Similarities in the symptoms of chronic fatigue syndrome (CFS) and inflammatory bowel disease (IBD) have been observed as follows: severe disease activity in IBD correlates with severe fatigue, major psychiatric signs, the common use of medication, and bacterial translocation. One of several hypotheses for explaining the mechanisms underlying CFS suggests a similarity to the impaired intestinal mucosa of IBD. “This study investigated the risk of incident CFS among patients with IBD”. We conducted a population-based retrospective cohort study by using Taiwan’s National Health Insurance Research Database to evaluate the subsequent risk of CFS in patients with IBD, according to demographic characteristics and comorbidities. The exposure cohort comprised 2163 patients with new diagnoses of IBD. Each patient was randomly selected and frequency matching according to gender and age with four participants from the general population who had no history of CFS at the index date (control cohort). Cox proportional hazards regression analysis was conducted to estimate the relationship between IBD and the subsequent risk of CFS. The exposure cohort had a significantly higher overall risk of subsequent CFS than that of the control group [adjusted hazard ratio (Christophi in Inflamm Bowel Dis 18(12):2342–2356, 2012 ) = 2.25, 95%, confidence interval (Aaron and Buchwald in Ann Intern Med 134(9 Pt 2):868–881, 2001 ; Farraye et al. in Am J Gastroenterol 112:241, 2017 ) 1.70–2.99]. Further analysis indicated a significantly higher risk of CFS in patients who were male (HR = 3.23, 95% CI 2.12–4.91), were older than 35 years, and had IBD but without comorbidity status, e.g. Cancers, diabetes, obesity, depression, anxiety, sleep disorder, renal disease (HR = 2.50, 95% CI 1.63–3.84) after adjustment. The findings from this population-based retrospective cohort study suggest that IBD, especially Crohn’s disease, is associated with an increased risk of subsequent CFS.

The onset of chronic fatigue syndrome (CFS) has been shown to be associated with several immunological conditions such as infections or atopy. The aim of this study was to clarify the risk of chronic fatigue syndrome following the diagnosis of psoriasis, an immune-related dermatological disease, by analyzing the National Health Insurance Research Database of Taiwan. 2616 patients aged 20 years or older with newly diagnosed psoriasis during 2004–2008 and 10,464 participants without psoriasis were identified. Both groups were followed up until the diagnoses of CFS were made at the end of 2011. The relationship between psoriasis and the subsequent risk of CFS was estimated through Cox proportional hazards regression analysis, with the incidence density rates being 2.27 and 3.58 per 1000 person-years among the non-psoriasis and psoriasis populations, respectively (adjusted hazard ratio [HR] = 1.48, with 95% confidence interval [CI] 1.07–2.06). In the stratified analysis, the psoriasis group were consistently associated with a higher risk of CFS in male sex (HR = 2.05, 95% CI 1.31–3.20) and age group of ≥ 60 years old (HR = 2.32, 95% CI 1.33–4.06). In addition, we discovered that the significantly increased risk of CFS among psoriasis patients is attenuated after they receive phototherapy and/or immunomodulatory drugs. The data from this population-based retrospective cohort study revealed that psoriasis is associated with an elevated risk of subsequent CFS, which is differentiated by sex and age.

Age-related bone diseases are partly caused by impaired bone integrity, which are closely related to osteoblasts’ activity and angiogenesis. Endothelial progenitor cells (EPCs) are the initiators of angiogenesis and found to have senescent-induced dysfunctions. The aim of this study is to investigate the effects of senescence in EPCs on osteogenesis and angiogenesis. Human primary EPCs and a murine osteoblast cell line (MC3T3-E1) are utilized in this study. The senescence of EPCs are induced by serial passages. When co-cultured with senescent EPCs, the osteoblasts demonstrate weakened alkaline phosphatase (ALP) activity and mineral deposition. On the other hand, osteoblast-induced migration decreases in senescent EPCs. As for the intracellular alterations of senescent EPCs, the activation of Akt/mTOR/p70S6K pathway, MnSOD and catalase are diminished. In contrast, the level of reactive oxygen species are significantly higher in senescent EPCs. Furthermore, senescent EPCs has decreased level intracellular ATP level and coupling efficiency for oxidative phosphorylation while the non-mitochondrial respiration and glycolysis are elevated. The senescence of EPCs impairs the functions of both osteoblasts and EPCs, suggesting EPCs’ role in the pathophysiology of age-related bone diseases. Targeting the alterations found in this study could be potential treatments.

Background: Early psychosis is marked by cortico-striatal and thalamocortical dysconnectivity, yet how aripiprazole modulates these circuits remains unclear. Methods: We examined putamen and thalamus functional connectivity (FC) in 30 early psychosis patients (ultra-high-risk, first-episode psychosis, schizophreniform disorder, or first-episode schizophrenia) and 30 matched healthy controls. At baseline, patients were naïve to dopamine receptor-targeting medication or minimally exposed (<12 weeks). All patients received flexible-dose aripiprazole, and symptoms were assessed using the Positive and Negative Syndrome Scale at baseline, days 14 and 28. Baseline resting-state functional MRI was acquired for patients and controls, and follow-up scans for patients after 41.6 ± 13.9 days of treatment. Results: Compared with controls, patients showed hypoconnectivity within/between bilateral putamen, between putamen and thalamus, and between thalamus and salience network (SN) nodes. In contrast, hyperconnectivity was observed between the putamen and both sensorimotor (SM) and default mode network (DMN) nodes, as well as between the thalamus and SM nodes. After treatment with aripiprazole, FC increased within/between bilateral putamen, between putamen and SN nodes, and between thalamus and SN nodes, and decreased between thalamus and SM nodes and between putamen and SM nodes. At the uncorrected level ( p < 0.05), increases in FC between the right ventral rostral putamen and bilateral putamen correlated with improvement in positive symptoms. Conclusion: Findings suggest aripiprazole partially normalizes aberrant striatal–thalamic coupling early in psychosis, and putaminal FC changes may relate to clinical response. Aripiprazole may achieve therapeutic benefits by restoring integration within striatal hubs and their crosstalk with large-scale networks implicated in psychotic symptom expression.