Skeletal muscle growth defect in human growth hormone transgenic rat is accompanied by phenotypic changes in progenitor cells

Growth hormone (GH) is known to have a pivotal role in the maintenance of skeletal muscle mass. Sarcopenia, the loss of skeletal muscle mass, is a common phenomenon in aging, and it is widely accepted that sarcopenia is largely attributed to age-related decline in GH secretion. In the present study, we tested if human growth hormone transgenic rats (GH-TG rats) whose plasma GH levels are maintained relatively low could be an appropriate model for sarcopenia. Analyses of GH-TG rats revealed that they exhibit skeletal muscle growth defect as well as atrophy of myofibers. The number of myofibers in tibialis anterior muscle was comparable to that of WT rats, while the proportion of type I slow myofibers in tibialis anterior muscle was increased in GH-TG rats after 5 months. Neither increased expression of ubiquitin ligases, MuRF1 and MAFbx, nor indication of apoptotic cell death was observed. Notably, myogenic differentiation potential of skeletal muscle progenitor cells in GH-TG rats was lower than WT rats, and this was accompanied by increased adipogenic potential. These results indicate that GH-TG rats could be a useful model to elucidate the mechanism of sarcopenia induced by reduced GH action and raised the possibility that decreased GH action may cause an alteration of differentiation potential of skeletal muscle progenitor cells.     

Occupational Rhinosinusitis and Upper Airway Disease: The World Trade Center Experience

The World Trade Center disaster and its recovery work involved a range of hazardous occupational exposures that have not been fully characterized but that can be reasonably assumed to have the potential to cause mucosal inflammation, preferentially (but not exclusively) in the upper airway. A high prevalence of rhinosinusitis and upper airway disease (UAD) symptoms was reported by several early surveys. Clinical studies demonstrated objective, clinically significant, and persistent chronic perennial rhinosinusitis and UAD—with or without seasonal exacerbation—in a large proportion of patients. Demonstration of an association between UAD and available exposure indicators has been limited. Atopy seemed to be associated with increased UAD symptom severity and to be a risk factor for upper, but not lower, airway disease. World Trade Center-related UAD is considered an irritant-induced disease but not, in many cases, of acute onset. No data thus far suggest an increased upper airway cancer incidence.     

Mitochondrial Dysfunction and Oxidative Damage to Sarcomeric Proteins

Hypertension is an important risk factor for the development of heart failure. Increased production of reactive oxygen species (ROS) contributes to cardiac dysfunction by activating numerous pro-hypertrophic signaling cascades and damaging the mitochondria, thus setting off a vicious cycle of ROS generation. The way in which oxidative stress leads to exacerbation of systolic and diastolic dysfunction is still unclear, however. In skeletal muscle and ischemic myocardium, increased ROS production causes preferential oxidation of myofibrillar proteins and provides a mechanistic link between oxidative damage and impaired contractility through disruption of actin-myosin interactions, enzymatic functions, calcium sensitivity, and efficiency of cross-bridge cycling. In this review, we summarize recent findings in the fields of heart failure and sarcomere biology and speculate that oxidative damage to myofibrils may contribute to the development of heart failure.     

The Potential Research Impact of Patient Reported Outcomes on Osteogenesis Imperfecta

Background  

Osteogenesis imperfecta (OI) is an inherited connective tissue disorder with many phenotypic presentations ranging from mild to severe. It is often called “brittle bone disease.” Treatment consists of physical therapy, surgical interventions, medications and, in some cases, experimental therapies. Because treatment is not standardized and is often experimental, information on the success of different methods is usually not available or well documented.     

Absence of Mycobacterium avium ss paratuberculosis-specific IS900 sequence in intestinal biopsy tissues of Indian patients with Crohn’s disease

Background and Objective  

The role of Mycobacterium avium ss paratuberculosis (MAP) in the etiopathology of Crohn’s disease (CD) remains controversial, because of conflicting reports demonstrating the presence of MAP-specific insertion sequence from intestinal biopsy tissues of patients clinically diagnosed for the disease. The present study was carried out to investigate the presence of MAP DNA in the intestinal tissues of CD patients to ascertain the relevance of MAP in Indian patients with CD.     

Double Giant Lambl’s Excrescence of aortic valve causing posterior circulation stroke

Diagnostic evaluation of embolic neurologic events requires the consideration of cardiac causes. Lambl’s Excrescences (LE)are filiform fronds that occur at sites of valvular closure due to “wear and tear” (Lambl Wien Med Wschr 6:244–247, 1856). The complex form of LE is “giant Lambl’s Excrescences” which results from the adherence of multiple adjacent excrescences that grow large. We recently had young male adult who presented with features of posterior circulation stroke (basilar) and detected to have two separate giant Lambl’s Excrescences on the aortic valve and treated successfully.     

Aortic root enlargement in patients undergoing double valve replacement for rheumatic etiology–preliminary results

Introduction  

Combined aortic and mitral valve disease is usually of rheumatic origin. In these patients we often encounter problem of small valve annuli particularly with aortic annulus. It is still debated whether a small prosthesis should be used or aortic root should be enlarged to prevent Patient Prosthesis Mismatch (PPM). This study was undertaken to review our strategy and feasibility of Aortic Root Enlargement (ARE) in patient undergo Double Valve Replacement (DVR) to avoid mismatch without increase in cost of treatment, morbidity or mortality.