Rochester Hills, MI, United States

Rochester College
Rochester Hills, MI, United States

Rochester College is a four-year, liberal arts college located in Rochester Hills, Michigan; a northern exurb of Detroit. The college was founded by members of Churches of Christ in 1959. Total enrollment for the fall 2011 semester is 1,084 students.Rochester College is primarily undergraduate and includes both residential and commuting student populations. The college also offers a degree completion program for adult students. The college is governed by a board of trustees who are members of the Churches of Christ. The Ennis and Nancy Ham Library provides service to students, faculty, staff, and others.Rochester College was founded in 1959 as North Central Christian College, then later renamed Michigan Christian College. In 1997, the board of trustees adopted the name Rochester College in order to more clearly portray the institution's nature as a liberal arts college in a Christian setting. Wikipedia.

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Murad M.H.,Rochester College
The Journal of clinical endocrinology and metabolism | Year: 2012

Osteoporosis and osteopenia are associated with increased fracture incidence. The aim of this study was to determine the comparative effectiveness of different pharmacological agents in reducing the risk of fragility fractures. We searched multiple databases through 12/9/2011. Eligible studies were randomized controlled trials enrolling individuals at risk of developing fragility fractures and evaluating the efficacy of bisphosphonates, teriparatide, selective estrogen receptor modulators, denosumab, or calcium and vitamin D. Reviewers working independently and in duplicate determined study eligibility and collected descriptive, methodological quality, and outcome data. This network meta-analysis included 116 trials (139,647 patients; median age, 64 yr; 86% females and 88% Caucasians; median follow-up, 24 months). Trials were at low to moderate risk of bias. Teriparatide had the highest risk reduction of fractures (odds ratios, 0.42, 0.30, and 0.50 for hip, vertebral, and nonvertebral fractures, respectively) and the highest probability of being ranked first for efficacy (probabilities of 42, 49, and 79% for hip, vertebral, and nonvertebral fractures, respectively). However, differences to denosumab, zoledronate, risedronate, ibandronate, and alendronate were not statistically significant. Raloxifene and bazedoxifene were likely less effective, although these data were limited. Calcium and vitamin D were ineffective given separately but reduced the risk of hip fractures if given in combination (odds ratio, 0.81; 95% confidence interval, 0.68-0.96). Teriparatide, bisphosphonates, and denosumab are most effective in reducing the risk of fragility fractures. Differences in efficacy across drugs are small; therefore, patients and clinicians need to consider their associated harms and costs.

The objective of this research is to gain a greater understanding of the cause of fasting and postprandial hyperglycemia in people with type 2 diabetes. Endogenous glucose production is excessive before eating and fails to appropriately suppress after eating in people with type 2 diabetes. This is due in part to impaired insulin-induced suppression of endogenous glucose production, which is observed early in the evolution of type 2 diabetes. Increased rates of gluconeogenesis and perhaps glycogenolysis contribute to hepatic insulin resistance. Insulin-induced stimulation of hepatic glucose uptake and hepatic glycogen synthesis are reduced in people with type 2 diabetes primarily due to decreased uptake of extracellular glucose presumably because of inadequate activation of hepatic glucokinase. Delayed insulin secretion results in higher peak glucose concentrations particularly when suppression of glucagon is impaired, whereas insulin resistance prolongs the duration of hyperglycemia, which can be marked when both hepatic and extra-hepatic insulin resistance are present. The premise of these studies, as well as those performed by many other investigators, is that an understanding of the pathogenesis of type 2 diabetes will enable the development of targeted therapies that are directed toward correcting specific metabolic defects in a given individual. I, as well as many other investigators, believe that such therapies are likely to be more effective and to have a lower risk than would occur if everyone were treated the same regardless of the underlying cause of their hyperglycemia. While we do not yet have sufficient knowledge to truly individualize therapy, in my opinion this approach will be the norm in the not too distant future. © 2010 by the American Diabetes Association.

Service F.J.,Rochester College
Diabetes | Year: 2013

The proposed contribution of glucose variability to the development of the complications of diabetes beyond that of glycemic exposure is supported by reports that oxidative stress, the putative mediator of such complications, is greater for intermittent as opposed to sustained hyperglycemia. Variability of glycemia in ambulatory conditions defi ned as the deviation from steady state is a phenomenon of normal physiology. Comprehensive recording of glycemia is required for the generation of any measurement of glucose variability. To avoid distortion of variability to that of glycemic exposure, its calculation should be devoid of a time component. © 2013 by the American Diabetes Association.

Burgess R.J.,Rochester College | Zhang Z.,Rochester College
Nature Structural and Molecular Biology | Year: 2013

Nucleosome assembly following DNA replication, DNA repair and gene transcription is critical for the maintenance of genome stability and epigenetic information. Nucleosomes are assembled by replication-coupled or replication-independent pathways with the aid of histone chaperone proteins. How these different nucleosome assembly pathways are regulated remains relatively unclear. Recent studies have provided insight into the mechanisms and the roles of histone chaperones in regulating nucleosome assembly. Alterations or mutations in factors involved in nucleosome assembly have also been implicated in cancer and other human diseases. This review highlights the recent progress and outlines future challenges in the field. © 2013 Nature America, Inc. All rights reserved.

Sine S.M.,Rochester College
Physiological Reviews | Year: 2012

The synapse is a localized neurohumoral contact between a neuron and an effector cell and may be considered the quantum of fast intercellular communication. Analogously, the postsynaptic neurotransmitter receptor may be considered the quantum of fast chemical to electrical transduction. Our understanding of postsynaptic receptors began to develop about a hundred years ago with the demonstration that electrical stimulation of the vagus nerve released acetylcholine and slowed the heart beat. During the past 50 years, advances in understanding postsynaptic receptors increased at a rapid pace, owing largely to studies of the acetyl-choline receptor (AChR) at the motor endplate. The endplate AChR belongs to a large superfamily of neurotransmitter receptors, called Cys-loop receptors, and has served as an exemplar receptor for probing fundamental structures and mechanisms that underlie fast synaptic transmission in the central and peripheral nervous systems. Recent studies provide an increasingly detailed picture of the structure of the AChR and the symphony of molecular motions that underpin its remarkably fast and efficient chemoelectrical transduction.

Petersen R.C.,Rochester College
New England Journal of Medicine | Year: 2011

A 70-year-old woman has been noticing increasing forgetfulness over the past 6 to 12 months. Although she has always had some difficulty recalling the names of acquaintances, she is now finding it difficult to keep track of appointments and recent telephone calls, but the process has been insidious. She lives independently in the community; she drives a car, pays her bills, and is normal in appearance. A mental status examination revealed slight difficulty on delayed recall of four words, but the results were otherwise normal. Does the patient have mild cognitive impairment? How should her case be managed? Copyright © 2011 Massachusetts Medical Society.

Kendrick M.L.,Rochester College
Cancer Journal (United States) | Year: 2012

Minimally invasive surgical approaches for pancreatic resection have been established as feasible and safe. Whereas widespread application of laparoscopic distal pancreatectomy is in progress, the utilization of laparoscopic pancreaticoduodenectomy is still localized to a few centers because of the added complexity and advanced laparoscopic skills required. Comparative studies have demonstrated the typical advantages of minimally invasive approaches for pancreatic resection, namely, less blood loss and shorter hospital stay. Robotic assistance for laparoscopic approaches is gaining interest, but the true value added is still undefined. Significant discussion revolves around the appropriateness of minimally invasive approaches in pancreatic cancer. Although limited data and only short-term follow-up engender ongoing skepticism, the technical feasibility, existing reports in pancreatic cancer, and the lack of negative outcomes in other gastrointestinal cancers spark ongoing clinical evaluation. Minimally invasive surgical approaches have significant potential to improve the outcomes of pancreatic resection especially in pancreatic cancer patients in whom an optimal recovery is important for adjuvant treatment options. Larger experiences are forthcoming, and controlled trials are eagerly awaited; however, the feasibility of such is questionable because of the low incidence of resectable pancreatic cancer and the small number of centers performing minimally invasive pancreatectomy for malignancy. Copyright © 2012 by Lippincott Williams &Wilkins.

Torres V.E.,Rochester College
Annual Review of Medicine | Year: 2015

The synthesis of nonpeptide orally bioavailable vasopressin antagonists devoid of agonistic activity (vaptans) has made possible the selective blockade of vasopressin receptor subtypes for therapeutic purposes. Vaptans acting on the vasopressin V2 receptors (aquaretics) have attracted attention as a possible therapy for heart failure and polycystic kidney disease. Despite a solid rationale and encouraging preclinical testing, aquaretics have not improved clinical outcomes in randomized clinical trials for heart failure. Additional clinical trials with select population targets, more flexible dosing schedules, and possibly a different drug type or combination (balanced V1a/V2 receptor antagonism) may be warranted. Aquaretics are promising for the treatment of autosomal dominant polycystic kidney disease and have been approved in Japan for this indication. More studies are needed to better define their long-term safety and efficacy and optimize their utilization. © 2015 by Annual Reviews.

Frye M.A.,Rochester College
New England Journal of Medicine | Year: 2011

A 26-year-old businesswoman seeks evaluation for a pattern of "hibernating away" each winter; this pattern began when she was in high school. Her current symptoms include excessive sleeping, a 20-lb (9-kg) weight gain related to an increased intake of sweets and excessive alcohol use, anhedonia, lack of motivation, negative ruminations, and decreased productivity at work. She reports a history of several-week periods in college when she had less need for sleep, with associated increases in mood, energy, and libido. During the last episode, she exceeded her credit-card limit and was evaluated at an emergency department for alcohol intoxication. How should she be evaluated and treated? Copyright © 2011 Massachusetts Medical Society. All rights reserved.

Borlaug B.A.,Rochester College
Nature Reviews Cardiology | Year: 2014

Approximately half of all patients with heart failure have preserved ejection fraction (HFpEF) and, as life expectancies continue to increase in western societies, the prevalence of HFpEF will continue to grow. In contrast to heart failure with reduced ejection fraction (HFrEF), no treatment has been proven in pivotal clinical trials to be effective for HFpEF, largely because of the pathophysiological heterogeneity that exists within the broad spectrum of HFpEF. This syndrome was historically considered to be caused exclusively by left ventricular diastolic dysfunction, but research has identified several other contributory factors, including limitations in left ventricular systolic reserve, systemic and pulmonary vascular function, nitric oxide bioavailability, chronotropic reserve, right heart function, autonomic tone, left atrial function, and peripheral impairments. Multiple individual mechanisms frequently coexist within the same patient to cause symptomatic heart failure, but between patients with HFpEF the extent to which each component is operative can differ widely, confounding treatment approaches. This Review focuses on our current understanding of the pathophysiological mechanisms underlying HFpEF, and how they might be mechanistically related to typical risk factors for HFpEF, including ageing, obesity, and hypertension. © 2014 Macmillan Publishers Limited. All rights reserved.

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