Utjecaj mangana na sinaptičku transmisiju

In the course of our investigations of the influence of metal ions on synaptic transmission and acetilcholine output, we have noticed that manganese ions cause a block of ganglionic transmission when added to the fluid perfusing the superior cervical ganglion.Dodatak mangana tekućini, kojom se vrši perfuzija izoliranog gornjeg vratnog simpatičnog ganglija mačke, izaziva smanjenje kontrakcija membrane niktitans na stimulaciju predganglijskih vlakana vratnog simpatikusa. Stimulacija postganglijskih vlakana izaziva normalne kontrakcije membrane usprkos prisutnosti manganovih iona. Kalcijevi ioni imaju antagonističke djelovanje na blokadu sinaptičke transmisije izazvanu dodatkom manganovih iona. Mangan izaziva sinaptičku blokadu u koncentraciji od 100 mikrograma na 1 ml

TAVR: A Review of Current Practices and Considerations in Low-Risk Patients

Transcatheter aortic valve replacement (TAVR) is an established treatment for severe, symptomatic, aortic stenosis (AS) in patients of all risk categories and now comprises 12.5% of all aortic valve replacements. TAVR is a less invasive alternative to traditional surgical aortic valve replacement (SAVR), with equivalent or superior outcomes. The use of TAVR has increased rapidly. The success and increase in use of TAVR are a result of advances in technology, greater operator experience, and improved outcomes. Indications have recently expanded to include patients considered to be at low risk for SAVR. While TAVR outcomes have improved, remaining challenges include the management of coexistent coronary artery disease, prevention of periprocedural stroke, and issue of durability. These issues are even more relevant for low-risk, younger patients

Apixaban as a Rare Cause of Leukocytoclastic Vasculitis

Apixaban is a rare cause of leukocytoclastic vasculitis (LCV). To our knowledge, there is only one other reported case due to apixaban in the literature. We present a case of apixaban-induced leukocytoclastic vasculitis in a 95-year-old male. He had been started on apixaban 12 days prior to presentation and developed worsening palpable purpura of his lower extremities. Possible etiologies of this new rash were excluded, with biopsy showing extensive purpura with superficial perivascular neutrophilic infiltrate and leukocytoclasis. Apixaban was discontinued, and the patient was started on a slow prednisone taper with subsequent resolution of his rash

Cardiovascular manifestations of renovascular hypertension in diabetic mice

Purpose. Type 2 diabetes is the leading cause of end stage renal disease in the United States. Atherosclerotic renal artery stenosis is commonly observed in diabetic patients and impacts the rate of renal and cardiovascular disease progression. We sought to test the hypothesis that renovascular hypertension, induced by unilateral renal artery stenosis, exacerbates cardiac remodeling in leptin-deficient (db/db) mice, which serves as a model of human type II diabetes. Methods. We employed a murine model of renovascular hypertension through placement of a polytetrafluoroethylene cuff on the right renal artery in db/db mice. We studied 109 wild-type (non-diabetic, WT) and 95 db/db mice subjected to renal artery stenosis (RAS) or sham surgery studied at 1, 2, 4, and 6+ weeks following surgery. Cardiac remodeling was assessed by quantitative analysis of the percent of myocardial surface area occupied by interstitial fibrosis tissue, as delineated by trichrome stained slides. Aortic pathology was assessed by histologic sampling of grossly apparent structural abnormalities or by section of ascending aorta of vessels without apparent abnormalities. Results. We noted an increased mortality in db/db mice subjected to RAS. The mortality rate of db/db RAS mice was about 23.5%, whereas the mortality rate of WT RAS mice was only 1.5%. Over 60% of mortality in the db/db mice occurred in the first two weeks following RAS surgery. Necropsy showed massive intrathoracic hemorrhage associated with aortic dissection, predominantly in the ascending aorta and proximal descending aorta. Aortas from db/db RAS mice showed more smooth muscle dropout, loss of alpha smooth muscle actin expression, medial disruption, and hemorrhage than aortas from WT mice with RAS. Cardiac tissue from db/db RAS mice had more fibrosis than did cardiac tissue from WT RAS mice. Conclusions. db/db mice subjected to RAS are prone to develop fatal aortic dissection, which is not observed in WT mice with RAS. The db/db RAS model provides the basis for future studies directed towards defining basic mechanisms underlying the interaction of hypertension and diabetes on the development of aortic lesions

A Rare Case of ARDS Caused by Bupropion Inhalation and Treated with Noninvasive Ventilation

Acute respiratory distress syndrome, characterized by the Berlin criteria, is associated with a high mortality rate. Its treatment includes addressing the underlying etiology, general supportive measures, and achievement of effective oxygenation. New key data indicates that in a subset of patients, noninvasive ventilation techniques can be a therapeutic and equivalent alternative to traditional invasive ventilation. We present a rare case of ARDS triggered by nasal bupropion inhalation and effectively treated with noninvasive positive pressure ventilation resulting in complete resolution

Cardiovascular phenotype in Smad3 deficient mice with renovascular hypertension

<div><p>Renovascular hypertension (RVH) has deleterious effects on both the kidney and the heart. TGF-β signaling through Smad3 directs tissue fibrosis in chronic injury models. In the 2-kidney 1-clip (2K1C) model of RVH, employing mice on the 129 genetic background, Smad3 deficiency (KO) protects the stenotic kidney (STK) from development of interstitial fibrosis. However, these mice have an increased incidence of sudden cardiac death following 2K1C surgery. The purpose of this study was to characterize the cardiovascular phenotype of these mice. Renal artery stenosis (RAS) was established in Wild-type (WT) and Smad3 KO mice (129 genetic background) by placement of a polytetrafluoroethylene cuff on the right renal artery. Mortality was 25.5% for KO mice with RAS, 4.1% for KO sham mice, 1.2% for WT with RAS, and 1.8% for WT sham mice. Myocardial tissue of mice studied at 3 days following surgery showed extensive myocyte necrosis in KO but not WT mice. Myocyte necrosis was associated with a rapid induction of <i>Ccl2</i> expression, macrophage influx, and increased MMP-9 activity. At later time points, both KO and WT mice developed myocardial fibrosis. No aortic aneurysms or dissections were observed at any time point. Smad3 KO mice were backcrossed to the C57BL/6J strain and subjected to RAS. Sudden death was observed at 10–14 days following surgery in 62.5% of mice; necropsy revealed aortic dissections as the cause of death. As observed in the 129 mice, the STK of Smad3 KO mice on the C57BL/6J background did not develop significant chronic renal damage. We conclude that the cardiovascular manifestations of Smad3 deficient mice are strain-specific, with myocyte necrosis in 129 mice and aortic rupture in C57BL/6J mice. Future studies will define mechanisms underlying this strain-specific effect on the cardiovascular system.</p></div

Mortality in Smad3 KO and WT mice on the 129 background observed at different time points following RAS or sham surgery.

<p>Mortality in Smad3 KO and WT mice on the 129 background observed at different time points following RAS or sham surgery.</p

Smad3 KO RAS mice showed significant induction in <i>Ccl2</i> mRNA expression at day 3 following RAS.

<p>*p<0.0001, **p = 0.0002.</p