NIW recommendation letter（medicine，life science）

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jim0212

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   NIW recommendation letter（medicine，life science）
   摘自加州大学论坛 ucbbs.org (Universities in California Bulletin Board System)  jim0212  2009-06-19 17:21
NIW recommendation letter-1（medicine，life science）

Dear friends, I have several recommendation letter samples and will share with you all. Hope they would be helpful for you!

Letter-1

(RE-TYPE ON EMPLOYER’S LETTERHEAD)

(Date)

Department of Homeland Security
U.S. Citizenship and Immigration Service
Texas Service Center
P. O. Box 852135
Mesquite, TX 75185-2135

     Re: XXX Ph.D.; national interest waiver
To Whom It May Concern:
I am writing this letter to express my strong support of Dr. XXX's application for permanent residency in the United States, based on the impact on the national interest of the United States of her research on the neuronal activity involved in such neurodegenerative diseases as Alzheimer’s disease. Her continued work in this area will promote the improvement of health care for such diseases, which will benefit the national interest of providing better health care to the American population while reducing the enormous health care costs associated with these prevalent and serious diseases.
I am the … in the Department of Molecular and Cellular Biology and Medicine at Baylor College of Medicine. I served from 1987 to 1998 as Senior Director, and later as Vice-President, for Basic Research at Merck Research Laboratories of Merck & Co., where I was involved primarily with identifying new drug targets for metabolic diseases and drugs to improve the quality of life for elderly persons. I have broad expertise in many therapeutic programs, including the neurodegenerative diseases of aging, osteoporosis, diabetes, atherosclerosis, obesity, and cancer. During my eleven-year career at Merck, I produced more than ten new compounds that met the strict criteria for the initiation of development studies. In 1998, I received the Merck Management Award for scientific leadership and excellence. Prior to joining Merck, I was a professor at Baylor College of Medicine where, in addition to conducting basic research, I directed the Endocrine Subspecialty OB/GYN Department and the AUA Fellowship Program in Urology. Since returning to Baylor, I have continued to work on the function of the orphan growth hormone secretagogue receptor that was cloned in my laboratory at Merck. I am an author of over 200 scientific papers and books. A copy of my curriculum vitae is attached, documenting my professional qualifications.
I came to know Dr. XXX when she joined our department in February 2004. Consequently, I believe that I am in a good position to evaluate Dr. XXX's research accomplishments. I was highly impressed with Dr. XXX's work entitled: "Audiogenic seizure susceptibility is induced by termination of continuous infusion of GABA or an NMDA antagonist into the inferior colliculus", which focused directly on the questions raised by some leading scientists in the field of epilepsy regarding whether the inferior colliculus is critical in audiogenic seizure initiation or merely an auditory structure, suggesting that seizures are initiated by structures efferent to the inferior colliculus. Dr. XXX's research established, for the first time, a focal model of sound induced-seizures using osmotic minipump technology. Her research provided vital insight into the mechanism of convulsive behaviors, by showing that an abnormality of synaptic transmission in the inferior colliculus elicits the susceptibility of sound triggered seizures, which is very critical in determining the neuronal network in this neurological disorder. Her results have been among the most substantial in confirming the theory that the inferior colliculus is critical in the initiation of sound triggered seizures.
Dr. XXX has continued to break new ground in studying the mechanisms underlying neurological disorders. She conducted another critical project involving the simultaneous evaluation of neuronal responses and the behavior during each phase of alcohol withdrawal convulsion in freely moving animals. The abnormal firing patterns were exhibited by neurons in two brainstem structures, the deep layers of superior colliculus and the periaqueductal gray that produce each discrete behavioral phase of the alcohol withdrawal convulsion. She demonstrated that these two structures are implicated in the generation of the wild running and tonic-clonic phase of seizures. This project produced vital data on amino acid transmitter alterations and neuronal firing abnormalities in these nuclei, establishing a complete network model of each phase of the generalized convulsion during alcohol withdrawal. Similar studies had never been conducted previously, due to the complicated processes and difficulties in conducting this single unit recording in a free-moving animal. Based on Dr. XXX’s findings, new therapeutic strategies for the prevention of convulsions may be achieved, utilizing the blockade of neuronal excitation at the brainstem level.
Dr. XXX's research has also elucidated the intracellular mechanisms of alcohol withdrawal syndromes. She was the first scientist to demonstrate the selective modification of membrane properties and synaptic activities of the periaqueductal gray nucleus during alcohol withdrawal. The data is extremely relevant and significant in the development of treatment modalities for alcoholism. The observed increased susceptibility to convulsion in animal models appears similar to the increased susceptibility to seizures observed in humans during alcohol withdrawal. Dr. XXX's studies indicate that convulsive behaviors can be blocked by the bilateral infusion of glutamate receptor antagonists into the deep layers of the superior colliculus and the periaqueductal gray, implicating the glutamate receptors in both structures in modulating the excitability of neurons during alcohol withdrawal. Thus, Dr. XXX has provided fundamental data for predicting the most sensitive therapeutic target for the prevention and treatment of alcohol withdrawal convulsion.

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Currently, Dr. XXX is working as a Research Scientist at the Huffington Center on Aging at Baylor College of Medicine, which is a research-intensive biomedical institution that is internationally respected for excellence in education, research, and patient care. The Huffington Center on Aging has one of the most advanced aging research programs in the country and is a John A. Hartford Foundation, Inc. of New York-designated Center of Excellence in Geriatrics. Dr. XXX is conducting an analysis of the synaptic activities changes in the central nerve system and its implications on Alzheimer's disease. The long-term goal of this research is to uncover novel pathways and to seek greater understanding of Alzheimer's disease pathogenesis using knockout mice as a model system. The long-term objective of her research is the development of novel therapeutics, and the progress of this research surely will have a significant impact on improving public health care for neurodegenerative diseases, particularly with regards to Alzheimer's disease.
Alzheimer's disease is a leading cause of senile dementia that is characterized by the loss of neurons and deposition of beta-amyloid plaques in the brain of affected individuals. Thus far, most studies have been focused on the molecular defects on the brain of Alzheimer's disease animal models. While, during the past decade, the genes causing familial forms of Alzheimer's disease have been identified and the protein pathways involving the gene products have been delineated, it is still not clear how these molecular factors affect normal brain functions. Alzheimer's disease usually begins with a remarkably pure impairment of the brain function, from which patients with this devastating disorder of the limbic and associated cortices lose their ability to encode new memories, first of trivial and then of important details of life. It has become clear that scientists must focus on the clinicopathological study of the earliest stages of the disorder. The synapses in the brain are the initial target in Alzheimer's disease. Attempts to decipher the subtle alterations in synaptic function that underlie the earliest cognitive features of Alzheimer’s disease are the most advanced example of the rapid progress in understanding the mechanisms of human neurodegerative diseases.
The hallmark of an outstanding scientist is not only to have an impact on the field of study, but also to do so consistently over a period of time. Dr. XXX has clearly demonstrated this ability. She is playing a leading and critical role in the central and crossing research project relating to Alzheimer's disease, a neurological disorder, at the Huffington Center on Aging. Dr. XXX is a fully qualified neuro-electrophysiologist. Electrophysiological recordings, including patch clamp recording, have been proven to be the most effective way to detect the functional activities of brain synapses. Dr. XXX’s studies utilize the knockout mice model, in which mice deficient in amyloid precursor protein (APP) are studied to determine which aspect of APP function predominates in vitro and in vivo, which will provide vital information that is critical for evaluating whether APP is a good therapeutic drug target for the treatment of neurodegenerative diseases. She developed an effective method of creating neuronal cultures, which is an important process in the study of synaptic activity, and established a sophisticated electrophysiological recording system to characterize the synaptic pathology in APP knockout mice, which is crucial to the early diagnosis and development of new and effective therapies for the treatment of Alzheimer's disease. She has brought new techniques to the lab and established sophisticated experimental procedures that only those who have had many years of training can operate, such as neuronal cultures; electrophysiological recording (including intracellular, extracellular and whole-cell patch recordings in neuronal cultures and slices); calcium images, and microdialysis that have become the cornerstone of these studies.
Dr. XXX's research showed, for the first time, that an increased hippocampal spontaneous neuronal firing in knock-out mice, as compared to the control mice models, and that a nicotinic receptor antagonist is more effective in the blockade of acetycholine-induced responses in neurons from the control mice than those of the mutants. Her studies demonstrated that the trans-membrane protein APP is required to maintain the normal cholinergic function of the central nervous system. This study will provide new concepts regarding Alzheimer's disease and eventually lead to the advent of novel treatments for this devastating disease. These are very promising studies and should be continued. Dr. XXX has played a leading role in these projects, which have made highly impressive progress. She has always displayed extreme enthusiasm in her work and has been deeply committed to the success of each research project. Since there are currently very few individuals who are capable of performing this cutting-edge research, the continued involvement of and contributions by Dr. XXX are vital to its success. In my opinion, she cannot be replaced by other researchers at her level of qualifications without a substantial impairment or interruption of the ongoing projects.
Dr. XXX has been the key scientist performing the above-described cutting-edge research and has provided rare and significant insights in understanding the brain mechanisms underlying neuronal disorders. She has published four first-author articles in Experimental Neurology, Brain Research and Neuropharmacology, which are major peer-reviewed journals with a worldwide circulation, and she has presented her research at many national and international leading conferences. Publication in these journals is an attestation of research of high quality and is respected internationally, which can be reflected by the fact that there have been thirty citations listed in the Science Direct database on Dr. XXX's work. As a result of her high quality studies and publications, the Editor-in-Chief, T. E. Salt, of Current Pharmacology, a journal that publishes reviews written by experts and leaders in the fields of molecular, cellular, and systems/behavioral aspects of neuropharmacology and neuroscience, invited Dr. XXX to contribute a review article for the journal. She was also invited by Bradley University to present a lecture to its biology students. She has been honored, since 1999, with a regular membership in the Society for Neuroscience, which accepts only those scientists "who (have) done meritorious research relating to neuroscience". These honors and awards are indications that Dr. XXX's research represents a very high and well-respected standard of accomplishment.
In the United States, over four million people have Alzheimer's disease; by 2010, an estimated six million and by 2050, fourteen million Americans are projected to develop Alzheimer's disease. Currently, 313,000 new cases will develop each year in the United States. Alzheimer's disease will constitute an American public health catastrophe if effective methods of therapy cannot be developed. Alzheimer's disease costs the American public approximately $250 billion each year, representing the third most expensive health problem after heart disease and cancer, and the toll in human suffering is immeasurable. These factors make Alzheimer's disease an urgent priority of great national interest to the United States. The development of interventions that can delay the onset and detect the early stages of this disease will have an enormously positive public health impact. Consequently, there is an all-out campaign funded by the federal government to develop the needed therapeutic strategies for controlling this disease. The Alzheimer's Association has narrowed the window of time to as little as ten years to find solutions to these issues in time to make a substantial difference in preventing the projections of Alzheimer’s disease incidence stated above. Baylor College of Medicine is a major contributor to this campaign against Alzheimer's disease, conducting vital research aimed at elucidating the basic mechanisms of this disease, as well as developing novel therapies for its prevention and treatment. Thus, the research being conducted by Dr. XXX will provide extensive benefits to the national interest of the United States in improving health care for the American public and in reducing the enormous health care costs associated with this disease.
Dr. XXX's has proven herself an outstanding neuroscientist in the field of neurological diseases. Because of her direct interaction in this type of research, she is better equipped and better qualified than other researchers in her field. The exceptional combination of highly specialized and sophisticated knowledge, technical abilities, experience, and discipline makes her uniquely qualified to conduct the extremely complex research funded by the NIH. The Huffington Center on Aging is a John A. Hartford Foundation, Inc. of New York-designated Center of Excellence in Geriatrics and has one of the most advanced aging research programs in the country. The Center and its faculty have received numerous awards and accolades. As one of the nation’s leading medical research organizations, the Center and Baylor College of Medicine are committed to recruiting the highest ranking scientists, such as Dr. XXX, into the competitive research programs aimed at uncovering the neurophysical mechanisms for Alzheimer's disease and developing better therapies for neuronal diseases. Dr. XXX plays a very significant role in conducting research on the central nervous system dysfunction of Alzheimer's disease. Her numerous research accomplishments to date indicate strongly that she will continue to make significant contributions in the future that will impact the national interest of the United States in advancing health care for neurological diseases. A scientist of her caliber, with her unique combination of skills and practical experience, is absolutely indispensable for the success of the Center’s research to elucidate the mechanisms of Alzheimer's disease and to develop novel strategies for the early diagnosis and treatment of the disease.
There is no doubt that Dr. XXX's research will benefit the health care for the American public, and the continuing presence of Dr. XXX in this country would be in the national interest of meeting this critical objective. The inability of Dr. XXX to remain in the US would have dramatic adverse consequences for those NIH projects and for those suffering from Alzheimer's disease. Therefore, I strongly support her application for the national interest waiver and permanent resident status in the United States.
Sincerely,

XXX Ph.D.
Professor, Department of Molecular and Cellular Biology and Medicine

   摘自加州大学论坛 ucbbs.org (Universities in California Bulletin Board System)  jim0212  2009-06-19 17:21