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Pancreatoduodenectomy is the only treatment with a promise of cure for patients with pancreatic head adenocarcinoma, and a negative resection margin is an important factor related to overall survival. Complete clearance of the medial margin with removal of the so-called mesopancreas may decrease the recurrence rate after pancreatic resection. Here, we present some important information about the mesopancreas, total mesopancreas excision, and technical aspects to achieve negative resection margins. The area named mesopancreas is defined as the tissue located between the head of the pancreas and the superior mesenteric vessels and the celiac axis and consists of the nerve plexus, lymphatic tissue, and connective tissue. The superior mesenteric and celiac arteries define the border of the mesopancreas. En bloc resection of anterior and posterior pancreatoduodenal nodes, hepatoduodenal nodes, along the superior mesenteric artery nodes, pyloric nodes, and nodes along the common hepatic artery is necessary.

Improved knowledge of the surgical anatomy of the region and technical refinements of excision of the mesopancreas along with standardized pathological examination are important to increase and to determine radical resection of pancreatic head cancer.

Improved knowledge of the surgical anatomy of the region and technical refinements of excision of the mesopancreas along with standardized pathological examination are important to increase and to determine radical resection of pancreatic head cancer.Cognition is shaped by signals from outside and within the body. Following recent evidence of interoceptive signals modulating higher-level cognition, we examined whether breathing changes the production and perception of quantities. In Experiment 1, 22 adults verbally produced on average larger random numbers after inhaling than after exhaling. In Experiment 2, 24 further adults estimated the numerosity of dot patterns that were briefly shown after either inhaling or exhaling. Again, we obtained on average larger responses following inhalation than exhalation. These converging results extend models of situated cognition according to which higher-level cognition is sensitive to transient interoceptive states.The intimate relationships between cell fate and metabolism have long been recognized, but a mechanistic understanding of how metabolic pathways are dynamically regulated during development and disease, how they interact with signalling pathways, and how they affect differential gene expression is only emerging now. We summarize the key findings and the major themes that emerged from the virtual Keystone Symposium 'Metabolic Decisions in Development and Disease' held in March 2021.Persistent loss of dietary protein usually signals a shutdown of key metabolic pathways. In Drosophila larvae that have reached a 'critical weight' and can pupariate to form viable adults, such a metabolic shutdown would needlessly lead to death. Inositol 1,4,5-trisphosphate-mediated calcium (IP3/Ca2+) release in some interneurons (vGlutVGN6341) allows Drosophila larvae to pupariate on a protein-deficient diet by partially circumventing this shutdown through upregulation of neuropeptide signaling and the expression of ecdysone synthesis genes. Here, we show that IP3/Ca2+ signals in vGlutVGN6341 neurons drive expression of Set2, a gene encoding Drosophila Histone 3 Lysine 36 methyltransferase. Furthermore, Set2 expression is required for larvae to pupariate in the absence of dietary protein. IP3/Ca2+ signal-driven Set2 expression upregulates key Ca2+-signaling genes through a novel positive-feedback loop. Transcriptomic studies, coupled with analysis of existing ChIP-seq datasets, identified genes from larval and pupal stages that normally exhibit robust H3K36 trimethyl marks on their gene bodies and concomitantly undergo stronger downregulation by knockdown of either the intracellular Ca2+ release channel IP3R or Set2. IP3/Ca2+ signals thus regulate gene expression through Set2-mediated H3K36 marks on select neuronal genes for the larval to pupal transition.The pandemic of Coronavirus disease (COVID)-19 is a global threat, causing high mortality, especially in the elderly. The main symptoms and the primary cause of death are related to interstitial pneumonia. Viral entry also into myocardial cells mainly via the angiotensin converting enzyme type 2 (ACE2) receptor and excessive production of pro-inflammatory cytokines, however, also make the heart susceptible to injury. In addition to the immediate damage caused by the acute inflammatory response, the heart may also suffer from long-term consequences of COVID-19, potentially causing a post-pandemic increase in cardiac complications. Although the main cause of cardiac damage in COVID-19 remains coagulopathy with micro- (and to a lesser extent macro-) vascular occlusion, open questions remain about other possible modalities of cardiac dysfunction, such as direct infection of myocardial cells, effects of cytokines storm, and mechanisms related to enhanced coagulopathy. In this opinion paper, we focus on these lesser appreciated possibilities and propose experimental approaches that could provide a more comprehensive understanding of the cellular and molecular bases of cardiac injury in COVID-19 patients. We first discuss approaches to characterize cardiac damage caused by possible direct viral infection of cardiac cells, followed by formulating hypotheses on how to reproduce and investigate the hyperinflammatory and pro-thrombotic conditions observed in the heart of COVID-19 patients using experimental in vitro systems. Finally, we elaborate on strategies to discover novel pathology biomarkers using omics platforms.Adult-onset Still's disease (AOSD) is a rare, but characteristic non-familial, multi-genic systemic auto-inflammatory disorder, characterized by high spiking fever, salmon-like evanescent skin rash, polyarthritis, sore throat, hyperferritinemia, and leucocytosis. The hallmark of AOSD is a cytokine storm triggered by dysregulation of inflammation. Nowadays, with advances in anti-cytokine biologic agents, the treatment of AOSD is no longer limited to nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, or conventional synthetic disease modifying anti-rheumatic drugs (csDMARDs). In this review, we focused on the roles of these cytokines in the pathogenesis of AOSD and summarized the current and emerging biological therapy.

Experimental findings on genetic disease mechanisms are scattered throughout the literature and represented in many ways, including unstructured text, cartoons, pathway diagrams, and network graphs. Integration and structuring of such mechanistic information greatly enhances its utility.

MecCog is a graphical framework for building integrated representations (mechanism schemas) of mechanisms by which a genetic variant causes a disease phenotype. A MecCog mechanism schema displays the propagation of system perturbations across stages of biological organization, using graphical notations to symbolize perturbed entities and activities, hyperlinked evidence tagging, a mechanism ontology, and depiction of knowledge gaps, ambiguities, and uncertainties. The web platform enables a user to construct, store, publish, browse, query, and comment on schemas. MecCog facilitates the identification of potential biomarkers, therapeutic intervention sites, and critical future experiments.

The MecCog framework is freely available at http//www.meccog.org.

Supplementary data are available at Bioinformatics online.

Supplementary data are available at Bioinformatics online.

To evaluate the quality of antimicrobial prescribing, at the Department of Internal Medicine University Hospital Centre Rijeka, by assessing the necessity for antimicrobial treatment and adherence to the local Guidelines for hospital antimicrobial drug use and to compare results with previously conducted point prevalence surveys (PPSs).

A PPS was conducted on 7th May 2019. Demographic and relevant clinical data of each patient receiving systemic antimicrobials were recorded anonymously in a patient-specific form. The appropriateness of antibiotic prescribing was assessed as adherence to the fourth edition of the Guidelines for hospital antimicrobial drug use.

One hundred and seventy-one patients were hospitalized at the Department of Internal Medicine; 37.4% (n = 64) of patients received 102 prescriptions for an antimicrobial drug [62.8% (n = 64) of prescriptions were for intravenous and 37.2% (n = 38) for oral administration]. Of these, 52 were treated for an identified existing infection, 5 were treatis for tailoring antimicrobial stewardship programs/activities.Obesity is a disease of the nervous system. While some will view this statement as provocative, others will take it as obvious. Whatever our side is, the pharmacology tells us that targeting the nervous system works for promoting weight loss. It works, but at what cost? Is the nervous system a safe target for sustainable treatment of obesity? What have we learned - and unlearned - about the central control of energy balance in the last few years? In this Mini-Review, we provide a thought-provoking exploration of obesity as a disorder of neurotransmission. We discuss the state of knowledge on the brain pathways regulating energy homeostasis that are commonly targeted in anti-obesity therapy and explore how medications affecting neurotransmission such as atypical antipsychotics, antidepressants and antihistamines relate to body weight. Our goal is to provide the endocrine community with a conceptual framework that will help expending our understanding of the pathophysiology of obesity, a disease of the nervous system.A relationship between bitter and fat taste sensitivity, CD36 rs1761667 and TAS2R38 has been demonstrated. However, research is scarce and does not take diet into account. This study aimed to explore associations between genetics, fat and bitter taste sensitivity and dietary fat intake in healthy UK adults. A cross-sectional study was carried out on 88 Caucasian participants (49 females and 39 males aged 35 ± 1 years; body mass index 24.9 ± 0.5 kg/m2). Bitter taste sensitivity was assessed using phenylthiocarbamide (PTC) impregnated strips and the general Labeled Magnitude Scale. Fat taste sensitivity was assessed by the Ascending Forced Choice Triangle Procedure and dietary intake with a semi-quantitative food frequency questionnaire. Tanespimycin concentration Genotyping for rs713598, rs1726866, rs10246939, and rs1761667 was performed. Participants with TAS2R38 PAV/PAV diplotype perceived PTC strips as more bitter than groups carrying AVI haplotypes (AVI/AVI, P = 1 × 10-6; AVI/AAV, P = 0.029). CD36 rs1761667 was associated with fat taste sensitivity (P = 0.008). A negative correlation between bitter taste sensitivity and saturated fat intake was observed (rs = -0.256, P = 0.016). When combining the CD36 genotypes and TAS2R38 diplotypes into one variable, participants carrying both TAS2R38 AVI haplotype and CD36 A allele had a higher intake of saturated fat compared to carriers of CD36 GG genotype or TAS2R38 PAV/PAV and PAV/AAV diplotypes (13.8 ± 0.3 vs. 12.6 ± 0.5%TEI, P = 0.047) warranting further exploration in a larger cohort.