Better Alzheimer's detection: new EU-funded project to develop nanoscope [Date: 2012-06-07]A new research project that will pioneer a nanoscope to screen patient cells and potentially help with the early detection of Alzheimer's disease has just kicked off.With a boost of more than EUR 4 million in funding from the 'Nanosciences, nanotechnologies, materials and new production technologies' Theme of the EU's Seventh Framework Programme (FP7), the LANIR ('Label free nanoscopy using infra red') project will bring together researchers from 11 partner institutes across Belgium, Germany, Ireland, France, Italy and Romania. The consortium is made up of both small and medium-sized enterprise (SME) and academic partners.Set to run until 2012, the central aim of LANIR is to help find a way of detecting Alzheimer's disease in its early stages, as this is critical to developing effective treatments for the condition. At present, there is no such test available, despite the 7.7 million new cases each year worldwide, as well as 800 000 new patients in Europe who are affected by other forms of dementia. Alzheimer's disease is also directly responsible for increasing dependency costs among the elderly.The LANIR team will develop a nanoscope technique that works by deploying infrared (IR) radiation as a source of detection. It would be able to see features as small as 70 nanometres in lateral dimension, which is comparable to the size of a virus. The LANIR prototype will allow direct imaging of the chemistry and the structure of very small 'buried' features, without having to destroy the surface of a cell or a material.Infrared nanoscopy (IRN) is based on Infrared reflection absorption spectroscopy (IRAS), which measures the IR absorption in a material by recording the IR light reflected by or transmitted through the sample. When an incident IR wavelength matches with the specific (vibrational) excitations of chemical bonds in the probed molecules or materials, the IR absorption increases resonantly. IR spectroscopy thus reveals characteristic signatures of the chemical structures and molecular species.IRN's two main features are advanced laser techniques and spatio-temporal optical patterning. Chemical fingerprints of a sample can be imaged point by point at nanometre resolution by scanning over the pump-probe pattern on the sample.CORDIS News spoke to Project Manager John Mulcahy from the Materials and Surface Science Institute at the University of Limerick, Ireland, the LANIR coordinating institution.He comments on the project: 'The infrared nanoscope being developed in LANIR will provide tools for use as an early diagnostic device for Alzheimer's disease, which will allow timely intervention against the causes of reversible dementias, the start of therapies that can slow disease progression, the start of therapies that can potentiate the cognitive performance of patients by exploiting the non-complete impairment of their neuronal circuits, and the implementation of measures that reduce the effects of the co-morbidity associated with dementia.'He also described how the nanoscope will help with the timely implementation by patients and their families of the measures necessary to solve problems related to the disease's progression.John Mulcahy outlined how important EU funding is to the success of the project and the significance of the participation of the six SME partners for getting the table-top prototype to market: 'The transnational nature of FP7 Collaborative projects such as LANIR is particularly beneficial to bring together leading microscopists, spectroscopists and biologists under one umbrella beside industry leaders, to develop a new nanoscope and relevant applications of the nanoscope. FP7 funding leverages significant funding to bring this groundbreaking technique to a commercial reality in the shortest possible time. The specific emphasis on SMEs in FP7 projects has also been important to ensure participation from innovative and research and development (R&D)-oriented SMEs, and interfacing them with top-level expertise and infrastructure available in academic and public research bodies, in order to bring forward this groundbreaking technology. It would not have been possible to progress the technology otherwise.'As well as the prototype, table-top, multimodal IRN, the project will also construct three research IR microscopes, which will routinely image at a resolution less than 1 000 nm in IR and less than 100 nm in visible light. These three research IR microscopes will be located in Limerick in Ireland, Bucharest in Romania and Genoa in Italy.Mr Mulcahy says this ensures the benefits of high-end nanoscopy will be spread out across the whole of Europe, a feat he describes as 'impossible without FP7 funding'.
Thursday, June 7, 2012
大江生醫 佈局上海百岳特生技…功能性飲料
大江生醫：知悉董事及經理人從事大陸地區之競業情形 鉅亨網新聞中心 2012-06-07 第三十四條 第22款 1.事實發生日:101/06/072.經理人或董事之名稱: 董事長:楊武男 董事:關淑君 董事兼經理人:林詠翔 3.所擔任該大陸地區事業之公司名稱及職務: 大陸地區事業之公司名稱:百岳特生物技術(上海)有限公司 董事長:楊武男 董事:關淑君 董事兼經理人:林詠翔 4.所擔任該大陸地區事業地址:上海市金山工業區月工路888號1幢24區。 5.所擔任該大陸地區事業營業項目:從事功能性飲料之生產製造等。 6.對本公司財務業務之影響程度: 該公司為本公司100%轉投資公司並採權益法認列，故無重大影響。 7.經理人如有對該大陸地區事業從事投資者，其投資金額及持股比例:不適用。 8.公司擬採行措施:將於最近一次董事會解除董事及經理人競業禁止之限制， 並於最近一次股東會解除董事競業禁止之限制。 9.其他應敘明事項:無。
推動空中醫療救援服務
2012-06-08 00:35 工商時報 【記者劉朱松／台中報導】 台中童綜合醫院與漢翔航空工業公司昨（7）日共同簽署「空中醫療救援服務合作」備忘錄，藉由雙方的合作，讓醫療與航空做緊密結合，且緊急醫療救護運送，更有效率，期許達到全程醫護的完整服務。該項備忘錄的簽署儀式，昨由童綜合醫院急診室主任盧立華，及漢翔公司飛航事業處處長朱泰樺，在漢翔沙鹿廠共同簽署，未來將由童綜合醫院提供醫療設備與人員；漢翔將飛機改裝醫療專機，以最安全、快速及經濟的方式，提供最高品質的空中醫療轉送服務。童綜合醫院具備航空醫學的專業背景及醫療團隊，具有10餘年的國際醫療轉送經驗，自2007年即率先投入國際醫療救援，及空中醫療轉運服務業務。朱泰樺說，改裝的醫療專機航程，最遠可達6小時，除離島和本島的醫療後送服務，也可提供國際航線的醫療轉運，對於加入空中醫療救援服務，有極大的優勢和方便。由童綜合醫院提供醫療設備與人員，以客製化的飛航服務方式，除可彌補國內在此領域的不足，也可救人濟世，造福社會。
risk genes for neurodegenerative diseases !
Mapping genes: Study finds new risk factors for neurodegenerative diseases June 7, 2012 in Genetics Using a new and powerful approach to understand the origins of neurodegenerative disorders such as Alzheimer's disease, researchers at Mayo Clinic in Florida are building the case that these diseases are primarily caused by genes that are too active or not active enough, rather than by harmful gene mutations. 1000s of cDNA Clones - cDNA clones,Order On-Line & Save! Lowest Price Worldwide Guaranteed - sinobiological.com/Human_cDNA_Clone In the June 7 online issue of PLoS Genetics, they report that several hundred genes within almost 800 brain samples of patients with Alzheimer's disease or other disorders had altered expression levels that did not result from neurodegeneration. Many of those variants were likely the cause. "We now understand that disease likely develops from gene variants that have modest effects on gene expression, and which are also found in healthy people. But some of the variants — elevating expression of some genes, reducing levels of others — combine to produce a perfect storm that leads to dysfunction," says lead investigator Nilufer Ertekin-Taner, M.D., Ph.D., a Mayo Clinic neurologist and neuroscientist. "If we can identify the genes linked to a disease that are too active or too dormant, we might be able to define new drug targets and therapies," she says. "That could be the case for both neurodegenerative disease as well as disease in general." Dr. Ertekin-Taner says no other lab has performed the extent of brain gene expression study conducted at Mayo Clinic's Florida campus. "The novelty, and the usefulness, of our study is the sheer number of brain samples that we looked at and the way in which we analyzed them. These results demonstrate the significant contribution of genetic factors that alter brain gene expression and increase risk of disease," she says. This form of data analysis measures gene expression levels by quantifying the amount of RNA produced in tissue and scans the genome of patients to identify genetic variants that associate with these levels. Mayo researchers measured the level of 24,526 transcripts (messenger RNA) for 18,401 genes using cerebellar autopsy tissue from 197 Alzheimer's disease patients and from 177 patients with other forms of neurodegeneration. The researchers then validated the results by examining the temporal cortex from 202 Alzheimer's disease patients and from 197 with other pathologies. The difference between these samples is that while the temporal cortex is affected by Alzheimer's disease, the cerebellum is relatively spared. Customised Knockout Mice - Designed to your specifications. Contact us for a free consultation - www.ozgene.com/knockouts From these analyses, the researchers identified more than 2,000 markers of altered expression in both groups of patients that were common between the cerebellum and temporal cortex. Some of these markers also influenced risk of human diseases, suggesting their contribution to development of neurodegenerative and other diseases regardless of their location in the brain. They identified novel expression "hits" for genetic risk markers of diseases that included progressive supranuclear palsy, Parkinson's disease, and Paget's disease, and confirmed other known associations for lupus, ulcerative colitis, and type 1 diabetes. "Altered expression of brain genes can be linked to a number of diseases that affect the entire body," Dr. Ertekin-Taner says. They then compared their eGWAS to GWAS data on Alzheimer's disease, conducted by the federally funded Alzheimer's Disease Genetics Consortium, to test whether some of the risk genes already identified promote disease through altered expression. "We found that a number of genes already linked to Alzheimer's disease do, in fact, have altered gene expression, but we also discovered that many of the variants in what we call the gray zone of the GWAS — genes whose contribution to Alzheimer's disease was uncertain — were also influencing brain expression levels," Dr. Ertekin-Taner says. "That offers us new candidate risk genes to explore. "This is a powerful approach to understanding disease," she says. "It can find new genes that contribute to risk, as well as new genetic pathways, and can also help us understand the function for a large number of genes and other molecular regulators in the genome that are implicated in very important diseases."
A better diagnostic tool for brain cancer
June 7, 2012 in Cancer A joint study by researchers at the National Neuroscience Institute (NNI), National University of Singapore (NUS), and Singapore Institute for Clinical Sciences (SICS), A*STAR, has uncovered the role of a new tumour suppressor – known as parkin – in brain cancer that promises to shed insights into why certain brain tumours are more aggressive than others. This multi-institutional collaborative work, led by Associate Professor Lim Kah Leong at the NUS Yong Loo Lin School of Medicine's Department of Physiology, and Dr Carol Tang, Research Scientist at NNI together with Associate Professor Ang Beng Ti, Consultant at the Department of Neurosurgery at NNI and Senior Principal Investigator at SICS, was published recently in the May 15 issue of Cancer Research, a leading international cancer journal. Forming the majority of adult malignant brain tumours, gliomas affect a significant number of individuals globally, including here in Singapore. The NNI sees about 50 new cases of malignant glioma each year and continues to manage its existing glioma caseload by means of a multi-disciplinary neuro-oncology clinic. The prognosis for the majority of these tumours remains grim, particularly for patients with glioblastoma multiforme (GBM), the most aggressive form of brain tumour. The late Senator Edward Kennedy was reportedly afflicted with this malignant form of glioma. Senator Kennedy died 15 months after his diagnosis. For reasons yet unclear, others readily succumbed to the disease within a much shorter time. Interestingly, the study showed that the level of parkin expression in glioma cells can determine the survival outcome and disease progression of patients, i.e. those who have high parkin expression in their cancer cells tend to survive longer with lower tumor grades than their parkin-deficient counterparts. "With this understanding, instead of generalising malignant brain cancer patients, we can now differentiate their tumours based on their molecular characteristics" commented A/Prof Lim and Dr Tang. Agreeing, A/Prof Ang added, "This is significant as the stratification would allow us to formulate the most appropriate treatment for each patient." Importantly, the investigators also found that the restoration of parkin expression inparkin-deficient cells can slow down their proliferation rate and decrease their tumour size significantly. They are currently testing drugs that can mimic parkin's protective function against the aggression of brain tumours. The study is funded by research grants from the Khoo Teck Puat Foundation and Singapore Institute for Clinical Sciences, A*STAR. Other key authors of the study are Mr Yeo Wee Sing, a graduate student at NUS Department of Physiology and Ms Felicia Ng, a bioinformatician previously at the Singapore Institute for Clinical Sciences, A*STAR. Journal reference: Cancer Research
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