Vitamin D deficiency (VDD) has been implicated in the pathogenesis of tuberculosis (TB), but most studies have not reported a significant association. We conducted a meta-analysis to explore the association between vitamin D status and TB in children. Web of Science, Ovid Medline, and EMBASE were searched for studies in English that discussed vitamin D status and TB in children before January 22, 2018. From the 585 initially identified studies, we selected those that addressed an association between vitamin D status and TB according to our preselected inclusion criteria. Our meta-analysis included 10 studies. According to the random effects model, TB was significantly associated with VDD (ORs, 1.70; 95% CI, 1.20–2.42; P < .05) in children. Vitamin D levels were significantly lower in TB patients than in controls, with a mean difference d = −5.49 nmol/L (95% CI, −10.42 to −0.55; P < .05), indicating that VDD was significantly associated with TB (OR, 1.78; 95% CI, 1.30–2.44; P < .05) in children. This study suggests that vitamin D levels are significantly lower in children with TB/latent TB infection than in controls. TB may contribute to VDD in children. Therefore, VDD may be associated with TB in children.

Objective To investigate the association between bronchopulmonary dysplasia (BPD) and the risk of cerebral palsy (CP) in children. Data sources We used EMBASE, PubMed and Web of Science to conduct a meta-analysis of studies published before 1 September 2017, written in English whose titles or abstracts discussed an association between BPD and CP. Study selection Observational studies, for example, case–control and cohort studies were included. Data extraction and synthesis All review stages were conducted by two reviewers independently. Data synthesis was undertaken via meta-analysis of available evidence. Main outcomes and measures The prevalence of developing CP was measured after exposure to BPD. Results Among 1234 initially identified studies, we selected those that addressed an association between BPD and CP according to our preselected inclusion criteria. Our meta-analysis included 11 studies. According to a random effect model, BPD was significantly associated with CP (ORs 2.10; 95% CI 1.57 to 2.82) in preterm infants. Factors explaining differences in the study results included study design, the definition of BPD, the time of diagnosis of CP and whether the studies adjusted for potential confounders. Conclusion This study suggests that BPD is a risk factor for CP. Further studies are required to confirm these results and to detect the influence of variables across studies.

Programmed cell death is an active extinction process, including autophagy, ferroptosis, pyroptosis, apoptosis, and necroptosis. m⁶A is a reversible RNA modification which undergoes methylation under the action of methylases (writers), and is demethylated under the action of demethylases (erasers). The RNA base site at which m⁶A is modified is recognized by specialized enzymes (readers) which regulate downstream RNA translation, decay, and stability. m⁶A affects many aspects of mRNA metabolism, and also plays an important role in promoting the maturation of miRNA, the translation and degradation of circRNA, and the stability of lncRNA. The regulatory factors including writers, erasers and readers promote or inhibit programmed cell death via up-regulating or down-regulating downstream targets in a m⁶A-dependent manner to participate in the process of disease. In this review, we summarize the functions of m⁶A with particular reference to its role in programmed cell death.

Calpains are a family of Ca²⁺‑dependent cysteine proteases that participate in various cellular processes. Calpain 3 (CAPN3) is a classical calpain with unique N‑terminus and insertion sequence 1 and 2 domains that confer characteristics such as rapid autolysis, Ca²⁺‑independent activation and Na⁺ activation of the protease. CAPN3 is the only muscle‑specific calpain that has important roles in the promotion of calcium release from skeletal muscle fibers, calcium uptake of sarcoplasmic reticulum, muscle formation and muscle remodeling. Studies have indicated that recessive mutations in CAPN3 cause limb‑girdle muscular dystrophy (MD) type 2A and other types of MD; eosinophilic myositis, melanoma and epilepsy are also closely related to CAPN3. In the present review, the characteristics of CAPN3, its biological functions and roles in the pathogenesis of a number of disorders are discussed.

Ferroptosis is morphologically characterized by shrunken mitochondria and biochemically characterized by iron overload, lipid peroxidation and lipid reactive oxygen species (ROS) accumulation; these phenomena are suppressed by iron chelation, genetic inhibition of cellular iron uptake, and intervention on other pathways such as lipid metabolism. The induction of ferroptosis may be related to pathological cellular conditions in the central nervous system (CNS); thus, ferroptosis may cause disability via CNS damage. Here, we review the role of ferroptosis in the main cells of the CNS, including glial cells, neurons, and pericytes; in various diseases of the CNS; and in the interaction of glia and neurons in CNS diseases. Some small molecules and traditional Chinese drugs which inhibit ferroptosis in cells of the CNS are shown as potential therapeutic strategies for neurological diseases.