Oxalate nephropathy in association with gastric bypass.

We present the case of a 46-year-old woman with a history of Roux-en-Y gastric bypass one year prior, who presented to the emergency room with vomiting and oliguria lasting 10 days. Initial evaluation revealed acute kidney injury with serum creatinine 14.9 mg/dL (normal range 0.

Angiotensin II Regulates Mitochondrial mTOR Pathway Activity Dependent on Acyl-CoA Synthetase 4 in Adrenocortical Cells.

Two well-known protein complexes in mammalian cells, mTOR type 1 and type 2 (mTORC1/2) are involved in several cellular processes such as protein synthesis, cell proliferation, and commonly dysregulated in cancer. An acyl-CoA synthetase type 4 (ACSL4) is one of the most recently mTORC1/2 regulators described, in breast cancer cells. The expression of ACSL4 is hormone-regulated in adrenocortical cells and required for steroid biosynthesis.

Inhibition of mitochondrial fission by Drp-1 blockade by short-term leptin and Mdivi-1 treatment improves white adipose tissue abnormalities in obesity and diabetes.

Background: Obesity and type 2 diabetes are chronic diseases characterized by insulin resistance, mitochondrial dysfunction and morphological abnormalities.

Objective: We have investigated if dysregulation of mitochondrial dynamics and biogenesis is involved in an animal model of obesity and diabetes.

Methods: The effect of short-term leptin and mdivi-1 - a selective inhibitor of Drp-1 fission-protein - treatment on mitochondrial dynamics and biogenesis was evaluated in epididymal white adipose tissue (WAT) from male ob/ob mice.

Type 1 diabetes and subcutaneous insulin resistance syndrome treated with pancreas transplantation.

We present a case of subcutaneous insulin resistance syndrome, a rare entity, consisting of subcutaneous and intramuscular insulin resistance, with normal or almost normal sensitivity to insulin when administered intravenously. Its cause is unknown and its treatment is challenging. Our patient required a pancreas transplant.

[Tibial brown tumor as a presentation of primary hyperparathyroidism].

Cystic fibrous osteitis is a complication of a very evolved hyperparathyroidism. Because the determination of calcium, parathyroid hormone and vitamin D have become routine studies, this bone complication is uncommon in western countries. However, it should be considered in the differential diagnosis of hypercalcemia and lytic bone lesions.

[Analysis of the first 100 patients with COVID-19 admitted to internal medicine wards at the Hospital de Clínicas José de San Martin, Buenos Aires University].

This retrospective descriptive study analyzes the clinical and epidemiological characteristics, the disease evolution and its association with laboratory markers of poor prognosis of the first 100 patients with COVID-19 admitted to internal medicine wards at the Hospital de Clínicas José de San Martín, University of Buenos Aires. Thirty-one patients were nursing home residents, the most common clinical manifestations were fever, cough and odynophagia. Regarding comorbidities, obesity was the most frequent one and hypertension was the most prevalent in patients with pneumonia.

[Emphysematous cystitis in an 87 year old man].

Emphysematous cystitis is a complicated form of urinary tract infection, characterized by the presence of air inside the wall and in the light of the bladder, affecting more diabetics, elderly and immunosuppressed. The microorganisms that most frequently cause this entity are Escherichia coli and Klebsiella pneumoniae. Its treatment is based on broad-spectrum antibiotics, bladder catheterization and partial or total cystectomy in severe cases.

Angiotensin II stimulation promotes mitochondrial fusion as a novel mechanism involved in protein kinase compartmentalization and cholesterol transport in human adrenocortical cells.

In steroid-producing cells, cholesterol transport from the outer to the inner mitochondrial membrane is the first and rate-limiting step for the synthesis of all steroid hormones. Cholesterol can be transported into mitochondria by specific mitochondrial protein carriers like the steroidogenic acute regulatory protein (StAR). StAR is phosphorylated by mitochondrial ERK in a cAMP-dependent transduction pathway to achieve maximal steroid production.

Fitz-Hugh-Curtis Syndrome Caused by Gonococcal Infection in a Patient with Systemic Lupus Erythematous: A Case Report and Literature Review.

BACKGROUND Fitz-Hugh-Curtis (FHC) syndrome is a perihepatitis linked to inflammatory pelvic disease. It can be caused by Neisseria gonorrhoeae or Chlamydia trachomatis infections. FHC syndrome usually presents with pain in the right hypochondrium and fever, associated with symptoms and signs of pelvic infection in women.

Treatment with liraglutide may improve markers of CVD reflected by reduced levels of apoB.

Background: Dislipidaemia and increased levels of apolipoprotein B (apoB) in individuals with obesity are risk factors for development of cardiovascular disease (CVD). The aim of this study was to investigate the effect of weight loss and weight maintenance with and without liraglutide treatment on plasma lipid profiles and apoB.

Methods: Fifty-eight individuals with obesity (body mass index 34.

Takotsubo Myocardiopathy and Hyperthyroidism: A Case Report and Literature Review.

BACKGROUND Takotsubo cardiomyopathy (TM), also called stress myocardiopathy or transient left ventricular apical ballooning syndrome, is characterized by acute left ventricular dysfunction with reversible wall motion abnormalities. TM resembles acute coronary syndrome (ACS) in the absence of coronary artery disease (CAD). In several reports, TM has been described in association with hyperthyroidism, suggesting the potential role of thyrotoxicosis in the pathophysiology.

Intravascular Large B Cell Lymphoma Presenting as Fever of Unknown Origin and Diagnosed by Random Skin Biopsies: A Case Report and Literature Review.

BACKGROUND Intravascular lymphoma (IVL) is a rare lymphoproliferative disorder characterized by the proliferation of large B lymphoma cells within the lumen of small-caliber blood vessels. Clinical features are nonspecific, presenting as a systemic disease with fever and may be life-threatening. Antemortem diagnosis is difficult but may be made with biopsies of affected tissues or with random skin biopsies.

Cardiac-specific overexpression of thioredoxin 1 attenuates mitochondrial and myocardial dysfunction in septic mice.

Sepsis-induced myocardial dysfunction is associated with increased oxidative stress and mitochondrial dysfunction. Current evidence suggests a protective role of thioredoxin-1 (Trx1) in the pathogenesis of cardiovascular diseases. However, it is unknown yet a putative role of Trx1 in sepsis-induced myocardial dysfunction, in which oxidative stress is an underlying cause.

The pan-caspase inhibitor Emricasan (IDN-6556) decreases liver injury and fibrosis in a murine model of non-alcoholic steatohepatitis.

Background & Aims: Hepatocyte apoptosis, the hallmark of non-alcoholic steatohepatitis (NASH) contributes to liver injury and fibrosis. Although, both the intrinsic and extrinsic apoptotic pathways are involved in the pathogenesis of NASH, the final common step of apoptosis is executed by a family of cysteine-proteases termed caspases. Thus, our aim was to ascertain if administration of Emricasan, a pan-caspase inhibitor, ameliorates liver injury and fibrosis in a murine model of NASH.

Abnormal mitochondrial fusion-fission balance contributes to the progression of experimental sepsis.

Sepsis-associated multiple organ failure is a major cause of mortality characterized by a massive increase of reactive oxygen and nitrogen species (ROS/RNS) and mitochondrial dysfunction. Despite intensive research, determining events in the progression or reversal of the disease are incompletely understood. Herein, we studied two prototype sepsis models: endotoxemia and cecal ligation and puncture (CLP)-which showed very different lethality rates (2.

Defective leptin-AMP-dependent kinase pathway induces nitric oxide release and contributes to mitochondrial dysfunction and obesity in ob/ob mice.

Aims: Obesity arises on defective neuroendocrine pathways that increase energy intake and reduce mitochondrial metabolism. In the metabolic syndrome, mitochondrial dysfunction accomplishes defects in fatty acid oxidation and reciprocal increase in triglyceride content with insulin resistance and hyperglycemia. Mitochondrial inhibition is attributed to reduced biogenesis, excessive fission, and low adipokine-AMP-activated protein kinase (AMPK) level, but lateness of the respiratory chain contributes to perturbations.

Mitochondrial nitric oxide synthase: a masterpiece of metabolic adaptation, cell growth, transformation, and death.

Mitochondria are specialized organelles that control energy metabolism and also activate a multiplicity of pathways that modulate cell proliferation and mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO) regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the production of superoxide anion from the mitochondrial electron transfer chain. In this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to oxidation-reduction reaction (redox)-dependent cell signaling.

Control of muscle mitochondria by insulin entails activation of Akt2-mtNOS pathway: implications for the metabolic syndrome.

Background: In the metabolic syndrome with hyperinsulinemia, mitochondrial inhibition facilitates muscle fat and glycogen accumulation and accelerates its progression. In the last decade, nitric oxide (NO) emerged as a typical mitochondrial modulator by reversibly inhibiting citochrome oxidase and oxygen utilization. We wondered whether insulin-operated signaling pathways modulate mitochondrial respiration via NO, to alternatively release complete glucose oxidation to CO(2) and H(2)O or to drive glucose storage to glycogen.

The biological significance of mtNOS modulation.

In the last years, nitric oxide synthases (NOS) have been localized in mitochondria. At this site, NO yield directly regulates the activity of cytochrome oxidase, O(2) uptake and the production of reactive oxygen species. Recent studies showed that translocated neuronal nitric oxide synthase (nNOS) is posttranslationally modified including phosphorylation at Ser 1412 (in mice) and myristoylation in an internal residue.

Modulation of liver mitochondrial NOS is implicated in thyroid-dependent regulation of O(2) uptake.

Changes in O(2) uptake at different thyroid status have been explained on the basis of the modulation of mitochondrial enzymes and membrane biophysical properties. Regarding the nitric oxide (NO) effects, we tested whether liver mitochondrial nitric oxide synthase (mtNOS) participates in the modulation of O(2) uptake in thyroid disorders. Wistar rats were inoculated with 400 microCi (131)I (hypothyroid group), 20 microg thyroxine (T(4))/100 g body wt administered daily for 2 wk (hyperthyroid group) or vehicle (control).