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Total well being inside patients together with IBD through the COVID-19 crisis within the Holland.
Of the 166 EP surveyed, 76% rated GH treatment as potentially improving quality of life (QoL), with 88% reporting a minimum 3-inch height increase as necessary to improve QoL. CONCLUSIONS Height comparisons were more likely to impact EP than PP in seeking height-related medical care for their children. EP had high expectations of QoL improvement with GH treatment, which are unlikely to be met with treatment of idiopathic short stature. Thus, clinicians should be prepared to support families in other ways that promote positive development in children with short stature. © 2020 S. Karger AG, Basel.Necrotizing enterocolitis (NEC) is a devastating inflammatory condition of the intestine, which affects premature infants and causes untold damage. Its pathogenesis has to do with how colonizing bacteria interact with the immature newborn intestine. An immature innate immune response with increased TLR-4 on the cell surface and increased signaling molecules, such as NF-κB, can cause excessive inflammation. This is in conjunction with a decrease in the appearance of regulatory molecules which effect the control of innate responses. This condition is so devastating that it must be prevented and not treated. Fortunately, breast milk and probiotics can affect the condition leading to reduced inflammation. How does this effect work? We have shown that breast milk tryptophan and Bifidobacterium infantis result in a metabolite (indole-3-lactic acid) response, which is anti-inflammatory via inhibition of the aryl hydrocarbon receptor transcription factor which stimulates an IL-8 response. We have also shown that breast milk complex carbohydrates interacting with Bacteroides fragilis can cause short-chain fatty acids which exert anti-inflammatory effects on the newborn intestine. These breast milk metabolites could help prevent NEC if shown to be effective clinically. © 2020 Nestlé Nutrition Institute, Switzerland/S. Karger AG, Basel.Social grooming is often exchanged between individuals in many primate species. Rates of bidirectional (or simultaneous mutual) grooming vary across primate species, and its function is not yet fully understood. For example, mutual grooming is frequent in chimpanzees but rare in most primate species including wild bonobos. There are, however, no quantitative data available in captive bonobos. Therefore, through the direct comparison between captive bonobos and chimpanzees, this study aimed to (i) compare the frequency of mutual grooming between Pan species, (ii) explore and compare the function of mutual grooming, and (iii) discuss the rarity of this behavior in wild bonobo populations. We tested three hypotheses following the previous literature in wild chimpanzees. The social bonding hypothesis states that mutual grooming facilitates the maintenance of strong dyadic bonds. The immediate investment hypothesis states that it serves to signal willingness to invest in the interaction. The switching hypothesis states that mutual grooming serves no function but only occurs as an overlap to change the direction of unidirectional grooming. Our findings strongly supported the immediate investment hypothesis, but not the others. Grooming bouts that included mutual grooming were longer and more equitable than bouts without, illustrating that captive Pan species use mutual grooming to maximize their short-term benefits and increase the social value of their interaction. Captive bonobos performed mutual grooming in similar proportions and for similar functions as captive and wild chimpanzees do. This contrasts with wild bonobos who engage in this behavior only rarely. We suggest that the differences in patterns of mutual grooming between captive and wild bonobos might be explained by different degrees of kinship or by a potential intraspecies variation. © 2020 S. Karger AG, Basel.Germinal center (GC) responses require B cells to respond to a dynamic set of intercellular and microenvironmental signals that instruct B cell positioning, differentiation, and metabolic reprogramming. ROCK2, a serine-threonine kinase that can be therapeutically targeted by ROCK inhibitors or statins, is a key downstream effector of RHOA-GTPases. While RHOA-mediated pathways are emerging as critical regulators of GC responses, the role of ROCK2 in B cells is unknown. Here, we find that ROCK2 was activated in response to key T cell signals like CD40 and IL21 and that it regulated GC formation and maintenance. Ruboxistaurin RNA-seq analyses revealed that ROCK2 controlled a unique transcriptional program in GC B cells that promoted optimal GC polarization and cholesterol biosynthesis. ROCK2 regulated this program by restraining AKT activation and subsequently enhancing FOXO1 activity. ATAC-seq and biochemical analyses revealed that the effects of ROCK2 on cholesterol biosynthesis were instead mediated via a novel mechanism. ROCK2 directly phosphorylated IRF8, a crucial mediator of GC responses, and promoted its interaction with SREBP2 at key regulatory regions controlling the expression of cholesterol biosynthetic enzymes, resulting in optimal recruitment of SREBP2 at these sites. These findings thus uncover ROCK2 as a multifaceted and therapeutically targetable regulator of GC responses.BACKGROUND Specific features of the tumor microenvironment (TME) may provide useful prognostic information. We conducted a systematic investigation of the cellular composition and prognostic landscape of TME in gastric cancer. METHODS We evaluated the prognostic significance of major stromal and immune cells within TME. We proposed a composite TME-based risk score and tested it in six independent cohorts of 1,678 patients with gene expression or immunohistochemistry measurements. Further, we devised a new patient classification system based on TME characteristics. RESULTS We identified natural killer cells, fibroblasts, and endothelial cells as the most robust prognostic markers. The TME risk score combining these cell types was an independent prognostic factor when adjusted for clinicopathologic variables (gene expression HR [95% CI] 1.42 [1.22-1.66]; immunohistochemistry 1.34 [1.24-1.45], P less then 0.0001). Higher TME risk scores consistently associated with worse survival within every pathologic stage (HR range 2.
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