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igm, our theoretical framework remains to be thought-provoking, and hypothesis-generating at the present time. Muscle coordination plays an important role in glenohumeral stability. The rotator cuff and the long head of the biceps are considered the primary dynamic stabilizers muscles. However, the fact that a subgroup of patients with a massive tear in the rotator cuff were able to keep a normal function, should make us question this traditional view. We hypothesize that the teres major which is also a monoarticular scapulohumeral muscle, although it is not part of the conjoined tendon of the rotator cuff, can play a role in glenohumeral stability by a direct support of the humeral head generated by the particular posteroanterior location of this muscle under the humeral head and which, as far as we know, has not been written up previously. This particular effect could appear while the arm is being lifted and the humeral head could be leaning on against the teres major muscle belly underneath it. An anatomical a radiological study was carried out to substantiate our hypothesis. Two cadaver specimens were used for the anatomical study. Frist body was studied through conventional dissection. The second body was analysed through sectional anatomy. Then a radiological study was carried out using magnetic resonance imaging in a healthy male volunteer. Both anatomically and radiologically, the anteroinferior surface of the humeral head was showed firmly resting against the muscle belly of the teres major, to the point of misshaping it from 110 degrees of arm elevation with external rotation. The specific contribution of this effect to the glenohumeral stability needs to be confirmed by further studies and can help us to prevent the high incidence of glenohumeral dislocations. Atherosclerosis and its fatal complications, such as myocardial infarction or stroke, represent the most common cause of morbidity or mortality in modern world. It was observed that an excess of reactive oxygen species (ROS) accompanies atherosclerosis. Under physiological circumstances, intracellular H+ accumulates and cell membrane depolarizes during ROS production, rendering ROS generation self-limiting and thus avoiding oxidative stress. However, the persistent production of ROS during atherosclerosis suggests that the physiologically self-limiting ROS-generating process was somehow disrupted and there may be an as-yet unknown mechanism supporting unlimited ROS generation. We thus postulated that an outward H+ conductance, which can efficiently export H+ from the cytosol and maintain membrane potential, may play a crucial role during atherosclerosis. So far, Hv1 channels were mainly found in immune cells (macrophages, neutrophils). As large quantities of vascular infiltrating macrophages exist, we proposed that Hv1-mediated oxidative stress promoted excessive ROS production and the formation of foam cells, contributing to atherosclerosis. In addition, we could not exclude the possibility that Hv1 channels may be upregulated in vascular cells under atherosclerotic conditions, which may also exert effects on vascular inflammation and fibrous cap formation. The present study will employ Hv1 knockout mice in combination with in vitro studies to explore the role of Hv1 channel in atherosclerosis and dissect the underlying mechanisms. The results are expected to offer novel insights into the pathogenesis of atherosclerosis as well as clues for developing novel therapeutic avenues. Skin microbial flora was believed to can implicate skin health, and many recent reports point out a close linkage between the dysbiosis of the microbiome with the disease. Changes of microbiota, including diversity, species, and abundance, have been demonstrated in disease states, and it was believed the changes may cause infection and chronicity of the debilitating wounds. And it was been found a reverse of the dysbiosis after the effective treatment, but it failed to find a positive effect of antibiotic therapy on skin disease without significant clinical infection. The microbiomes were compared to the ‘second gene reservoir’, and indicated that their co-existing with the human being is a result of co-evolution. The current studies have shown that the microbial community on the skin surface should have an ideal optimal state, which can effectively regulate the immune tolerance and help to avoid the invasion of external pathogenic bacteria, then the body can be in a relatively healthy state. In this paper, we hypothesized that failing to maintain the harmonious relationship between microbes and human beings is the reason we suffering from most skin diseases, including chronic non-healing wounds. Thus, the dysbiosis of skin microbiota theory can help us better understand the mechanism of wound formation and problems encountered in wound treatment. Quality metrics in the healthcare sector have become a key component of ensuring improved health outcomes and care equity. Alongside the emergence of information technology in healthcare (eg. electronic health records), the primary method utilized to infer “quality” has been the development of measures for healthcare processes and outcomes. Engaging with the specific case of sepsis treatment and sepsis quality metrics, this paper traces how quality is defined, measured, and codified in a 600-bed acute-care hospital in New York City. Sepsis is a severe health condition, primarily managed in the emergency department, that is caused by infection and can result in multi-organ shutdown and mortality. Multiple government agencies have established metrics that regulate New York hospitals based on their compliance with specific sepsis treatment procedures. I draw on data from a 15-month ethnography and in-depth interviews with clinicians and administrators, to show how quality measurement is reshaping the ways healthcare is delivered and organized. BMS-927711 order I reveal how, at Borough Hospital, efforts to treat sepsis based on quality metrics have constrained clinician expertise, prioritized compliance, and reoriented workflow towards standardized treatment protocols. This reorientation leads to, what I term abstracted surveillance protocols, that increasingly regulate definitions of healthcare quality. I demonstrate that abstracted surveillance protocols enable highly complex clinical processes to be measured based on metric compliance rather than clinical pathways, therefore moving definitions of quality away from the bedside.