An insidious internal hernia 30 years after jejunoileal bypass: a case report.

Jejunoileal bypass (JIB) was an early bariatric procedure that involved bypassing most of the small bowel resulting in malabsorption and weight loss. Due to serious complications associated with the procedure, JIB was largely discontinued by the mid-1980s. We report the case of a 77-year-old woman with a history of JIB 31 years earlier. In 2022, she was hospitalized for acute abdominal pain. A computed tomography (CT) scan revealed a suspicion of internal hernia (IH) with a typical swirl sign. Due to the quick relief of symptoms an emergency surgery was not considered at the time. Nevertheless, a subsequent operation revealed a large mesenteric defect, adhesions and 100 cm of effective small bowel left. Although the procedure is no longer performed, some patients with JIB are still alive and develop late complications. To our knowledge, this is the first case report describing an IH in a patient who has undergone JIB.

High-volume evacuation mitigates viral aerosol spread in dental procedures.

Dental healthcare personnel (DHCP) are subjected to microbe-containing aerosols and splatters in their everyday work. Safer work conditions must be developed to ensure the functioning of the healthcare system. By simulating dental procedures, we aimed to compare the virus-containing aerosol generation of four common dental instruments, and high-volume evacuation (HVE) in their mitigation. Moreover, we combined the detection of infectious viruses with RT-qPCR to form a fuller view of virus-containing aerosol spread in dental procedures. The air-water syringe produced the highest number of aerosols. HVE greatly reduced aerosol concentrations during procedures. The air-water syringe spread infectious virus-containing aerosols throughout the room, while other instruments only did so to close proximity. Additionally, infectious viruses were detected on the face shields of DHCP. Virus genomes were detected throughout the room with all instruments, indicating that more resilient viruses might remain infectious and pose a health hazard. HVE reduced the spread of both infectious viruses and viral genomes, however, it did not fully prevent them. We recommend meticulous use of HVE, a well-fitting mask and face shields in dental procedures. We advise particular caution when operating with the air-water syringe. Due to limited repetitions, this study should be considered a proof-of-concept report.

Dynamics of adipose tissue macrophage populations after gastric bypass surgery.

OBJECTIVE: This case-control study aimed to analyze the dynamics of macrophage infiltration in subcutaneous adipose tissue following bariatric surgery or conservative treatment of obesity and to clarify whether these features predict the weight loss outcome after the surgery. METHODS: Subcutaneous tissue samples taken before and 12 months after laparoscopic Roux-en-Y gastric bypass surgery (n = 39) or conservative (n = 43) treatment for obesity were analyzed. Fat cell size was determined, and with CD68 immunohistochemistry, crown-like structures (CLS) were counted and single macrophages were quantitated. RESULTS: A major decline in CLS density from 4.1 (SD 3.5) to 1.1 (SD 0.8) per 1000 fat cells (p < 0.000) was found, regardless of the degree of weight loss after the surgery. Surgery had no effect on the fraction of infiltrating single-cell macrophages in subcutaneous adipose tissue. The abundance of these macrophage populations before the intervention did not predict the degree of postsurgery weight loss or suboptimal response to the surgery. CONCLUSIONS: The effect of gastric bypass on adipose tissue inflammatory status associates closely with CLS density even in subjects with suboptimal weight loss. The study suggests that factors related to bypass surgery other than weight loss modify the inflammatory response in adipose tissue.

A Straightforward Method for Adipocyte Size and Count Analysis Using Open-source Software QuPath.

Changes in adipose tissue morphology, depicted by cell morphology alterations such as enlargement of fat cells, always accompany over-weight and obesity. The variables related to cell size have been shown to associate with low-grade inflammation of adipose tissue and common obesity-related comorbidities including metabolic syndrome and type 2 diabetes. Quantifying fat cell morphology from images of histological specimens can be tedious. Here, we present a straightforward method for the task using the free open-source software QuPath with its inbuilt tools only. Measurements of human adipose tissue samples with the described protocol showed an excellent correlation with those obtained with ImageJ software with Adipocyte Tools plugin combined with manual correction of misdetections. Intraclass correlation between the two methods was at good to excellent level. The method described here can be applied to considerably large tissue areas, even whole-slide analysis.

Neuroanatomical mapping of juvenile rat brain regions with prominent basal signal in [(35)S]GTPgammaS autoradiography.

[(35)S]GTPgammaS autoradiography represents a powerful functional approach to detect receptor-dependent G(i/o) protein activity in anatomically defined brain structures. Inherent to this technique, however, is the notable basal signal evident in several brain regions in the absence of receptor stimulation by exogenously added agonist. In the rat brain, much of this basal labelling derives from tonic activation of adenosine A(1) and lysophosphatidic acid LPA(1) receptors in the gray and white matter regions, respectively. Despite the elimination of the two receptor activities, prominent basal [(35)S]GTPgammaS labelling is still evident in discrete brain structures, possibly reflecting regional enrichment of G(i/o) and/or constitutive receptor activity or the presence of still unknown endogenous ligands activating their orphan receptors. Here, the anatomical distribution of the enhanced basal signal was systematically mapped in brain sections of 4-week-old male Wistar rats. Regions with prominent basal [(35)S]GTPgammaS labelling represented neuroanatomically distinct structures, in particular various thalamic and hypothalamic nuclei. For instance, the paraventricular thalamic nucleus, the bed nucleus of the stria terminalis and the subfornical organ were highly labelled, as were the periaqueductal gray and the nucleus of the solitary tract. Pre-treatment with N-ethylmaleimide (NEM), an alkylating agent preventing all known receptor-driven G protein activity in cryostat sections markedly decreased the basal binding in all examined regions. In preliminary screening, selective antagonists for various brain-enriched G(i/o)-coupled receptors failed to suppress the basal signal in any of the studied regions.

Visualization of 2-arachidonoylglycerol accumulation and cannabinoid CB1 receptor activity in rat brain cryosections by functional autoradiography.

In neuronal signalling mediated by the endocannabinoid 2-arachidonoylglycerol, both synthetic and inactivating enzymes operate within close proximity to the G(i/o)-coupled pre-synaptic CB(1) receptors, thus allowing for rapid onset and transient duration of this lipid modulator. In rat brain, 2-arachidonoylglycerol is inactivated mainly via hydrolysis by serine hydrolase inhibitor-sensitive monoacylglycerol lipase activity. We show in this study that comprehensive pharmacological elimination of this activity in brain cryosections by methyl arachidonylfluorophosphonate or hexadecylsulphonyl fluoride results in endocannabinoid-mediated CB(1) receptor activity, which can be visualized by functional autoradiography. URB597, a specific inhibitor of anandamide hydrolysis proved ineffective. TLC indicated that the bioactivity resided in 2-arachidonoylglycerol-containing fraction and gas chromatography-mass spectroscopy detected elevated levels of monoacylglycerols, including 2-arachidonoylglycerol in this fraction. Although two diacylglycerol lipase inhibitors, tetrahydrolipstatin (THL) and RHC80267, blocked the bulk of 2-arachidonoylglycerol accumulation in methyl arachidonylfluorophosphonate-treated sections, only THL reversed the endocannabinoid-dependent CB(1) receptor activity. Further studies indicated that at the used concentrations, THL rather specifically antagonized the CB(1) receptor. These findings confirm that in brain sections there is preservation of enzymatic pathways regulating the production of endogenous receptor ligands. Furthermore, the presently described methodology may serve as an elegant and intuitive approach to identify novel membrane-derived lipid modulators operating in the CNS.

URB754 has no effect on the hydrolysis or signaling capacity of 2-AG in the rat brain.

Previous studies indicate that in brain tissue the endocannabinoid 2-AG is inactivated by monoglyceride lipase (MGL)-catalyzed hydrolysis, and a recent report has indicated that MGL activity could be specifically inhibited by URB754 . In the present study, URB754 failed to inhibit 2-AG hydrolysis in rat brain preparations. In addition, brain cryosections were employed to assess whether URB754 could facilitate the detection of 2-AG-stimulated G protein activity. Nevertheless, whereas pretreatment with PMSF readily allowed detection of 2-AG-stimulated G protein activity, URB754 was ineffective. In contrast to previous claims, brain FAAH activity was also resistant to URB754. Thus, in our hands URB754 was not able to block the endocannabinoid-hydrolyzing enzymes and cannot serve as a lead structure for future development of MGL-specific inhibitors.

The basic secretagogue compound 48/80 activates G proteins indirectly via stimulation of phospholipase D-lysophosphatidic acid receptor axis and 5-HT1A receptors in rat brain sections.

The basic secretagogues, such as compound 48/80 (c48/80) and mastoparans, are widely used histamine-releasing agents and their mechanism of action is commonly attributed to a direct, receptor-bypassing property to activate the G(i/o) class of G proteins. We tested here whether c48/80 could directly stimulate [(35)S]guanosine-5'-[gamma-thio]triphosphate ([(35)S]GTPgammaS) binding to rat brain sections in an attempt to visualize the entire signaling pool of G(i/o) in its native neuroanatomical context. Instead of direct G(i/o) activation, c48/80 (100 microg ml(-1)) from various suppliers stimulated brain phospholipase D (PLD) activity, leading to the generation of endogenous phospholipids capable of activating brain white matter-enriched, G(i/o)-coupled lysophosphatidic acid (LPA) receptors. This response was sensitive to 1-butanol and was potently reversed by the LPA(1)/LPA(3) receptor-selective antagonist Ki16425 (IC(50) 59+/-13 nM, mean+/-s.e.m.), and showed age-dependent decline, closely reflecting known developmental regulation of the PLD-LPA(1) receptor axis in the CNS. In addition, c48/80 was found to modestly activate hippocampal 5-HT(1A) receptors in a pH-dependent and antagonist-sensitive manner. Consistent with the lack of direct G(i/o)-activating properties in brain sections, c48/80 showed no activity in classical membrane [(35)S]GTPgammaS binding assays. Instead, c48/80 from one particular manufacturer elicited non-specific effect in these assays, therefore challenging the previous interpretations regarding the compound's ability to activate G proteins directly. We conclude that c48/80 is not a receptor-bypassing general G protein activator but rather activates PLD, leading to generation of endogenous LPA receptor-activating phospholipids. This property may also contribute to the compound's ability to release histamine from mast cells.