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A new relation between the maximum geometric concentration factor C and the angular acceptance interval for asymmetrical ideal non-imaging concentrators is proposed. A generalization of the well-known relation for the two-dimensional case, sin [[theta].sub.c] = 1/C where [[theta].sub.c] is the acceptance half-angle, results in the proposed relation sin [[theta].sub.2]-sin [[theta].sub.1] = 2/C, where [[theta].sub.1] and [[theta].sub.2] are the angles of the acceptance interval limits relative to the normal of the entrance aperture. The proposed relation is valid for any ideal 2D concentrator, symmetrical or asymmetrical. A proof based on conservation of phase space is provided. Keywords: Concentration; Radiation; Asymmetrical; Angular acceptance

Background: Alteration of the host-microbiota cross talk at the intestinal barrier may participate in the pathophysiology of irritable bowel syndrome (IBS). Therefore, we aimed to determine effects of fecal luminal factors from IBS patients on the colonic epithelium using colonoids., Methods: Colon-derived organoid monolayers, colonoids, generated from a healthy subject, underwent stimulation with fecal supernatants from healthy subjects and IBS patients with predominant diarrhea, phosphate-buffered saline (PBS), or lipopolysaccharide (LPS). Cytokines in cell cultures and fecal LPS were measured by ELISA and mRNA gene expression of monolayers was analyzed using Qiagen RT 2 Profiler PCR Arrays. The fecal microbiota profile was determined by the GA-map ™ dysbiosis test and the fecal metabolite profile was analyzed by untargeted liquid chromatography/mass spectrometry., Key Results: Colonoid monolayers stimulated with fecal supernatants from healthy subjects (n = 7), PBS (n = 4) or LPS (n = 3) presented distinct gene expression profiles, with some overlap (R 2 Y = 0.70, Q 2  = 0.43). Addition of fecal supernatants from healthy subjects and IBS patients (n = 9) gave rise to different gene expression profiles of the colonoid monolayers (R 2 Y = 0.79, Q 2  = 0.64). Genes (n = 22) related to immune response (CD1D, TLR5) and barrier integrity (CLDN15, DSC2) contributed to the separation. Levels of proinflammatory cytokines in colonoid monolayer cultures were comparable when stimulated with fecal supernatants from either donor types. Fecal microbiota and metabolite profiles, but not LPS content, differed between the study groups., Conclusions: Fecal luminal factors from IBS patients induce a distinct colonic epithelial gene expression, potentially reflecting the disease pathophysiology. The culture of colonoids from healthy subjects with fecal supernatants from IBS patients may facilitate the exploration of IBS related intestinal micro-environmental and barrier interactions., (© 2022 The Authors. Neurogastroenterology & Motility published by John Wiley & Sons Ltd.)

Altered bacterial composition and small intestinal bacterial overgrowth (SIBO) may be associated with irritable bowel syndrome (IBS). This study aimed to determine the fecal and mucosa-associated bacterial composition along the gastrointestinal (GI) tract and to assess SIBO in IBS. Bacterial composition of feces, and mucosa of the duodenum and sigmoid colon was determined by 16S rRNA-amplicon-sequencing. SIBO was evaluated by bacterial culture of duodenal aspirate, glucose and lactulose breath tests. Mucosal antibacterial gene expression was assessed by PCR Array. The bacterial profiles of feces and the mucosa of sigmoid colon, but not duodenum, differed between IBS patients (n = 17) and HS (n = 20). The IBS specific bacterial profiles were linked to the colonic antibacterial gene expression. Fecal bacterial profile differed between IBS subtypes, while the mucosa-associated bacterial profile was associated with IBS symptom severity and breath tests results at baseline (H 2 and/or CH 4  ≥ 15 ppm). The prevalence of SIBO was similar between IBS patients and HS. This study demonstrates that alterations in the bacterial composition of the sigmoid colon of IBS patients were linked to symptoms and immune activation. While breath tests reflected the mucosa-associated bacterial composition, there was no evidence for high prevalence of SIBO or small intestinal bacterial alterations in IBS.

Background: This study aimed to determine whether patients with IBS displayed altered mucosal mast cell (MC) numbers and proportions of MCs co-localizing with nerves compared with healthy subjects (HS) and whether these MC characteristics correlated with IBS symptoms, elements of the epithelial barrier, or visceral sensitivity., Methods: Mucosal MC characteristics were determined using immunoassay. IBS symptoms, gene expression of elements of the epithelial barrier, fecal serine protease activity, and visceral sensitivity were assessed., Key Results: The MC numbers per mm 2 were 2.0 (0.0-6.0) in patients with IBS (n = 43) and 3.5 (1.1-9.1) in HS (n = 20, P = .26). Of these, MCs were 0.0 (0.0-20) % vs 3.1 (0.0-18) % (P = .76) in IBS and HS, respectively, in co-localization with nerve fibers. MC characteristics were equivalent in the different IBS subtypes. Hierarchical cluster analysis identified two distinct groups among patients with IBS: MC high (higher MC numbers and proportions of MCs co-localizing with nerves) and MC low (lower MC numbers and proportions of MCs co-localizing with nerves). The MC high and MC low groups could not be discriminated with regard to IBS symptoms, parameters of visceral sensitivity, gene expression of elements of the epithelial barrier, and fecal protease activity., Conclusion and Inferences: There was no evidence of increased infiltration or altered localization of MCs in the colonic mucosa of patients with IBS. These MC characteristics were not linked to global IBS symptoms or mucosal expression of elements of the epithelial barrier. These findings indicate that quantity and location of mucosal MCs are factors not involved in the pathophysiology of IBS., (© 2019 John Wiley & Sons Ltd.)

The intestinal microbiota influences immune maturation during childhood, and is implicated in early-life allergy development. However, to directly study intestinal microbes and gut immune responses in infants is difficult. To investigate how different types of early-life gut microbiota affect immune development, we collected fecal samples from children with different allergic heredity (AH) and inoculated germ-free mice. Immune responses and microbiota composition were evaluated in the offspring of these mice. Microbial composition in the small intestine, the cecum and the colon were determined by 16S rRNA sequencing. The intestinal microbiota differed markedly between the groups of mice, but only exposure to microbiota associated with AH and known future allergy in children resulted in a T helper 17 (Th17)-signature, both systemically and in the gut mucosa in the mouse offspring. These Th17 responses could be signs of a particular microbiota and a shift in immune development, ultimately resulting in an increased risk of allergy.

1 Possibly acting via mu-opioid receptors (MORs), morphine inhibits the formation of experimentally induced postoperative abdominal adhesions in rats. Mesothelial cells may participate in adhesion formation by secreting mediators that interfere negatively with fibrinolysis. Morphine may prevent adhesions by inhibiting the release of pro-adhesion mediators from mesothelial cells. This study aimed to investigate whether human mesothelial cells express MOR-1; if so, such could constitute a site of action for morphine in adhesion prevention. 2 Cells from Met-5A, a human mesothelial cell line were seeded and prepared for immunocytochemistry and Western blotting. 3 Immunocytochemistry showed MOR-1 expression in mesothelial cells, predominantly in the nuclei. Western blotting showed two bands (c. 35 and 50 kDa) which correspond to those obtained with a control lysate from cells known to express MORs. In addition, we found MOR-1 expression with nuclear and cytoplasmatic localization in biopsies from human abdominal adhesions. 4 The current findings may suggest that morphine could interact directly with mesothelial cells via MOR-1 receptors, and thereby modulate adhesion formation, possibly by interfering with the release of pro-adhesion factors from these cells.

Thirty-four patients with gallstone disease were examined with cholescintigraphy and gastroscopy before and after cholecystectomy. Sixteen patients had a functioning and 23 a non-functioning gallbladder at cholescintigraphy. At scintigraphy 99Tcm-activity was found over the gastric fundus in 28% before and in 22% after cholecystectomy and there was no difference between the groups with and without a functioning gallbladder regarding bile reflux. Before cholecystectomy bile-stained contents in the stomach was significantly more often found among those with a non-functioning gallbladder (87%) than in those with a functioning gallbladder (44%). After cholecystectomy the number of patients with bile-stained contents in the stomach was high in both groups (92% and 82% respectively). No correlation could be found between the two methods to detect bile in the stomach. Before cholecystectomy patients with a functioning gallbladder had inflammatory changes in the antral as well as the fundic mucosa in 31%. Patients with a nonfunctioning gallbladder had inflammatory changes in the antral mucosa in 47% and in the fundic mucosa in 56%. These differences were however not statistically significant. No correlation could be found between bile-stained contents in the stomach and chronic gastritis or scintigraphically detected bile in the stomach and chronic gastritis. The degree and distribution of chronic gastritis was virtually unchanged one year after cholecystectomy.