Disappearing choroidal mass: Ophthalmic manifestations of a Presumed Kikuchi-Fujimoto disease.

PURPOSE: to report our findings in a patient with presumed Kikuchi-Fujimoto disease. METHODS: report of clinical findings, fundus images, OCT, and ultrasonography. RESULTS: a 19-year-old female patient who presented with an unusual form of symptoms that fit a disease called Kikuchi-Fujimoto disease (KFD). A large choroidal mass was observed in the posterior pole, a month later the mass was completely gone. CONCLUSION: large choroidal masses can occur in patients with Kikuchi-Fujimoto disease, these do not warrant treatment as they are self-limiting.

Customizable Collagen Vitrigel Membranes and Preliminary Results in Corneal Engineering.

Corneal opacities are a leading cause of visual impairment that affect 4.2 million people annually. The current treatment is corneal transplantation, which is limited by tissue donor shortages. Corneal engineering aims to develop membranes that function as scaffolds in corneal cell transplantation. Here, we describe a method for producing transplantable corneal constructs based on a collagen vitrigel (CVM) membrane and corneal endothelial cells (CECs). The CVMs were produced using increasing volumes of collagen type I: 1X (2.8 µL/mm2), 2X, and 3X. The vitrification process was performed at 40% relative humidity (RH) and 40 °C using a matryoshka-like system consisting of a shaking-oven harboring a desiccator with a saturated K2CO3 solution. The CVMs were characterized via SEM microscopy, cell adherence, FTIR, and manipulation in an ex vivo model. A pilot transplantation of the CECs/CVM construct in rabbits was also carried out. The thickness of the CVMs was 3.65-7.2 µm. The transparency was superior to a human cornea (92.6% = 1X; 94% = 2X; 89.21% = 3X). SEM microscopy showed a homogenous surface and laminar organization. The cell concentration seeded over the CVM increased threefold with no significant difference between 1X, 2X, and 3X (p = 0.323). The 2X-CVM was suitable for surgical manipulation in the ex vivo model. Constructs using the CECs/2X-CVM promoted corneal transparency restoration.

Intermittent Fasting as Possible Treatment for Heart Failure.

Western-style diet often leads to food overconsumption, which triggers the development of comorbidities, such as obesity, insulin resistance, hypercholesterolemia, hypertriglyceridemia, type 2 diabetes, and heart failure (HF). Several studies suggest that intermittent fasting (IF) protects against the development of those morbidities. This study presents evidence of the beneficial effects of IF on HF. Based on the current evidence, we discuss the potential molecular mechanisms by which IF works and where liver ketone bodies (KBs) play important roles. There is evidence that IF promotes a metabolic switch in highly metabolic organs, such as the heart, which increases the use of KBs during fasting. However, besides their role as energy substrates, KBs participate in the signaling pathways that control the expression of genes involved in oxidative stress protection and metabolism. Several molecular factors, such as adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferatoractivated receptor, fibroblast growth factor 21 (FGF21), sirtuins, and nuclear factor erythroid 2-related factor 2 (Nrf2) are involved. Furthermore, IF appears to maintain circadian rhythm, which is essential for highly metabolically active organs. Finally, we highlight the important research topics that need to be pursued to improve current knowledge and strengthen the potential of IF as a preventive and therapeutic approach to HF.

Glucolipotoxicity-induced Oxidative Stress is Related to Mitochondrial Dysfunction and Apoptosis of Pancreatic ß-cell.

Glucolipotoxicity-induced oxidative stress and mitochondrial dysfunction of pancreatic ß-cells are some of the mechanisms that have been related to the low insulin secretion and cell death during diabetes development. In early or non-chronic stages, the pancreatic ß-cells respond to hyperglycemia or hyperlipidemia, stimulating insulin secretion. However, the chronic effect of both leads to glucolipotoxicity, which induces constant overstimulation of pancreatic ß-cells, a condition that leads to cell death by apoptosis. The mechanism described, at this moment, is the accelerated mitochondrial dysfunction triggered by the high production of reactive oxygen species (ROS) due to excess nutrients. At first, mitochondria respond to over-nutrition accelerating oxygen consumption and consequently increasing the ATP synthesis. A permanent increase of ATP/ADP ratio leads to a constant inhibition of K+ ATP-channel and, therefore, a continuous insulin secretion accompanied by an increase in ROS. Finally, ROS accumulation compromises mitochondrial function due to the uncontrolled oxidation of proteins, lipids, and DNA generating functional alterations such as a drop of membrane potential, deregulation of mitochondrial dynamics, low rate of ATP synthesis and consequently the cell death. This review aims to describe the effect of glucolipotoxicity- induced oxidative stress and its relationship with mitochondrial dysfunction in ß-cell during type 2 diabetes development.

A single session of physical activity restores the mitochondrial organization disrupted by obesity in skeletal muscle fibers.

BACKGROUND: Several studies have proved that physical activity (PA) regulates energetic metabolism associated with mitochondrial dynamics through AMPK activation in healthy subjects. Obesity, a condition that induces oxidative stress, mitochondrial dysfunction, and low AMPK activity leads to mitochondrial fragmentation. However, few studies describe the effect of PA on mitochondrial dynamics regulation in obesity. AIM: The present study aimed to evaluate the effect of a single session of PA on mitochondrial dynamics regulation as well as its effect on mitochondrial function and organization in skeletal muscles of obese rats (Zucker fa/fa). MAIN METHODS: Male Zucker lean and Zucker fa/fa rats aged 12 to 13 weeks were divided into sedentary and subjected-to-PA (single session swimming) groups. Gastrocnemius muscle was dissected into isolated fibers, mitochondria, mRNA, and total proteins for their evaluation. KEY FINDINGS: The results showed that PA increased the Mfn-2 protein level in the lean and obese groups, whereas Drp1 levels decreased in the obese group. OMA1 protease levels increased in the lean group and decreased in the obese group. Additionally, AMPK analysis parameters (expression, protein level, and activity) did not increase in the obese group. These findings correlated with the partial restoration of mitochondrial function in the obese group, increasing the capacity to maintain the membrane potential after adding calcium as a stressor, and increasing the transversal organization level of the mitochondria analyzed in isolated fibers. SIGNIFICANCE: These results support the notion that obese rats subjected to PA maintain mitochondrial function through mitochondrial fusion activation by an AMPK-independent mechanism.

[Update in the endoscopic management of benign esophageal stenoses]. / Actualidades en el manejo endoscópico de las estenosis benignas del esófago.

Correction of dysphagia in benign esophageal stenosis without the need for surgery is a task that has been tried to be resolved for more than three centuries; in the last three decades this management has evolved with the development of pneumatic dilators and, more recently, alternative and adjuvant treatments like local steroid injection, electrocoagulation, use of argon plasma and the use of expandable stents have been added. The most common causes of benign esophageal stenosis are peptic esophagitis in first place followed by the ingestion of caustic substances; other less frequent etiologies are medication ingestion, stenosis secondary to a surgical anastomosis of the esophagus and stenosis related to mediastinal radiotherapy; the rarest causes include esophageal rings and membranes, sclerotherapy for esophageal varices, the prolonged use of a nasogastric tube, Crohn's disease, among others. A complete clinical, radiological and endoscopic evaluation of the patient is required to make the diagnosis, with the respective complimentary histopathologic study. At present, traditional esophageal dilatations, as well as pneumatic dilatations are the most common and effective treatments, the previously mentioned alternative and adjuvant treatments are used in exceptional cases, some with advantages over the others depending on each patient in particular and on the characteristics and etiology of the stenosis. The future seems to be aimed at the use of temporary expandable stents.

Función inadecuada del esfinter de ODDI: Tratamiento endoscópico y evaluación a largo plazo / Inadequate function of Oddi-s sphincter. Endoscopic treatment and long term follow up

El síndrome de función inadecuada de esfinter de Oddi, es una entidad clínica de difícil diagnóstico y tratamiento controvertido. El diagnóstico se sospecha con bases clínicas, bioquímicas, ultrasonográficas y endoscópica, pero se corrobora solamente con la manometría. Estudiamos a 35 pacientes, 23 mujeres y 12 hombres con edad promedio de 56.4 años. Todos tenian antecedentes de colecistectomía y continuaban con dolor similar, 33 tenían elevación de la fosfatasa alcalina, en todos se demostro dilatación de la vía biliar mayor a 12 mm y retardo en el vaciamiento del medio de contraste mayor a 45 minutos. La manometría demostró presión elevada de esfinter de Oddi mayor a 30 mmHg. En todos los casos realizamos una esfinterotomía endoscópica amplia sin complicaciones. Hicimos evaluación clínica, bioquímica y endoscópica cada 3 meses durante el primer año y cada 6 meses durante el segundo y tercer año. Treinta y un pacientes (89.6