An individual’s profile of schizophrenia risk genes is associated with an increased risk of cannabis use. This is the main finding in a paper from an international team of researchers published today as an advanced online publication in the journal Molecular Psychiatry. The findings do not rule out a causal relationship between cannabis use and risk of developing schizophrenia but do suggest that the relationship may also work the other way, i.e. that genetic predisposition to schizophrenia may also increase the likelihood of using cannabis.

Cannabis is the most commonly used illegal drug internationally. In some countries, there is intense debate on the issue of legalising and controlling cannabis use, so increased insight into the health risks associated with cannabis are more pressing than ever. Schizophrenia is a devastating psychiatric disorder which affects about 1% of the population and commonly features auditory hallucinations and delusions. There is substantial evidence to suggest that cannabis is one causal component for schizophrenia, however there is debate around whether this is completely due to cannabis increasing psychosis risk or whether the genes that contribute to increased risk of psychosis also contribute to increased risk of cannabis use.

In an attempt to address this debate, the research team recruited 2082 healthy individuals of whom 1011 had used cannabis. They established the ‘schizophrenia genetic risk profile’ for each person, i.e. the number of genetic variants considered to be predisposing to schizophrenia. The results indicated that individuals who had a genetic predisposition to cancer were more likely to use cannabis and in greater quantities than those who did not have the schizophrenia genetic risk factors.

First author Robert Power, of King's College London, explains the significance of the results: "We know that cannabis increases the risk of schizophrenia. Our study certainly does not rule this out, but it suggests that there is likely to be an association in the other direction as well – that a pre-disposition to schizophrenia also increases your likelihood of cannabis use." Mr Power concludes: "Our study highlights the complex interactions between genes and environments when we talk about cannabis as a risk factor for schizophrenia. Certain environmental risks, such as cannabis use, may be more likely given an individual's innate behaviour and personality, itself influenced by their genetic make-up. This is an important finding to consider when calculating the economic and health impact of cannabis."

So the debate continues on the complex links between cannabis use and schizophrenia risk and should be an important consideration in discussions of cannabis legalisation.

Sources:
Power, R.A. et al. (2014). Genetic predisposition to schizophrenia associated with increased use of cannabis. Molecular Psychiatry advance online publication 24 June 2014; doi: 10.1038/mp.2014.51

Press release: King’s College London; available from http://www.eurekalert.org/pub_releases/2...062314.php [Accessed 24 June 2014]

Hello everyone,

My name is Masino and I am studying Bio- and Nanotechnology in Iserlohn, Germany. I am starting to work on my bachelor thesis in which I have to bind biotin on interleukin 1 antibodies. After that I need a method to check which antibodies binded the biotin and which not. Does someone of you have an idea? Thanks !

International Association of Plant Biotechnology Congress 2014

Organisers: International Association for Plant Biotechnology

Dates: August 10th-15th, 2014

Location: Melbourne Convention and Exhibition Centre, Melbourne, Australia

Website: http://www.iapb2014congress.com/

The website gives all the necessary information on conference agenda, hotel, exhibitions and other important facts.

The congress features a comprehensive programme covering multiple aspects of plant biotechnology with an international line-up of plenary and keynote speakers.

Symposia topics:
• Abiotic stress
• Bioenergy
• Bioinformatics
• Biopharma, bioproducts and bioprospecting
• Biosafety and acceptance
• Biotic stress
• Cereals
• Communicating innovation
• Crop biofortification & nutritional enhancement
• Economics and social benefits
• Emerging technologies
• Forages
• Forestry
• Gene expression
• Gene stacking
• Genomics
• Grain legumes
• Horticulture and ornamentals
• Innovations in in vitro culture/propagation
• Metabolomics & proteomics
• Microbiomes & plant-microbe interactions
• Molecular breeding
• Next-generation breeding technologies & innovations in gene transfer to plants
• Nutrient uptake & phytoremediation
• Oil and fibre crops
• Phenomics
• Regulation of new breeding technologies
• Tuber and root crops
• Yield

Plenary and Keynote Speakers
• Tom Adams, USA
• Julian Adams, USA
• Arie Altman, Israel
• Marilyn Anderson, Australia
• Jim Birchler, USA
• Stevens Brumbley, USA
• Jorge Canhoto, Portugal
• Henry Daniell, USA
• Swapan Datta, India
• Barbara De Coninck, Belgium
• Sacco de Vries, Netherlands
• Sharon Doty, USA
• Nina Fedoroff, Saudi Arabia
• Brett Ferguson, Australia
• Geoff Fincher, Australia
• Rainer Fischer, Germany
• Richard Flavell, USA
• Robert Furbank, Australia
• Stanton Gelvin, USA
• Yuri Gleba, Germany
• Jonathan Gressel, Israel
• Wilhelm Gruissem, Zurich
• Robert Hall, Netherlands
• Robert Henry, Australia
• Bertrand Hirel, France
• Jeanne Jacobs, New Zealand
• Beat Keller, Switzerland
• Jens Kossmann, South Africa
• Juergen Logemann, Germany
• Cathie Martin, United Kingdom
• Ying Miao, China
• Maurice Moloney, Australia
• Hilde Nelissen, Belgium
• David Ow, China
• James Petrie, Australia
• Ingo Potrykus, Switzerland
• Elibio Rech, Brazil
• Philippe Rigault, Canada
• Patrick Schnable, USA
• Lakshmi Sastry-Dent, USA
• Patrick Schnable, USA
• Kazuo Shinozaki, Japan
• Alex Sorokin, Singapore
• Erin Sparks, USA
• Satoshi Tabata, Japan
• Acram Taji, Australia
• Marc Van Montagu, Belgium
• Rajeev Varshney, India
• Ry Wagner, USA
• Zeng-Yu Wang, USA
• Jim Whelan, Australia
• William Wilson, USA
• Zhongchao Yin, Singapore
• Ulrich Zimmermann, Germany

Efforts to advance production of environmentally friendly transportation fuels from plant biomass should be aided by a new glycosyltransferase clone collection compiled by researchers at the U.S. Department of Energy (DOE)’s Joint BioEnergy Institute (JBEI). A paper on the collection has been accepted for publication in The Plant Journal. The aim of the JBEI GT collection is to provide a functional genomic for researchers in the field of sugar extraction from plant biomass to product fuels.

Glycosyltransferases (GT) are the enzymes responsible for catalysis of simple plant monosaccharides into complex polysaccharides needed for many plant cells function and structures. Large GT families have evolved in plants but their chemical nature has hampered efforts to understand specific functions of the majority of GTs. This hinders bioenergy research efforts to modify plant biomass with a goal to produce maximum amounts of transportation fuels.

In an attempt to address this issue, the JBEI team, led by Dr Joshua Heazlewood, director of the JBEI Plant Systems Biology Programme, have cloned and verified the new clone collection which contains 403 Arabidopsis GTs (the reference plant for poplar and other similar species) and 96 rice GTs (the reference plant for grasses). This represents about 88% of the known Arabidopsis GTs but only about 15% of rice GTs, so the team aim to extend this. Dr Heazlewood explains the ethos and utility behind the clone collection: “Using the unique infrastructure and resources at JBEI, we have provided a collection of high quality GT clones, all of which have been verified by sequencing and are available in easy to use cassettes…We’re making this entire collection available to the plant research community and expect it to drive our basic understanding of GTs and enable the manipulation of cell walls.”

As well as the GT clone collection, the team have produced a set of so-called ‘pBullets’ which are particle bombardment plasmids that mark targeted protein location with high efficiency when shot into cells. The JBEI pBullets are designed to mark elements of the plant endomembrane system, which separates the functional and structural plant cell components. Dr Heazlewood explains how this system could be useful: “Our pBullet vector series is custom designed for efficient bombardment…Researchers generally use large unwieldy plasmids that perform badly when it comes to localizing proteins.”
More information on the JBEI GT collection and the pBullets can be found on the JBEI Website at http://gt.jbei.org/

Sources

Lao, J. et al. (2014). The Plant Glycosyltransferase Clone Collection for Functional Genomics. The Plant Journal (accepted article); DOI: 10.1111/tpj.12577

Press release: The Berkeley Lab; available from https://newscenter.lbl.gov/2014/06/23/th...ollection/ [Accessed 24 June 2014].

The architecture of the key regulatory protein beta-arrestin in complex with a G-protein coupled receptor (GPCR) has been elucidated by a combination of electron microscopy and mass spectrometry in a paper published in the journal Nature. The study comes from a research team from Duke Medicine, the University of Michigan and Stanford University. The study should help advance understanding of how cells transmit signals and how signalling is controlled in the body's response to stimuli including light and pain.

GPCRs are seven transmembrane spanning structures which operate in a multitude of cell signalling pathways. As a group, they represent the largest drug target family for human diseases as disparate as cardiovascular disease, neurological disease and cancer. Co –senior author on the paper, Dr Robert J. Lefkowitz of Duke University School of Medicine and the Howard Hughes Medical Institute, explains the importance of insights into the structure of GPCRs: "It is crucial to visualize how these receptors work to fully appreciate how our bodies respond to a wide array of stimuli, including light, hormones and various chemicals." Dr Lefkowitz shared the Nobel Prize for Chemistry in 2012 with one of the other senior co-authors on the paper, Dr Brian K. Kobilka, of Stanford University School of Medicine, for their work on GPCRs.

In this paper, the authors presented a visualisation of the protein beta-arrestin in complex with the ‘fight-or-flight’ associated beta 2-adrenergic receptor. Beta-arrestins function to desensitise and therefore cap GPCR signalling and to initiate a new wave of GPCR-independent signalling. Another co-senior author, Dr Georgios Skiniotis of the University of Michigan further explains: "Arrestin's primary role is to put the cap on GPCR signaling. Elucidating the structure of this complex is crucial for understanding how the receptors are desensitized in order to prevent aberrant signalling." The research team formed and purified a functional human β2AR–β-arrestin-1 complex. Using mass spectrometry, cross-linking analysis and electron microscopy, they were able to confirm a previously suspected but not demonstrated bimodal binding, involving two separate interactions between beta-arrestin and both the intracellular carboxy tail of the GPCR and with its 7 transmembrane core.

The authors now plan to bring X-ray crystallography into play in order to attain atomic level insights into this architecture. These details could then be harnessed in experiments aimed at novel drug design and for gaining improved understanding of the fundamentals of GPCR biology. Co-lead author Arun K. Shukla concludes: “This is just a start and there is a long way to go…We have to visualize similar complexes of other GPCRs to develop a comprehensive understanding of this family of receptors."

Sources

Shukla, A.K. et al (2014). Visualization of arrestin recruitment by a G-protein-coupled receptor. Nature (June 22 2014); doi:10.1038/nature13430

Press release: Duke University Medical Center; available from http://www.eurekalert.org/pub_releases/2...061914.php

Could the Isis Pharmaceuticals trial drug ISIS-APOCIIIRx, which is currently in Phase 2 trials for the rare disease familial chylomicronemia syndrome (FCS), have wider implications for reduction of heart disease risk? The results of two new studies in the New England Journal of Medicine, from research groups in the USA and in Denmark, suggests that this may be the case.

ISIS-APOCIIIRx targets the APOC3 protein, a key mediator in triglyceride metabolism. Triglycerides are elevated to dangerously high levels in FCS. Until now, there has been controversy about whether triglycerides, which tend to be elevated in in people with heart attacks, were a causative agent or simply associated with other risk-associated factors. The doubt was increased when trials of drugs that caused a small reduction in triglycerides failed to have any effect on heart attack rates. However, the two recent studies appear to have ended the speculation as they point to a number of mutations in the APOC3-encoding gene which are associated with both an approximately 40% reduced level of triglycerides and a 40% reduction in heart attack risk. The results of the two independent studies were “eerily consistent”, according to the senior author on the American paper, Dr. Sekar Kathiresan of Massachusetts General Hospital and the Broad Institute.

A previous smaller study from the University of Maryland in 2008 on Amish people had shown that one in twenty Amish carried a mutation in APOC3 compared to one in 150 in the general American population and had substantially reduced triglyceride levels. The data, while interesting, were difficult to extrapolate to determine any impact on heart disease risk due to both the need to follow people over a substantial time period and also cultural reasons such as the tendency for Amis people to attend hospital less frequently than the general population, making cause of death more difficult generally to establish. The new studies were much larger, with the American study from researchers at the Broad Institute of Harvard and M.I.T mapping genes from 3734 Americans and the Danish study from researchers in Copenhagen University Hospital, using data from 75,725 people to investigate whether low triglyceride levels associated with reduced heart attack risk. In both studies APOC3 stood out as mutations in the gene encoding it was associated with both reduced triglycerides and reduced heart attack risk of between 36% to 40%.

The findings of these studies point the way to the development of new drugs for heart attack reduction for the first time essentially since the development of LDL-cholesterol targeting statins in the 1980s. This is where the Isis Pharmaceuticals ISIS-APOCIIIRx may come in. While the drug is currently in Phase 2 trials for FCS, and is targeted at APOC3, the company is keeping its options open regarding a wider indication in heart disease. However, the kind of huge, long-lasting study that would be needed would be beyond the scope of a small company like Isis and would require the resources of a larger company. Isis CEO Stanley Cooke said to Bloomberg"We're weighing how we want to take full advantage of this breakthrough, and as we do that we have to consider the potential broader development of the follow on product…We have a great deal of licensing interest for this drug." However, some industry analysts suggest that the potential of this drug and the underperformance of some other Isis products leaves them vulnerable to a hostile takeover. Whatever the outcome, t
he results of these important new studies raise hope of a new strategy to tackle the risk of heart disease.

Sources

The TG and HDL Working Group of the Exome Sequencing Project, National Heart, Lung, and Blood Institute. Loss-of-Function Mutations in APOC3, Triglycerides, and Coronary Disease. N Engl J Med (18 June 2014), doi:10.1056/nejmoa1307095

Jørgensen, A. B., R. Frikke-Schmidt, B. G. Nordestgaard, and A. Tybjærg-Hansen. N Engl J Med (18 June 2014), doi:10.1056/nejmoa1308027

Kolata, G. In Single Gene, a Path to Fight Heart Attacks. New York Times (18 June 2014), available from http://www.nytimes.com/2014/06/19/health...t_now&_r=1

http://www.fiercebiotech.com/story/isis-...2014-06-20

A search for large-scale DNA rearrangements has revealed a surprising genetic phenomenon associated with the deadly paediatric brain tumour, Group 3 medulloblastoma. The study from a research team in the European Molecular Biology Laboratory (EMBL), the German Cancer Research Centre (DKFZ), both in Heidelberg, Germany, and Sanford-Burnham Medical Research Institute in San Diego, USA, is published online today in the journal Nature. The results reveal that a ‘DNA shuffling’ event places the genes growth factor independent 1 transcription repressor (GFI1) or growth factor independent 1b transcription repressor (GFI1b) in proximity with enhancer elements that dramatically increase their expression.

Group 3 medulloblastoma is the most common paediatric brain tumour and has a higher rate of metastasis and a poorer prognosis than other types of this tumour. It has different subtypes and currently available treatments only cure a subset of patients and are associated with significant morbidity in the long-term. Therefore, increased insight into the mechanisms of this disease are vital in moving towards new therapies. Up until now, only the oncogene MYC had been firmly established as playing an important part in Group 3 medulloblastoma but this couldn’t explain many aspects of the disease. In the current study, the research team endeavoured to identify other genes involved. To do this they exploited the large known number of medulloblastoma sequences.

The team took a different approach to that usually used in identifying genetic changes in solid tumours. Instead of looking at individual gene changes, they concentrated on large-scale rearrangements in the areas between the genes. DNA from different patients was revealed to harbour a multitude of changes, among them inversions, deletions and duplications and importantly complex ‘DNA shuffling’ events. These events had one outcome in common; they placed GFI1b in close proximity to gene enhancer elements which are drivers of gene transcription, so that the expression of the GFI1b gene was now switched on in situations and cells where it would normally be switched off. While GFI1b was not affected in all patients, in many where it wasn’t a related gene called GFI1, which is on a different chromosome, was similarly shuffled so that it was in proximity to an enhancer. The research team suggest that it is these shuffling events that drive formation of the tumours. Study first author Dr Paul Northcott commented: “Nobody has seen such a process in solid cancers before…although it shares similarities with a phenomenon implicated in leukaemias, which has been known since the 80s.”

To further elucidate the role of GFI1b and GFI in medulloblastoma, the team engineered neural stem cells to express either GFI1b or GFI1 along with MYC and introduced these stem cells into the brains of healthy mice. These mice went on to develop aggressive, metastatic brain tumours very similar to human Group 3 medulloblastoma. These mice represent a genetic model for Group 3 medulloblastoma that can now be used to test potential therapies based on the study findings. For example, an existing class of drugs called bromodomain inhibitors can be used to target enhancer elements. The study has also created a potential diagnostic tool as GPI1b and GPI1 are not normally expressed in the brain.

The mice studies also left a puzzle for the research team to solve. For tumours to develop, the mice had to have MYC switched on as well as activation of GFI1B or GFI1. However, the groups established a statistical association between GFI1 and MYC but not between GFI1b and MYC. Further studies are addressing this puzzle. Senior author Dr Jan Korbel concluded: “What we’re learning from this study is that clearly one has to think outside the box when trying to understand cancer genomes.”

Sources

Northcott, P.A., Lee, C., Zichner, T. et al. Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma. Published online in Nature on 22 June 2014. DOI: 10.1038/nature13379.

Press release: European Molecular Biology Laboratory; available from http://www.embl.de/aboutus/communication...eidelberg/ [Accessed 23 June 2014]

A new study has shown that newer equine influenza A viruses from strains generated in the early 2000s can infect isolated dog tracheas and that reassorted viruses combining gene fragments from human influenza A virus (hIAV) and canine influenza virus (CIV) are viable. The study from researchers in the USA and UK, published online ahead of print in the Journal of Virology, suggests that dogs could act as a ‘mixing vessel’ for novel viruses with the potential to cause pandemics.

CIV is a relatively recent disease which was first observed in 2003 when a single equine influenza virus was transferred to dogs in a greyhound training facility in the USA and then was spread by the infected greyhounds to other states. Other similar transfers occurred from horses to foxhounds in the UK and from infected horses to nearby dogs in Australia in 2007. Influenza A viruses generally have the ability to be transferred between species, as for example with the H1N1pdm09 ‘swine flu’ pandemic of 2009 in which a virus originating in pigs became combined with human and avian gene segments. It became just antigenically different enough to evade immune recognition by human antibodies against previous H1N1 seasonal strains.

The current study used a model of infection of dog tracheas with different equine and human influenza A viruses in order to study efficiency of cross-species infection with different viral strains. The research team found that equine viruses from the early 2000s infected dog tracheas efficiently to give a CIV-like phenotype in terms of infectivity and tissue damage while those from the 1960s were not effective. Some human influenza virus A strains were also effective. Furthermore, engineered influenza viruses carrying gene segments from human and canine strains were effective as was a virus engineered by combining the human 2009 pandemic virus with the haemagglutinin (HA) and neuraminidase (NA) genes of CIV. It is the HA and NA genes that are often targeted by antibodies and vaccines. The authors point out that a virus combining CIV HA with seven genomic segments of the human H1N1 has been recently detected in dogs and would be poorly- if at all- recognised by human antibodies to seasonal H1N2 strains.

Corresponding author Dr Pablo Murcia and of the University of Glasgow explains the significance of the results with engineered chimeric canine-human influenza viruses: “We showed that the genes are indeed compatible, and we also showed that chimeric viruses carrying human and canine influenza genes can infect the dog tracheas." He explains that this implies such chimera could occur in nature and infect dogs, which could then act as “mixing vessels” for viruses with pandemic potential. The final edition of the article is due to appear in the August 2014 edition of the Journal of Virology. Given the high exposure of humans to dogs, the research team are currently investigating the burning question of whether these chimeric viruses can infect human lungs.

Sources

Gonzalez, G. et al., 2014. Infection and pathogenesis of canine, equine and human influenza viruses in canine tracheas. Journal of Virology, Published ahead of print, 4 June 2014, doi: 10.1128/JVI.00887-14

Press release: American Society for Microbiology, available from http://www.eurekalert.org/pub_releases/2...061914.php

A new mathematical and computational method combining elements of criminal geographical profiling and Bayesian methods used in epidemiology has been developed by researchers in Queen Mary University of London and Texas State University in the USA to determine infection sources by geographical location of disease cases. The method, described in a paper in the journal Methods in Ecology and Evolution, had improved search efficiency compared to either of the other two methods in both simulations and real world situations.

In criminology, investigators use a method called geographical profiling in which they use information on the spatial locations of linked crimes such as murder or rape in order to determine the area where the perpetrator is most likely to live. This provides a way to narrow down the search, for example in cases which generate large numbers of names of potential suspects such as that of the Yorkshire Ripper. This method uses an algorithm called criminal geographic targeting (CGT). In recent times this method has been applied to identification of infection sources for diseases by using information on the locations of disease cases. This facilitates targeted intervention, for example in the case of malaria outbreaks. However, issues arise when trying to identify multiple sources, particularly when the number of sources is not known.

In the current study, the researchers claim to have solved the issue of identifying multiple sources, even when the number of sources is unknown. They tested their new model on both simulations and on real world situations such as data from a malaria outbreak in Cairo. Study author Dr Steve le Comber explained the effectiveness of the new model in identifying the breeding sites of the mosquitoes responsible for this outbreak: malaria. "The experts working in the field had to search almost 300 square km to find seven breeding sites, but our model found the same sites after searching just two thirds of this area…In fact our model found five of the seven sites after searching just 10.7 square km. This is potentially important since there is a lot of evidence suggesting that the best way to control outbreaks of malaria is to attack the mosquito breeding sites – but it is incredibly difficult to do in practice."

Another key advantage of the technique is that it takes only minutes to carry out on a computer, suggesting its potential in the important early stages of epidemics when control efforts are most likely to bear fruit. Thus an outbreak could be stopped in its tracks before it has the opportunity to spread. Dr le Comber concludes: "The model has potential to identify the source of other infectious diseases as well, and we're now working with public health bodies to develop it further for use with TB, cholera and Legionnaires' disease."

Sources

Verity, R., Stevenson, M. D., Rossmo, D. K., Nichols, R. A., and Le Comber, S. C. (2014). Spatial targeting of infectious disease control: identifying multiple, unknown sources. Methods Ecol Evol (1 April 2014), pp. n/a-n/a, doi:10.1111/2041-210x.12190

Press release: Queen Mary, University of London; available from http://www.eurekalert.org/pub_releases/2...061914.php [Accessed 22 June 2014]

Hi everyone,
Hope all are doing good.....

Guys, I completed my masters in biotechnology in 2011 from India. Now, I want to pursue my further career in biotech mixed with any computer related subjects (like Bioengineering). So can anyone please suggest me are there any courses in masters and also universities which are offering subjects as I asked before.

Also please suggest me that "Is it better to opt now for masters in the previously mentioned subjects (biotech mixed up with computers) or Ph.D. (purely biotechnology), so that I want to earn a good job in biotech field itself.

Hoping for the quick and best answer...

Thank You for reading my query...

Have a nice time guys.

Hello all,

Shell scripting has been an indispensable part of Bioinformatics. Thought to initiate a thread for discussing problems/codes/useful one-liners/anything that can ease the life of the Bioinformaticians!

Here are some of the useful one-liners one can use for various purposes ( assuming actions on tab separated text file):

Transpose of a File :
awk '{ for (i=1; i<=NF; i++) { a[NR,i] = $i }}NF>p { p = NF }END { for(j=1; j<=p; j++) {str=a[1,j];for(i=2; i<=NR; i++){str=str" "a[i,j];}print str}}'

Number of Columns and Rows in a matrix
awk '{print NF}' (For Columns)
awk '{print NR}' (For Rows)

Print Even and Odd Numbered Columns and Rows in a matrix
awk '{NR%2==0}' For Even Rows
awk '{NR%2==1}' For odd Rows
awk '{NF%2==0}' For Even Columns
awk '{NF%2==1}' For Odd Columns

Fastq to Fasta conversion
Use FASTX Toolkit from Hannon Lab: Click Here for the link.

The Magic of !!
Double exclamation is a very useful command in Shell (those who have used it, would agree). Whenever you type !! in your terminal, it will print and execute the Last Shell Command you used on your Linux Terminal. Now this puts forward an array of possibiliies using !!.

Just for an example:
Use !! to add your last used command into any file or even a shell script you want to update.
If I use:
perl abc.pl
and then
!! (it will print following)
perl abc.pl

So, you can do echo !! >> filename (this will append the last used command to your file.

Delete First Line of a File
All you have to do is:
sed '1d' Filename

Delete all lines having a particular string
sed '/STRING/d' Filename

So, these were some of the tips for today. I'll keep it posted. And, let's share tips and problems here.

i know that glyoxalate cycle is a shunt pathway of krebs cycle..and important enzymes malate synthase and isocitrate dehydrogase which play vital role in the glyoxalate pathway.

can any one help me in knowing micro organisms which has this two enzymes?

what are the enzymes that can be produced by ecoli ?

i mean genes present in ecoli genome which produces enzymes or enzyme producing genes present in ecoli DH5 alpha strain?

how i can isolate a required enzyme gene from a bacterial source?

A ‘sex-distorting’ approach to control malaria-spreading mosquitoes, first proposed in theory sixty years ago, my be closer to reality. A new study in the journal Nature Communications from an international team led by researchers in Imperial College London, describes use of an endonuclease from slime mould to selectively shred the X chromosome of the malaria mosquito vector Anopheles gambiae. This has a two-fold effect as it results in males having almost exclusively male offspring, leading to reductions in population over time and also reduces malaria spread as only female mosquitoes bite humans and transmit malaria.

Malaria remains a serious public health issue, most notably in sub-Saharan Africa. The disease kills hundreds of thousands of people every year. In mosquitoes, like humans, normal sperm contains 50% X and 50% Y chromosomes. The current study exploited the fact that the endonuclease I-Ppol selectively targets cutting sites located exclusively on the X chromosome of Anopheles gambiae. The research team used a combination of protein engineering and molecular genetics to produce male mosquitoes in which the I-Ppol was turned on only during spermatogenesis. Therefore, these males produced almost no X chromosome-containing sperm as the X chromosomes were shredded by the endonuclease, and hence very few female offspring. Importantly, the modification was heritable so that many of the male offspring of the original males also produced few female offspring.

The results were striking. In five test cages originally containing 50 males and 50 females each, introduction of 150 sex-distorter males resulted in a major reduction in females over 4 generations and in complete loss of the population after another 2 generations in 4 out of 5 cages. The results are promising and are unlikely to have a serious impact on the surrounding ecosystem as, for example, it specifically targets the malarial mosquito unlike pesticides which are more indiscriminate. However, the system is some years away from deployment in the field.

Commentators have welcomed the study but point out that targeting the Y chromosome would represent a better long-term strategy as the modified males would pass the change on to all of their male offspring and there would be less dilution of the effect than would be likely with the system in the current study, which would probably need ‘topping up’ over time. The authors of the current paper agree with this analysis and in fact have been working on gene insertions in the mosquito Y chromosome. Thus the future looks promising for harnessing of sex-distorting strategies to control spread of malaria.

Sources

Galizi, R., Doyle, L. A., Menichelli, M., Bernardini, F., Deredec, A., Burt, A., Stoddard, B. L., Windbichler, N., and Crisanti, A. (2014). A synthetic sex ratio distortion system for the control of the human malaria mosquito. Nature Communications, Vol. 5 (10 June 2014), doi:10.1038/ncomms4977

BBC News; available from http://www.bbc.com/news/science-environment-27765974 [Accessed 13 June 2014]

A study to be presented today at the European League Against Rheumatism Annual Congress (EULAR 2014; Abstract Number: OP0187) sheds light on how biomarkers identified from whole blood gene expression profiles in children with juvenile idiopathic arthritis (JIA) could be harnessed to predict disease status at 12 months. The study highlights the fact that long-term disease status could only be accurately predicted after treatment initiation in newly diagnosed patients.

Juvenile idiopathic arthritis is the most common of the childhood (i.e. under 16 years of age) rheumatic diseases, affecting between 16-150 out of every 100,000 children. The causes of this devastating condition are not well understood. The symptoms include pain and swelling in joints, tenderness and stiffness lasting for more than six weeks and can also affect the eyes and lymph nodes. While gene expression profiling has brought the rheumatology field forward, it has so far only been possible to use biomarkers to predict therapeutic outcome at 6 months. Longer term predictions have proved elusive. Lead author on the current study, Professor James Jarvis of the University of Buffalo explains the importance of advancing biomarker profiling to allow longer-term predictions: "By predicting disease progression in these young children we can better understand the course of the disease and how best to treat the individual."

In the study, researchers constructed whole blood gene expression profile from children enrolled in the NIH-funded TREAT study, which is a clinical trial comparing methotrexate (MTX) with MTX + etanercept in children with newly-diagnosed JIA. The profiles were used to identify genes whose expression best predicted the twelve month outcome in terms of presence of active versus inactive disease. The research team found that while baseline expression profiles could be used to predict disease status at six months, they could not accurately predict the twelve month status. However, samples collected at 4 months after diagnosis from children on treatment were strongly predictive of the 12 months status. The study uncovered differences in response mechanisms between children who were positive for Rheumatoid Factor versus those who were negative, shedding light on the relative refractoriness of Rheumatoid Factor positive patients to therapies that are effective in other patients.

Sources

Yao J, Jiang K, Franks MB et al. Developing prognostic biomarkers from whole blood expression profiling in Juvenile Idiopathic Arthritis: Influence of early therapy on treatment outcome. EULAR 2014; Paris: OP0187

Press release: European League against Rheumatism; available from http://www.eurekalert.org/pub_releases/2...061114.php [Accessed 13 June 2014]

A new study from researchers in Trinity College Dublin could help predict and overcome resistance to the HER2 targeted cancer drug Herceptin and other newer anti-HER2 drugs. The results of the study, published in the journal Cancer Research, indicates that an extracellular vesicle biomarker called neuromedin U (NmU) is strongly associated with resistance to hercepin and newer drugs against HER2 positive cancers.

Levels of HER2, one of the family of receptors for epidermal growth factor, are elevated in about 25% of breast cancer patients. HER2 positive breast cancer is associated with relatively poor prognosis. However, a number of HER2 cancer targeted drugs have become available in recent years, among them the well-known Herceptin, but also including newer examples such as lapatinib, neratinib, afatinib, pertuzumab and T-DM1.

While these drugs are effective in many HER2 positive breast cancer patients, others are resistant to these therapies or develop resistance over time. Dr Lorraine O’Driscoll, senior author on the study, explains the problem further: "Many patients with HER2 positive tumours gain huge benefit from these drugs. Unfortunately, however, some who seem suitable candidates based on a HER2 test, don't gain the maximum intended benefit from these treatments. They may have a natural level of resistance to the treatment which is not detectable with currently available tests, while some other patients respond at first but may then become unresponsive or develop resistance to the treatments."

Thus there is an urgent need for biomarkers which could predict which patients are likely to be responsive to Herceptin and other anti-HER2 positive cancer drugs. This is where the new finding of a strong association between NmU and resistance to these drugs may be of vital importance. Furthermore, the blood levels of NmU are reflective of the intracellular levels, introducing the possibility of a minimally invasive blood test to measure NmU levels when considering the treatment options in patients with HER2 positive breast cancer.
In functional tests, the research team discovered that adjusting the levels of NmU could restore sensitivity to Heceptin and other anti-HER2 drugs. Also, blocking NmU could significantly reduce tumour growth. Studies are ongoing in this area. Meanwhile, the group has two patents pending in the USA and in Europe, in the context of facilitation of translation of their discoveries for patient benefit. This will be helped by the team's collaboration with the All Ireland Oncology Research Group (ICORG).

Sources

Rani, S., Corcoran, C., Shiels, L., Germano, S., Breslin, S., Madden, S., McDermott, M. S., Browne, B. C., O'Donovan, N., Crown, J., Gogarty, M., Byrne, A. T., and O'Driscoll, L. (2014). Neuromedin u: a candidate biomarker and therapeutic target to predict and overcome resistance to HER kinase inhibitors. Cancer Research. Cancer Research (29 May 2014), doi:10.1158/0008-5472.can-13-2053

Press release: Trinity College Dublin, available from http://www.eurekalert.org/pub_releases/2...061014.php

EHFPI, a database of Essential Host Factors (EHFs) for Pathogenic Infections. EHFs are a group of host cellular genes identified from (genome-wide) RNA interference (RNAi) screens, the knockdown effect of which greatly influences the infection of a pathogen but not the viability of host cells (designated as "confirmed hits", see the workflow chart below for detailed information). less http://lnkd.in/bgekf4f

Two new studies in the journal Biomedical Optics describe biometric watches that rely on changing patterns of scattered light. One study from researchers in Israel's Bar-Ilan University describes a device to measure glucose concentration and dehydration while the other from Delft University of Technology in the Netherlands describes a watch to monitor pulse. The watches could be used in the future by those looking to monitor their performance and well-being during physical activity.

Both devices depend on the so-called ‘speckle’ effect, which are the grainy interference patterns that result on images when laser light is reflected from uneven surfaces or is scattered from an opaque material. For example, in the case of the pulse-measuring watch, the blood flowing is scattering the light which the study authors claim results in a pulse monitoring system that is less sensitive to motion than other currently available devices.

The glucose measuring watch consists of a laser which generates a light wavefront that can illuminate a patch of skin on the wrist near an artery and a camera to monitor changes in the back-scattered light from the skin. A magnet attached to the device creates an external magnetic field which results in glucose molecules altering the wavefront polarisation and hence changing the speckle patterns. The study authors claim that this is the first non-invasive device which can be used to monitor glucose levels and relative hydration.

The pulse measuring watch uses a newly developed method to non-invasively monitor pulse in a way that is not sensitive to the movement of the wearer. The research team used simulated heart beats in milk and performed their measurements on the finger of a volunteer. They were able to show that flow pulsations could be accurately measured via speckle pattern changes even if the light source creating the pattern was also moving. Lead author Dr Mahsa Nemati explained: "This paper shows for the first time that a speckle pattern generated from a flowing liquid can give us the pulsation properties of the flow in spite of motion-induced artifacts…Sophisticated optics is not necessary to implement this, so the costs for devices can be kept low. Another advantage is that the devices can be non-contact or far from the sample."

Both devices may have future applications both in the clinic and in sports. The research teams involved are working on potential
commercialisation of their devices.

Sources

"Improved noncontact optical sensor for detection of glucose concentration and indication of dehydration level," N. Ozana et al., Biomedical Optics Express, Vol. 5, Issue 6, pp. 1926-1940 (2014). http://www.opticsinfobase.org/boe/abstra...e-5-6-1926

"Dynamic light scattering from pulsatile flow in the presence of induced motion artifacts," M. Nemati et al., Biomedical Optics Express, vol. 5, Issue 7, pp. 2145-2156 (2014). http://www.opticsinfobase.org/boe/abstra...e-5-7-2145

Press release: The Optical Society, available from http://www.eurekalert.org/pub_releases/2...061014.php