Bilateral pneumothorax after general anesthesia in patient with pleomorphic sarcoma of soft tissue

The occurrence of a pneumothorax using supraglottic device is a rare complication during general anesthesia. Moreover, less than 2% of pneumothoraxes can be related to lung metastases, most due to soft tissue sarcoma. We present the case of a 45-year-old female diagnosed with metastatic sarcoma who developed a bilateral pneumothorax after general anesthesia with supraglottic device. Different causes of pneumothorax were discussed

A partition-free approach to transient and steady-state charge currents

We construct a non-equilibrium steady state and calculate the corresponding current for a mesoscopic Fermi system in the partition-free setting. To this end we study a small sample coupled to a finite number of semi-infinite leads. Initially, the whole system of quasi-free fermions is in a grand canonical equilibrium state. At t = 0 we turn on a potential bias on the leads and let the system evolve. We study how the charge current behaves in time and how it stabilizes itself around a steady state value, which is given by a Landauer-type formula.Comment: 14 pages, submitte

Caspase-independent programmed cell death triggers Ca2PO4 deposition in an in vitro model of nephrocalcinosis

We provide evidence of caspase-independent cell death triggering the calcification process in GDNF-silenced HK-2 cells

Albumin uptake in human podocytes: a possible role for the cubilin-amnionless (CUBAM) complex

Abstract Albumin re-uptake is a receptor-mediated pathway located in renal proximal tubuli. There is increasing evidence of glomerular protein handling by podocytes, but little is known about the mechanism behind this process. In this study, we found that human podocytes in vitro are committed to internalizing albumin through a receptor-mediated mechanism even after exposure to low doses of albumin. We show that these cells express cubilin, megalin, ClC-5, amnionless and Dab2, which are partners in the tubular machinery. Exposing human podocytes to albumin overload prompted an increase in CUBILIN, AMNIONLESS and CLCN5 gene expression. Inhibiting cubilin led to a reduction in albumin uptake, highlighting its importance in this mechanism. We demonstrated that human podocytes are committed to performing endocytosis via a receptor-mediated mechanism even in the presence of low doses of albumin. We also disclosed that protein overload first acts on the expression of the cubilin-amnionless (CUBAM) complex in these cells, then involves the ClC-5 channel, providing the first evidence for a possible role of the CUBAM complex in albumin endocytosis in human podocytes

Outcome predictors and quality of life of severe burn patients admitted to intensive care unit

<p>Abstract</p> <p>Background</p> <p>Despite significant medical advances and improvement in overall mortality rate following burn injury, the treatment of patients with extensive burns remains a major challenge for intensivists. We present a study aimed to evaluate the short- and the long-term outcomes of severe burn patients (total body surface area, TBSA > 40%) treated in a polyvalent intensive care unit (ICU) and to assess the quality of life of survivors, one year after the injury using the EuroQol-5D (EQ-5D) questionnaire.</p> <p>Methods</p> <p>A prospective-observational study was performed in an ICU of a University-affiliated hospital. Logistic regression analysis was used to identify the factors predicting in-hospital mortality. The EQ-5D questionnaire was used to asses participant's long term self-reported general health.</p> <p>Results</p> <p>During a period of five years, 50 patients participated in the study. Their mean age was 53.8 ± 19.8; they had a mean of %TBSA burned of 54.5 ± 18.1. 44% and 10% of patients died in the ICU and in the ward after ICU discharge, respectively. Baux index, SAPS II and SOFA on admission to the ICU, infectious and respiratory complications, and time of first burn wound excision were found to have a significant predictive value for hospital mortality. The level of health of all survivors was worse than before the injury. Problems in the five dimensions studied were present as follows: mobility (moderate 68.5%; extreme 0%), self-care (moderate 21%; extreme 36.9%), usual activities (moderate 68.5%; extreme 21%), pain/discomfort (moderate 68.5%; extreme 10.5%), anxiety/depression (moderate 36.9%; extreme 42.1%).</p> <p>Conclusions</p> <p>In severe burn patients, Baux index, severity of illness on admission to the ICU, complications, and time of first burn wound excision were the major contributors to hospital mortality. Quality of life was influenced by consequences of injury both in psychological and physical health.</p

Genetics and phenotypic heterogeneity of Dent disease: the dark side of the moon

Dent disease is a rare genetic proximal tubulopathy which is under-recognized. Its phenotypic heterogeneity has led to several different classifications of the same disorder, but it is now widely accepted that the triad of symptoms low-molecular-weight proteinuria, hypercalciuria and nephrocalcinosis/nephrolithiasis are pathognomonic of Dent disease. Although mutations on the CLCN5 and OCRL genes are known to cause Dent disease, no such mutations are found in about 25-35% of cases, making diagnosis more challenging. This review outlines current knowledge regarding Dent disease from another perspective. Starting from the history of Dent disease, and reviewing the clinical details of patients with and without a genetic characterization, we discuss the phenotypic and genetic heterogeneity that typifies this disease. We focus particularly on all those confounding clinical signs and symptoms that can lead to a misdiagnosis. We also try to shed light on a concealed aspect of Dent disease. Although it is a proximal tubulopathy, its misdiagnosis may lead to patients undergoing kidney biopsy. In fact, some individuals with Dent disease have high-grade proteinuria, with or without hematuria, as in the clinical setting of glomerulopathy, or chronic kidney disease of uncertain origin. Although glomerular damage is frequently documented in Dent disease patients' biopsies, there is currently no reliable evidence of renal biopsy being of either diagnostic or prognostic value. We review published histopathology reports of tubular and glomerular damage in these patients, and discuss current knowledge regarding the role of CLCN5 and OCRL genes in glomerular function

Cell death in the kidney

Apoptotic cell death is usually a response to the cell&rsquo;s microenvironment. In the kidney, apoptosis contributes to parenchymal cell loss in the course of acute and chronic renal injury, but does not trigger an inflammatory response. What distinguishes necrosis from apoptosis is the rupture of the plasma membrane, so necrotic cell death is accompanied by the release of unprocessed intracellular content, including cellular organelles, which are highly immunogenic proteins. The relative contribution of apoptosis and necrosis to injury varies, depending on the severity of the insult. Regulated cell death may result from immunologically silent apoptosis or from immunogenic necrosis. Recent advances have enhanced the most revolutionary concept of regulated necrosis. Several modalities of regulated necrosis have been described, such as necroptosis, ferroptosis, pyroptosis, and mitochondrial permeability transition-dependent regulated necrosis. We review the different modalities of apoptosis, necrosis, and regulated necrosis in kidney injury, focusing particularly on evidence implicating cell death in ectopic renal calcification. We also review the evidence for the role of cell death in kidney injury, which may pave the way for new therapeutic opportunities