to explain the purpose of the lines. The Nazca Lines in Peru were used as a source of water, and the Nazca people depended on them for freshwater.
- In recent years, the discovery of the Cahuachi people has provided new insight into the mysterious lines. Just south of Nazca, scientists have discovered the lost city of the line builders. It is said that this was built around 2000 years ago and abandoned around 500 years later. The artifacts found in view are giving researchers new information about the people who are now believed to have built the lines. Until now no one knows why the lines were built and for what purpose, and we may never know.
There is no doubt that the global understanding of the Nasca lines will continue to evolve with the passing of the years and new technological advances. The Nazca lines are one of the most symbolic archaeological sites in the ancient world and their importance is reflected in their growing popularity. Likewise, it is never too late for you to fly over the Nazca lines and put together your own theories about how they were made.
THEORIES SURROUNDING THE NAZCA LINES
Some of the Nazca theories can be anything but reasonable, while others seem to maintain certain scientific criteria. Due to the mystery surrounding the question of how the Nazca lines were made, many conspiracy theories emerged to make sense of it. In addition, given that at ground level it is not possible to perceive whether the figures are correctly drawn or not, it is thought that the construction had to be directed from a high place.
Although many think that these lines can only be seen from the air, they can also be found in the hills that surround the pampas (plains) and valleys. Figures up to nearly 300 meters long look perfect there. This sighting from the land makes it the main aspect to confirm that the creators of these feats were the Nazca people. Even so, the perfection of the plot unleashed more than one theory, among which are solstices, constellations, and extraterrestrial sun gods.
Over the years a wide variety of Nazca Line Theories have appeared that attempt to explain the purpose of the site. A book published in 1968 supported the theory that the lines were landing fields for aliens and the lines were created by aliens many thousands of years ago. Archaeologist Johan Reinhardt believes that the lines have a religious purpose and were to worship the gods. But the truth is that many archaeologists and scientists have studied the lines and many pieces of the puzzle are still missing. There are still many unanswered questions surrounding the site. From what the lines are for, who built them, and when they were built. Despite this, thanks to ancient cultures, today we can see the lines and marvel at the magnificence of the site.
“HAVE STORIES TO TELL, NOT STUFF TO SHOW.”
The Nazca lines represent much more than a popular tour on the air. It is the manifestation of one of the most incredible works made by cultures older than the Incas. It is a perfect opportunity to learn a little more about the history of man before the arrival of the conquerors. We hope together with the experts from Machu Travel Peru to have been of help. We believe that the best way to answer the question of how the Nazca lines were made is with a complete journey through them. Do not miss the mystical and magical experience of walking these amazing geoglyphs. If you want to know more about our tours of the lines, you can consult with our charming advisors. They will be happy to help you with everything regarding your next trip to Peru.


Activity for ages 6 to 8.
Long vowels are tricky! There are numerous ways to spell them out so it takes time and practice for kids to become confident. These long vowel clip cards are an easy and fun way to show long vowel words spelled in different ways. They’re great puzzlers for first and second graders.
To prepare, I printed the clip cards onto cardstock, cut to separate them and used a marker to put a small dot behind each correct answer so they’d be self-checking.
Then I grabbed some small clothespin pegs and a couple of big books that contained words with long vowels.
Long Vowels in Books
Before introducing the cards, we read through a couple of big books, trying to hear and see long vowels along the way.
When students heard a long vowel, they’d raise their hand and then, after finishing the sentence, we’d go back and look at how the word was spelled.
This was a good activity for helping kids intentionally focus on long vowels and see how much spelling variety there is.
Each child who picked a word wrote it on our butcher paper, writing it near words that used the same spelling pattern. By the time we were finished there were big clusters of words.
Long Vowel Clip Cards
When we were finished, I pulled out the clip card basket. We looked at a few of them together, sounding out each written word to see what they sounded like. Mostly, they sounded very much the same! It was a really great a-ha kind of moment… seeing how sounds work.
Of course, since the sounds are so similar, choosing the correct word comes from developing familiarity through lots of reading and writing, and knowing when each pattern is more likely to be found (for example ‘ew’ is commonly found at the end of a word such as in ‘flew’ and ‘blew’).
Although the back of each card had the answer in the form of a dot, our kids used the activity as a chance to work with dictionaries. If they had any doubt as to which word was correct, they tried to find it in their dictionaries. The follow up step was a simple way to extend the learning value of the cards.


Description - AutoCAD Workbook for Architects and Engineers by Shannon R. Kyles
Students need a book about drawing, not software and this step-by-step guide offers the basics on how to produce a range of drawings types with a wide variety of AutoCAD commands and sequences. This focus of this book is producing 2D drawings for engineering and architectural designs. It is not about every AutoCAD command and the many options, variables and command sequences that go into that command. There are a great many very good reference books on the market that discuss these aspects of the AutoCAD program, and all of that information is found within the Help files of the program. Each chapter - or teaching module - contains a brief introduction to the commands and many exercises. Many students are not familiar with basic drawing types: working drawings as opposed to presentation drawings, orthographic projection as opposed to pictorial views, sections and reverse sections, etc. This book will show how to produce all these using 'walk-throughs' on how to approach different situations. Only a few commands are covered in each chapter, with between 4 and 20 exercises per chapter illustrating how the commands can be employed.
This book concentrates on useable exercises that provide completed drawings - and explanations on the software is secondary.
Buy AutoCAD Workbook for Architects and Engineers by Shannon R. Kyles from Australia's Online Independent Bookstore, Boomerang Books.
(294mm x 210mm x 16mm)
John Wiley & Sons Ltd
Publisher: John Wiley and Sons Ltd
Country of Publication:
Book Reviews - AutoCAD Workbook for Architects and Engineers by Shannon R. Kyles
Author Biography - Shannon R. Kyles
Shannon R. Kyles is Professor of Architecture at Mohawk University, Ontario and teaches on the Bachelor of Technology at McMaster University. She has over 30 years experience teaching drawing to design students.