Annular pancreas as a cause of neonatal duodenal obstruction, a case report.

The annular pancreas (AP) is an uncommon congenital anomaly, characterised by a circumferential envelope in the second portion of the duodenum. In recent years, some genetic component has been found in the etiology. A newborn full-term male, weighing at 1910 g at birth, had a history of intrauterine growth restriction and diagnosis of tetralogy of Fallot, Down syndrome and congenital hypothyroidism. Duodenal membrane is suspected after persistent postprandial vomiting and abdominal distension; his abdomen was distended, hyperresonant and soft. The gastroduodenal series showed data compatible with a duodenal membrane so exploratory laparotomy was performed, finding the pancreas completely wrapping the second portion of the duodenum, so a diamond-shaped-duodenoduodenostomy anastomosis was performed. The AP should be considered, especially in male neonates with postprandial vomiting, abdominal distension, who show some other congenital anomaly, and in the abdominal X-ray, the sign of the double bubble is observed.

Interactions of the molecular assembly of polysaccharide-protein systems as encapsulation materials. A review.

Studying the interactions of biopolymers like polysaccharides and proteins is quite important mainly due to the wide number of applications such as the stabilization and encapsulation of active compounds in complex systems. Complexation takes place when materials like proteins and polysaccharides are blended to promote the entrapment of active compounds. The interaction forces between the charged groups in the polymeric chains allow the miscibility of the components in the complex system. Understanding the interactions taking place between the polymers as well as between the wall material and the active compound is important when designing delivery systems. However, some features of the biopolymers like structure, functional groups, or electrical charge as well as extrinsic parameters like pH or ratios might affect the structure and the performance of the complex system when used in encapsulation applications. This work summarizes the recent progress of the polysaccharide/protein complexes for encapsulation and the influence of the pH on the structural modifications during the complexation process.

Importancia del uso adecuado del equipo de protección individual y la implementación de protocolos de seguridad perioperatorios durante la pandemia de COVID-19 / Importance of the Proper use of Personal Protective Equipment and the Implementation of Perioperative Safety Protocols During the COVID-19 Pandemic

RESUMEN El panorama que se presenta en la actualidad es un reto sin precedentes para el manejo de los pacientes quirúrgicos, la toma de decisiones y el empleo de recursos en cuanto a material y equipos de protección en el contexto de la pandemia por COVID-19. Por lo que el presente artículo pretende dar a conocer los lineamientos para el correcto actuar en el quirófano, el uso del equipo de protección individual, las indicaciones de cirugía y el mejor abordaje en el marco de esta situación. El principal objetivo de seguir estas recomendaciones es mitigar el riesgo de contagio y educar al personal de salud médico-quirúrgico para que esté preparado para hacer frente a esta pandemia.

ABSTRACT The current landscape represents an unprecedented challenge in managing surgical patients, decision-making and the use of resources such as protective equipment in the context of the COVID-19 pandemic. Therefore, the objective of this article is to provide guidelines for good conduct in the operating room, the use of personal protective equipment, suggestions for surgeries and the best approach in the context of this situation. The main objective of these recommendations is to mitigate the risk of contagion and to educate medical-surgical health personnel in how to deal with this pandemic.

Comparative transcriptional network modeling of three PPAR-α/γ co-agonists reveals distinct metabolic gene signatures in primary human hepatocytes.

AIMS: To compare the molecular and biologic signatures of a balanced dual peroxisome proliferator-activated receptor (PPAR)-α/γ agonist, aleglitazar, with tesaglitazar (a dual PPAR-α/γ agonist) or a combination of pioglitazone (Pio; PPAR-γ agonist) and fenofibrate (Feno; PPAR-α agonist) in human hepatocytes. METHODS AND RESULTS: Gene expression microarray profiles were obtained from primary human hepatocytes treated with EC(50)-aligned low, medium and high concentrations of the three treatments. A systems biology approach, Causal Network Modeling, was used to model the data to infer upstream molecular mechanisms that may explain the observed changes in gene expression. Aleglitazar, tesaglitazar and Pio/Feno each induced unique transcriptional signatures, despite comparable core PPAR signaling. Although all treatments inferred qualitatively similar PPAR-α signaling, aleglitazar was inferred to have greater effects on high- and low-density lipoprotein cholesterol levels than tesaglitazar and Pio/Feno, due to a greater number of gene expression changes in pathways related to high-density and low-density lipoprotein metabolism. Distinct transcriptional and biologic signatures were also inferred for stress responses, which appeared to be less affected by aleglitazar than the comparators. In particular, Pio/Feno was inferred to increase NFE2L2 activity, a key component of the stress response pathway, while aleglitazar had no significant effect. All treatments were inferred to decrease proliferative signaling. CONCLUSIONS: Aleglitazar induces transcriptional signatures related to lipid parameters and stress responses that are unique from other dual PPAR-α/γ treatments. This may underlie observed favorable changes in lipid profiles in animal and clinical studies with aleglitazar and suggests a differentiated gene profile compared with other dual PPAR-α/γ agonist treatments.

A critical review of the pharmacology of the plant extract of Pygeum africanum in the treatment of LUTS.

Despite an unremitting increase in the number of patients presenting symptoms of benign prostate hyperplasia (BPH), the viable treatment options remain relatively limited when compared to other disorders of aging. This has spurred an interest in so-called alternative medicines, many of which continue to be used in spite of the more recent emergence of rationally targeted therapies. Nonetheless, in the case of plant extracts, the vast majority of these have not been subjected to the same rigorous pre-clinical pharmacological testing and large-scale clinical trials now required by health authorities. Furthermore, demonstration of their clinical efficacy in BPH has been hindered by trials of limited duration with a high placebo response. Beginning with a preliminary demonstration of in vitro inhibition of growth factor-mediated fibroblast proliferation with Pygeum africanum extract, a detailed series of in vitro and in vivo studies on prostate growth and bladder function were undertaken. These studies, reviewed herein, have permitted the identification of putative molecular targets of Pygeum africanum extract affecting both growth factor-mediated prostate growth as well as specific parameters of bladder function. These results, corroborated in part by short-term clinical efficacy, set the stage for a large-scale clinical trial to investigate the efficacy of Pygeum africanum extract in the treatment of lower urinary tract symptoms.

Opposite regulation of the rat and human cytosolic aspartate aminotransferase genes by fibrates.

Fenofibrate, a peroxisome proliferator-activated receptor alpha (PPARalpha) activator, increases the expression of the cytosolic aspartate aminotransferase (cAspAT) gene in human liver cells, which may partially explain the increase of this enzyme in the serum of individuals undergoing fenofibrate treatment. Conversely, in rodents, fenofibrate represses the expression of the cAspAT gene. We compared the mechanisms of fenofibrate action in human and rat hepatoma cells. Transfection assays of the wild-type and mutated rat promoters in Fao and H4IIEC3 cells established a critical role for sequences similar to nuclear receptor responsive elements in the -404/-366 bp region. Nuclear proteins bound to these sequences and the amounts of protein bound were decreased by fenofibrate treatment, probably accounting for the decreased gene expression. Pharmacological studies confirmed the involvement of PPARalpha. However, this receptor did not bind directly to these sequences. The human promoter was cloned and the regulatory region localized between -2663/-706 bp. Co-transfection assays suggested that, in humans, the PPARalpha was also involved in the increase in expression of the cAspAT gene due to fibrates, without the presence of a canonical PPAR responsive element.

Fenofibrate induces a selective increase of protein-bound homocysteine in rodents: a PPARalpha-mediated effect.

Elevated levels of plasma homocysteine (Hcy) are associated with increased risk of cardiovascular disease though it is uncertain whether increases in Hcy represent a cause or a consequence of the disease process. Plasma Hcy exists in reduced, free oxidized, and protein-bound forms, that together comprise total Hcy (tHcy). Free reduced Hcy is thought to be the atherogenic, though minor, sub-fraction of tHcy. Recent reports have indicated that fenofibrate and other fibrates are capable of moderately increasing plasma tHcy. As many of the effects of fibrates are known to be mediated by the nuclear receptor PPARalpha, we determined the effect of fenofibrate on tHcy in PPARalpha-deficient mice. We further examined the effect of fenofibrate and fenofibrate plus folate supplementation on total as well as protein-bound Hcy in rats. Fenofibrate significantly increased serum tHcy in wild-type mice but not in PPARalpha deficient mice. In rats, fenofibrate increased serum tHcy by 69%, while the co-administration of folate with fenofibrate increased tHcy by only 7%. In spite of the above increase in tHcy in rats, only the protein-bound fraction of Hcy was increased. In a further study, fenofibrate also induced a significant increase in tHcy, while in spite of this, ex vivo peroxidation of VLDL+LDL was beneficially lowered and the lag time prolonged. In summary, fenofibrate increases serum tHcy in rodents in a PPARalpha-dependent manner. The increase in rats is solely due to protein-bound Hcy as atherogenic, reduced Hcy was unchanged. While awaiting corroboration in human, our results suggest that the extent and mechanism of the increase in total Hcy in patients treated with fenofibrate should not a priori be associated with relevant risk.