Depressive symptoms in caregivers immediately after stroke.

Background: Caregivers of stroke survivors often suffer depressive symptoms that interfere with their own health. Early recognition may lead to attenuation of symptoms and better health and well-being for caregivers.

Objective: We examined characteristics of caregivers and stroke survivors associated with caregivers' depressive symptoms in the early poststroke period.

Musical and Cognitive Abilities in Older Adults with Mild Cognitive Impairment.

The objective of this cross-sectional study was to determine the extent and nature of self-reported musical abilities in persons with mild cognitive impairment (MCI). We recruited 60 older adults with a diagnosis of MCI from the Alzheimer's disease Core Center. We evaluated self-reported musical abilities using the Goldsmiths General Musical Sophistication Index.

Effects of Uncertainty on Perceived and Physiological Stress in Caregivers of Stroke Survivors: A 6-Week Longitudinal Study.

Caregivers' stress following a family member's stroke is likely accentuated by its associated uncertainty. The purpose of the current study was to examine the effect of uncertainty on caregivers' perceived and physiological stress (i.e.

Caregiving Immediately After Stroke: A Study of Uncertainty in Caregivers of Older Adults.

Background: Caregivers of stroke survivors experience high rates of mental and physical morbidity. Stroke has sudden onset, and the outcome is not immediately known. Uncertainties surrounding the new caregiving role may not only necessitate major changes in the lives of family caregivers but also contribute to negative health outcomes for the caregiver.

Advancing LGBT Health at an Academic Medical Center: A Case Study.

Academic health centers are strategically positioned to impact the health of lesbian, gay, bisexual and transgender (LGBT) populations by advancing science, educating future generations of providers, and delivering integrated care that addresses the unique health needs of the LGBT community. This report describes the early experiences of the Penn Medicine Program for LGBT Health, highlighting the favorable environment that led to its creation, the mission and structure of the Program, strategic planning process used to set priorities and establish collaborations, and the reception and early successes of the Program.

Self-care and health outcomes of diabetes mellitus.

Studies show that self-care improves diabetes mellitus (DM) outcomes; however, previous studies have focused on self-care maintenance, and little is known about self-care management. The objective of this study is to examine the influence of DM self-care maintenance and management on number of hospitalizations and hospitalization days. A cohort design with secondary analysis of data from the Health and Retirement Study 2002-2004 was used.

Biomarkers of myocardial stress and systemic inflammation in patients who engage in heart failure self-care management.

Background: Self-care is believed to improve heart failure (HF) outcomes, but the mechanisms by which such improvement occurs remain unclear.

Methods: We completed a secondary analysis of cross-sectional data collected on adults with symptomatic HF to test our hypothesis that effective self-care is associated with less myocardial stress and systemic inflammation. Multivariate logistic regression modeling was used to determine if better HF self-care reduced the odds of having serum levels of amino-terminal pro-B-type natriuretic peptide and soluble tumor necrosis factor α receptor type 1 at or greater than the sample median.

The influence of heart failure self-care on health outcomes: hypothetical cardioprotective mechanisms.

Lapses in self-care are commonly cited as a major cause of poor outcomes in persons with heart failure (HF). Not surprisingly, self-care is assumed to be central to improving health outcomes in this patient population. Empirically, however, this assumption is not well supported, and mechanistically, relationships between self-care and outcomes in HF have not yet been described.

Current concepts of neurohormonal activation in heart failure: mediators and mechanisms.

Neurohormonal activation is a commonly cited array of phenomena in the body's physiologic response to heart failure. Although various neurohormones and pharmacologic agents that moderate their pathophysiologic effects have been reviewed in the nursing literature, both the mechanisms of neurohormonal system activation and cellular and organ system effects have been described only in brief. Accordingly, this article reviews mechanisms of neurohormonal activation and describes cellular and cardiovascular effects of the (1) sympathetic nervous system, (2) renin-angiotensin-aldosterone system, (3) kallikrein-kininogen-kinin system, (4) vasopressinergic system, (5) natriuretic peptide systems, and (6) endothelin in the context of heart failure.

Insulin sensitivity, food intake, and cravings with premenstrual syndrome: a pilot study.

Objective: The objective of this pilot study was to evaluate possible differences in insulin sensitivity, food intake, and cravings between the follicular and luteal phases of the menstrual cycle in women with premenstrual syndrome (PMS).

Methods: Subjects were screened for PMS using the Penn Daily Symptom Rating (DSR) scale. Each subject had two overnight admissions (once in each cycle phase) to the Hospital of the University of Pennsylvania.

Cognitive influences on self-care decision making in persons with heart failure.

Background: Despite advances in management, heart failure is associated with high rates of hospitalization, poor quality of life, and early death. Education intended to improve patients' abilities to care for themselves is an integral component of disease management programs. True self-care requires that patients make decisions about symptoms, but the cognitive deficits documented in 30% to 50% of the heart failure population may make daily decision making challenging.

Methods of measuring insulin sensitivity.

Insulin resistance is a component of several health disorders, most notably impaired glucose tolerance and type 2 diabetes mellitus. Insulin-resistant individuals have an impaired biological response to the usual action of insulin; that is, they have reduced insulin sensitivity. Various methods are used to assess insulin sensitivity both in individuals and in study populations.

Hypoglycemia activates arousal-related neurons and increases wake time in adult rats.

Hypoglycemia resulting from excess of exogenous or endogenous insulin elicits central nervous system activation that contributes to counterregulatory hormone secretion. In adult humans without diabetes, hypoglycemia occurring during sleep usually produces cortical activation with awakening. However, in adult humans with type 1 diabetes, hypoglycemic arousal appears blunted or absent.

Menstrual cycle effects on insulin sensitivity in women with type 1 diabetes: a pilot study.

Background: Many women complain of difficulty maintaining euglycemia during the luteal phase of the menstrual cycle. This pilot study's objective was to evaluate possible differences in insulin sensitivity between follicular and luteal phases in women with type 1 diabetes.

Methods: Women using insulin infusion pumps (n = 5, mean age 29.

From bedside to bench and back again: research issues in animal models of human disease.

To improve outcomes for patients with many serious clinical problems, multifactorial research approaches by nurse scientists, including the use of animal models, are necessary. Animal models serve as analogies for clinical problems seen in humans and must meet certain criteria, including validity and reliability, to be useful in moving research efforts forward. This article describes research considerations in the development of rodent models.

Cortical Fluoro-Jade staining and blunted adrenomedullary response to hypoglycemia after noncoma hypoglycemia in rats.

Intensive insulin therapy in patients with type 1 diabetes mellitus reduces long-term complications; however, intensive therapy is also associated with a three-fold increase in hypoglycemic episodes. The present study in conscious rats characterizes the physiologic and neuropathologic consequences of a single episode of moderate hypoglycemia. In this model, intravenous insulin is used to reduce plasma glucose to 30 to 35 mg/dL for 75 mins.

Development of posttraumatic hyperthermia after traumatic brain injury in rats is associated with increased periventricular inflammation.

Posttraumatic hyperthermia (PTH) is a noninfectious elevation in body temperature that negatively influences outcome after traumatic brain injury (TBI). We sought to (1) characterize a clinically relevant model and (2) investigate potential cellular mechanisms of PTH. In study I, body temperature patterns were analyzed for 1 week in male rats after severe lateral fluid percussion (FP) brain injury (n=75) or sham injury (n=17).

Obesity-prone rats have preexisting defects in their counterregulatory response to insulin-induced hypoglycemia.

Rats that develop diet-induced obesity (DIO) on a 31% fat [high-energy (HE)] diet have defective sensing and responding to altered glucose levels compared with diet-resistant (DR) rats. Thus we postulated that they would also have defective counterregulatory responses (CRR) to insulin-induced hypoglycemia (IIH). Chow-fed selectively bred DIO and DR rats underwent three sequential 60-min bouts of IIH separated by 48 h.

A single episode of central glucoprivation reduces the adrenomedullary response to subsequent hypoglycemia in rats.

Hypoglycemia-associated autonomic failure (HAAF) is a complication of recurrent hypoglycemia in patients with diabetes. The present experiments were performed to study the contribution of brain glucose-sensitive structures to HAAF. In conscious rats, brain glucoprivation was elicited by injection of 2 deoxy-D-glucose (2-DG) into the third cerebral ventricle (intracerebroventricular, ICV), while controls received saline ICV.

Hyperthermia following traumatic brain injury: a critical evaluation.

Hyperthermia, frequently seen in patients following traumatic brain injury (TBI), may be due to posttraumatic cerebral inflammation, direct hypothalamic damage, or secondary infection resulting in fever. Regardless of the underlying cause, hyperthermia increases metabolic expenditure, glutamate release, and neutrophil activity to levels higher than those occurring in the normothermic brain-injured patient. This synergism may further compromise the injured brain, enhancing the vulnerability to secondary pathogenic events, thereby exacerbating neuronal damage.

Presumed apoptosis and reduced arcuate nucleus neuropeptide Y and pro-opiomelanocortin mRNA in non-coma hypoglycemia.

Hypoglycemia reduces sympathoadrenal responses to subsequent hypoglycemic bouts by an unknown mechanism. To assess whether such hypoglycemia-associated autonomic failure is due to actual brain damage, male Sprague-Dawley rats underwent 1-h bouts of insulin-induced (5 U/kg i.v.

Immune stimulation induces Fos expression in brainstem amygdala afferents.

Adaptation to infectious diseases or models of infectious diseases such as immune stimulation with exogenous administration of bacterial lipopolysaccharide (LPS) or cytokines involve complex autonomic, endocrine, and behavioral responses mediated by the central nervous system. The purpose of this study is to determine the neural pathways from the brainstem activating the central nucleus of the amygdala after LPS injections in rats. Fos immunohistochemistry was performed as a marker of neuronal activation in rats prepared with injections of the retrograde tracing agents Fluorogold or cholera toxin B subunit directed at the central nucleus of the amygdala, and subsequently treated with intravenous LPS.

Identification of pressor regions activated by central cholinergic stimulation in rat brain.

The acetylcholinesterase inhibitor neostigmine (2 microg) was microinjected into the lateral cerebral ventricle (i.c.v.

Central amygdala Fos expression during hypotensive or febrile, nonhypotensive endotoxemia in conscious rats.

The distribution and time course of Fos expression in neurons in the central nucleus of the amygdala (CeA) were studied in endotoxemic rats in two separate experiments. In each case, the severity of the endotoxin (lipopolysaccharide; LPS) challenge was characterized by using physiological outcome variables, including blood pressure and heart rate. Throughout the rostrocaudal extent of the CeA, extensive Fos staining was found 3 hours after injection with a hypotensive dose of Salmonella enteritidis LPS.