Harakeke and Wharariki
In this section
|Māori names||harakeke, kōrari (Northland)|
|Other common names||flax, New Zealand flax, swamp flax|
|Scientific name||Phormium tenax|
|Family||Hemerocallidaceae (day-lily family)|
Few New Zealanders would fail to recognise harakeke, one of our most distinctive native plants. It is the principal weaving plant, and many weavers use named forms selected for leaf pliability, colour and fibre quality.
Leaf strips are used in raranga, the plaiting of kete (containers) and whāriki (mats). Extracted fibre (muka or whītau) is used to make traditional kākahu (cloaks), and for cordage. Today, harakeke is also used in non-traditional ways to create original and exciting works of art.
Harakeke grows throughout New Zealand, from sea level to about 1300 m in altitude. It is commonly found in lowland wetlands and along rivers, and in coastal areas on estuaries, dunes and cliffs. A hundred years ago, harakeke was much more abundant in many regions, but large wild stands today are diminished and scattered. Harakeke is often seen in gardens, is used widely in landscaping projects and in wetland restoration plantings, and as shelter belts on farmland.
Harakeke is said to be native also to Norfolk Island, though may have been introduced by Māori. The harakeke found on the subantarctic Campbell and Auckland islands was taken there by Māori and sealers in the 1800s.
Harakeke is a herbaceous plant, meaning its growth form is soft, not woody. The robust, sword-like leaves are arranged in two adjoining sets around the growing point (rito) to form a fan. A unique feature of harakeke and related plants is that the lower third or so of each leaf is folded together along its midrib or keel. This creates a stiff, heavy butt.
Fans develop from the stout, fleshy underground rhizome or rootstock. The rhizome has many reddish yellow roots of varying lengths that extend laterally or downwards. Hundreds of fans can develop from the rootstock to create the flax bush. Because these offshoots are of the same genetic stock, they exhibit the same leaf and fibre qualities.
The number of fans produced in a bush varies a lot and is one of the characteristics that can help identify different weaving cultivars. For instance, the weaving cultivar 'Māeneene' quickly produces many fans set closely together. 'Ngaro', a tall variety with strong fibre, produces fewer, bulkier fans that are set wider apart.
In older plants the rootstocks branch, generally away from the centre, and new fans arise that may eventually create a ring around the original plant. Sometimes as the plant ages, the rootstock is exposed above the ground and new fans develop that are less thrifty, through receiving fewer nutrients and moisture. Some strains are more prone to this ‘perching’ behaviour (e.g. the weaving variety 'Paoa').
Most fans produce about eight mature leaves, four on each side of the rito, before they start to yellow and die off.
The look and feel of the leaf is what draws a weaver to consider its worth for raranga or whatu. Harakeke leaves are variable in length (1–4 m), width (2–12 cm), and rigidity. Some bushes have stiff, upright leaves, others are softer and lax. The fibre bundles within the leaf run parallel to the keel. Sometimes these striations show clearly on the surface and the leaf feels rigid and tough. Other leaves are quite smooth to the touch. Leaf colour varies from blue-green, green, yellow-green through to bronze. The leaf underside is often glaucous, with a blue bloom like a plum.
Harakeke has coloured leaf margins and keel, with orange, red, brown and black being the most common. Colours can vary between young and old leaves, even within a bush. Coloured edges are narrow, thick or smudged. Young leaves in particular are sometimes smudged with colour (particularly reddish brown) at the tips.
Black-edged varieties are regarded by some weavers as having the best muka. The well-known varieties 'Kōhunga', 'Taeore' and 'Tapamangu' fall into this category. However, having a black edge and/or keel is not necessarily indicative of good fibre. There are excellent varieties with orange keels and margins, such as 'Arawa' and 'Makaweroa'.
Harakeke flowers from late October through to February. Each spectacular flower stalk (kōrari) grows up to five metres tall from the centre of the fan, which dies after flowering has taken place. The new kōrari is heavy with sap, but dries out over the summer months and becomes very light.
Each kōrari has a group of peduncles, like little branches, that grow out from each side of the main stem. These peduncles branch further and carry clusters of dull red flowers.
Each individual flower has both male and female parts. The copious orange pollen is carried on a thin stalk that sticks up above the flower tepals (the fleshy ‘petals’). The pollen on a particular flower matures before the female parts below are ready to receive it.
The flowers are designed to be pollinated by nectar-feeding native birds – tūī, korimako (bellbirds) and pihipihi (waxeyes). Today, starlings, mynahs and honeybees are also frequent visitors.
When a bird visits a flower, it pushes its beak down into the flower tube to feed on the nectar. Pollen brushes onto the top of the bird’s head. The pollen is then transferred to the next receptive flower the bird visits – that is, a flower where the pollen has already been shed, and the stigma and style (female parts) have pushed forward to collect the pollen. The fertile pollen travels down the style to the ovaries at the base. The fertilised ‘eggs’ or ovules then develop into seed, contained in the pod that develops from the flower.
The flower bunches on a kōrari do not open all at once. Their opening spreads over about 6 weeks.
Ecologists John Craig and Ann Stewart carried out some experiments on harakeke reproduction and found that harakeke is largely ‘self-incompatible’. Seeds produced from outcrossed flowers (where pollen comes from a different plant) are much more numerous and are larger than those produced by flowers from different kōrari on the same bush. In turn, the latter seeds are larger and more viable than those produced from flowers on the same kōrari. Perhaps compounds exist in the flowers that inhibit the development of plants of the same genetic composition.
There are likely to be some changes in genetic composition though, even in the course of vegetative reproduction. For example, leaves of the striking variegated Parekoretawa will, on some fans over time, revert from yellow stripes to green.
How often does harakeke flower?
We still do not know for sure what triggers harakeke flowering. Bushes do not flower consistently each year, and even in a seemingly prolific year there are regional variations. It was thought that harakeke flowered well about every three years, triggered by high temperatures the previous autumn, but this is not always the case. The cues seem to be more subtle and are not yet well understood.
For instance, in the summer of 2007/08, most harakeke in the Orchiston reference collection at Manaaki Whenua, Lincoln, flowered. However, in a nearby trial block of 36 Orchiston cultivars of a similar age, not a single bush flowered. Included in this block are three plants of the cultivar ‘Paoa’, which over many years has been a consistent early flowerer, even in ‘bad’ flowering years.
The seed capsules on harakeke form in the summer months, and are upright on the branches. This is the main feature that distinguishes harakeke from wharariki (Phormium cookianum). The pods can be short and stout, or long and narrow, and are triangular in cross section. Each pod contains dozens of black, glistening seeds. When the dry pods burst open, the seed is scattered, and can be carried by water and wind.
Harakeke is easy to grow from seed, but to ensure a plant has the same properties as the parent bush, it is best to take a fan with some root material attached. Seedlings also take longer to mature, about 6–8 years. Plants grown from root stock take about half that time. See Establishing a Pā Harakeke for detailed information on establishing a pā harakeke – a planting of selected varieties for weaving.
|Other common names||mountain flax|
|Scientific name||Phormium cookianum|
|Family||Hemerocallidaceae (day-lily family)|
Wharariki is found throughout New Zealand, on cliffs and mountain slopes. It is more tolerant of lower temperatures than harakeke. Horticulturalists have developed many coloured ornamental forms that are widely used in gardens and landscaping projects.
Wharariki is generally a smaller plant than harakeke, and the leaves are not as stiff. The leaves are usually less than 2 m in length and inclined to droop. Often there is little or no colour on the margins and keel of wild forms.
The leaves are not as stiff because they do not contain such strong fibre bundles. It is more difficult to extract fibre from the leaves of wharariki, and it is weaker and finer. Because the leaves are softer, they are useful for learners. However, they would not make strong kete or whāriki, and with the lack of extractable fibre, wharariki plants are not used for muka.
Flowers and seeds
The flowers are greenish, with tones of orange or yellow (as opposed to the red of harakeke). The most obvious distinguishing feature is the seed pods. The pods of wharariki are long, narrow, and hang down, often with a twist. They curl and become papery with age.
Wharariki tends to flower earlier than harakeke, and more prolifically.
Harakeke and wharariki are usually found in different environments. The two species can, however, interbreed easily (hybridise). Plant breeders take advantage of this when developing new ornamental strains. Recent molecular work carried out by Rob Smissen and Peter Heenan confirms that there are stable populations of wild hybrids. There may be other species (such as the Chatham Islands flax). Work on the extent of variation in flax species is ongoing.
Some of the well-known cultivars used by weavers are hybrids, such as 'Mawaru' and 'Wharanui'. Their leaves are light green and relatively soft. The pods have a twist and are not erect like harakeke or as long, curled and papery in old age as wharariki.


No it's not the weather, it's the species. The first issue is identification, Hylocereus and Selenicereus can be difficult to distinguish. The second is the common 'wild' plant that occurs on the east coast is usually referred to as "Queen of the night" cactus, this plant flowers but will not produce fruit. That being said it is a great grafting stock:)
My Cacti Blog, please come visit me.


Water is much more than we know. Many scientists and leading edge researchers, from around the planet, are continuing to report, that there is much more to know about this ancient substance that supports and sustains our lives.
This information is leading us to alter our perceptions, and thereby our relationships and responsibilities to this miraculous and life giving element. What we do know is that we live on a water planet, unique and unlike any other in our Solar System. All of the humans, animals, trees and all life forms that coexist with, come from water, and are made of water. Almost all of the surface of this planet is water. Our bodies are about seventy percent of this life giving substance. There are about 326 trillion gallons of water on planet Earth. Ninety-seven percent of that vast amount is salt water. Only three percent is fresh water and nearly eighty percent of what is fresh, is frozen in the polar ice caps and glaciers around the globe.
What we have left is less than one percent of all of the available water on the planet for people, plants and animals to use, to sustain our lives.
As we all live together on this water planet, in our water bodies, we are inherently, and naturally attracted to healthy water. We also know that what were once abundant sources of healthy and alive water are becoming increasingly scarce and, in several scenarios, severely compromised.
Scientists and researchers are continuing to show us that our thoughts affect our own vibrational energy which directly affects the structure of the very water within our bodies and in our environment. It has been proven that water, in it's natural and healthy state of purity and integrity, is intelligent and highly responsive to all other forms of life. It is no longer just theory, that water, like everything else, has consciousness.
We believe the following articles will assist you in understanding the importance of this enigmatic substance. These articles contain information pertaining to the many mysterious aspects and faces of water, and water research, including: structured water, clustered water, healthy water, toxic water, dehydration, detoxifying with water, cleansing the lymphatic system with water, water flow forms, water cycles, living water, healthy community water systems, healing water, water remedies, water cures, regeneration with water, health tips, and information on bottled water, water filters, shower filters, tap water and much more. We will be continually making many additions to the Water articles index in the coming weeks and months.
Healthy Wealth Blogger continues to be deeply involved in researching, developing and publishing information on this very important subject matter. We are working closely with many notable water resources and researchers and will be publishing several exciting and vital articles in the weeks ahead, detailing these findings.
We invite you to sit back... relax... and explore at your leisure, choosing your own path through this array of excellent articles. We encourage you to print these articles and enjoy them at your leisure, perhaps finding a grand old tree to sit with as you do. If you would care to share any of these with a friend, please note the option of notifying them by email at the bottom of each page. As always, we welcome your comments. Please remember to bookmark our site, and return often.


100 most important questions in Plant Biology
A1. How do we feed our children’s children?
A2. Which crops must be grown and which sacrificed, to feed the billions?
A3. When and how can we simultaneously deliver increased yields and reduce the environmental impact of agriculture?
A4. What are the best ways to control invasive species including plants, pests and pathogens?
A5. Considering two plants obtained for the same trait, one by genetic modification and one by traditional plant breeding techniques, are there differences between those two plants that justify special regulation?
A6. How can plants contribute to solving the energy crisis and ameliorating global warming?
A7. How do plants contribute to the ecosystem services upon which humanity depends?
A8. What new scientific approaches will be central to plant biology in the 21st Century?
A9. (a) How do we ensure that society appreciates the full importance of plants?
A9. (b) How can we attract the best young minds to plant science so that they can address Grand Challenges facing humanity such as climate change, food security, and fossil fuel replacement?
A10. How do we ensure that sound science informs policy decisions?
A11. How can we translate our knowledge of plant science into food security?
A12. Which plants have the greatest potential for use as biofuels with the least effects on biodiversity, carbon footprints and food security?
A13. Can crop production move away from being dependent on oil-based technologies?
A14. How can we use plant science to prevent malnutrition?
A15. How can we use knowledge of plants and their properties to improve human health?
A16. How do plants and plant communities (morphology, colour, fragrance, sound, taste etc.) affect human well-being?
A17. How can we use plants and plant science to improve the urban environment?
A18. How do we encourage and enable the interdisciplinary that is necessary to achieve the UN’s Millennium Development Goals, which address poverty and the environment?
B1. How can we test if a trait is adaptive?
B2. What is the role of epigenetic processes in modulating response to the environment during the life span of an individual?
B3. Are there untapped potential benefits to developing perennial forms of currently annual crops?
B4. Can we generate a step-change in C3 crop yield through incorporation of a C4 or intermediate C3 ⁄C4 or crassulacean acid metabolism (CAM) mechanism?
B5. How do plants regulate the proportions of storage reserves laid down in various plant parts?
B6. What is the theoretical limit of productivity of crops and what are the major factors preventing this being realized?
B7. What determines seed longevity and dormancy?
B8. How can we control flowering time?
B9. How do signalling and cross-talk between the different plant hormones operate?
B10. Can we develop salt ⁄ heavy metal ⁄ drought-tolerant crops without creating invasive plants?
B11. Can plants be better utilized for large-scale remediation and reclamation efforts on degraded and ⁄ or toxic land?
B12. How can we translate our knowledge of plants and ecosystems into ‘clever farming’ practices?
B13. Can alternatives to monoculture be found without compromising yields?
B14. Can plants be bred to overcome dry land salinity or even reverse it?
B15. Can we develop crops that are more resilient to climate fluctuation without yield loss?
B16. Can we understand (explain and predict) the succession of plant species in any habitat, and crop varieties in any location, under climate change?
B17. To what extent are the stress responses of cultivated plants appropriate for current and future environments?
B18. Are endogenous plant adaption mechanisms enough to keep up with the pace of man-made environmental change?
B19. How can we improve our cultivated plants to make better use of finite resources?
B20. How do we grow plants in marginal environments without encouraging invasiveness?
B21. How can we use the growing of crops to limit deserts spreading?
C1. What are the best ways to control invasive species including plants, pests and pathogens?
C2. Can we provide a solution to intractable plant pest problems in order to meet increasingly stringent pesticide restrictions?
C3. Is it desirable to eliminate all pests and diseases in cultivated plants?
C4. What is the most sustainable way to control weeds?
C5. How can we simultaneously eradicate hunger and conserve biodiversity?
C6. How can we move nitrogen-fixing symbioses into non-legumes?
C7. Why is symbiotic nitrogen fixation restricted to relatively few plant species?
C8. How can the association of plants and mycorrhizal fungi be improved or extended towards better plant and ecosystem health?
C9. How do plants communicate with each other?
C10. How can we use our knowledge of the molecular biology of disease resistance to develop novel approaches to disease control?
C11. What are the mechanisms for systemic acquired resistance to pathogens?
C12. When a plant resists a pathogen, what stops the pathogen growing?
C13. How do pathogens overcome plant disease resistance, and is it inevitable?
C14. What are the molecular mechanisms for uptake and transport of nutrients?
C15. Can we use nonhost resistance to deliver more durable resistance in plants?
D1. How do plant cells maintain totipotency and how can we use this knowledge to improve tissue culture and regeneration?
D2. How are growth and division of individual cells coordinated to form genetically programmed structures with specific shapes, sizes and compositions?
D3. How do different genomes in the plant talk to one another to maintain the appropriate complement of organelles?
D4. How and why did multicellularity evolve in plants?
D5. How can we improve our understanding of programmed developmental gene regulation from a genome sequence?
D6. How do plants integrate multiple environmental signals and respond?
D7. How do plants store information on past environmental and developmental events?
D8. To what extent do epigenetic changes affect heritable characteristics of plants?
D9. Why are there millions of short RNAs in plants and what do they do?
D10. What is the array of plant protein structures?
D11. How do plant cells detect their location in the organism and develop accordingly?
D12. How do plant cells restrict signalling and response to specific regions of the cell?
D13. Is there a cell wall integrity surveillance system in plants?
D14. How are plant cell walls assembled, and how are their strength and composition determined?
D15. Can we usefully implant new synthetic biological modules in plants?
D16. To what extent can plant biology become predictive?
D17. What is the molecular ⁄ biochemical basis of heterosis?
D18. How do we achieve high-frequency targeted homologous recombination in plants?
D19. What factors control the frequency and distribution of genetic crossovers during meiosis?
D20. How can we use our knowledge about photosynthesis and its optimization to better harness the energy of the sun?
D21. Can we improve algae to better capture CO2 and produce higher yields of oil or hydrogen for fuel?
D22. How can we use our knowledge of carbon fixation at the biochemical, physiological and ecological levels to address the rising concentrations of atmospheric CO2?
D23. What is the function of the phenomenal breadth of secondary metabolites?
D24. How can we use plants as the chemical factories of the future?
D25. How do we translate our knowledge of plant cell walls to produce food, fuel and fibre more efficiently and sustainably?
E14. What is the answer to Darwin’s ‘abominable mystery’ of the rapid rise and diversification of angiosperms?
E15. How has polyploidy contributed to the evolutionary success of flowering plants?
E16. What are the closest fossil relatives of the flowering plants?
E17. How do we best conserve phylogenetic diversity in order to maintain evolutionary potential?
Have a look at these question - which ones interest you? It might help you decide how to pick a university degree or dissertation/thesis topic!
Humans and plants
Plant adaptation and agriculture
Plant pathogens, fungi and nutrient transportation
Molecular biology, epigenetics and photosynthesis
Biodiversity, speciation and evolution
E1. How much do we know about plant diversity?
E2. How can we better exploit a more complete understanding of plant diversity?
E3. Can we increase crop productivity without harming biodiversity?
E4. Can we define objective criteria to determine when and where intensive or extensive farming practices are appropriate?
E5. How do plants contribute to ecosystem services?
E6. How can we ensure the long-term availability of genetic diversity within socio-economically valuable gene pools?
E7. How do specific genetic differences result in the diverse phenotypes of different plant species? That is, why is an oak tree an oak tree and a wheat plant a wheat plant?
E8. Which genomes should we sequence and how can we best extract meaning from the sequences?
E9. What is the significance of variation in genome size?
E10. What is the molecular and cellular basis of plants’ longevity and can plant life spans be manipulated?
E11. Why is the range of life spans in the plant kingdom so much greater than in animals?
E12. What is a plant species?
E13. Why are some clades of plants more species-rich than others?


Tanacetum parthenium, known as feverfew or bachelor's buttons, is a flowering plant in the daisy family Asteraceae. It is a traditional medicinal herb which is commonly used to prevent migraine headaches.
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What symptoms did you experience with cervical cancer?
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Cervical cancer may not produce any symptoms or signs. In particular, early stage cervical cancers, like precancerous changes, typically do not produce symptoms. Symptoms may develop when the cervical cancer cells start to invade surrounding tissues.
Symptoms and signs of cervical cancer include:
Abnormal vaginal bleeding
Vaginal bleeding after menopause
Vaginal bleeding after sex
Bleeding or spotting between periods
Longer or heavier menstrual periods than usual
Other abnormal vaginal discharge
Pain during sexual intercourse
It is important to note that these symptoms are not specific for cervical cancer and can be caused by a variety of conditions.


The process of polar auxin transport, central to a plant's auxin relations, can be inhibited by a group of synthetic compounds that apparently act by binding to a plasma membrane protein known as the naphthylphthalamic acid (NPA) receptor. No endogenous ligand to the NPA receptor, capable of affecting polar auxin transport in plants, has yet been found. It is now shown that a group of flavonoids - including quercetin, apigenin, and kaempferol - can specifically compete with [3H]NPA for binding to its receptor and can perturb auxin transport in a variety of plant tissues and transport systems in a manner closely paralleling the action of synthetic transport inhibitors. Because the active flavonoids are widely distributed in the plant kingdom and exert their effects at micromolar concentrations approximating likely endogenous levels, they may act as natural auxin transport regulators in plants.
|Original language||English (US)|
|Number of pages||4|
|State||Published - 1988|
ASJC Scopus subject areas


Oil pastel on paper by Beverley Dancy. Worm lettering and border by Andrea Choe.
View the full size version.
Oil pastel on paper by Beverley Dancy. Worm lettering and border by Andrea Choe.
View the full size version.
N1 still disgruntled over Brenner’s choice (Cambridge UK). Disproving the popular maxim that time heals all wounds, N1 made clear in a statement today that it is every bit as annoyed about not becoming the “chosen strain” as it was nearly 50 years ago. “Bristol had nothing on me then and it’s got nothing on me now,” said the visibly petulant Caenorhabditis elegans isolate obtained from Sidney Brenner’s backyard. “Mushroom compost? Give me a break,” added the derisive strain, referring to the humble origins of N2. According to N1, “It was totally political from the very beginning. These things always are. Anyway, it’s not like I really wanted to be prodded, mutagenized, starved, bleached and ultimately autoclaved by a bunch of sadistic scientists,” the transparently begrudging nematode added. “So the joke’s on you, N2. Hope you’ve enjoyed the last 50 years, because you’ve got a lot more of the same coming.”
Project dies peaceful death surrounded by loved ones (University of Davis, CA). Following a prolonged, uphill and often painful battle, NIH proposal GM052937 is finally at rest according to sources close to the proposal. Whereas the termination of the project came as something of a shock to its long-term collaborators, those closest to the revised R01 had expressed serious concerns in the months leading up to its death. “The signs were all there,” said one of the postdocs intimately familiar with the well-being of the project. “Insufficient preliminary data, a delay in publications, and a lack of connectivity to the aims. It was clear enough if you just looked.” The proposal’s brave but futile struggle was accompanied by emotions typical of end-of-project scenarios including a denial of experimental flaws, anger at reviewers and funding agencies, bargaining with editors, depression of summer salaries, and ultimately acceptance into a journal of significantly lower impact than was expected. Still, in all endings new beginnings may find their genesis. “It’s hard to know what lies beyond the mythical ‘great wall’,” stated one of the lead investigators after learning of the project’s demise. “Perhaps there’s nothing whatsoever. But maybe the Hindus have it right, and reincarnation awaits all things that pass.” As of press time, the project’s PIs were rumored to be heavily favoring the “theory of rebirth” in the form of an R21.
Worm theologians ponder meaning of ‘Pick of Fate’ (Petri dish). Ancient mythological narratives within the C. elegans community have long included fanciful tales of shining objects that descend from the sky, arbitrarily removing “chosen members” of the population. “Though it’s considered an ill omen to speak of, the Pick Gods must be appeased once in every generation,” proclaimed one worm elder, who spoke on condition of anonymity. Although reasons for the apparent sacrifices continue to elude the nematode clerics, it has been noted that virgin L4s appear to “please the giant gleaming spade” above all others. Some survivors of the choosing ceremony have reported approaching a bright light or flame. Still others claim that it is a form of alien abduction in which individuals are subjected to painful gonadal probing by a giant clear needle. Such survivors have described recovering consciousness on a completely different plate while smeared from nose to tail in a kind of viscous oily substance, possibly of an inter-dimensional or protoplasmic nature. Conspiracy theorists within the worm community have gone so far as to suggest that these individuals may have been “implanted” with a “seed of foreign origin”, although this theory remains controversial. Nevertheless, universal agreement behind the meaning of “Shovel Selection” is likely to remain unresolved. Stated one wizened post-gravid hermaphrodite, “We can only hope that a divine and loving intelligence is controlling the pick and that it does not merely represent the whims of some dispassionate cosmic manipulator.”
The C. elegans Development, Cell Biology & Gene Expression meeting is in Nara, Japan this July15th-19th, 2014. This meeting is in association with the 6th Asia-Pacific C. elegans Meeting.
Meeting Website: http://cedevap2014.sakura.ne.jp/
Abstract and registration opened March 9, 2014. Please pay attention to the deadlines.
Early registration: May 9
Late registration: June 30
**On and after May 10, registration fee will be higher
Abstract Deadline: May 9
Financial Aid: We have received several grants to cover travel expenses of presenters (posters or talks). Please apply for this financial aid if needed.
Hotels: You must make your own hotel reservations by June 30th.
Hope to see you there!
Ahna Skop, Asako Sugimoto & Andrew Chisholm, Head Organizers
Our lab has previously developed a combination of single-step SNP mapping and whole genome sequencing (WGS) methods to pinpoint phenotype-causing sequence variants (Doitsidou et al., 2010). The mapping part of the single-step procedure is essential to separate the phenotype-causing, mutagen-induced sequence variant from background sequence variants. WGS data can be analyzed with CloudMap, a free, cloud-based software analysis tool that we recently developed (Minevich et al., 2012). We have previously provided proof-of-concept studies for the use of CloudMap, and we report here our experience with using CloudMap on a routine basis.
We have found over the last two years that the SNP/WGS strategy and ensuing CloudMap-based data analysis can reproducibly and accurately pinpoint phenotype-causing mutations to mapping regions as small as 0.5 Mb and that the method can work with very few recombinants. Fig. 1 shows the mapping plots from a selection of 16 EMS mutagenized strains from 8 different EMS-induced screens for loss of neuronal identity (thanks to many members of the Hobert lab for providing the mapping data). The tallest histograms indicate the regions containing the largest amount of normalized pure parental alleles following an outcross to the Hawaiian CB4856 mapping strain. For 14 of the causal variants in 13 strains (ot628 is a confirmed double mutant) we have either cloned the causal variant or have strong evidence for its identity and are in the process of confirming. For 8/14 of the causal variants, CloudMap correctly identified the 0.5 Mb where the causal variant resides. In the 6 cases where the 0.5 Mb bins did not correctly identify the causal variant, CloudMap was off by an average of 0.54 Mb.
The accuracy of CloudMap in identifying mapping intervals depends on strict adherence to the Hawaiian SNP mapping protocol and also on the number of F2 recombinants that are pooled for sequencing. In addition, Mendelian ratios should be calculated to identify whether the causal variant resides at one locus or many and if it is dominant or recessive. We also recommend thawing an ancestral Hawaiian strain once a year to minimize variants introduced by genetic drift and to maximize mapping accuracy.
In a number of cases where the Hawaiian mapping protocol was strictly followed, CloudMap was able to identify the correct 0.5 Mb mapping interval with very few recombinants. For example, both hu80 and hu97 were correctly mapped to a 0.5 Mb mapping interval with as few as 16 and 34 F2 recombinants respectively.
We consistently noted that the previously described incompatibility region between Bristol and Hawaian strains on the left arm of LG I (Seidel et al., 2008) is largely not visible relative to the peak of the causal variant due to the normalization procedure we use to compute the frequency of pure parental alleles. In cases where the causal variant is also on LG I (ot740, the taller peak contains the causal variant), CloudMap was able to separate the incompatibility peak from the causal variant peak.
Transgenes contained in the strain background and required to observe a mutant phenotype can generate a mapping signal if the transgene is re-homozygosed in the F2 generation. We find that this mapping signal is virtually eliminated if as few as 50% of the picked F2 recombinants are heterozygous for the transgene.
CloudMap is available via the Galaxy web platform, requires no installation when run on the cloud, and can also be run locally or via the Amazon Elastic Compute Cloud (EC2) service (http://usegalaxy.org/cloudmap and http://hobertlab.org/cloudmap).
Mutation mapping by whole-genome sequencing (WGS) is becoming increasingly popular with C. elegans researchers. Pioneering studies from several worm labs have laid the foundations for this trend by providing proofs of concept (Sarin et al., 2008; Flibotte et al., 2010), working out experimental strategies (Doitsidou et al., 2010, Zuryn et al., 2010), and contributing tools and workflows for the analysis of mapping-by-sequencing data (Minevich et al., 2012).
Yet even though many good bioinformatic tools for WGS data analysis exist, almost all of them seem daunting to biologists. The CloudMap collection of workflows and tools for Galaxy is a notable exception here, but it requires the upload of huge experimental datasets to the main Galaxy server (http://usegalaxy.org), which is time-consuming and not well-suited for maintaining an archive of data from several experiments. Hence, most people in the field still do not consider analyzing WGS data themselves, and the resulting need to establish collaborations prevents a more rapid spread of mapping-by-sequencing approaches in the community.
We have recently developed MiModD, a comprehensive software package for the identification and annotation of mutations in the genomes of model organisms from whole-genome sequencing data, with the specific goal to enable biologists/geneticists with limited bioinformatical knowledge to analyze genome-wide sequencing data locally on (relatively) standard desktop computers. The current beta version of MiModD enables short-reads alignment from several input formats, variant calling, post-processing (i.e., filtering and annotating lists of variants), and the generation of summary reports with hyperlinks to biological databases including Wormbase. It also supports various mapping-by-sequencing approaches by producing CloudMap-ready output, i.e., variant lists produced by MiModD can be used directly with the CloudMap EMS Variant Density, Variant Discovery Mapping, and Hawaiian Variant Mapping tools. By default, the package is controlled through a command line interface, but can be fully integrated, with a single command, into a local installation of Galaxy to obtain a beginner-friendly graphical user interface and a lab-internal WGS analysis server.
In principle, MiModD can be used to analyze WGS data from any organism, but its memory requirements are dependent on genome size. To analyze C. elegans data we recommend a system with 16GB of memory (though 8GB will do for testing). The package runs on Linux and Mac OS systems without any further strict hardware requirements. Obviously, performance will depend on the exact configuration of the system MiModD is running on, but on our development machine – a desktop PC equipped with a 3rd generation Intel Core i7 processor, 16 GB RAM and an Ubuntu 12.04 operating system – the complete analysis of a 30x covered worm genome finishes in less than 1 hour, which should be good enough for the occasional user.
MiModD is free, open-source and actively developed, and labs interested in WGS analysis are encouraged to download and test the software. We offer assistance with installing and using the package to users of the beta version and are looking forward to receiving your feedback. Further information is available at www.celegans.de/mimodd.
Flibotte S, Edgley ML, Chaudhry I, Taylor J, Neil SE, Rogula A, Zapf R, Hirst M, Butterfield Y, Jones SJ, et al. (2010). Whole-genome profiling of mutagenesis in Caenorhabditis elegans. Genetics 185, 431-441.


Why Your Meals Should Contain Calcium
Have you ever wondered why your teeth suddenly break on their own? Have you once in a while felt like your bones are as feeble as that of a nonagenarian even while you are as young as 25? Have you knowingly or unknowingly been excluding calcium from your meals? Are you among those who think calcium is an insignificant nutrient, and if it is not included in your diet, there would be no problems at all? Do your pedicurist and manicurist sly you as a result of your brittle, ugly looking nails each time you book an appointment? The cause of your funny ‘nonagenarian feeling’ and sudden break of teeth, as well as feeble and weak bones, teeth, and nails, are pointers to the deficiency of calcium in your body. This could be really dangerous to your health, as it could land you in places you least expect.
Why You Need Calcium
You do not want to begin to complain of waist pain at the age of 35. You do not want to have severe bone fractures upon any little fall you have. You do not want to lose all your teeth at 35 while making a dentist a do-or-die friend in your life. You also do not want to use artificial teeth, knowing fully well that the reason for your massive loss of teeth is your fault.
If you seek reasons why calcium is essential to your wellbeing, you have come to the right place. This article has within it the health benefits of calcium, causes of calcium deficiency, the symptoms of calcium deficiency, and the major topic of the article, which is the risks you expose yourself to when you refuse to include calcium in your diet. However, before we begin, the most explicit definition of calcium deficiency is the extreme lack of calcium in the body. Got that?
Health Benefits of Calcium
Let me present the benefits of the nutrients you treat as insignificant. Most people lack this nutrient so much that it becomes a big deal in their bid to restore it into their bodies; at this point, its status changes from insignificant to ‘quintessential.’
- Calcium is well known for its function for the development, growth, and strengthening of the teeth.
- It also aids in making the bones stronger.
- It helps the heart function properly.
- It ensures that the muscles stay strong and healthy and prevents muscle contraction.
- Calcium and Vitamin D combined help protect your body against cancer, diabetes, and high blood pressure.
- The record holds that calcium sees to the efficient functioning of some key enzymes.
- Calcium also helps generate blood clotting and ensures that the blood vessels work perfectly.
- It helps nerves pass the right messages to the brain.
- Generally, calcium generates strength for the whole body.
- Your body does not produce calcium. You can only get calcium from meals, and having appropriate amounts of calcium in your body would help keep you away from your Doctor (except the Doctor is a close friend.)
Sources of Calcium
Calcium can be found in foods, and some of these foods include;
- Soy products with added calcium
- Bread and other fortified flour products
- Bony fishes
- Broccoli, spinach, and other green leafy vegetables
- Beans and lentils also contain decent amounts of calcium
- Fortified drinks
Quickly note that;
- The medical record holds that people who eat the bones of fishes and other meats tend to grow healthy teeth, nails and bones as these animal bones they eat contain high levels of calcium that are sufficient for the body.
Causes of Calcium Deficiency
- The primary and most apparent cause of calcium deficiency is the lack of calcium intake for a long time, this has to do with the absence of the inclusion of calcium in diets. It happens mainly when you do not eat calcium-giving foods.
- Also, another reason found to be the cause of calcium deficiency is Vitamin D deficiency. Vitamin D ensures the absorption of calcium, so no matter how much calcium content you have if you lack Vitamin D to absorb it, you would suffer from the health risks attached to calcium deficiency. This automatically means that the idea of calcium in the body depends on an existing and functioning Vitamin D; without this, there would be no calcium content in your body.
Other Causes Include;
- Medications: Some medications are used repeatedly, tamper with the calcium content in your body. One of these medications is chemotherapy medications. They do this by affecting the Vitamin D content, which eventually makes it impossible to absorb calcium.
- Hormonal changes also cause calcium deficiency. This is very common with the womenfolk.
- Another cause of calcium deficiency could also be genetic factors.
- Excessive consumption of magnesium can also lead to calcium deficiency as it alters the proper absorption and functioning of calcium.
- The record holds that excessive sodium and protein intake would cause calcium excretion, thereby making your body lose calcium.
- Some digestive diseases have also been found to cause calcium deficiency.
- Body activities that eliminate calcium through sweat or urine can also cause calcium deficiency.
- High coffee and alcohol consumption.
- Kidney and thyroid diseases.
- Age is also a factor. Wondering how this is possible? Infants are known to absorb 60% of the calcium they get in foods; however, as they grow, the absorption level reduces to about 20%
Effects of Calcium Deficiency
- Constant muscle cramps, contraction, and spasm
- Excess and continuous fatigue and sluggishness
- Dry skin, skin irritation, and skin infections like eczema
- Osteopenia; the reduction of the mineral density in the bone
- Osteoporosis; this makes the bones thinner. Both osteopenia and osteoporosis cause severe pain and acute disability as well as bad posture
- Rickets in children
- Extremely painful menstruation
- Weak bones, nails, and muscles
- Heart diseases
- Some forms of cancer
- Severe dental issues
- Poor blood clotting
- Delayed growth and development in children
- Heart-related illnesses
These are the health risks of the lack of calcium in the body. Little or no amounts of calcium in the body would lead to any of the following health issues mentioned above. This automatically means that one way to keep a healthy medical record lies in supplying your body with necessary nutrients like calcium.
Symptoms of Calcium Deficiency
- Memory loss which is closely linked with confusion
- Numbness in the face, feet, and hands
- Weak nails
- Constant muscle cramps
- Easy fracture of bones
- Easy breakage of teeth
- Extreme and continuous fatigue and fainting
- Itchy and dry skin which can lead to eczema
- Brittle nails
- Extremely painful menstruation
- Difficulty swallowing
The excellent news about calcium deficiency is that its treatment process is not complicated. It has to do with changes in lifestyle and diet and dedication to the treatment routine. With all of these in place, the lost calcium in your body would return, and you would see yourself strong and healthy again.
How Do You Treat It?
- To begin with, change your diet. Make sure your diet includes calcium-giving foods like dairy products, soy products, beans, fish bones, fortified bread, green leafy vegetables, and so on. All of these are have calcium contents in them.
- Furthermore, after you must have started out with your calcium diet, make sure that every physical activity you engage in does not make you lose excess calcium through sweat or urine.
- Avoid excessive intake of magnesium, sodium, protein, and phosphate.
- Eat foods that contain Vitamin D, as Vitamin D is a key factor in the absorption of calcium into your body.
- Then eat more and more meals that contain calcium and Vitamin D. Also, do not forget to chew biscuit bones as they contain calcium as well.
Now that you know that calcium is not so insignificant after all, would you still ignore it? Ignoring it would be extremely detrimental to your health. Remember that calcium is not part of your body’s makeup. To supply your body with calcium, you have to eat calcium-giving foods and foods rich in Vitamin D, which would also help your body absorb calcium. These foods include dairy and soy products, fortified flour products, bones, and many more. The illnesses associated with calcium deficiency is not favorable; however, its treatment process is relatively easy and more advantageous than its symptoms and effects. Your health is a very important part of you, hence the need to take care of it by protecting it from deficiencies as little as calcium deficiency.


Turtles feed predominantly on plants. However, animal proteins in the form of insects and fish should also be regularly on the menu. With a one-sided and unbalanced diet, the animals are quickly prone to deficiency symptoms. These are often noticeable in the form of shell deformation or can lead to organ damage. Turtle feed should therefore contain an appropriate mixture of plants and animal proteins. In addition, you can equip the terrarium with water lettuce or floating aquatic plants. Even though they are so unassuming, turtles are also good hunters. In addition to turtle feed, there are also a few water fleas, amphipods or mosquito larvae that you can place in the terrarium.


Title: Studies on prevalence of gastrointestinal helminthic infections and their associated risk factors in dairy animals of semi-arid eastern plains of Rajasthan
Authors: Monika, Abhishek Gupta, PK Pilania, N Kumar, KP Parmar and GS Manohar
Source: Ruminant Science (2017)-6(1):55-62.
Cite this reference as: Monika, Gupta Abhishek, Pilania PK, Kumar N, Parmar KP and Manohar GS (2017).Studies on prevalence of gastrointestinal helminthic infections and their associated risk factors in dairy animals of semi-arid eastern plains of Rajasthan. Ruminant Science 6(1):55-62.
A total of 649 faecal samples comprising of 392 samples from cattle (215; native and 177; crossbred) and 257 from buffaloes were collected randomly from dairy animals of semi-arid eastern plains of Rajasthan during summer, rainy and winter seasons from March 2016 to January 2017. Coprological examination of samples revealed an overall prevalence of 55.62% for gastrointestinal helminthic (GIH) infections. Among various helminthes, highest prevalence reported was of strongyles (55.01%), followed by amphistomes (14.02%), Strongyloides sp. (12.48%), Trichuris sp. (10.01%), Moniezia sp. (1.38%) and Fasciola sp. (1.08%) in the decreasing order of prevalence. Quantitative analysis revealed mild to high severity of infections in terms of EPG with strongyles, Strongyloides sp. amphistome and Moniezia sp. ranging from 200-5500, 100-1700, 100-700 and 200-3400 with an average of 1218.92±249.37, 700±205.17, 244.44±66.90 and 1300±1051.64 eggs per gram, respectively. Statistical analysis using multivariate binary logistic regression model revealed highly significant difference (P<0.01) in the prevalence of GIH infection in the different types of dairy animals, among different seasons from different districts of the study area. Coprolculture analysis revealed the presence of larvae of genera Haemonchus, Oesophagostomum, Trichostrongylus, Bunostomum, Strongyloides, Cooperia and Nematodirus in the decreasing order of prevalence in the dairy animals of semi-arid eastern plain zone of Rajasthan.
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A Child's Life
Volume 25 Number 2
Ora Hirsch Pescovitz
Photo by Office of Visual Media, IU School of Medicine
Not Just an Apple a Day
When it comes to 21st-century pediatric problems, there are few researchers moreinvolved or thoughtful than Ora Hirsch Pescovitz, executive associate dean for research affairs at the Indiana University School of Medicine. Also director of pediatric endocrinology and diabetology and the Edwin Letzter Professor of Pediatrics, Pescovitz is both clinical and basic investigatorshe has published in 150 scientific publications and has served as president of the Society for Pediatric Research, the world's largest pediatric research organization.
Pausing between dean's office meetings, hospital visits, and time on the lab bench, Pescovitz offered her expert take on the causes and consequences of some of thorniest issues affecting childhood health: widespread diabetes, puberty as early as 6 or 7, and growth hormone use.
Since Pescovitz began concentrating on this area 20 years ago, researchers have learned a tremendous amount about growth hormone and achieved major advances in understanding the genetic causes of growth disorders. Prior to 1985, the only way doctors could get their hands on growth hormone involved harvesting human cadavers.
"That obviously restricted the availability," Pescovitz says. "And in fact there were some significant complications associated with its use, which is why it was withdrawn." Some children whose families resorted to this treatment died of a serious neurological disorder closely related to Mad Cow disease. Growth hormone extracted from cadavers was later replaced by genetically engineered versions.
Of course, children with growth disorders don't always respond to growth hormone treatments. "There are still a number of situations where we don't understand why children do not grow," says Pescovitz.
Pescovitz's research in the growth hormone area led her to discover a new polypeptide, present in the hypothalamus and testes, that is related to a factor called growth hormone-releasing hormone. She holds an intellectual property status patent for the find. At present, she and other researchers know this polypeptide plays a role in regulating normal spermatogenesis (sperm formation) and normal hematopoiesis (blood cell formation). She also knows the polypeptide is made by the hypothalamus and has actions in the pituitary gland. The polypeptide's full physiological functions in human adults and children remain to be seen, however: "We're still in the stage of evaluating its role in rodents," Pescovitz says.
The puzzles of growth hormone research are complicated by difficult bioethical questions that parents and pediatricians alike must consider, as the development of growth hormone products continues: What is normal stature, what is genetic short stature, and should we treat children to make them taller just because we can?
"What if you said you could treat every child under the fifth percentile (for height)?" Pescovitz muses. "Then what would you do with everyone in the new fifth percentile after the shift?"
In recent years, controversy over children's sexual development has hit the newsstand headlines. Is puberty in the 21st century becoming "precocious," and is such early development O.K? While some pediatric endocrinologists have argued that puberty as early as age 7 is normal, Pescovitz remains firm that puberty in a girl younger than age 8 or a boy younger than 9 is clearly precocious.
But she questions whether there is really a "trend" toward early puberty at all.
"Personally, I'm not 100 percent convinced there are significant trends toward earlier onset of puberty, with the exception of children with increased obesity," Pescovitz says. "If you look at the age of onset from the early 1900s to the early 2000s, there is no question the age has decreased," she concedes. "But the latter half of the 20th century isn't exactly clear."
Pescovitz's research in this area has shown that once nutritional gains made in the first half of the 20th century that affected the entire American population are accounted for, no additional triggers appeared to lower the age of puberty.
Such thinking saved one 7-year-old girl whose family practitioner labeled her early development normal; Pescovitz's evaluation revealed a brain tumor causing the early puberty signs.
One consequence of true precocious pubertyif left untreatedis what the medical community calls premature epiphyseal fusion. Although a child may be tall at age 6, the growth plates fuse prematurely, leading to a shorter-than-normal adult who finished achieving height at the same time her peers shot up. "It's a major handicap in adult life to (be a male) under 5'2 or (a female) under 4'8," Pescovitz sympathizes.
Not to mention the psychosocial experiences that precocious children have to endure in gym lockers, public swimming pools, pajama parties, and other common gatherings. In light of these consequences, Pescovitz says treatments like Lupron injections, which reduce the progression of secondary sexual characteristics such as breasts, pubic hair, and menstrual cycles in children, are "miraculous." But she still seeks answers to the basic question: Why do some children enter puberty on the ends of the bell curve? At present, she notes, environmental disrupters have been implicated in affecting human reproductive system functions and the onset of puberty, but far more investigation is needed to determine the impact of chemicals, toxins, diet, and other environmental factors.
Although Pescovitz says she consider each of the disorders she treats serious, diabetes among America's youth alarms her, since it carries the most significant risk for morbidity and, despite major advances toward diagnosis and control, still lacks a cure. In her trademark upbeat fashion, Pescovitz translates this into an opportunity.
"As scientists who are interested in the well-being of children," she says, "we have to look at the disorders that have the greatest affliction, cause the most harm, the most pain, the most suffering, the most short- and long-term morbidity.
"Diabetes is all-encompassing for families," she continues. "I don't really know if I could do what we ask most parents of children with diabetes to do in their lives." Pescovitz ticks off the hurdles: a regimented lifestyle that requires set sleeping hours and diets, the constant risk of blood sugars plummeting too low or skyrocketing, the glucose checks as often as 10 times per day.
Then there's the financial impact that the lobbyist in Pescovitz can't ignore. As president-elect of the Society for Pediatric Research in 2001, Pescovitz testified before the House of Representatives Committee on Appropriations' Subcommittee on Labor, Health and Human Services, and Education. At the time, the combined costs of cardiovascular, endocrine, nutritional, and metabolic diseases were estimated to be $232.1 billion annually, more than 12 times the size of the NIH budget. "Imagine the economic and societal savings that are possible if we invest in preventing these diseases during childhood and adolescence," she pleaded with representatives on Capitol Hill.
That's partially why her team follows more than 1,000 children with diabetes based at the Riley Hospital for Children. Thanks to researchers such as Linda DiMeglio, assistant professor of pediatrics at the IU School of Medicine, Riley stands in the forefront of using insulin pumps in children and toddlers, an advance that introduces more flexibility into the sleeping hours of a diabetic child.
And Pescovitz's husband, Mark, IU professor of surgery, immunology, and microbiology, has spearheaded development of a novel approach to preventing progression of Type 1 diabetes. He is on an IU team that has received a $2 million National Institutes of Health grant to participate in a seven-year Type 1 diabetes trial. If they can halt autoimmunity from destroying the pancreas, the hope is they can stop the disease's progression in children.
"We have advances, but not cures. There is no magic bullet," Pescovitz reiterates. That's why she is delving once again into questions whose answers could prevent more children from streaming into her office to receive a diabetes diagnosis.
"When I started in pediatric endocrinology, we never saw Type II diabetes in children. It was unheard of, and today it's not uncommon," Pescovitz reports. "We know our genes haven't changed in that 20 years, so it means there is something environmental influencing this."
Pescovitz observes that public schools have decreased physical education classes in the budget-cutting crises sweeping their districts, that schools now boast vending machines stocked with potato chips and pop, that meal portions in America have super-sized in the past two decades.
"Just look at the portions people eat today compared to what they eat in other countries or what you put on your plate as a child," she says. "It's a matter of finding which environmental aspects are the bigger triggers. I don't think it's a toxin in the air or water▀it's something we are doing to ourselves and to our children."
Yet Pescovitz shuns the image of herself as Chicken Little, alarming parents over every study, every finding. Instead, she urges education interpreted according to a family's own genetic propensities. For example, families whose members never struggle with obesity or diabetes shouldn't sweat an occasional trip through McDonald's drive-thru. If diabetes is present in your family tree, vigilance is crucial.
"Individualize the risks," Pescovitz says. "The public shouldn't conclude there's too much confusing information, so (they will) ignore it. Just the opposite."
Julie Sturgeon is a freelance journalist in Indianapolis.


Pancreatic ductal adenocarcinoma is really a devastating disease having a dismal prognosis. set off by these microenvironmental cues through association with intracellular signaling cascades. While these ideas have already been founded for additional malignancies tightly, proof offers emerged just that ion stations are motorists of PDAC aggressiveness recently. Particularly, they may actually donate to two of the quality PDAC features: the substantial fibrosis from the tumor stroma (desmoplasia) as well as the effective immune system evasion. Our important overview of the books clearly demonstrates there’s still an extraordinary lack of understanding with regards to the contribution of ion stations to both of these normal PDAC properties. However, we are able to draw parallels from ion channel research in other inflammatory and fibrotic diseases. Evidence can be accumulating that pancreatic stellate cells communicate exactly the same profibrotic ion stations. Similarly, it really is at least partly known which main ion stations are indicated in those innate and adaptive immune system cells that populate the PDAC microenvironment. We explore potential restorative avenues produced thereof. Since medicines focusing on PDAC-relevant ion stations are in medical make use of currently, we propose to repurpose those in PDAC. The search for ion route targets can be both motivated and difficult by the actual fact that a number of the relevant stations, for instance, KCa3.1, are expressed within the tumor functionally, stroma, and immune system cells. Only research will disclose which equip of the total amount we should place our weights on when developing channel-targeting PDAC therapies. Enough time can be up to explore the effectiveness of ion route focusing on in (transgenic) murine PDAC versions before launching medical tests with repurposed medicines. by inhibitor clofazimine Zaccagnino et al. (2017) Reduced manifestation in PDAC, connected with metastatic tumors Brevet et al. (2009) mitoKV1.3Apoptosis of tumor cells, tumor MA-0204 development, and development in mouse types of PDAC Leanza et al. (2017) and Zaccagnino et al. (2017) KV10.1 (hEAG)Inhibition of route activity by monoclonal antibodies; inhibition of tumor cell development in mouse xenograft style of pancreatic tumor Gmez-Varela et al. (2007) KV11.1 (hERG)Manifestation in PDAC samples Zhou et al. (2012) Cell development and invasiveness Feng et al. (2014) PDAC malignancy and and style of severe pancreatitis (Han et al., 2016). In severe pancreatitis, IL-6 promotes ANO1 manifestation via IL-6R/STAT3 signaling. ANO1 overexpression, subsequently, raises IL-6 secretion via IP3R/Ca2+/NFB signaling activation (Wang et al., 2020a). Therefore, ANO1 is apparently involved with a positive responses loop with this inflammatory disorder. CFTR and ANO1 are indicated in Capan-1 cells extremely, where they mediate ATP/UTP-regulated Cl? secretion (Wang et al., 2013). ANO1 can be overexpressed in a number of PDAC cell lines when its manifestation can be in comparison to that in HDPE cells that are recommended to represent a style of the normal human being pancreatic ductal epithelium (Sauter et al., 2015). Certainly, the evaluation of patient materials demonstrates ANO1 mRNA and protein are up-regulated in 75% from the cases. That is associated with an unhealthy Rabbit Polyclonal to ANXA10 probability of success (Crotts et al., 2019). An EGFR-related signaling pathway, needing ANO1, regulates Cl? and Ca2+ homeostasis in pancreatic tumor cells. This EGF-induced store-operated Ca2+ admittance is necessary for the migration of pancreatic tumor MA-0204 cells (Crotts et al., 2019). Oddly enough, ANO1 includes MA-0204 a promigratory part in PDAC cells but does not have any influence on cell proliferation. Whole-cell patch-clamp tests reveal practical ANO1 as a significant mediator of PDAC CaCC currents. While knockdown of ANO1 using siRNA totally abolishes the CaCC-mediated currents almost, the three examined ANO1 inhibitors T16Ainh-A01, CaCCinh-A01, and NS3728 display unspecific unwanted effects and limited specificity (Sauter et al., 2015). Ion Route Participation in Desmoplasia Fibrosis is really a pathological result common for most chronic inflammatory illnesses including chronic pancreatitis (Wynn and Ramalingam, 2012). The abundant stroma response (desmoplasia) is really a hallmark common to both persistent pancreatitis and PDAC (Haeberle et al., 2018). Chronic pancreatitis is known as a risk element for pancreatic tumor, and even, it regularly evolves to a genuine PDAC (McKay et al., 2008). In both full cases, the standard pancreatic parenchyma can MA-0204 be markedly remodeled (as demonstrated in Shape 1) so the regular organ function can be eventually dropped. The badly vascularized desmoplastic.


Liver regenerating cells discovered
August 14, 2015
These newly discovered cells are in a more excellent way at regenerating tissue than ordinary liver cells, moreover known as hepatocytes.
Previously, researchers believed that a clump of adult stem cells known similar to oval cells were responsible for the liver’s illustrious regenerative properties, but it has seeing that been proven that these stem cells exhibit into bile duct cells.
Instead, the researchers at the University of California-San Diego School of Medicine be favored with revealed that “hybrid hepatocytes” are backward the liver’s regeneration. Their tools and materials are published in Cell.
“Hybrid hepatocytes delineate not only the most effective room for passing to repair a diseased liver, but that also the safest way to hinder fatal liver failure by cell transplantation,” says direct author Michael Karin, distinguished professor of pharmacology and pathology.
Such are the regenerative powers of the liver that diseases piteous the organ – such as cirrhosis and hepatitis – are frequently treated by transplanting a piece of wholesome liver from a donor.
Cirrhosis – scarring of the liver – be able to lead to a number of freedom from disease problems, including enlarged veins in the pharynx and stomach, jaundice and kidney failure. In the US, the greatest part common causes of cirrhosis are alcoholism and hepatitis – heat of the liver.
For the study, the researchers examined the liver cells involved in the regeneration of tissue following injury caused ~ means of exposure to an environmental toxin called carbon tetrachloride. They discovered the hermaphrodite hepatocytes in an area of the liver known in the same proportion that the portal triad.
After chronic liver hurt, these unique cells proliferate extensively and provide liver tissue. While they are resembling in many ways to regular hepatocytes, they unambiguous far lower levels of bile channel cell-specific genes.
“Although hybrid hepatocytes are not stem cells, thus far they seem to be the in the greatest degree effective in rescuing a diseased liver from clean failure,” explains first author Joan Font-Burgada.
Hybrid hepatocytes renew the liver without giving rise to cancer
At not past nor future, many researchers are testing the capabilities of induced pluripotent pedigree cells (iPSCs) to repair damaged livers and have lodgings liver failure from occurring. Using iPSCs can be difficult, however, as it can be hard to stop these cells from proliferating once they have completed their therapeutic business.
As iPSCs continue to proliferate, the jeopardize of them forming cancerous tumors moreover increases.
The researchers then tested to perceive whether the newly discovered hybrid hepatocytes had homogeneous tumor-forming properties by examining tumors in three diverse mouse models of liver cancer. After decline to find evidence of hybrid hepatocytes in a single one of the tumors, the researchers concluded that the cells did not give to certain forms of liver cancer.
While the full age of the research was conducted using search models, the researchers were also versed to identify cells similar to the look closely hybrid hepatocytes in human livers.
Experts waiting under the possibility of fulfilment that one day, cell-based therapies choose replace the use of liver transplants. Previously, Medical News Today reported forward a groundbreaking study in which scientists managed to compensate organ function in a live animal’s distressingly damaged liver by transplanting stem cells grown in a laboratory.
A form into ~s of liver stem cells known to the degree that hepatic progenitor cells (HPCs) were transplanted into mice and, in excess the following months, the cells spurred greater areas of the liver to converted, improving both the structure and the form of the liver. http://bit.ly/1DQfnlO
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Invitae is interested in companies that can contribute positively to its revenues in the next two to three quarters, according to CEO Sean George.
The acquisitions will enable Invitae to add reproductive health genetic testing to its portfolio and become what it calls a "comprehensive genomic information company."
Dubbing itself a "telegenomics company," San Francisco startup Genome Medical announced the launch this week of its genetic consultation services offering.
The company said it now has payor coverage for more than 130 million individuals.
Genome Medical will provide genetic counseling support for Good Start Genetics' VeriYou carrier screening service.
Under the agreement, Roche Diagnostics will offer Good Start's GeneVu carrier screening test along with its Harmony NIPT.
Couples can now buy cystic fibrosis and spinal muscular atrophy carrier screening tests through Amazon, though a doctor will have to approve the order.
The firms found that NGS-based carrier screening is more cost effective than genotyping-based testing for 14 disorders and results in fewer affected births.
The partnerships are in the areas of consumer applications in reproductive health, and genetics-focused educational programs and entrepreneurship support.
Good Start will serve as an in-network laboratory partner for a variety of genetic screening tests.
Sometimes genetic tests give inconclusive results and provide little reassurance to patients, the Associated Press reports.
Vox wonders whether gene-editing crops will be viewed similarly as genetically modified organisms of if people will give them a try.
In Science this week: research regulation and reporting requirement reform, and more.
With H3Africa, Charles Rotimi has been working to bolster the representation of African participants and African researchers in genomics, Newsweek reports.


By De-Yuan Hong
Codonopsis and its allied genera, are a bunch of crops that are vital in financial system and horticulture. A Monograph of Codonopsis and Allied Genera (Campanulaceae s. str.) deals its viewers complete wisdom of those crops together with palynology, cytology, inhabitants biology, morphological description, geographical distribution with vouchers brought up, first-class ink illustrations, and colour images, and keys to genera and to species.
This first-class paintings will facilitate identity of appropriate vegetation, use of plant assets, evaluation of endangered states, the improvement of conservation options, and should advertise systematic and evolutionary study of this group.
- Provides entire descriptions and classifications of Codonopsis and allied genera
- Richly illustrated with line drawings and top quality colour photographs
- Delineates and clarifies the relationships of Codonopsis and its allied teams in accordance with the analyses utilizing info from exterior morphology, pollen morphology, chromosomes, and molecular biology
Read or Download A Monograph of Codonopsis and Allied Genera PDF
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Extra resources for A Monograph of Codonopsis and Allied Genera
Moeliono (1960) merged Campanumoea (including Cyclocodon) with Codonopsis. Hong and Pan (1998) restored Cyclocodon as genus based on observations on pollen grains and seed-coat of two species in Campanumoea sect. Campanumoea and two species in Campanumoea sect. Cyclocodon. Recent molecular works (Eddie etÂ€al. 2003; Haberle etÂ€al. 2009; Wang etÂ€al. 2013) indicated that the closest relative of Cyclocodon is Platycodon, not Codonopsis. Our observations in the present work show that the three species of Cyclocodon are consistent in seed morphology and deserve an independent seed type (Figures.
2011), but they are different in respect of ovary position. In C. inflata, the calyx and corolla are both epigynous but in the other the corolla is epigynous, while the calyx is hypogynous (Figure II 1:6a & b, and Figure IV 1: 45B). In the Codonopsis pilosula / C. tangshen complex, the corolla is epigynous, but the position of calyx varies from typically hypogynous, and thus calyx looks like five free sepals, gradually to half-epigynous (Figure II 1:6f and Figure IV 1: 23B d-g). Corolla: Shape The corolla is rather polytypical in Codonopsis and its allies.
Campanumoea sect. Cyclocodon 32â•… A Monograph of Codonopsis and Allied Genera Type III. 4–6-colpate, with short colpi, long spinules, and thin nexine. Codonopsis subg. Pseudocodonopsis Kom. (= Pseudocodon D. Y. Hong & H. Sun) Type IV. 5–7-colpate, with medium-long colpi, small spinules, and thin nexine. Codonopsis subg. Obconicicapsula D. Y. Hong (= Himalacodon D. Y. Hong & Q. , 2011) strict sense is heterogeneous in pollen morphology, Codonopsis subg. Codonopsis belonging to Type I, subg. Pseudocodonopsis Kom.


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Allison recalled that time lag between treatment and effect when he learned of results from early clinical trials of a CTLA-4 drug. While the therapy worked for some patients within the first 12 weeks of treatment, others responded later, often after the tumors had progressed. “When I heard this, it reminded me of the mice and the fact that tumors first grew prior to shrinking,” says Allison. “I thought, this is exactly what you should expect.”
Clinicians of course hope for a timely response to chemotherapy. Allison worried that rapid efficacy might be an impossible requirement for immunotherapy to meet, since T cells must detect cancer cell debris, multiply, and then trigger attack before the tumors will shrink. A few years ago, thanks to steady rallying by Allison and many clinical colleagues, the criteria for immunological trials changed so that patients were given more time to respond to drugs.
In the trial presented at ASCO, the benefit of ipilimumab began to show after four months. A total of 676 patients with stage III or IV melanoma received ipilimumab alone, ipilimumab with an anticancer vaccine (gp100, which targets a protein on the melanoma’s cell surface), or the vaccine alone. Patients taking ipilimumab alone or ipilimumab with the vaccine lived an average 10.1 and 10 months, respectively; those given only the vaccine lived an average 6.4 months.
The advantage of ipilimumab became more notable over time. At one year, 46 percent of patients taking ipilimumab were alive compared with 25 percent of those receiving the vaccine only. The study was published June 5, 2010, in an online edition of the New England Journal of Medicine.
“Look at the survivors at the tail of the curve,” urges Allison referring to the lines in a graph representing overall survival of stage III and IV cancer patients taking ipilimumab. “People who are alive at two years are alive after four years—usually, no one survives that long.”
“I’ve been in the field [of immunotherapy] for a long time and I’ve seen the waves of enthusiasm followed by disappointment,” says Lloyd Old, a cancer immunologist at MSKCC. “But Jim’s research on CTLA-4 has led to a discovery of the first magnitude.”
Although 60 percent of study participants given the drug experienced autoimmunity issues such as colitis or diarrhea, the symptoms usually resolved within two weeks of corticosteroid treatments.
In late June, Bristol-Myers Squibb applied to the FDA for regulatory approval of ipilimumab. If approved, it could be the second cancer immunotherapy available. The drug is also being tested in Phase III trials for hormone refractory prostate cancer and Phase II trials for lung cancer.
For an approach so heavily scrutinized in its early days, Allison was wise to trust the data and carry on. At MSKCC since 2004, he’s sticking to his guns, digging ever deeper into the immunological frontier.


…we may conclude that Philip K Dick wrote nonfiction.
Reading another person’s mind is impossible. But it is now possible to see what’s going on in there visually, thanks to scientists at the University of California-Berkeley, who on Thursday announced they had managed to decode the brain signals of three individuals into watchable movies. YouTube movies, to be exact.
The scientists used MRI to record the brain activity of subjects as they watched movie trailers.
Then, the team took the recorded brain signals and ran them through a database of 18-million-seconds of random YouTube clips, but specifically didn’t include clips of the trailers that the subjects had been watching in the first place.
Berkley’s computer program was able to pick out new clips visually similar to the subjects’ brain imagery and mash them together into composites, creating eerie, hallucinatory new movies that replicate with startling accuracy the exact scenes that subjects saw in the trailers, frame-for-frame.


Mark Jit elected a Fellow of the Academy of Medical Sciences18 May 2023 London School of Hygiene & Tropical Medicine London School of Hygiene & Tropical Medicine https://lshtm.ac.uk/themes/custom/lshtm/images/lshtm-logo-black.png
Professor Mark Jit from the London School of Hygiene & Tropical Medicine (LSHTM) has been elected as a Fellow of the Academy of Medical Sciences this year.
Professor Jit, a professor of vaccine epidemiology and head of the department of infectious disease epidemiology, is one of 59 influential biomedical and health scientists who have been awarded the prestigious fellowship.
Fellows were chosen from 353 candidates from UK institutions, with their research expertise spanning from molecular imaging to biostatistics and public health policy.
They are being recognised for their contributions to advancing biomedical and health science, cutting-edge research and translating developments into benefits for society.
Professor Jit said: “I'm honoured to be elected as a Fellow of the Academy of Medical Sciences. The Academy brings together scientists who are working on some of the greatest health challenges facing our world. The last few years of the COVID-19 pandemic have been especially difficult for us all, but scientists have played a vital role our struggle against the virus. I'm excited to be part of this incredible community of Fellows and help us recover from the pandemic and build a better world.”
Professor Jit is a leading academic in the field of vaccine epidemiology with his research focusing predominantly on understanding the epidemiological and economic impact of vaccines and other methods of infectious disease control in order to inform decision-making in public health.
He is a co-Director of the Global Health Economics Centre at LSHTM, and is also affiliated with the Centre for the Mathematical Modelling of Infectious Diseases (CMMID) and the Vaccine Centre. He also holds affiliations at schools of public health at the University of Hong Kong and the National University of Singapore.
Professor Jit will be formally admitted to the Academy on Wednesday 12th July at an event that will also be celebrating the 25th anniversary of the organisation. He will join a network of 1,400 Fellows who play a central role in the Academy’s work.
Professor Dame Anne Johnson PMedSci, President of the Academy of Medical Sciences said: “These new Fellows are pioneering biomedical research and driving life-saving improvements in healthcare, from understanding the spread of infectious diseases to developing mental health interventions. It’s a pleasure to recognise and celebrate their exceptional talent by welcoming them to the Fellowship.
“This year, we are celebrating our 25th anniversary. The Fellowship is our greatest asset, and their broad expertise and dynamic ability has shaped the Academy to become the influential, expert voice of health. As we look to the future, the collective wisdom our new Fellows bring will be pivotal in achieving our mission to create an open and progressive research sector to improve the health of people everywhere.”
In 2021, Professor Beate Kampman was another LSHTM researcher who was elected as a Fellow of the Academy of Medical Sciences with Professors Matthew Burton and Mike Blackman also being awarded the title last year.
Further information on this year’s fellowships can be found on the Academy of Medical Sciences website.
LSHTM's short and specifically designed courses provide the opportunity for intensive study in specialised topics.
These courses enable participants to refresh their skills and keep up to date with the latest research and knowledge in public and global health.


Former PhD Student, 2018-2023
Department of Bioengineering
Dave is a former Ph.D student who joined our lab in Auguest 2018, and successfully defended his thesis on March 22nd, 2023.
He is interested in the field of Deep Learning and can be found typing ferociously on the computer, both in lab and at home.
D. Le, M. Alam, B. A. Miao, J. I. Lim, and X. Yao, “Fully automated geometric feature analysis in optical coherence tomography angiography for objective classification of diabetic retinopathy”. Biomedical Optics Express, 10(5): 2493-2503 (2019) [Full text]
Research Currently in Progress
Quantitative OCTA analysis and AI classification of eye diseases


Fungal trunk pathogens associated with Juglans regia in the Czech Republic.
Juglans regia L. (English walnut) trees with cankers and dieback symptoms were observed in two regions in the Czech Republic. Isolations were made from diseased branches. In total, 138 fungal isolates representing 10 fungal species were obtained from wood samples and identified based on morphological characteristics and molecular methods: Cadophora novi-eboraci, Cadophora spadicis, Cryptovalsa ampelina, Diaporthe eres, Diplodia seriata, Dothiorella omnivora, Eutypa lata, Eutypella sp., Peroneutypa scoparia, and Phaeoacremonium sicilianum. Pathogenicity tests conducted under field conditions with all species using the mycelium-plug method indicated that Eutypa lata and Cadophora spp. were highly virulent to woody stems of walnut. This is the first study to detect and identify fungal trunk pathogens associated with diseased walnut trees in Europe.