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New York City, NY, United States

Albany Medical College is a medical school located in Albany, New York, United States. It was founded in 1839 by Alden March and James H. Armsby and is one of the oldest medical schools in the nation. The college is part of the Albany Medical Center, which includes the Albany Medical Center Hospital.Along with Albany College of Pharmacy, Albany Law School, the Dudley Observatory, the Graduate College of Union University, and Union College, it is one of the constituent entities of Union University.Over its 170 year history, Albany Medical College has attracted and produced many leaders in medicine and research. Among its present and past faculty, researchers, and alumni count two Nobel Prize winners, two Lasker Award winners, two MacArthur Fellowship recipients, one Gairdner Foundation International Award winner, former Surgeon General of the United States Army, former Surgeon General of the United States Air Force, several presidents and CEOs of major academic hospitals, as well as an early president and co-founder of the American Medical Association. AMC is attributed as the site where David S. Sheridan perfected the modern-day disposable catheter, among other major discoveries and innovations. Among AMC alumni accomplishments include the discovery of the hormone leptin, the invention of computed tomography, and the discovery of oral rehydration therapy. Wikipedia.


Smith H.S.,Albany Medical College
Pain physician | Year: 2012

Opioid therapy is one of the most effective forms of analgesia currently in use. In the past few decades, the use of opioids as a long-term treatment for chronic pain has increased dramatically. Accompanying this upsurge in the use of long-term opioid therapy has been an increase in the occurrence of opioid associated endocrinopathy, most commonly manifested as an androgen deficiency and therefore referred to as opioid associated androgen deficiency (OPIAD). This syndrome is characterized by the presence of inappropriately low levels of gonadotropins (follicle stimulating hormone and luteinizing hormone) leading to inadequate production of sex hormones, particularly testosterone. Symptoms that may manifest in patients with OPIAD include reduced libido, erectile dysfunction, fatigue, hot flashes, and depression. Physical findings may include reduced facial and body hair, anemia, decreased muscle mass, weight gain, and osteopenia or osteoporosis. Additionally, both men and women with OPIAD may suffer from infertility. While the literature regarding OPIAD remains limited, it is apparent that OPIAD is becoming increasingly prevalent among chronic opioid consumers but often goes unrecognized. OPIAD can have a significant negative impact on the the quality of life of opioid users, and clinicians should anticipate the potential for its occurrence whenever long-term opioid prescribing is undertaken. Once diagnosed, treatment for OPIAD may be offered utilizing a number of androgen replacement therapy options including a variety of testosterone preparations and, for female patients with OPIAD, dehydroepiandrosterone (DHEA) supplementation. Follow-up evaluation of patients receiving androgen replacement therapy should include a review of any unresolved symptoms of hypogonadism, laboratory evaluation, and surveillance for potential adverse effects of androgen replacement therapy including prostate disease in males.: Source


Argoff C.E.,Albany Medical College
Mayo Clinic Proceedings | Year: 2013

Oral analgesics are commonly prescribed for the treatment of acute and chronic pain, but these agents often produce adverse systemic effects, which sometimes are severe. Topical analgesics offer the potential to provide the same analgesic relief provided by oral analgesics but with minimal adverse systemic effects. This article describes the results of a systematic review of the efficacy of topical analgesics in the management of acute and chronic pain conditions. A literature search of MEDLINE/PubMed was conducted using the keywords topical analgesic AND chronic pain OR acute pain OR neuropathic pain and focused only on individual clinical trials published in English-language journals. The search identified 92 articles, of which 65 were eligible for inclusion in the review. The most commonly studied topical analgesics were nonsteroidal anti-inflammatory drugs (n=27), followed by lidocaine (n=9), capsaicin (n=6), amitriptyline (n=5), glyceryl trinitrate (n=3), opioids (n=2), menthol (n=2), pimecrolimus (n=2), and phenytoin (n=2). The most common indications were acute soft tissue injuries (n=18), followed by neuropathic pain (n=17), experimental pain (n=6), osteoarthritis and other chronic joint-related conditions (n=5), skin or leg ulcers (n=5), and chronic knee pain (n=2). Strong evidence was identified for the use of topical diclofenac and topical ibuprofen in the treatment of acute soft tissue injuries or chronic joint-related conditions, such as osteoarthritis. Evidence also supports the use of topical lidocaine in the treatment of postherpetic neuralgia and diabetic neuropathy. Currently, limited evidence is available to support the use of other topical analgesics in acute and chronic pain. © 2013 Mayo Foundation for Medical Education and Research. Source


Singer H.A.,Albany Medical College
Journal of Physiology | Year: 2012

Vascular smooth muscle (VSM) undergoes a phenotypic switch in response to injury, a process that contributes to pathophysiological vascular wall remodelling. VSM phenotype switching is a consequence of changes in gene expression, including an array of ion channels and pumps affecting spatiotemporal features of intracellular Ca 2+ signals. Ca 2+ signalling promotes vascular wall remodelling by regulating cell proliferation, motility, and/or VSM gene transcription, although the mechanisms are not clear. In this review, the functions of multifunctional Ca 2+/calmodulin-dependent protein kinase II (CaMKII) in VSM phenotype switching and synthetic phenotype function are considered. CaMKII isozymes have complex structural and autoregulatory properties. Vascular injury in vivo results in rapid changes in CaMKII isoform expression with reduced expression of CaMKIIγ and upregulation of CaMKIIδ in medial wall VSM. SiRNA-mediated suppression of CaMKIIδ or gene deletion attenuates VSM proliferation and consequent neointimal formation. In vitro studies support functions for CaMKII in the regulation of cell proliferation, motility and gene expression via phosphorylation of CREB1 and HDACIIa/MEF2 complexes. These studies support the concept, and provide potential mechanisms, whereby Ca 2+ signalling through CaMKIIδ promotes VSM phenotype transitions and vascular remodelling. © 2012 The Author. The Journal of Physiology © 2012 The Physiological Society. Source


Smith H.S.,Albany Medical College
Pain Physician | Year: 2011

Up to 90% of patients with metastatic or advanced stage cancer will experience significant cancer-related pain. Approximately half or more of patients diagnosed with cancer may experience bone pain. It has been estimated that tumor metastases to the skeleton affect roughly 400,000 United States citizens annually. Carcinoma from breast, lung, and prostate cancers account for about 80% of secondary metastatic bone disease. Bone metastases may cause devastating clinical complications associated with dramatic reductions in quality of life, mobility, and independence as well as excruciating refractory pain. Associated complications from osseous metastases also present a substantial economic burden. Currently, there is still a significantly high number of patients suffering with unrelieved pain from osseous metastases. Treatments for painful osseous metastases may not only diminish pain, but may also improve quality of life and independence/mobility, and reduce skeletal morbidity, potential pathologic fractures, spinal cord compression, and other "skeletalrelated events." Treatment strategies for painful osseous metastases include systemic analgesics, intrathecal analgesics, glucocorticoids, radiation (external beam radiation, radiopharmaceuticals), ablative techniques (radiofrequency ablation (RFA) and cryoablation), bisphosphonates, chemotherapeutic agents, inhibitors of RANK-RANKL interaction (e.g., denosumab), hormonal therapies, interventional techniques (e.g., kyphoplasty), and surgical approaches. Although the mechanisms underlying the development of bone metastases are not completely understood, there appears to be important bi-directional interactions between the tumor and the bone microenvironment. A greater understanding of the pathophysiology of painful osseous metastases may lead to better and more selective targeted analgesic therapy. Additionally, potential future therapeutic approaches to painful osseous metastases may revolutionize approaches to analgesia for this condition, leading to optimal outcomes with maximal pain relief and minimal adverse effects. Source


Trebak M.,Albany Medical College
Journal of Physiology | Year: 2012

Stromal interaction molecules (STIM1 and STIM2) are single pass transmembrane proteins located mainly in the endoplasmic reticulum (ER). STIM proteins contain an EF-hand in their N-termini that faces the lumen side of the ER allowing them to act as ER calcium (Ca2+) sensors. STIM1 has been recognized as central to the activation of the highly Ca2+ selective store-operated Ca2+ (SOC) entry current mediated by the Ca2+ release-activated Ca2+ (CRAC) channel; CRAC channels are formed by tetramers of the plasma membrane (PM) protein Orai1. Physiologically, the production of inositol 1,4,5-trisphosphate (IP3) upon stimulation of phospholipase C-coupled receptors and the subsequent emptying of IP3-sensitive ER Ca2+ stores are sensed by STIM1 molecules which aggregate and move closer to the PM to interact physically with Orai1 channels and activate Ca2+ entry. Orai1 has two homologous proteins encoded by separate genes, Orai2 and Orai3. Other modes of receptor-regulated Ca2+ entry into cells are store-independent; for example, arachidonic acid activates a highly Ca2+ selective store-independent channel formed by heteropentamers of Orai1 and Orai3 and regulated by the PM pool of STIM1. Here, I will discuss results pertaining to the roles of STIM and Orai proteins in smooth muscle Ca2+ entry pathways and their role in vascular remodelling. © 2012 The Author. The Journal of Physiology © 2012 The Physiological Society. Source

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