In individuals with irritable bowel syndrome (IBS), eliminating dietary triggers can alleviate symptoms but may lead to nutrient deficiencies and overall health decline. Although various nutritional supplements show promising results in relieving IBS symptoms due to their potential to alter the microbiome, conclusive scientific evidence remains lacking. This exploratory study aims to assess the bifidogenic properties of four nutritional supplement interventions and their impact on IBS-symptoms, faecal microbiota composition, faecal short-chain fatty acid (SCFA) concentrations, stool pattern, and quality of life (QoL), compared to a placebo control. Seventy subjects with IBS, meeting the ROME IV criteria, participated in this randomised, double-blind, placebo-controlled parallel intervention study. Subjects were assigned to one of the four treatment groups, receiving either resistant starch, pea fibre, chondroitin sulfate, protein hydrolysate, or placebo daily for four weeks. Daily reports on stool pattern and gastrointestinal complaints were collected. Stool samples and questionnaires on dietary intake, symptom severity, QoL, and anxiety and depression were collected at baseline and after the 4-week intervention. The results show no significant increase in Bifidobacterium abundance or faecal SCFA levels after the 4-week intervention with any of the four nutritional supplement interventions. While some improvements in symptom severity and QoL were observed within-groups, these were not significantly different from changes observed with placebo. In conclusion, the tested nutritional supplements did not increase Bifidobacterium abundance in subjects with IBS within four weeks. Furthermore, we conclude that future studies should consider a run-in period and a larger sample size to study improvements in IBS symptoms.

We aimed to identify risk factors related to COVID-19 reinfection in Hong Kong. We performed a population-based retrospective cohort study and reviewed case-based data on COVID-19 infections reported to the Centre for Health Protection from 8 January 2020 to 29 January 2023. We analyzed the epidemiology of COVID-19 infections and performed a Cox regression analysis. In this period, 3.32% (103,065/3,106,579) of COVID-19 infections recorded were classified as reinfection. Compared with primarily infected cases, a higher proportion of re-infected cases had chronic diseases (33.54% vs. 27.27%) and were residents of residential care homes (RCH) (10.99% vs. 1.41%). The time interval between the two episodes ranged from 31 to 1,050 days (median 282 days). Cox regression analysis of Omicron cases with the adjustment of covariates showed that being female (Hazard Ratio [HR] 1.12, 95% CI 1.11–1.13), chronic diseases (HR 1.18, 95% CI 1.16–1.20) and RCH residents (HR 6.78, 95% CI 6.61–6.95) were associated with reinfection, while additional vaccination after primary infection was protective (HR 0.80, 95% CI 0.79–0.81). Further analytical studies on the risk factors and protectors of COVID-19 reinfection are needed to guide targeted interventions.

Acute pancreatitis (AP) is an acute-onset gastrointestinal disease characterized by a significant inflammation of the pancreas. Most of the time, AP does not leave substantial changes in the pancreas after the resolution of the symptoms but the severe forms are associated with local or systemic complications. The pathogenesis of AP has long been investigated and, lately, the importance of intracellular mechanisms and the immune system has been described. The initial modifications in AP take place in the acinar cell. There are multiple mechanisms by which cellular homeostasis is impaired, one of the most important being calcium overload. Necrotic pancreatic cells initiate the inflammatory response by secreting inflammatory mediators and attracting immune cells. From this point on, the inflammation is sustained by the involvement of innate and adaptive immune systems. Multiple studies have demonstrated the importance of the first 48 h for identifying patients at risk for developing severe forms. For this reason, there is a need to find new, easy-to-use and reliable markers for accurate predictions of these forms. This review provides an overview of the main pathogenetic mechanisms involved in AP development and the most promising biomarkers for severity stratification.

Recent developments have indicated a potential association between tinnitus and COVID-19. The study aimed to understand tinnitus following COVID-19 by examining its severity, recovery prospects, and connection to other lasting COVID-19 effects. Involving 1331 former COVID-19 patients, the online survey assessed tinnitus severity, cognitive issues, and medical background. Of the participants, 27.9% reported tinnitus after infection. Findings showed that as tinnitus severity increased, the chances of natural recovery fell, with more individuals experiencing ongoing symptoms (p < 0.001). Those with the Grade II mild tinnitus (OR = 3.68; CI = 1.89–7.32; p = 0.002), Grade III tinnitus (OR = 3.70; CI = 1.94–7.22; p < 0.001), Grade IV (OR = 6.83; CI = 3.73–12.91; p < 0.001), and a history of tinnitus (OR = 1.96; CI = 1.08–3.64; p = 0.03) had poorer recovery outcomes. Grade IV cases were most common (33.2%), and severe tinnitus was strongly associated with the risk of developing long-term hearing loss, anxiety, and emotional disorders (p < 0.001). The study concludes that severe post-COVID tinnitus correlates with a worse prognosis and potential hearing loss, suggesting the need for attentive treatment and management of severe cases.

Serum troponin is often elevated in patients with acute stroke and its mechanism is unknown. In a retrospective single-center cohort study, we evaluated the association between stroke severity and serum troponin in 187 patients with acute stroke using multivariable modified Poisson models. A one-point increase in the National Institutes of Health Stroke Scale (measure of stroke severity) was associated with a marginally higher serum troponin level in adjusted models (aIRR 1.03; 1.01–1.05, P = 0.001). The modest, yet potentially independent, association between stroke severity and serum troponins could suggest a neurogenic basis for a cardiac injury in patients with acute stroke.

Since the emergence of Omicron variant of SARS-CoV-2 in late 2021, a number of sub-lineages have arisen and circulated internationally. Little is known about the relative severity of Omicron sub-lineages BA.2.75, BA.4.6, and BQ.1. We undertook a case–control analysis to determine the clinical severity of these lineages relative to BA.5, using whole genome sequenced, PCR-confirmed infections, between 1 August 2022 and 27 November 2022, among those who presented to emergency care in England 14 days after and up to one day prior to the positive specimen. A total of 10,375 episodes were included in the analysis; of which, 5,207 (50.2%) were admitted to the hospital or died. Multivariable conditional regression analyses found no evidence of greater odds of hospital admission or death among those with BA.2.75 (odds ratio (OR) = 0.96, 95% confidence interval (CI): 0.84–1.09) and BA.4.6 (OR = 1.02, 95% CI: 0.88– 1.17) or BQ.1 (OR = 1.03, 95% CI: 0.94–1.13) compared to BA.5. Future lineages may not follow the same trend and there remains a need for continued surveillance of COVID-19 variants and their clinical outcomes to inform the public health response.

A robust association has been reported between childhood adverse life events (ALEs) and risky substance use in adolescence. It remains unclear, however, what the impact of type and timing of these ALEs is. We investigated the association between ALEs and substance use in adolescents. ALEs were operationalized as broad (e.g., moving, parental divorce, family sickness) or physically threatening (physical and/or sexual abuse). First, we examined lifetime ALEs, followed by an investigation into their timing. The sample consisted of 909 adolescents (aged 12–18 years) from a cohort oversampled on high levels of emotional and behavioral problems. The primary caregiver indicated which ALEs each adolescent experienced across their lifetime. Adolescents self-reported on number and frequency of substances used. Poisson and ordinal regression models were used to model the associations. The associations between lifetime ALEs and a substance used were observed only for physical ALEs (incidence rate ratio 1.18 [1.03, 1.35], p = 0.02). When investigating timing, physical ALEs after the age of 12 predicted number of substances used (IRR 1.36 [1.13, 1.63], p < .001). Recent ALEs (occurring after age 12) seem to have considerable impact on substance use. Alcohol and drugs as a coping mechanism were considered a plausible explanation for the results.

Criteria for assessing the severity of scientific procedures in laboratory rodents include the loss of body mass. However, guidance is limited for passerine birds and application of criteria developed for mammals risks poor welfare decisions. Here, I ask whether, and how, body mass criteria could be incorporated into laboratory welfare assessment of passerines. Passerine birds strategically adjust their body mass to minimise combined mortality risk from starvation and predation. A systematic literature review found that strategic mass changes can be sizeable (sometimes > 10%) even over short timescales. Many aspects of a bird's current or past environment, including husbandry and experimental procedures, may alter perceived starvation or predation risks and thus drive strategic mass change via evolved mechanisms. Therefore, body mass criteria used for rodents may be too stringent for passerines, potentially leading to over-estimated severity. Strategic mass changes might obscure those stemming from experimental interventions yet could also offer insights into whether birds perceive an intervention or altered husbandry as a threat. Mass criteria for severity assessment should be species- and context-specific in order to balance needs for refinement and reduction. To guide the development of appropriate criteria, a future research priority is for greater data collection and sharing based on standardised routine monitoring of mass variation under a representative range of husbandry conditions and procedures.

The ongoing Coronavirus disease 19 (Covid-19) pandemic and associated mortality in children led to an effort to address risk factors and develop protective measures. Observational studies in adults showed that vitamin D deficiency is associated with Covid-19 severity. The aim of this review was to summarise data regarding the role of serum vitamin 25(OH)D concentration in the severity of Covid-19 and the associated multisystem inflammatory syndrome in children (MIS-C). Many studies noted lower concentrations of vitamin 25(OH)D in children with Covid-19 compared with healthy controls; however, studies that assessed vitamin 25(OH)D suboptimal concentrations as a risk factor for Covid-19 severity were scarce. There was no high-quality evidence that vitamin 25(OH)D concentrations are associated with Covid-19 severity. Similarly, for MIS-C, a few studies with a small number of patients found that vitamin D deficiency was associated with more severe MIS-C. Vitamin D has many immunomodulatory actions and is consumed in the immunomodulatory cells, especially in infections such as the Covid-19 which is associated with increased inflammation and cytokine storm. Therefore, decreased concentrations of plasma vitamin 25(OH)D have been proposed to be the result of vitamin use by immunomodulatory cells in severe Covid-19, rather than a predisposing factor. In conclusion, the available data cannot prove that vitamin D deficiency is a risk factor for severe Covid-19 disease. More studies, of prospective design, are needed to investigate the role of this marker independently of other risk factors.

The present study examined the intergenerational transmission of internalizing and externalizing symptom severity, which indexes comorbidity, and symptom directionality, which indicates differentiation toward externalizing versus internalizing problems. Data are from 854 male and female, same-sex adult twin pairs born between 1926 and 1971 (32–60 years old, M = 44.9 years, SD = 4.9 years) from the Twin and Offspring Study in Sweden and their adolescent offspring (11–22 years old, M = 15.7 years, SD = 2.4 years, 52% female). Children-of-twins models revealed additive (9%) and dominant (45%) genetic and nonshared environmental (47%) influences on twins’ symptom severity, and additive genetic (39%) and nonshared environmental (61%) influences on twins’ symptom directionality. Both comorbid problems and preponderance of symptoms of a particular – internalizing versus externalizing – spectrum were correlated across parent and child generations, although associations were modest especially for directionality (i.e., transmission of specific symptom type). By interpreting findings alongside a recent study of adolescent twins, we demonstrate that the intergenerational transmission of symptom severity and symptom directionality are both unlikely to be attributable to genetic transmission, are both likely to be influenced by direct phenotypic transmission and/or nonpassive rGE, and the intergenerational transmission of symptom severity is also likely to be influenced by passive rGE.