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Aim: This study aimed to assess the potential role of physical activity (PA) in reducing the risk of developing inflammatory bowel diseases (IBDs) and in their management. Subject and methods: A systematic review of literature was conducted up to October 2023 using the PubMed, Scopus, Web of Science and Cochrane Library databases. Observational studies, semi-experimental and experimental studies reporting PA effects were considered eligible. Data on disease status and PA characteristics, main outcomes and possible confounders were collected in a database. The Newcastle–Ottawa Quality Assessment Scale was used to assess risk of bias. Results: Of the 29 articles included, six investigated PA and risk of IBDs and four of them showed an inverse relationship. Among the others, seven reported positive effects of PA on IBD symptoms, while all showed improvements in comorbidities, complications and quality of life. Conclusion: PA seems to be effective in preventing or treating IBDs and their complications. Owing to the low quality of the majority of the studies and their heterogeneity, further research is needed to better understand which type and level of PA may be useful in the prevention and treatment of these diseases.

•Review of reticulospinal systems implicated in control of motor and autonomic functions.•Advocate the need for single-cell recording to decipher reticulospinal activity across behaviors.•Draw attention on studies that exploit developmental identity of reticulospinal neurons to study their physiological roles.

Serotonin-producing neurons profusely innervate brain regions via long-range projections. However, it remains unclear whether and how endogenous serotonergic transmission specifically influences regional or global functional activity. We combined designed receptors exclusively activated by designed drugs (DREADD)-based chemogenetics and functional magnetic resonance imaging (fMRI), an approach we term “chemo-fMRI,” to causally probe the brain-wide substrates modulated by endogenous serotonergic activity. We describe the generation of a conditional knockin mouse line that, crossed with serotonin-specific Cre-recombinase mice, allowed us to remotely stimulate serotonergic neurons during fMRI scans. We show that endogenous stimulation of serotonin-producing neurons does not affect global brain activity but results in region-specific activation of a set of primary target regions encompassing corticohippocampal and ventrostriatal areas. By contrast, pharmacological boosting of serotonin levels produced widespread fMRI deactivation, plausibly reflecting the mixed contribution of central and perivascular constrictive effects. Our results identify the primary functional targets of endogenous serotonergic stimulation and establish causation between activation of serotonergic neurons and regional fMRI signals.

BackgroundPrevious cross-sectional studies have demonstrated that fat-free mass (FFM) is an important determinant of left ventricular mass (LVM) in athletes. However, cross-sectional investigations have not the ability to detect the dynamic adaptation occurring with training. We hypothesized that LVM adapts concurrently with the increase of FFM induced by exercise conditioning. We sought to study the relationship between the variations of LVM and of FFM occurring in top-level soccer players during the season.MethodsTwenty-three male top-level athletes were recruited. LVM was assessed by echocardiography and FFM by dual-energy X-ray absorptiometry. Serial measurements were performed pre-season, after 1 month, at mid- and end-season, and after 2 months of detraining.ResultsLVM significantly increased at mid-season versus pre-season values, reaching the highest value at the end of the season (p < 0.05). While body weight did not vary during the study period, FFM significantly increased (p < 0.05 for mid-/end-season vs. pre-season data). After the detraining, no significant differences were observed between pre-season and detraining echocardiographic data. The only independent predictors of LVM were left ventricular stroke volume and FFM (R = 0.36, p = 0.005; R = 0.35, p = 0.005, respectively). When ΔLVM index was set as dependent variable, the only independent predictor was ΔFFM (R = 0.87, p = 0.002).ConclusionsChanges in LVM occur in close association with changes in FFM, suggesting that the left ventricle adapts concurrently with the increase of the metabolically active tissue induced by training, i.e. the FFM. Therefore, the dynamic changes in FFM and LVM may reflect a physiological adaptation induced by intensive training.

OBJECTIVE: To report a case of acute cholestatic hepatitis associated with the selective cyclooxygenase-2 inhibitor celecoxib.CASE SUMMARY: A 41-year-old white man was hospitalized for jaundice after 2 doses of celecoxib 200 mg for pain associated with right-knee trauma. Laboratory workup showed hyperbilirubinemia, mildly elevated serum transaminase concentrations, and cholestasis. Abdominal imaging showed no dilation of the biliary tree. Histology showed cholestasis, with bile plugs in dilated bile canaliculi and a mild portal infiltrate that are highly suggestive of drug-induced cholestasis.DISCUSSION: This is the fourth report in the English-language literature describing cholestatic hepatitis temporally related to celecoxib use, the second supported by histologic findings typical of drug-induced cholestasis, and the first in a patient who denied use of alcoholic beverages and was taking no other drugs or herbal products at the time of the reaction. The Naranjo probability scale indicated that celecoxib was a probable cause of acute cholestatic hepatitis in this patient.CONCLUSIONS: Cholestatic hepatitis is a well-recognized adverse effect of several drugs. Although celecoxib is considered to have a very low potential for hepatic toxicity, well-documented reports of adverse reactions can contribute significantly to the definition of more accurate safety profiles for new drugs introduced into clinical practice.