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Contact: Jordan Reese
jreese@upenn.edu
PHILADELPHIA— Researchers with the University of Pennsylvania School of Veterinary Medicine have demonstrated the process by which the cancer-causing chemical dioxin attacks the cellular machinery, disrupts normal cellular function and ultimately promotes tumor progression.
The team identified for the first time that mitochondria, the cellular sub-units that convert oxygen and nutrients into cellular fuel, are the target of tetrachlorodibenzodioxin, or TCDD. The study showed that TCDD induces mitochondria-to-nucleus stress signaling, which in turn induces the expression of cell nucleus genes associated with tumor promotion and metastasis.
The mechanism the research team has described is directly relevant to understanding incidences of breast and other cancers in human populations exposed to these chemicals. With a better understanding of this underlying cellular mechanism, researchers hope to improve their understanding of tumor growth and promotion.
"Now that we have identified this signaling mechanism we can look at ways to disrupt this complex chain of events," said Narayah Avadhani, chair of the Department of Animal Biology at Penn's School of Veterinary Medicine and the study's lead investigator. "Our ultimate goal is to block the propagation of this mitochondrial stress signaling and inhibit the expression of the proteins that combine to assist cancer growth."
A well-characterized mechanism of TCDD action occurs through activation of arylhydrocarbon receptors, AhR, by directly binding to the protein subunits. Activated AhR mediates the transcriptional activation of many genes including those involved in fatty acid metabolism, cell cycle regulation and immune response. The present study, however, shows that TCDD starts the chain of events that promote tumor progression in vivo by directly targeting mitochondrial transcription and induction of mitochondrial stress signaling. A unique feature of this TCDD-induced signaling is that it does not involve the action of AhR but occurs through increased calcium levels in cells and activation of calcium responsive factors. A net result of signaling cascade is slowing down of cellular apoptosis, increased cell proliferation and tumor cell metastasis. Taken together, this study describes a novel mechanism of TCDD-induced tumor progression and emergence of metastatic cancer cells.
TCDD is the most toxic compound in the dioxin family. Formed as a by-product during waste incineration, paper, chemical and pesticide manufacturing, it was the toxic ingredient in Agent Orange and closed the Love Canal in Niagara Falls. The public health impact of dioxin, according to the Environmental Protection Agency, compares to that of the pesticide DDT.
The study appears online and in the Dec. 17 issue of the Proceedings of the National Academy of Sciences and was performed by Avadhani, Gopa Biswas, Satish Srinivasan and Hindupur Anandatheerthavarada of the Penn School of Veterinary Medicine.
The research was supported by a grant from the National Cancer Institute and the National Institutes of Health.
December 18, 2007 Posted by FMS Global News | Cancer, Cancer Biology, FMS Global News, Global, Global News, London, London UK Feed, National Cancer Institute, NIH, Ottawa, Ottawa City Feed, PTSD, RSS Feed, Toronto, Toronto City Feed, Washington DC, Washington DC City Feed, World News	| Combat Related, Global News, PTSD, Soldiers, Vietnam | Leave a comment
USC researcher identifies stem cells in tendons that regenerate tissue in animal model
Finding promise new treatments for tendon injury and disease
Los Angeles, Sept. 7, 2007—Athletes know that damage to a tendon can signal an end to their professional careers. But a consortium of scientists, led in part by University of Southern California (USC) School of Dentistry researcher Songtao Shi, has identified unique cells within the adult tendon that have stem-cell characteristics—including the ability to proliferate and self-renew. The research team was able to isolate these cells and regenerate tendon-like tissue in the animal model. Their findings hold tremendous promise for the treatment of tendon injuries caused by overuse and trauma.
The results of their research will be published in the October 2007 issue of the journal Nature Medicine and will be available online at http://www.nature.com/nm on Sunday, September 9, 2007.
Tendons, the tough band of specialized tissues that connect bone to muscle, are comprised of strong collagen fibrils that transmit force allowing the body to move. Tendon injuries are a common clinical problem as damaged tendon tissue heals slowly and rarely regains the integrity or strength of a normal, undamaged tendon.
"Clinically, tendon injury is a difficult one to treat, not only for athletes but for patients who suffer from tendinopathy such as tendon rupture or ectopic ossification," Shi says. "This research demonstrates that we can use stem cells to repair tendons. We now know how to collect them from tissue and how to control their formation into tendon cells."
Prior to this research, little existed on the cellular makeup of tendons and their precursors. By looking at tendons at the molecular level, the research team identified a unique cell population—termed tendon stem/progenitor cells (TSPCs) in both mice and adult humans—that when guided by a certain molecular environment, form into tendon cells. The team included leading scientists from the National Institute of Dental and Craniofacial Research at the National Institutes of Health, Johns Hopkins University and the University of Maryland School of Medicine.
Songtao Shi, a researcher for USC's Center for Craniofacial Molecular Biology, a Division within the USC School of Dentistry, has published numerous studies on the role of stem cells in regeneration. He was part of an international research team that successfully generated tooth root and supporting periodontal ligaments to restore tooth function in the animal model. Earlier this year, his research was published in the journal Stem Cells after he and his team discovered that mesenchymal stem cells are capable of regenerating facial bone and skin tissue in the mouse and swine models.
Funding for the study came from the USC School of Dentistry and the National Institutes of Health.
Yanming Bi, Driss Ehirchiou, Tina M Kilts, Colette A Inkson, Mildred C Embree, Wataru Sonoyama, Li Li, Arabella I Leet, Byoung-Moo Seo, Li Zhang, Songtao Shi & Marian F Young. "Identification of tendon stem/progenitor cells and the role of the extracellular matrix in their niche." Nature Medicine, http://www.nature.com/nm
USC's Center for Craniofacial Molecular Biology
USC's Center for Craniofacial Molecular Biology is a research laboratory located on the Health Sciences Campus of the University of Southern California in Los Angeles. Administratively, CCMB is part of the USC School of Dentistry. The laboratory is funded through multiple research grants, including several from the National Institutes of Health, under which research is conducted into development, biochemical and molecular biological aspects of human development, with a special emphasis on craniofacial structures in both health and disease. Current investigations include the molecular etiology of cleft palate, the molecular genetics of tooth development and lung development in the premature infant.
Contact: Angelica Urquijo
urquijo@usc.edu
September 9, 2007 Posted by FMS Global News | Global Health Vision, Global News, Health, News, NIH, Science, Tendons, USC	| 1 Comment
The memories you want to forget are the hardest ones to lose
CHAPEL HILL – Painful, emotional memories that people would most like to forget may be the toughest to leave behind, especially when memories are created through visual cues, according to a new study by the University of North Carolina at Chapel Hill.
"When you're watching the news on television and see footage of wounded soldiers in Iraq or ongoing coverage of national tragedies, it may stick with you more than a newspaper headline," said the study's lead author, Keith Payne, an assistant professor of psychology in the College of Arts and Sciences.
It is adaptive to be able to intentionally forget neutral events such as wrong directions, a friend's outdated phone number or a switched meeting time. Intentional forgetting helps update memory with new information, Payne said.
But Payne and former psychology graduate student Elizabeth Corrigan found that even "mild" emotional events, like getting a bad grade on a test or a negative comment from a coworker, can be hard to forget. Their study, "Emotional constraints on intentional forgetting," appears in the September 2007 print issue of the Journal of Experimental Social Psychology.
When people are trying to intentionally forget information, they need to mentally segregate that information and then block off the information they don't want to retrieve, Payne said.
Emotion undermines both of those steps. "You make a lot of connections between emotional events and other parts of your life, so it might be difficult to isolate them. As far as blocking retrieval of an unwanted event, emotion makes events very salient and therefore highly accessible," Payne said.
Their results contrast with previous studies of emotional events and intentional forgetting, but those studies used emotion-laden words as stimuli, like "death" and "sex." The UNC study took a new approach, asking 218 participants to react to photographs instead of text.
"The word 'murder,' for instance, may or may not make you afraid, but if you see a graphic, violent picture, it may be powerful enough emotionally to change the way you feel," Payne said.
The researchers found that their subjects could not intentionally forget emotional events as easily as mundane ones. They also found that both pleasant and unpleasant emotional memories were resistant to intentional forgetting.
The UNC findings contribute to understanding the ways that emotion constrains mental control and to the question of whether intentional forgetting can be helpful in coping with painful or traumatic experiences.
"Our findings add to accumulating evidence that emotion places limits on the ability to control the contents of the mind," Payne said. "Our results suggest that even a relatively mild emotional reaction can undermine intentional forgetting. But this doesn't necessarily mean that emotional memories can never be intentionally forgotten. If the motivation to forget is powerful enough, individuals might be able to overcome the effects of emotion by enlisting additional coping strategies."
A different study would be needed to examine what treatment and coping strategies might be effective in helping people voluntarily forget an unwanted memory, he added.
Web site: The study can be found online at http://www.sciencedirect.com.
Note: Payne can be reached on his cell phone (919) 951-9177 or by email payne@unc.edu. He will be in San Francisco at the American Psychological Association convention until Sunday, Aug. 19 but will be taking calls and checking email. After Aug. 19, Payne can be reached at (919) 962-2055 or by email.
College of Arts and Sciences contact: Kim Spurr, (919) 962-4093, spurrk@email.unc.edu
News Services contact: Clinton Colmenares, (919) 843-1991, clinton_colmenares@unc.edu
Contact: Clinton Colmenares
clinton_colmenares@unc.edu
August 15, 2007 Posted by FMS Global News | Global Health Vision, Global News, Journal of Experimental Social Psychology, Medical Journals, News Canada, News US, News USA, NIH, University of North Carolina	| Leave a comment
Multicenter study nets new lung tumor-suppressor gene
BOSTON–Collaborating scientists in Boston and North Carolina have found that a particular gene can block key steps of the lung cancer process in mice. The researchers report in the journal Nature that LKB1 is not only a "tumor-suppressor" gene for non-small cell lung cancer in mice, it also may be more powerful than other, better-known suppressors. The study will be published on the journal's Web site on Aug. 5 and later in a print version.
If further research shows LKB1 has a similar effect in human lung cells, it could influence the way non-small cell lung cancer is diagnosed and treated, says the study's senior author, Kwok-Kin Wong, MD, PhD, of Dana-Farber, one of three institutions, along with Massachusetts General Hospital and the University of North Carolina School of Medicine, leading the work. If tumors with LKB1 mutations are found to be especially fast-growing, for example, patients with such tumors might be candidates for more aggressive therapy.
People born with defective versions of LKB1 often develop Peutz-Jeghers syndrome, which is marked by intestinal growths and an increased risk for certain cancers. Non-inherited mutations of the gene have been found in some lung cancers. This suggested that LKB1 normally thwarts tumors from forming. Mutated versions may be unable to act as a brake on cancer.
To find out, the investigators ran a series of experiments in mice with a defective form of a gene called Kras, which drives the formation and growth of lung cancer. They tracked the development of lung cancer in animals with mutated LKB1 and compared it to the experience of animals with abnormalities in either of two well-known tumor-suppressor genes.
They found that while Kras "cooperated" with the mutated tumor-suppressor genes to produce lung cancer, it cooperated even more strongly with mutated LKB1. "The LKB1-deficient tumors grew more rapidly and spread more frequently than the others, and comprised all three types of non-small cell lung cancer — squamous cell carcinoma, large-cell carcinoma, and adenocarcinoma — rather than just one or two," Wong says. "This suggests that LKB1 plays a role at major stages of the tumors' development: initiation, differentiation of normal lung cells into cancer cells, and metastasis."
An examination of human non-small-cell lung tissue suggests LKB1 mutations play a role there as well. Of 144 samples analyzed, 34 percent of the lung adenocarcinomas and 19 percent of the squamous cell carcinomas contained abnormal versions of the gene, researchers report.
"We were surprised at how significant a role LKB1 mutations play in non-small cell lung cancer development in mice," say Wong, who is also an assistant professor of medicine at Harvard Medical School. "This suggests there may be additional lung tumor-suppressor genes yet to be discovered. We're currently examining whether these results apply to human lung cancers as well and, if so, how such information can improve treatment."
The lead author of the study was Hongbin Ji, PhD, of Dana-Farber. Other Dana-Farber co-authors include Dongpo Cai, PhD, Liang Chen, PhD, Pasi Janne, MD, PhD, Bruce Johnson, MD, Jussi Koivunen, MD, PhD, Danan Li, Mei-Chih Liang, PhD, Kate McNamara, Matthew Meyerson, MD, PhD, Samanthi Perera, PhD, Geoffrey Shapiro, MD, PhD, and Takeshi Shimamura, PhD. Other authors were based at Children's Hospital Boston, Brigham and Women's Hospital, Broad Institute of Harvard University and Massachusetts Institute of Technology, University of Tennessee Health Science Center, and the University of Texas Southwestern Medical Center.
The research was supported by the National Institutes of Health, the Sidney Kimmel Foundation for Cancer Research, the American Federation of Aging, the Joan Scarangello Foundation to Conquer Lung Cancer, the Flight Attendant Medical Research Institute, the Waxman Foundation, the Harvard Stem Cell Institute, and the Linda Verville Foundation.
Dana-Farber Cancer Institute (www.dana-farber.org) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.
Contact: Bill Schaller
william_schaller@dfci.harvard.edu
August 5, 2007 Posted by FMS Global News | Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Cancer, Cancer Biology, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Human Genome, LKB1, Lung Cancer, Medical History, Medical Journals, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Peutz-Jeghers syndrome, University of North Carolina, World News	| 2 Comments
Flip of genetic switch causes cancers in mice to self-destruct, Stanford researchers find
STANFORD, Calif. – Killing cancerous tumors isn't easy, as anyone who has suffered through chemotherapy can attest. But a new study in mice shows that switching off a single malfunctioning gene can halt the limitless division of tumor cells and turn them back to the path of their own planned obsolescence.
The surprising possibility that a cell's own natural mechanism for ensuring its mortality could be used to vanquish tumors opens the door to a new approach to developing drugs to treat cancer patients, according to Dean Felsher, MD, PhD, associate professor of medicine (oncology) and of pathology at the Stanford University School of Medicine. Felsher is the senior author of the study to be published July 30 in the advance online version of the Proceedings of the National Academy of Sciences.
"Our research implies that by shutting off a critical cancer gene, tumor cells can realize that they are broken and restore this physiologic fail-safe program," said Felsher.
Cancer can be notoriously resistant to medical treatment. Not only do cancer cells proliferate uncontrollably, they somehow circumvent the mechanism that causes normal cells to die when they get old or malfunction. That makes cancer cells effectively immortal unless doctors manage to squelch them.
The gene Felsher's team studied produces a protein called Myc (pronounced "mick"), which promotes cell division. A mutation of the gene causes cells to overproduce the protein, prompting perpetual cell division and tumor growth. By turning off the mutated gene, the researchers found that not only did uncontrolled cell division cease, but the cells also reactivated a normal physiological mechanism, called senescence, which makes it possible for a cell to eventually die.
"What was unexpected was just the fact that cancer cells had retained the ability to undergo senescence at all," said Felsher. Cancer researchers had long thought the senescence process had to be irreversibly disrupted for a tumor to develop.
The researchers worked with a series of mice engineered to have Myc-triggered cancers of either the liver, blood or bones, along with a specially constructed version of the Myc gene that they could switch off by feeding the mice antibiotics. When the mice dined on doses of the drugs, invariably, the tumors ceased growing and then diminished, with some disappearing over the course of just a few days.
Although Felsher's lab had previously shown that mouse tumors diminished and disappeared when Myc was switched off, they hadn't been sure how the process actually worked. Historically, most research involving genetic methods of battling cancer cells has focused on reactivating genes called tumor-suppressor genes, which are generally overcome by a proliferating cancer. No one had explored the idea that senescence might play a key role in diminishing tumors.
Felsher described senescence as acting like a fail-safe mechanism to stop cancer. When a cell detects a deleterious mutation, it launches the senescence process, resulting in the permanent loss of the cell's ability to proliferate, thus halting any cancer.
"In order to become tumor cells, those cells have to overcome senescence," said Chi-Hwa Wu, PhD, postdoctoral researcher in Felsher's lab and first author of the study. Wu had the inspiration to explore whether the sudden diminishment they had observed in the tumors might be due to the reactivation of some latent remnant of the trigger for senescence.
Through a series of experiments looking at enzymes associated with the senescence process, as well as some molecular markers, Wu confirmed her suspicion. And not only was senescence occurring in cells that had been thought to be incapable of it, the process was reactivated in all the different tumors they studied.
Consider it a cell version of the Jekyll-and-Hyde transformation. "It's sort of like Mr. Hyde realizing that there's something wrong with him and then being able to put himself back into his normal state as Dr. Jekyll," Felsher said.
In addition to the deepened understanding of how the process of senescence works, Felsher and Wu see a lot of potential for new approaches to treating cancer, beyond the traditional tactic of trying to kill cancer cells directly. "This work implies that maybe part of the strategy should involve figuring out how to get the cancer cells to just be allowed to do what they originally wanted to do anyway, which is to not be proliferating endlessly and growing uncontrolled," said Felsher.
The next step for the team is to see how well the approach works in human cancer cells. "And we're also trying to figure out what the mechanism is," Felsher said. "What are the molecular mechanisms of this, so that we can figure out how to better treat cancer""
Other authors on the research paper are Jan van Riggelen, PhD, postdoctoral researcher; Alper Yetil, graduate student in cancer biology; Alice Fan, MD, instructor in medicine (oncology), and medical student Pavan Bachireddy.
The study was funded by the National Cancer Institute, the National Institutes of Health, the Leukemia and Lymphoma Society, the Burroughs Wellcome Fund, the Damon Runyon Lilly Clinical Investigator Award, the Lymphoma Research Foundation and the Howard Hughes Medical Institute.
Stanford University Medical Center integrates research, medical education and patient care at its three institutions – Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children's Hospital at Stanford. For more information, please visit the Web site of the medical center's Office of Communication & Public Affairs at http://mednews.stanford.edu.
Contact: Lou Bergeron
louisb3@stanford.edu
Stanford University Medical Center
July 31, 2007 Posted by FMS Global News | acute lymphoblastic leukemia, Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Cancer, Cancer Biology, Cancer Biology and Therapy, Childhood Lukemia, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Howard Hughes Medical Institute, Human Genome, Italy, Japan, Leukemia, Medical Journals, Molecular Biology, National Cancer Institute, National Institutes of Health, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, non-Hodgkin's lymphoma, Nova Scotia, Nunavut, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Toronto, UK, US, Virginia, Washington DC, Washington DC City Feed, Wellcome Trust, World News	| Leave a comment
New studies on goat milk show it is more beneficial to health than cow milk
-It helps to prevent diseases such as anaemia and bone demineralisation
-UGR researchers have carried out a comparative study on the properties of goat milk compared to those of cow milk. Rats with induced nutritional ferropenic anaemia have been used in the study
-Goat milk helps digestive and metabolic utilisation of minerals such as iron, calcium, phosphorus and magnesium
-Part of the results of this research have been published in the prestigious scientific journals International Dairy Journal and Journal Dairy Science
C@MPUS DIGITAL Research carried out at the Department of Physiology of the University of Granada has revealed that goat milk has more beneficial properties to health than cow milk. Among these properties it helps to prevent ferropenic anaemia (iron deficiency) and bone demineralisation (softening of the bones).
This project, conducted by Doctor Javier Díaz Castro and directed by professors Margarita Sánchez Campos, Mª Inmaculada López Aliaga and Mª José Muñoz Alférez, focuses on the comparison between the nutritional properties of goat milk and cow milk, both with normal calcium content and calcium enriched, against the bioavailability of iron, calcium, phosphorus and magnesium. To carry out this study, the metabolic balance technique has been used both in rats with experimentally induced nutritional ferropenic anaemia and in a control group of rats.
In order to know how the nutritive utilisation of these minerals may affect their metabolic distribution and destination, the UGR researcher has determined the concentration of these minerals in the different organs involved in their homeostatic regulation and different haematological parameters in relation to the metabolism of the minerals.
Better results with goat milk
Results obtained in the study reveal that ferropenic anaemia and bone demineralisation caused by this pathology have a better recovery with goat milk. Due to the higher bioavailability of iron, calcium, phosphorus and magnesium, the restoration of altered haematological parameters and the better levels of parathyroid hormone (PTH), a hormone that regulates the calcium balance in the organism was found in the rats that consumed this food.
Javier Díaz Castro points out that the inclusion of goat milk with normal or double calcium content in the diet "favours digestive and metabolic utilisation of iron, calcium and phosphorus and their deposit in target organs – parts of the organism to which these minerals are preferably sent – involved in their homeostatic regulation".
According to this researcher, all these conclusions reveal that regular consumption of goat milk – a natural food with highly beneficial nutritional characteristics – "has positive effects on mineral metabolism, recovery from ferropenic anaemia and bone mineralisation in rats. In addition, and unlike observations in cow milk, its calcium enrichment does not interfere in the bioavailability of the minerals studied".
Although there is no doubt that these findings may be a base for further in depth study of the multiple health benefits of goat milk, the UGR researcher warns that "studies in humans are still required in order to confirm the findings obtained in rats and to promote goat milk consumption both in the general population and in the population affected by nutritional ferropenic anaemia and pathologies related to bone demineralisation". Part of the results of this research has been published in the prestigious scientific journals International Dairy Journal and Journal Dairy Science.
Reference: Dr Javier Díaz Castro. Department of Physiology of the University of Granada.
Tel.: +34 958248319. Mobile: +34 654574434. Email: javierdc@ugr.es
July 30, 2007 Posted by FMS Global News | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Bone Demineralisation, Bone Diseases, Calgary, Canada, France, Germany, Global, Global Health Vision, Global News, Italy, Japan, Medical History, Medical Journals, Molecular Biology, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Nova Scotia, Nunavut, Nutritional Anthropology, Ottawa, Pennsylvania, Prince Edward Island, Quebec, Research, RSS, RSS Feed, Slovakia, Toronto, UK, University of Granada, US, Virginia, Vitamin D, Washington DC, Washington DC City Feed, World News	| Leave a comment
Research links genetic mutations to lupus
WINSTON-SALEM, N.C. – A gene discovered by scientists at Wake Forest University School of Medicine has been linked to lupus and related autoimmune diseases. The finding, reported in the current issue of Nature Genetics, is the latest in a series of revelations that shed new light on what goes wrong in human cells to cause the diseases.
"This research is a huge leap toward understanding the cause of lupus and related autoimmune diseases," said Fred Perrino, Ph.D., a co-author on the paper and a professor of biochemistry at Wake Forest. "There had been few clues before now."
Perrino, who discovered the gene in 1998, said he suspected it was involved in human disease, but it took a group of researchers from around the world collaborating to put the puzzle together.
"We've known that lupus was a complex disease, but now we have a specific protein and a particular cellular process that appears to be one of the causes," said Perrino. "We're connecting the dots to understand the biology of what's going on with the disease."
In Nature Genetics, lead author Min Ae Lee-Kirsch, M.D., from the Technische Universität Dresden in Dresden, Germany, and colleagues report finding variations of the TREX1 gene discovered by Perrino in patients with systemic lupus erythematosus. The study involved 417 lupus patients from the United Kingdom and Germany. Mutations were found in nine patients with lupus and were absent in 1,712 people without lupus.
"Our data identify a stronger risk for developing lupus in patients that carry variants of the gene," said Lee-Kirsch.
In recent years, the gene was also linked to Aicardi-Goutieres syndrome, a rare neurological disease that causes death in infants, and to chilblain lupus, an inherited disease associated with painful bluish-red skin lesions that occur during cold weather and usually improve in summer. The current research also links it to Sjogren's syndrome, a form of lupus.
The diseases are all autoimmuine diseases, which means that the body makes antibodies against itself. In lupus, these antibodies cause pain and inflammation in various parts of the body, including the skin, joints, heart, lungs, blood, kidneys and brain. The disease is characterized by pain, heat, redness, swelling and loss of function.
Perrino began studying the protein made by the gene more than 14 years ago.
"We basically cracked open cells to locate the protein and find the gene," said Perrino. "In the 14 years since, we've learned a lot about the protein and how it functions."
The gene manufactures a protein, also known as TREX1, whose function is to "disassemble" or "unravel" DNA, the strand of genetic material that controls processes within cells. The "unraveling" occurs during the natural process of cells dying and being replaced by new cells. If a cell's DNA isn't degraded or unraveled during cell death, the body develops antibodies against it.
"If the TREX1 protein isn't working to disassemble the DNA, you make antibodies to your own DNA and can end up with a disease like lupus," said Perrino.
Perrino and colleagues at Wake Forest have been studying the gene and its protein since 1993. Thomas Hollis, Ph.D., an assistant professor of biochemistry at Wake Forest, is credited with solving the structure of both TREX1 and a similar protein, TREX2. Perrino has also developed a way to measure the function of the proteins.
In a study reported in April in the Journal of Biological Chemistry, Hollis and Perrino found that three variations of the gene reduced the activity of the protein by four- to 35,000-fold.
"Now that we have the structure, we can understand how it disassembles DNA and how mutations in the gene may affect that process," said Hollis.
The researchers hope that understanding more about the gene's mutations and the structure of the protein may lead to drug treatments to help ensure that mutant copies of the gene are inactive.
Media Contacts: Karen Richardson, krchrdsn@wfubmc.edu; Shannon Koontz, shkoontz@wfubmc.edu; at 336-716-4587.
Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university's School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in primary care and 44th in research among the nation's medical schools. It ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.
Contact: Karen Richardson
krchrdsn@wfubmc.edu
Fibromyalgia Support
July 29, 2007 Posted by FMS Global News | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Clinical Trials, France, Genes, Genetic, Genetic Link, Genetic Marker C allele of rs10505477, Genetics, Genome, Genomic, Global, Global Health Vision, Global News, Health Canada, Human Genome, Italy, Japan, Lupus, Nature Genetics, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Nova Scotia, Nunavut, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, US, Virginia, Wake Forest University Baptist Medical Center, WASHINGTON, Washington DC, Washington DC City Feed, World Health Organisation, World News	| 1 Comment
One man's junk may be a genomic treasure
Scientists have only recently begun to speculate that what's referred to as "junk" DNA – the 96 percent of the human genome that doesn't encode for proteins and previously seemed to have no useful purpose – is present in the genome for an important reason. But it wasn't clear what the reason was. Now, researchers at the University of California, San Diego (UCSD) School of Medicine have discovered one important function of so-called junk DNA.
Genes, which make up about four percent of the genome, encode for proteins, "the building blocks of life." An international collaboration of scientists led by Michael G. Rosenfeld, M.D., Howard Hughes Medical Investigator and UCSD professor of medicine, found that some of the remaining 96 percent of genomic material might be important in the formation of boundaries that help properly organize these building blocks. Their work will be published in the July 13 issue of the journal Science.
"Some of the 'junk' DNA might be considered 'punctuation marks' – commas and periods that help make sense of the coding portion of the genome," said first author Victoria Lunyak, Ph.D., assistant research scientist at UCSD.
In mice, as in humans, only about 4 percent of the genome encodes for protein function; the remainder, or "junk" DNA, represents repetitive and non-coding sequences. The research team studied a repeated genomic sequence called SINE B2, which is located on the growth hormone gene locus, the gene related to the aging process and longevity. The scientists were surprised to find that SINE B2 sequence is critical to formation of the functional domain boundaries for this locus.
Functional domains are stretches of DNA within the genome that contain all the regulatory signals and other information necessary to activate or repress a particular gene. Each domain is an entity unto itself that is defined, or bracketed, by a boundary, much as words in a sentence are bracketed by punctuation marks. The researchers' data suggest that repeated genomic sequences might be a widely used strategy used in mammals to organize functional domains.
"Without boundary elements, the coding portion of the genome is like a long, run-on sequence of words without punctuation," said Rosenfeld.
Decoding the information written in "junk" DNA could open new areas of medical research, particularly in the area of gene therapy. Scientists may find that transferring encoding genes into a patient, without also transferring the surrounding genomic sequences which give structure or meaning to these genes, would render gene therapy ineffective.
Contributors to the paper include Lluis Montoliu, Rosa Roy and Angel Garcia-Díaz of the Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología in Madrid, Spain; Christopher K. Glass, M.D., Ph.D., UCSD Department of Cellular and Molecular Medicine; Esperanza Núñez, Gratien G. Prefontaine, Bong-Gun Ju, Kenneth A. Ohgi, Kasey Hutt, Xiaoyan Zhu and Yun Yung, Howard Hughes Medical Institute, Department of Molecular Medicine, UCSD School of Medicine; and Thorsten Cramer, Division of Endocrinology, UCSD Department of Medicine.
The research was funded in part by the Howard Hughes Medical Institute and the National Institutes of Health.
Contact: Debra Kain
ddkain@ucsd.edu
University of California – San Diego
July 13, 2007 Posted by FMS Global News | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Chile, DNA, Genes, Genetic, Genetics, Genome, Genomic, Global, Global Health Vision, Global News, Howard Hughes Medical Institute, Human Genome, Irvine, Italy, Japan, National Institutes of Health, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Nova Scotia, Osaka, Ottawa, Pennsylvania, Prince Edward Island, Proteins, Quebec, Research, Research Australia, RSS, RSS Feed, Slovakia, Spain, Toronto, UCSD, University of California, Virginia, WASHINGTON, Washington DC, Washington DC City Feed, World News	| Leave a comment
Place of death shifting for children with complex chronic conditions
Contact: Rachel Salis-Silverman
JAMA and Archives Journals
It is becoming more common for children with complex chronic conditions to die in their home than in a hospital, although black and Hispanic children with these conditions are less likely to die in their home, according to a study in the June 27 issue of JAMA, a theme issue on chronic diseases of children.
Chris Feudtner, M.D., Ph.D., M.P.H., of Children's Hospital of Philadelphia, presented the findings of the study at a JAMA media briefing in New York.
Many pediatric palliative care clinicians suggest that the preferred place of death, by the family, of an infant, child, or adolescent with a medically complex chronic condition is the home. Advances in home-based medical technology and changes in attitudes about pediatric palliative care and hospice services may be making this a more viable option, according to background information in the article.
Dr. Feudtner and colleagues conducted a study to determine if the proportion of complex chronic condition-related deaths occurring at home among children and adolescents increased between 1989 and 2003, and to assess if there were any race and ethnicity disparities in the location of death. The researchers analyzed data from the National Center for Health Statistics' Multiple Cause of Death Files.
Among the 22.1 percent of deaths (198,160 of 896,509 total deaths) attributed to a complex chronic condition between 1989 and 2003, the percentage of deaths occurring at home increased significantly for all age groups (overall, from 10.1 percent in 1989 to 18.2 percent in 2003), but with larger increases for deaths beyond infancy. The odds of death occurring at home increased by 3.8 percent annually.
The percentage of individuals dying at home increased significantly over time for infants (4.9 percent home deaths in 1989 to 7.3 percent in 2003); 1 to 9-year-olds (17.9 percent to 30.7 percent), and 10 to 19-year-olds (18.4 percent to 32.2 percent). During this same period, there was a significant decline in the percentage of deaths occurring in the hospital for each of these three age categories.
The authors suggest that this gradual change in place of death may be occurring because of advances in medical technology in the home setting and broad shifts in attitudes and decision-making processes regarding palliative and end-of-life care in U.S. culture.
The child's race, ethnicity, and region of home residence were significantly associated with death occurring at home. The odds of dying at home were reduced by 50 percent among black individuals, and reduced by 48 percent among Hispanic individuals, when compared with whites.
Concerning possible reasons for the observed racial and ethnic differences, " … differential access to health care services or medical technology, divergent cultural attitudes or approaches to palliative and end-of-life care decision making, or differing levels of financial or other support within the patient's or family's social network may make dying at home more or less likely."
"… as efforts to improve understanding of the sources and remedies of racial and ethnic disparities in pediatric end-of-life care are completed, medical and other concerned professionals need to ensure that all patients have access to necessary care and that all dialogue and interactions regarding decisions about care—whether curative, life-extending, or palliative—are built on mutual understanding, trust, and respect," the authors conclude.
(JAMA. 2007;297:2725-2732. Available pre-embargo to the media at http://www.jamamedia.org)
Editor's Note: The conduct of this study was supported in part by grants from the Agency for Healthcare Research and Quality and the National Institute of Nursing Research of the National Institutes of Health. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, etc.
For More Information: Contact the JAMA/Archives Media Relations Department at 312-464-JAMA or email: mediarelations@jama-archives.org.
June 27, 2007 Posted by FMS Global News | Alberta, Baltimore, Bethesda, Calgary, Cancer, Chronic, Chronic Multisymptom Illnesses, Complex Chronic Conditions, End Of Life Care, Global, Global Health Vision, Global News, JAMA, Medical Journals, News, News Australia, News Canada, News Israel, News Jerusalem, News UK, News US, NIH, Palliative Care, Pediatric Palliative Care, Research, Virginia, WASHINGTON, Washington DC, World News	| Leave a comment


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Speak Schmeak: Are you willing to have your beliefs challenged?
Are you willing to have your beliefs challenged?
This past weekend I attended the World Tea Expo to present a workshop on business networking. Also, to drink a ton of tea. This was my fifth or sixth time attending the conference and my second time speaking; what better way to combine two of my favorite things!
One of the sessions I attended was presented by Kevin Gascoyne, professional tea taster and owner of of Camellia Sinensis, a tea company in Canada. His presentation was called "A Step Toward Caffeine and Antioxidant Clarity." I was intrigued by this topic because there is an overabundance of information about the caffeine and antioxidant contents of various teas, and it's confusing and inconsistent.
Kevin (whose slides I hope to be showing you soon) quickly cleared up one mystery about caffeine testing in tea: Caffeine and antioxidant levels are not tested in tea that's prepared the way people actually drink it.
When people prepare tea for drinking (in case you're not a tea drinker), they first boil water, then depending on the kind of tea (white, green, oolong, black or puerh), infuse a tea bag or loose tea leaves in the water -- either immediately or after it's cooled a bit. Tea is steeped anywhere from a few seconds to five minutes, and then consumed. Many factors, in addition to the kind of tea, play into how a particular tea is steeped, including the kind of pot one is using, the amount of tea, the amount of water, the temperature of the water, and more.
To test caffeine, tea is ground up, mixed with distilled water (which one would never use for steeping as it renders tea flavorless) or other liquid, and possibly chemical compounds, and components are separated through liquid chromatography (the common denominator in both traditional research and Kevin's tests). Right there, you can see the problem. The caffeine content of tea processed in this way has nothing to do with the caffeine content of leaves prepared for drinking.
Kevin decided to hire a lab to test caffeine levels in teas prepared in the same way as we drink them, using common pots, regular water, typical steeping times and typical ratios of tea to water. He chose a couple dozen teas from his company to test.
Here's what we've all been told up till now about the caffeine content of tea: The amount of caffeine in tea is a direct result of how it's processed and its level of oxidation. This means that, in general, caffeine levels are expected to be highest in black teas, then diminish in order of oxidation levels: oolong, green, white. Puerh falls somewhere in the middle (puerh is a black tea that's been fermented after processing).
Kevin showed us that this "conventional wisdom" is FALSE. His results chart showed a white tea in the eighth position after several black and green teas. There were green and white teas all up and down the list, and black teas near the bottom. There was no discernible pattern. In fact, one first flush darjeeling was at the top of the chart, while an autumn flush darjeeling from a different area of the same tea garden was near the bottom. There was a sencha (green) high on the list and a sencha low on the list.
The purpose of this post is not to go into detail about why these teas had differing levels of caffeine (similar results were shown on the antioxidant test chart), but to point out that, for once, a speaker challenged conventional wisdom!
How many times have I heard the tired old statistic that people fear public speaking more than death -- even though there is no recent study to prove this? But speakers and writers continue to blather on about this as though there were substantial evidence to support it. Certainly, many people fear public speaking, and as social anxiety goes, it's right there at the top. But more than death? No.
In this case, Kevin took matters into his own hands, and paid for the research himself. The results were particularly eye-opening for him; he confessed to having steered customers who were caffeine-sensitive toward white tea, for example, because of the common belief that it was low in caffeine. In fact, I had gotten into a friendly argument with a fellow attendee the night before who insisted that her company's white teas had very little caffeine. But had she tested them? No.
By sponsoring this research, Kevin was willing to have his own long-standing beliefs challenged. And they were. And thanks to him (and his book where the research is published TEA: History,Terroirs, Varieties), we have all had our eyes opened.
As a result of this research, Kevin suggested that "the act of drinking tea must be appreciated for its own sake," regardless of caffeine and antioxidant quantities and that, if we're caffeine-sensitive, we stick with herbal tisanes. Sounds right to me!
If you're a speaker or writer, do you repeat the same statistics you've heard over and over, without looking into their validity? Do you continue to repeat statistics even when you can't find any proof? It's easy to play on the emotions of your audiences, and boy do we love a shocking statistic. But when your statistics can't be backed up (and these days, your audience can Google your stats while you're stating them), you are the one who ends up losing credibility.
Thank you, Kevin Gascoyne, for being willing to challenge conventional wisdom in this area. I was surprised that the session wasn't standing-room-only, but perhaps some attendees didn't want to have their worlds shaken and their beliefs tested. It's much easier to stick with the tried and true than re-educate yourself, your staff, your clients, your customers and your audiences.


Celebrity Jersey Cards is a regular series in which I create virtual trading cards for celebrities wearing sports jerseys. Today, we continue our alphabetical journey through all Major League Baseball teams.
Eric Stonestreet might be best known for his role on tv's Modern Family. A native of Kansas City, KS, Stonestreet attended Kansas State University and is a huge fan of Kansas City sports teams. He even wore the powder blues when he made an appearance on Jimmy Kimmel's show to earn his Celebrity Jersey Card.
Born in Connecticut, James Van Der Beek rose to fame as an actor, most notably on tv's Dawson's Creek. Van Der Beek participates in a lot of charitable events, including many baseball-related ones. He's not afraid of getting dirty while playing either, as seen on his Celebrity Jersey Card.


Crafted with the same precision and attention to detail as you would expect to find in one of the worlds most renowned luxury sports cars. Lines as sleek and elegant as you would expect from the Italian designers of Lamborghini automobiles. The Lamborghini Precisione Cigar Cutters feature a patented, spring-loaded, horizontal double blade made from surgical steel. The Precisione Cigar Cutter cuts cigars up to 58 ring gauge and has a scratch-resistant lacquer.


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Home » Wine Center » Red Wine » Geoff Merrill - Merlot "Wickham Park" - Mc Laren Vale - Australia
Geoff Merrill - Merlot "Wickham Park" - Mc Laren Vale - Australia
Australia, McLaren Vale
Celebration, Birthday, Business, Dinner With Family/Friends/Colleagues, Get Together, Gifting, Home, Home Party, Wedding
Geoff Merrill
James Halliday (JH) Australian Wine Companion 88/100
Wine Enthusiast Award 88/100
Wine Spectator Award 90/100
Deep brick red with garnet hues. Full of fruit cake, some musk, earth, cinnamon and meaty notes. The palate displays an exciting array of flavours including tart cherry, coffee, dark chocolate and rhubarb which is really showing the complexity that comes with maturation. The tannins are fine and firm & the acidity perfectly balanced to provide structure and length.
Best enjoyed between 15° & 18°
Beijing Hot Pot, Cantonese Rice Noodles With Beef, Taiwanese Beef Noodle Soup
Cold Cuts, Veal Parmigiana, Hamburger
Australia's winemaking regions are huddled into one or two pockets of the country. The state of South Australia, which produces about 60% of the country's wine, also has the most wineries and sub-regions, including McLaren Vale, Clare Valley, Coonawarra and Barossa Valley. New South Wales is home to the Hunter Valley, while the smaller, southern state of Victoria is best known for theYarra Valley. Head way west to the very large state of Western Australia and you'll find the tiny region of Margaret River at the southern tip. Vine cuttings from South Africa were first brought in Australia in 1788, and though the settlers took a while to get to grips with the new conditions, wine exports began in 1822. By the 1880s, Australian wines were winning prizes in Europe, but then phylloxera struck, and the industry subsided into producing fortified wines for the domestic market. Then the interest in table wines came back and culminated in 2000 when Australia sold more wine to the United Kingdom than did France. While early Australian wines, the Chardonnays in particular, were criticized for being over-oaked and over-ripe, Australian winemaking is now some of the most sophisticated in the world, with vineyards increasingly planted in cooler climates, such as Pinot Noir in Tasmania, and un-oaked wines becoming popular.
MCLAREN VALE - The McLaren Vale wine region is located approximately 35 km South of Adelaide in South Australia. The region was named after either David McLaren, the Colonial Manager of the South Australia Company or John McLaren who surveyed the area in 1839.
Although initially the region's main economic activity was the growing of cereal crops, John Reynell and Thomas Hardy planted grape vines in 1838 and the present-day Seaview and Hardy wineries were in operation as early as 1850.
Famous for producing some of the best Shiraz Australia has to offer, McLaren Vale is arguably one of the premier Shiraz-growing regions of the world. Shiraz is by far the most important variety for the region, accounting for about 50% of the total crush. The area's thin soils, limited water, and warm summers harness Shiraz's natural vigor and produce intense flavored fruit, and wine with a deep purple color that can last decades in the bottle.
McLaren Vale wines are distinguished by their ripeness, elegance, structure, power and complexity. McLaren Vale has 3,218 hectares of Shiraz under vine. Other major varieties include Cabernet Sauvignon with 1,288 ha planted, Chardonnay with 722 ha planted and Grenache with 402 ha- much of this dry-grown (non-irrigated) bush vines.
Geoff Merrill - Australia
In 1980, Geoff Merrill and business partner Trevor Stratton established Stratmer Vineyards, parent company of Geoff Merrill, Owens Estate and Mount Hurtle Wines. In the early years, Geoff Merrill wines were crafted at various locations across the South Australian wine regions, including Chateau Reynella and Pirramimma in McLaren Vale, and Peter Lehmann Wines in the Barossa Valley. A modern processing plant was established at McLaren Flat in 1984 in a joint venture with fellow winemaker, Goe DiFabio, which centralised the production of Geoff Merrill wines and allowed greater control over the winemaking process.
Trevor Stratton eventually sold his share of Stratmer Vineyards in 1992 to Alister Purbrick of Chateau Tahbilk, who remained a 50% partner until 2005. Geoff is now the sole owner of the company and continues to develop and produce exceptional wines.
GEOFF MERRILL, THE MAN
Young Geoff Merrill was raised on a sheep station in the far north of South Australia, until his family moved to the Barossa Valley in 1964 when Geoff was just 11 years old. Unsurprisingly, this is where Geoff's links with the wine industry were first forged.
At age 17, Geoff joined B Seppelt & Son where he embarked on a 4 year winemaking traineeship. Following this, he was lured to South Africa in 1974 with the opportunity to work as an Experimental Winemaker with Stellenbosch Farmers Winery, after which he set off to explore Europe.
Returning to Australia in late 1975, Geoff joined Chateau Reynella as Assistant Winemaker and was promoted to Senior Winemaker just 2 years later. He held this position until 1985 when he became a Consultant Winemaker for Thomas Hardy & Sons, who bought Chateau Reynella in 1982.
While working at Chateau Reynella, Geoff began to make wines under his own "Geoff Merrill" label; his first release in 1983 included a 1980 Cabernet and 1981 Semillon. With a view to establishing his own operation, Geoff purchased the beautiful, but run-down Mount Hurtle Winery in 1985 and, after restoring the property to its full potential, Geoff left Hardy's in 1988 to embark on his own venture.
Geoff's signature style eventually took his winemaking career to the international stage when, in 1993, he accepted a Consultant Winemaker position in Italy for UK supermarket Sainsbury, and Gruppo Italian Vini in Italy. Geoff continues to gain national and international recognition for his distinctive style of winemaking and zest for life.
Geoff Merrill Wines has vineyards in two of Australia's classic viticultural regions: "Pimpala Vineyard" and "Wickham Downs" in McLaren Vale, and "Graymoor" in the Coonawarra. Individual growing conditions at each site provide an exciting opportunity to highlight the very best of what each region has to offer by skilfully blending single varietals such as McLaren Vale Shiraz and Coonawarra Cabernet for a superb result.
Chateau Le Puy - Duc Des Nauves - AOC Cotes de Bordeaux
France, Bordeaux, AOC Cotes de Bourg
Cab. Sauvignon, Cabernet Franc, Merlot
Chateau Le Puy
Frontera - Merlot by Concha y Toro Vineyards
Chile, Central Valley
Domaine Pacalet - Pernand-Vergelesses "Les Belles Filles"
France, Burgundy, AOC Pernand Vergelesses
P. Pacalet
Mid-Autumn Gift Set- Loudenne Le Chateau - Cru Bourgeois - Medoc AOC - Rouge - 2 Bottles & Gift Bag
France, Bordeaux, AOC Medoc
Cab. Sauvignon, Merlot
Loudenne
Jacqueline Demi-Sec French Sparkling Wine
Colombard, Ugni Blanc

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Sprint offers DirecTV customers free year of…
Sprint offers DirecTV customers free year of phone service
By Anick Jesdanun and The Associated Press |
NEW YORK — Sprint is offering DirecTV customers one free year of cellphone service in a bold move aimed at the satellite TV company"s new owner, AT&T.
AT&T, which bought DirecTV for $48.5 billion in July, has been promoting a bundle that knocks $10 a month off a combined bill for video and wireless phone service. For a single line, the value of Sprint"s promotion is about $50 a month. It"s Sprint"s way of offering DirecTV customers a bundle without actually owning a video company.
Sprint, which is in the midst of a turnaround effort, has been making a range of promotional offers to lure customers. But so far, the Overland Park, Kansas, company hasn"t been as successful as T-Mobile, which went through its own turnaround. In the April-June quarter, Sprint lost 12,000 customers in "postpaid" phone plans, the ones offered to customers with good credit, while T-Mobile gained 760,000. But Sprint says it"s been reducing the size of its quarterly losses in customers and even saw gains in the months of May, June and July.
The offer is good for up to five lines on a single account, with each getting 2 gigabytes of data each month and unlimited calls and texts. It begins Friday and runs through Sept. 30. DirecTV customers must show some proof, like a DirecTV bill from the past 60 days, when signing up. But people can still sign up for DirecTV now to get the Sprint offer.
— Existing Sprint customers must add a new line of service to qualify. And both new and existing customers must buy or lease a new phone through Sprint; they cannot use one they already own.
— Customers must pay a one-time activation fee of $36, plus some monthly taxes and surcharges. Some taxes and surcharges are based on the number of lines rather than the cost of the plan, so customers wouldn"t save anything by paying nothing for service. But similar taxes and surcharges would apply at AT&T.
— The free offer is only good for a year, but phones typically take two years to pay off. For the second year, customers would pay $50 a month for a single line to $180 for five lines. That"s comparable to current rates.
— There"s no option for data beyond 2 gigabytes without paying higher fees for exceeding the cap — 1.5 cents per megabyte, or $15 per gigabyte. And these aren"t shared plans, so overage fees apply even if family members are below the cap. That said, 2 gigabytes is plenty for most people, unless they stream video.
Price should be only one factor in comparing services. Sprint"s network isn"t as extensive as Verizon"s or AT&T"s, particularly in rural areas; free service isn"t good if it won"t work where you need it.
The free service will cost Sprint $600 per line, plus any charges to pay off rivals" contract-termination fees or to finish off payments under monthly installment plans.
Nonetheless, the latest promotion shows how aggressive phone companies have become as they try to lure customers from each other, given that most Americans now have cellphones.
Dallas-based AT&T Inc. has been using the DirecTV service as a way to package wireless access and entertainment. Sprint Corp., which doesn"t have the entertainment component, isn"t willing to cede those customers to AT&T.
"DirecTV customers love their TV service — but they shouldn"t have to settle for AT&T wireless," said Kevin Crull, Sprint"s chief marketing officer.
Vacaville Planning Commission to vote on Alamo mixed-use development
Proceedings advance toward prelim for Vaca man accused of attempted murder
Psychologist believes Corral isn"t faking it
Anick Jesdanun
January 23, Arts and Entertainment Source: Ottmar brings Zen approach to music


Books & other thoughts: How do you keep track of the books you read?
Or (shocking to me as it might be to me) maybe you don't bother keeping track at all?
I had a notebook where I used to write down books that I read, starting back in 1988 (if that was before you were born, gentle reader, there is no need to mention that little fact :-D) . I later found a list I made that dated from 1980 (yes, being retentive starts early I suppose), so I added that, too. But as my notebook filled up, and my list grew longer and longer, I found it more and more difficult to find titles I was trying to locate (especially to see which book I was supposed to read next in a series).
So one day I sat down and transferred everything into a Word document. Now if I want to see all the books I've read by an author, I can just do "edit, find" by the author's name, and it takes me right down the list. It would be kind of fun to make a database out of it, but right now I just don't have the time (although the geek in me is delighted at the prospect). I also have a very complex system I use so I know if the book was a winner: I put a little happy face next to it. Yes, bleeding edge technology, I know - but I can still do a search and see what my favorite books are - which comes in very handy when I don't know what I feel like reading next, because I can bring up favorites and then head over to Amazon to see if the authors have published anything recently.
One unexpected benefit to being a retentive list maker is that, when I look through the list of books I've read, it brings back that time in my life quite forcefully. I remember reading this book while I was stuck in an airport in Denver, that book on the beach in Hawaii, this one when I was nursing my first child, etc. Kind of a cool time portal.
What about you? How do you keep track, if you do at all? If you don't, why not? Have you ever wished you did? Here is an interesting article about someone creating a virtual library through Google's new virtual library service. This service is similar to Library Thing, but includes book searches via Google's Book Search capabilities.
That whole idea is very appealing to me. I've noticed that since I began blogging about the books I read, they remain fresher in my mind, and I think that taking time to really think about them and write a short review about them enhances my reading experience. It makes me read more attentively. I don't know that I have the time right now to invest in taking advantage of putting together a virtual library. But I'd sure like to!
I've done that, especially with mysteries & thrillers.
As I have the books I own catalogued on my local computer, I use Library Thing as a reading list, which I find really useful. It only goes back about 3 years though, to when I started recording my reading on the computer.
However, you've reminded me of those notebooks I have safely stored somewhere of my reading in the '80s. The covers have got tattered and I'm not even sure if I have all of them, but I feel the need to go and find them now and relive that part of my life.
Amazingly, I didn't start keeping track until three or four years ago. After experimenting with different things, I now keep an html text file on my computer for each year, and periodically post it the updated list on my blog. Before I had a blog, I had a word file, but I like the html better.
Hey, Julian - thanks for stopping by! You are right - it is easy to get plots and characters mixed up. The worst is when I pick up a book and get about halfway through, and then I realize I've read it before. Bummer when it's a mystery! I enjoyed visiting your blog, btw - my kids are going to go nuts over that morphing cats thing!
Kerry - good to see you! I hope you can find those notebooks, and I wonder if you'll have the same reaction I did to reading through book lists from the old days. I hope so - it's lots of fun!
And Jen - that is interesting that you keep your list in HTML. Do you put all those picture books you read on it? That's one thing I haven't done, although I'm sort of wishing I did, because it would come in handy at work when I do children's programs at the library. It's something to think about, at any rate.
This is a great post Darla :) I've never kept track of my books before, and learned the hard way that I should! I've always bought my books, so my way of keeping track of what I've read was to put them on the shelf after I read them! Unfortunately, Katrina took the majority of my books, so it's hard for me to recall every book I read. Of course, I recall them when they're brought up or when I see a copy and there are those books that I'll never forget or that have already been replaced, but I sure do wish I would've kept a written account of them.
Now, I blog about my books, so I do indeed have a written account of them, and even have a separate blog dedicated just to books read. And a LibraryThing...I think I may start a notebook too just to have a hard copy!
I've been keeping a reading journal for several years now--it's basically a Word document where I jot down my thoughts about a particular book I've read. I also keep a table of contents that is basically a quick glance at my reading during any given year. My table of contents is basically an Excel document. I call if a table of contents because it's the basic information regarding the books I journaled about for the year.
I tried merging my table of contents lists once, but it got to be too much for me. I do catolog all of my books on Library Thing, something I just started doing this past December.
My grandpa suggested keeping track about five years ago and I'm so glad he did, because you really do start to forget titles or authors and sometimes I only remember the story, but when I look at the list it all comes back to me.
I write it down, pen and paper, the old fashion way.
I have not one but several spreadsheets that I use to keep track of things.
One is a list of what I have read this year and includes analysis of publishers, settings, genre etc.
Another is just a list of all the books I have read and bought (but not yet read), another lists all the books I want to read, another all the books I have out from the library and when they are due back and another yet is which series I am in the middle of reading or waiting for books in!
Of course, then there Library Thing, but I am a bit behind in that one!
Wow, Literary Feline - you sure are organized! I'd long been meaning to put annotations next to the books on my list, but somehow never got around to it. This blog works much better, since I get feedback and other book recommendations, too!
VA Gal - does your grandfather write down his books, too? I bet that would be an interesting list to look at!
Marg - It is amazing that you manage to keep track of all that! I also have a list of books I want to read. I started that one on the computer, and now I'm embarrassed when I see how very long it is. A few years ago I had the depressing realization that I could probably never get to them all in my lifetime - not to mention all the books to be published that I'll end up putting on there, too!
And Heather - maybe your blogs are your lists? One look there, and you can see the tons of books you've read!
I have also noticed that the books stay fresh for me once I started blogging about them.
I have kept lists at different points in my life about what I'm reading but for the past two years I've kept a record on my computer that I've found very useful. True, I have read books before that aren't on the list but it doesn't bother me that badly.
It bothers me when I forget to add a book - inevitably I need to know the author or something, and I know I've read it, but it's not there!
I keep a notebook of books I've read. My records go back to 1978, although I started keeping lists around 1973 - but I lost those because they were on index cards in a little file box. My system for noting whether or not I liked the book is to write beside the title "G" (good), "VG" (very good), "B" (bad), or "VB" (very bad). If I don't write anything, then the book was okay. Some I don't write down at all, if I really hated them, but I need to stop doing that. It's extremely low-tech (and I do love LibraryThing for keeping track of the books I have) but it's a system that has worked well for me for over 30 years, so I feel no need to change it.
Like you, I remember what I was reading when a particular child of mine was born, or when I was dating my soon-to-be-husband, or when I went on a trip with a friend, etc. I loved seeing that you do that, too.
And I agree with you that blogging reviews of books I read has helped me remember what I read better.
My dad was the one who got me started making a list of what I've read. Starting at about age 10, I used to pester him to take me to the library at the university. I'd check out armloads of books, then want to go back for more sooner than he believed I could have read what I had. When I was 12 he told me he wanted me to use index cards to record the title and a brief summary of each book I read, and show it to him. I did that for a couple of years and he finally believed that I was actually reading the books I borrowed from the library. It was good discipline for me. Unfortunately, I stopped the summaries when I was around 14, and didn't start doing it again until I started blogging a little over a year ago.
But I don't blog a review of every book I read. That would seriously cut into my reading time!
Wow, Laura - I love that story about your father having you write the index cards!
I had a similar experience as a child (although it didn't result in anything nearly as productive as your father's suggestion). My beloved children's librarian was absent one day, and a librarian from upstairs (the adult section) was subbing for her. It was summertime, and they had given all the children charts for their books, and we got a star sticker for every one we read. Well, she did not believe that I'd read the huge stack of books I'd brought back (MY librarian would have, though!) and so I just started telling her about each one. I got to the sixth or seventh and she sort of rolled her eyes and said, "All right, all right," and gave me my stickers. It kind of hurt my feelings, but I felt vindicated. I take special care not to ever do that to any of the kids who come into my library with their list of summer books!
Thanks for the insight into your methods. I like your rating scale - much higher tech than my happy face/frownie face one!


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All posts tagged "la cage aux folles"
Home / Posts tagged "la cage aux folles"
On Your Feet! star Mauricio Martínez brings his voice and his truth to APO's Jerry Herman tribute
By André Hereford on May 16, 2019
The actor and Broadway star beat the tabloids at their own game when they tried to out him
Editor's Picks: Unsinkable Molly Brown, La Cage, Toni Braxton, more
By Randy Shulman on January 31, 2019
Our picks of the best arts and entertainment in the D.C. area this week!
Exclusive Photos: La Cage Aux Folles at Signature Theatre
By Doug Rule on June 9, 2016
Signature's La Cage Aux Folles is a spectacle with heart. And a lot of feathers, sequins and mascara.
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Got a busy little person you need to occupy? Try one of these 25 no prep toddler activities, that don't require you to do anything to prep for the activity.
When you have a 2.5-year-old and an 18-month-old, things can get a little cray cray! In the past week, my 18 month old has pulled down two sets of curtains off my wall, shattered my glass top table, broke the glass bottle of Tabasco sauce from the fridge, poured balsamic vinegar all over my kitchen floor, took his diaper off and peed all over the carpet, dumped out the entire (family size!!!) Lucky Charms box all over the couch, I mean I could go on and on! I'm about to lose my freaking mind! He is out of control! This age is so dang hilarious, but man alive am I exhausted.
I have searched the web to find easy, no prep toddler activities! I'm all about quick, easy, and fast. With little to no mess. Which I know you are probably too! Toddlers have an attention span of a fly so I have tried to find the best ones that will keep your toddler busy for longer than 5 minutes!
I have the ABC ones on my fridge and when I get them out they love them. They are also great to learn with. You can find some HERE.
Have your toddler "paint" on colored construction paper. No mess and they love it.
I had plastic cups left over from a party and brought them out for them to stack and build. They had a blast and it can't get easier than that.
Asher's favorite part was to destroy it. Piper was not pleased.
Buy some glow sticks from the dollar store or HERE and turn the lights off! Or put them in the bath water with the lights off.
Gather your old jewelry that you don't care about anymore and let them play with it. My little ones especially love big chunky necklaces and bracelets. You can find super cheap ones at yard sales too.
I love this idea from Busy Toddler.
Put a bunch of toys in the bathtub with no water! They think this is so cool and good for you there's no water clean up! WINNING!
Put colored paint in a Ziploc and tape it to their high chair. Let them finger paint their little hearts out.
Get a plastic bin and fill with rice. Hide any toys your kids make want to find in the rice bin. I love these little rakes to help them search for the items.
I LOVE this no prep toddler activity idea from Adventures and Play.
Great idea for learning your letters and working on your fine motor skills.
In Vegas, it's so hot during the summer so sometimes I hate to send my kids outside to eat a popsicle. Put them in the bath instead! No mess and it will keep them entertained. It would also be great for teething babies or sick kids.
I did this no prep toddler activity with my kids and they LOVED it. Such a great idea from Busy Toddler. She has amazing ideas!
Save an old egg carton and put little toys or items in each egg slot.
On paper write the ABC's and then have them use ABC stickers, ABC cookies, ABC magnets, etc. to match the letters to the letters on the paper.
Get out your plastic eggs from Easter and put little items inside. They love opening and closing the eggs and seeing a surprise. It's great for learning fine motor skills too!
Use painters tape and make a road on the floor for their cars! You can get creative with this!
My kids LOVE playing with my wallet and taking out and putting back my credit cards. Find an old wallet and expired cards or old gifts cards and fill up the wallet!
Use an old paper tube and tape it to the wall/fridge/etc., and have them drop things down the tube! So fun and easy!
I have feather pillows and my kids love to blow the feathers! Grab a straw and some feathers (or felt balls!) and let them blow it across the floor or table.
Grab a cookie sheet and some magnets and let them go to town!
Make a start and finish line and have them push each other in the laundry basket.
Get out your pots, pans, utensils and let them have at it. If I put a little water in a bowl and give them a whisk or mixing spoon, they think it's the greatest thing ever. This is a great one to do outside.
Show them how to fold them and throw them in the air!
Have them thread pipe cleaners through a strainer. So easy and fun! Side note: You can also help them learn their colors by asking what color are each pipe cleaner.
Give them scrap paper or fabric and have them cut away! Use kid safety scissors of course.
Loved this cute idea. So great for summertime!
Use chalk and draw big circles outside in a circle and have them hop to each one. I love What Moms Love 101 sidewalk chalk ideas!
You can usually find old landline phones at Goodwill or any second-hand stores. They love punching the big number buttons and hanging it up.
What other no prep toddler activities would you add?
Giving children that young a real hammer to crush ice cubes is dangerous. They can hurt themselves or each other severely. God forbid you take your eyes off them for a millisecond. Also, if an object fits through a toilet paper roll or paper towel roll, it could pose a choking hazard. Nonetheless, there were some good ideas here.
I disagree hammers aren't quite as dangerous as you think. They are only as strong as the toddler using them. I've used hammers with young children for years and never once had an issue. I have however seen the very dangerous outcome of learned self helplessness from an overly protected environment.
Wow! Someone brave enough to say the truth. Nice to hear it.
These are great! I'm an active grandmother who will be incorporating these into my playtime with my sweet grandson.
Maybe instead of crushing the ice, give them salad tongs. Let them pick up the ice with the tongs and put it in a bowl…kept my little guy entertained for half an hour.
I actually thought that was what he was using in the photo at first glance! But a hammer? um… no.
Did the ice one with my son but using a large metal spoon instead of a hammer. As the ice starts to melt, it breaks apart easier and he loved banging away at the ice.
Ice smash thing is great until they hit a toe or finger with that heavy hammer.
Obviously you would be paying attention to your toddler while performing these activities. I have 3 children, and even from a young age of 2, my boys wanted "real tools." So I let them, and you know what, with a watchful eye, they actually use them correctly and safely. Children are brilliant and not letting them explore real world objects is what's wrong with today!
These are great! I love the "wet painting" idea! Messes drive me nuts!
Thanks for sharing! I like the painters tape race track! The kids will love designing their own track!


text:
По́жня — деревня в Торопецком районе Тверской области. Административный центр Пожинского сельского поселения.

География
Расположена в 22 километрах к северо-западу от районного центра Торопец, на реке Оке, притоке Куньи.

Климат

Деревня, как и весь район, относится к умеренному поясу северного полушария и находится в области переходного климата от океанического к материковому. Лето с температурным режимом +15…+20 °С (днём +20…+25 °С), зима умеренно-морозная −10…−15 °С; при вторжении арктических воздушных масс до −30…-40 °С.

Среднегодовая скорость ветра 3,5—4,2 метра в секунду.

Улицы
Уличная сеть деревни представлена восемью (8) улицами:

 ул. Гавриленко
 ул. Октябрьская
 ул. Комсомольская
 ул. Партизанская
 ул. Лесная
 ул. Речная
 ул. Советская
 ул. Первомайская

Главные улицы — Советская и Гавриленко.

Транспорт
Находится на автодороге «Торопец — Плоскошь», от которой здесь отходит дорога «Пожня — Наговье — Бологово».

Расстояние по автодорогам:

 До Торопца — 23 км:
 До Плоскоши — 20 км;
 До Наговья — 26 км.

Население

Население по переписи 2002 года — 418 человека, 184 мужчины, 234 женщины.

История
В 1714 году в селе Пожня была построена каменная трёхпрестольная церковь Казанской Иконы Божией Матери. В настоящее время не сохранилась.

В Списке населенных мест Псковской губернии в Торопецком уезде на почтовом тракте «Торопец — Холм» значится сельцо Пожни (2 двора, 12 жителей) с почтовой станцией и погост Пожни (или Богородицкое; 4 двора, 10 жителей), здесь православная церковь, лавка, винокуренный завод, водяная мельница на Оке.В 1940 году село Пожня — центр Пожинского сельсовета Торопецкого района Калининской области. Во время Великой Отечественной войны Пожня была оккупирована в августе 1941 года, освобождена в январе 1942 года.

В 1970—1980-е годы деревня Пожня — центральная усадьба совхоза «Пожинский».

В 1997 году — 229 хозяйств, 520 жителей; администрация сельского округа, правление кооператива «Пожинский», межлесхоз, средняя школа, детсад, ДК, библиотека, музей партизанской славы, участковая больница, аптека, отделение связи, магазины.

Достопримечательности

Музей партизанской славы открыт 7 мая 1977 года, филиал Тверского государственного объединённого музея.

С 5 сентября 1941 года до середины января 1942 года на территории Торопецкого района вели активную борьбу с оккупантами Торопецкий, Плоскошский, Сережинский партизанский отряды. После освобождения, 16 июля 1942 года при Военном Совете Калининского фронта был создан штаб партизанского движения (д. Шейно в 3 км от Пожни), который 6 сентября 1942 года был переименован в представительство Центрального Штаба партизанского движения при Военном Совете Калининского фронта. Здесь в 1942—1943 годах проходили подготовку, а затем забрасывались во вражеский тыл связные, диверсионные группы, партизанские отряды. Осуществлялось руководство боевой деятельностью партизанских отрядов и бригад на оккупированных территориях Калининской области (включая Великолукскую), Белоруссии и Латвии.

В экспозиции музея представлены фотографии, документы, оружие, личные вещи партизан, подпольные газеты, листовки, портативная типография и другое.

Инфраструктура

 Администрация сельского поселения (ул. Советская, 56).
 Магазины.
 Поженская средняя общеобразовательная школа (ул. Советская, 30). Основана в 1895 году.
 Отделение связи (почта).
 Сельский дом культуры.
 Библиотека (ул. Гавриленко, 4) — филиал Торопецкой центральной.

Примечания

Ссылки

 Музей партизанской славы
Панорамы деревни Пожня на Гугл-картах

Населённые пункты Торопецкого района

redpajama_set_name: RedPajamaWikipedia


text:
April 26, 2017 Article
Pinhole Effect in Confocal Microscopes
When operating a confocal microscope, or when discussing features and parameters of such a device, we inescapably mention the pinhole and its diameter. This short introductory document is meant to explain the significance of the pinhole for those, who did not want to spend too much time to dig into theory and details of confocal microscopy but wanted to have an idea about the effect of the pinhole.
Rolf T. Borlinghaus , Dr.
What is a pinhole?
Lens-based optical instruments are mainly concerned with two parameters: the lens curvature and the diameter. The curvature defines in which directions parallel rays are deflected, the diameter defines how much of those rays contribute to the resulting image. The diameter could simply be the frame of the lens, in many cases it is a separate diaphragm delimiting the beam diameter. Common diaphragms are made of lamellae by which the diameter of the diaphragm is controlled. Very tiny diaphragms, though, do not fit to current lamella-technology. The simplest way to generate a very tiny diaphragm is, to prick a cardboard or an aluminum foil with a needle (pin), therefore called a pin-hole. Such pinholes are the working principle of a "camera obscura"[1]
What is the purpose of the pinhole in a confocal microscope?
Confocal microscopes allow to optically separate slices of the sample's response and record theses slices as images. Optimally, the slices cover just the depth of focus generated in the microscope.
To achieve this task, the sample is scanned by a tiny light point. The smallest shape that can be generated is a diffraction limited spot. A diffraction limited spot in the focal plane of the microscope is the image of a spot-shaped light source and therefore called "point spread function, psf". The psf is the distribution of light in the focus of an optical device when imaging a dimensionless spot. As all conventional light sources are usually not spot-shaped but have a significant extension, the light source is projected on a tiny aperture, the pinhole, acting as a spot-shaped source.
On the detection side, the sensor must follow in an equal manner. That is, the sensing region should as well be a diffraction limited spot, at all times coinciding with the illumination spot. This is achieved by a similar arrangement: the emission light is fed through a tiny aperture, the detection pinhole, before recorded by a sensing element. It is this detection pinhole, which usually is referred to when we mention the "pinhole" in a confocal microscope.
The term "confocal" refers to exact this arrangement: both illumination and detection are focused to the same spot [2]typo3/. The foci coincide. The image is then generated by scanning the field of view spotwise, like the electron beam in a tv-screen of the last century. The scanning is usually performed by an arrangement of pivotable mirrors.
As illustrated in Figure 1 [3], the detection pinhole removes all emission not originating from the focal plane. It is therefore also referred to as "spatial filter", filtering the depth of focus and blocking extrafocal signal. As the device cuts out sections from the sample by optical means, it is also called the "optical knife".
Figure 1: The optical knife. a) a compound microscope generates an intermediate image (iim) by an objective lens (obj), containing both focal (red) and extrafocal (pink) signal emanated by the sample (prp). When imaging a single spot, the detector (det) will record both a spot-shaped feature from the focal plane and extended blurry discs from other regions. b) by introducing a pinhole aperture (ph) in the intermediate image plane, nearly all extrafocal signal is cut off and solely the emission from the focal plane can reach the detector. The spatial filter generates an optical section.
Why is the pinhole's diameter variable?
For general confocal imaging, the recommendation is to just transmit the inner part of the diffraction limited feature by the pinhole. This inner part is called the "Airy disc". The size of Airy disc in the intermediate image depends on the wavelength (color), on the numerical aperture NA, the magnification of the objective lens and the magnification of internal optics of the microscope. The NA and objective magnification is engraved on the lens barrel. Consequently, the required pinhole diameter is different for various colors and for different objective lenses which have different NA and/or magnification.
Figure 2: Pinhole diameter and diffraction pattern. On the left: red circle indicates a circular pinhole adjusted to 1 AU. This pinhole will cut out the inner disk of the diffraction pattern and generate an optical section of the dimension dz. AU = "Airy Unit". On the right: for image rescanning microscopy, a series of subsets of the diffraction pattern is recorded. These images are combined and show increased lateral resolution (compared to widefield). The optical sectioning performance will still assume the equivalent of the rescanned area, i.e. is equivalent to a pinhole set to a size indicated by the red ring.
In addition, a variable pinhole offers the freedom to the user to increase the optical sectioning sharpness by lessening the diameter or to reduce optical sectioning performance by increasing the diameter.
What happens, if the pinhole is larger?
As stated above, the pinhole for general confocal imaging should just pass the Airy disc. The diameter in this case is referred to as "Airy Unit, AU". This is a good and practical compromise, not a law by nature. When the pinhole is increased, more and more extrafocal contributions will reach the sensor and increasingly fog the sharp focal information [4]typo3/. The overall intensity is thus increasing and apparently the signal to noise ratio (SNR) seems improving. But the increase is due to collecting unwanted blurry signal from layers outside the focal plane. If the pinhole is (virtually) infinity, the microscope behaves like a non-confocal widefield microscope (see Figure 3). It is therefore generally not recommended to open the pinhole just for the benefit to reduce the noisiness of the image.
Figure 3: Axial response to pinhole diameter. A practical setting for confocal microscopy is a diameter of 1 AU (grey vertical). When increasing the diameter, the detector will pick up extrafocal signal, the z-sectioning performance is deteriorated, although the intensity might increase. For pinhole diameters below 1 AU the sectioning performance will still increase, but assume a finite diffraction limited value at diameter zero.
The lateral resolution not affected and stays always at the value that is also true for widefield imaging and given by Abbe's formula: d=λ/2NA (See Figure 4).
What happens, if the pinhole is smaller?
The thinnest optical slices, at the diffraction limit in axial direction, are obtained when the pinhole diameter assumes zero. This is, of course, not practical. As a matter of fact, the thickness of the slice at the diffraction limit is only 25% better [4] than at 1 AU.
Other than for pinhole diameters above 1 AU, also the lateral resolution is affected when the pinhole is closed. At pinhole zero, one can expect an increase in lateral resolution4 of ca. 30%. This improvement can be partially exploited by closing the pinhole somewhat below the recommended 1 AU. For example at 0,6 AU, we already gain 58% of the possible resolution increase. To still ensure good signal to noise ratio, we should use a microscope with very good efficiency for the emitted fluorescence and virtually noise-free sensors.
Figure 4: Lateral response to pinhole diameter. The lateral resolution at 1 AU is constant for increasing diameters and corresponds to ordinary widefield microscopy resolution (diffraction limited resolution). If the pinhole diameter is below 1 AU, the lateral resolution is improved. The maximum increase in resolution is some 30% at pinhole diameter zero. Already at pinhole diameter 0,6 AU about 60% of the possible resolution increase is exploited (red vertical).
How does this relate to small fractions of psfs in image scanning?
An alternative to closing the pinhole for increasing lateral resolution is a method, called "image rescanningtypo3/" [5]. Here, the diffraction pattern itself is scanned again and the fractions are redistributed to neighbouring pixels (see Figure 2, right side). By computing a new synthetic image, the lateral resolution can be increased by about a factor of 1.4-fold as compared to widefield microscopy, nearly independent of the equivalent pinhole diameter. The optical sectioning performance, though, will assume the optical sectioning performance of the whole scanned area and follow the relations shown in Figure 3.
Pinhole Camera https://en.wikipedia.org/wiki/Pinhole_camera (retrieved Feb. 21st 2017)
C.J.R. Sheppard, A. Choudhury: Image Formation in the Scanning Microscope. In: Optica Acta: International Journal of Optics. 24, 1977, S. 1051–1073, doi:10.1080/713819421
Borlinghaus RT: The White Confocal – Microscopic Optical Sectioning in all Colors. Springer International, Heidelberg (2017) ISBN 978-3-319-55561-4 (in press).
Wilson T: Resolution and optical sectioning in the confocal microscope. Journal of Microscopy, Vol. 244, Pt 2 2011, pp. 113–121 doi: 10.1111/j.1365-2818.2011.03549.x
de Luca GMR et al.: Re-scan confocal microscopy scanning twice for better resolution. Optics Express 4: 2644–56 (2013).
Pinhole Geometry: Four Corners are Perfect
Confocal Optical Section Thickness
Pinhole Controls Optical Slicing
Confocal Microscopes
Microscope Objective & Leitz OEM Optics
With the STELLARIS confocal platform, we have re-imagined confocal microscopy to get you closer to the truth.


Dr. Wei Hu is an associate professor at Department of Computer Science and Technology, Nanjing University, China. He received his PhD degree in Computer Software and Theory in 2009, and his BS degree in Computer Science and Technology in 2005, both from Southeast University. He joined the faculty of Nanjing University in Dec. 2009.
Wei Hu appointed as the visiting student at Vrije Universiteit Amsterdam from Nov. 2007 to May 2008, advised by Prof. Frank van Harmelen. He interned at IBM Research - China from Sep. 2008 to Dec. 2008. He appointed as the visiting scholar/professor at Stanford University from Sep. 2014 to Sep. 2015, working with Prof. Michel Dumontier, University of Texas at Arlington from Nov. 2016 to May 2017, working with Prof. Chengkai Li, and University of Toronto from Jun. 2017 to Nov. 2017, working with Prof. Sheila McIlraith.
* I am always looking for highly-motivated, hard-working PhD and master students interested in the aforementioned areas.
© Copyright 2013 by the Websoft Research Group, Nanjing University, PR China. All rights reserved.


text:
Does Good Rice Add to a Good Life?
The country that computes Gross National Happiness as its measure of national success also produces special Bhutanese Red Rice.
By Kristin Belz September 13, 2011
Bhutan, the country that measures its Gross National Happiness, still produces material wealth such as fluffy, nutty red rice to export.
We all know that Rice A' Roni is the "San Francisco treat." Uncle Ben is the friendly white-haired man on the box of converted rice. And Minute Rice helped feed many a family in nary a minute for decades. But does Bhutan have it all over Ben and the gang?
Bhutanese Red Rice is nutty, fluffy and delicious (which is not to say that it's anything like Fluffernutter; it's not, thank goodness). And the country of Bhutan is much in the news these days because of the government's attempt to quantitatively value citizens' happiness, not just their accumulation of financial and material wealth.
Sounds like another way of saying money can't buy you love. Instead of measuring the Gross National Product (how many new widgets did we produce this month?), other factors – how satisfied are we with our lives? – count in the calculation as well.
It's quite a radical notion, and Western economists are eating it up – the notion, that is. Me, I'm wondering about the rice. What has generated this elevated state of mind in the Bhutanese? Could it be the red rice grown at 8,000 foot elevation fed by Himalayan 1,000 year old glacier waters?
My experiment with the red rice of these advanced people is too recently begun for any conclusions as of yet. Short-term results, however, indicate that this rice is unusually yummy and has potential to make the consumption of many future meals a happier occasion for me and my fellow diners.
With its ruddy color and short grain, Bhutanese rice would be excellent for a pilaf or as a companion to the strong flavors of woodsy mushrooms or hearty root vegetables. Possibilities range from breakfast porridge to dessert pudding. People's Co-op in Southeast Portland carries the red rice from importer Lotus Foods whose website includes many recipes.
Lotus takes a progressive stance on rice and global food production in general. The several types of rice it sells include those labeled "SRI" – for System of Rice Intensification. It's a method and movement of efficiently and healthily producing more rice with fewer seeds and less water. It addresses the fact that, "According to the United Nations Food and Agriculture Organization, almost one- third of the world's population depends on rice and its products for 60-70% of their daily calories."
With SRI, rice fields don't have to be flooded, which produces great savings, since "in Asia, where most rice is grown and eaten, about 84% of water withdrawal is for agriculture, mostly in flooded rice."
I figure it's worth keeping up the Bhutanese red rice experiment and maybe boosting the happiness quotient for all of us. SRI rice is next in my rice test kitchen.
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12/15/2021 By Cami Hughes
Omicron Hasn't Peaked in Oregon Yet, at Least Not According to Our Poop


text:
Q: System.Windows.Forms.WebBrowser login dialog doesn't appear When I navigate to an intranet site requiring windows authentication, the WinForms WebBrowser control isn't displaying a login dialog.  But it will display (after refreshing the page) if I first open Internet Explorer and view the same page.
Also, if I make the URL refer to my local IIS instance, the login dialog will appear.
Any ideas?  Thanks!

A: You can send credentials via IAuthenticate. You can either extend the winform webbrowser site or write your own webbrowser wrapper.

redpajama_set_name: RedPajamaStackExchange


Erie Insurance sells auto, home, business and life insurance through our network of independent agents in 12 states and the District of Columbia. Innovative Insurance Group was established in 2007 in Green Lane, Pennsylvania. The agency specializes in commercial insurance. Innovative Insurance Group also offers personal insurance including homeowners, renters, auto, boat, life insurance and more.
Principal agent Robert McVaugh has over 28 years of insurance experience. He and his six-agent staff serve over 1,600 clients and have more than 100 years of combined insurance experience. "I believe in old-fashioned service. I will come to you, your home, your business, day or night -- 24 hours a day, 7 days a week. I give all of our clients my personal cell phone number so that they can contact me for any insurance-related questions or problems. As principal agent, I am committed 100 percent to all of our clients," says Robert.
Innovative Insurance Group is located in beautiful Green Lane, Pennsylvania, in Montgomery County. It is surrounded by beautiful parks that are used by many outdoorsmen and fishermen year round. The agency can be found right off Main Street, also known as Sumneytown Pike, and their office is ADA compliant.