Background The causal association between the gut microbiome and the development of migraine and its subtypes remains unclear. Methods The single nucleotide polymorphisms concerning gut microbiome were retrieved from the gene-wide association study (GWAS) of the MiBioGen consortium. The summary statistics datasets of migraine, migraine with aura (MA), and migraine without aura (MO) were obtained from the GWAS meta-analysis of the International Headache Genetics Consortium (IHGC) and FinnGen consortium. Inverse variance weighting (IVW) was used as the primary method, complemented by sensitivity analyses for pleiotropy and increasing robustness. Results In IHGC datasets, ten, five, and nine bacterial taxa were found to have a causal association with migraine, MA, and MO, respectively, (IVW, all P < 0.05). Genus.Coprococcus3 and genus.Anaerotruncus were validated in FinnGen datasets. Nine, twelve, and seven bacterial entities were identified for migraine, MA, and MO, respectively. The causal association still exists in family.Bifidobacteriaceae and order.Bifidobacteriales for migraine and MO after FDR correction. The heterogeneity and pleiotropy analyses confirmed the robustness of IVW results. Conclusion Our study demonstrates that gut microbiomes may exert causal effects on migraine, MA, and MO. We provide novel evidence for the dysfunction of the gut-brain axis on migraine. Future study is required to verify the relationship between gut microbiome and the risk of migraine and its subtypes and illustrate the underlying mechanism between them.

Introduction Cardiovascular disease (CVD) is associated with higher morbidity and mortality rates in patients with chronic kidney disease (CKD). Studies have shown that vascular calcification is a major predictor of CVD. Vascular calcification in the CKD population is associated with various risk factors, and changes in bone and mineral metabolism have been linked to an increased risk of atherosclerosis. Therefore, we aimed to investigate the correlation between vascular calcification and bone metabolism, which is necessary to improve the survival and prognosis of patients with CKD. Methods We included 146 patients with CKD who received coronary artery calcification (CAC) scores at our hospital from May 2017 to November 2018. Spearman rank correlation analysis, Mann–Whitney U test, and Kaplan–Meier method were used to analyze laboratory data and all-cause mortality. Results In the 146 patients, chronic glomerulonephritis accounted for the most common cause of CKD, at approximately 39.0%. Spearman rank correlation analysis on the factors influencing vascular calcification in patients with CKD showed that CAC score was significantly and positively correlated with C-reactive protein, N-terminal/midregion osteocalcin (N-MID), N-terminal peptide of type 1 procollagen (P1NP), β-cross-linked C-telopeptide of type 1 collagen (β-CTx), and parathyroid hormone (P = 0.0423, P = 0.0432, P = 0.0235, P = 0.0061, P < 0.0001, respectively). Serum calcium levels were positively correlated with N-MID, P1NP, β-CTx, and iPTH (r = 0.19, r = 0.24, r = 0.21, r = 0.21, respectively), and serum phosphorus levels were positively correlated with N-MID, P1NP, β-CTx, and iPTH (r = 0.50, r = 0.37, r = 0.50, r = 0.55, respectively). However, no difference was found in CVC scores among patients with CKD in different stages and receiving different treatments. In the Kaplan–Meier analysis of all-cause hospitalization and mortality rates, patients with CAC > 400 had a higher risk. Conclusion We found that the primary cause of CKD is glomerulonephritis, and the CAC score is positively correlated with inflammatory and bone metabolism markers, with a higher risk of all-cause mortality and cardiovascular hospitalization when the CAC score is greater than 400.

Background Among the histiocytic disorders, anaplastic lymphoma kinase (ALK)-positive histiocytosis emerged in 2008. As more and more cases of the novel entity are reported, our understanding of it is deepened. However, only a few cases with central nervous system (CNS) involvement have been reported. Furthermore, the lesion in the suprasellar region has not been documented.  Case presentation We presented a case of ALK-positive histiocytosis involving the suprasellar region of a one-year-and-four-month-old boy. Through clinical, neuropathological, and genomic analyses, the patient was diagnosed with ALK-positive histiocytosis. After lesions were resected he started treatment with a combination of the three compounds vincristine, prednisolone, and crizotinib, but they did not work. Cytarabine was then added as an additional chemotherapy drug for him, and the lesions in the brain and lungs were shrunk by combining treatment of crizotinib, dexamethasone, vincristine, and cytarabine according to the RECIST (esponse Evaluation Criteria In Solid Tumours). Conclusions Additional adjuvant chemotherapy drugs are needed when ALK-inhibitor treatment is ineffective.

BackgroundMultiple risk factors of stroke have been identified in previous studies; however, the causal role of snoring in the onset of stroke is less investigated. To clarify the causal association of snoring on stroke and its subtypes, this study is performed.MethodsThe single nucleotide polymorphisms in relation to snoring were retrieved from the UK biobank cohort with 408,317 participants. The data for stroke and its subtypes of European ancestry (67,162 cases and 453,702 controls) were obtained from the MEGASTROKE consortium. In single-variable Mendelian randomization (SVMR) and multivariable MR (MVMR) analyses, inverse variance weighting was used as the primary estimate, complemented with sensitivity analyses more robust to pleiotropy.ResultsGenetically predicted snoring increased the risk of stroke (odds ratio [OR] = 2.69, 95% confidence interval [CI] = 1.19–6.08, P = 0.016) and ischemic stroke (IS) (OR = 2.82, 95% CI = 1.23–6.44, P = 0.013), but not large artery stroke (LAS) (OR = 3.02, 95% CI = 0.31–29.44, P = 0.339), cardioembolic stroke (CES) (OR = 1.51, 95% CI = 0.58–3.92, P = 0.395). We provide novel genetic evidence that snoring increases the risk of stroke and IS, but not LAS, CES, and SVS.ConclusionOur findings provide novel genetic evidence that snoring increases the risk of stroke and IS, but not LAS, CES, and SVS.