Exenatide for obesity in children and adolescents: Systematic review and meta-analysis.

Objectives: There is no curative treatment for childhood obesity. We aim to synthesize published Randomized Controlled Trials (RCTs) evidence on the efficacy of exenatide in obese children and adolescents. Methods: We conducted a comprehensive search and analysis of relevant studies in popular databases such as PubMed, Web of Science, Embase, and Cochrane Library. Our focus was on RCTs that examined the effectiveness of exenatide for treating obesity in children. We primarily assessed changes in body weight, body mass index (BMI), fasting plasma glucose (FPG), or HbA1c levels. Additionally, we considered any adverse events reported during the treatment period, with particular attention to hypoglycemia. To evaluate the quality of RCTs included in our study, we employed the Cochrane bias assessment tool. Results: Five studies met the inclusion criteria. A group of 100 children were assigned to receive treatment with exenatide. Compared with controls, exenatide therapy reduced body weight and BMI by -0.6% (95% CI -0.93, -0.27), -1.11% (95% CI -1.91, -0.31), respectively. Undesirable consequences encompass gastrointestinal symptoms, with the majority of instances being characterized by mild severity. Conclusion: Exenatide demonstrates efficacy in the treatment of pediatric and adolescent obesity. Systematic Review Registration: PROSPERO https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=413706.

A 11-year-old boy with Blastocystis hominis infection, presents as immune thrombocytopenia.

BACKGROUND: Some causes of first-line treatment failure for ITP are often closely related to infections. But parasitic infections are rarely mentioned and easily overlooked. The case is the first to describe a boy with immune thrombocytopenia associated with blastocystis hominis. CASE PRESENTATION: The case involved a boy presenting with bleeding skin spots and ecchymosis and accompanied by intermittent epigastric pain and constipation. After a series of complete examinations, the platelet count was found to be decreased to 13 × 109/L and immune thrombocytopenia was diagnosed. After first-line treatment with gamma globulin and prednisolone, the thrombocytopenia remained unchanged. Blastocystis hominis was subsequently found in the patient's stool and then the treatment of metronidazole was provided. One week later, the patient's thrombocytopenia was completely relieved. He was followed up for six months and was found to have recovered well. CONCLUSIONS: The screening for potential predisposing factors is very important for immune thrombocytopenia patients with poor response to first-line treatment, and the best treatment strategy should include the management of potential diseases.

The role of mitochondrial transfer via tunneling nanotubes in the central nervous system: A review.

Tumour necrosis factor alpha-induced protein 2 (TNFAIP2) is a gene induced by tumor necrosis factor in endothelial cells. TNFAIP2 has important functions in physiological and pathological processes, including cell proliferation, adhesion, migration, angiogenesis, inflammation, tunneling nanotube (TNT) formation and tumorigenesis. Moreover, TNFAIP2 is the key factor in the formation of TNTs. TNTs are related to signal transduction between different cell types and are considered a novel means of cell-to-cell communication. Mesenchymal stem cells (MSCs) are pluripotent cells that exhibit self-renewal, multidirectional differentiation, paracrine function and immune-regulating ability. MSCs can transfer mitochondria through TNTs to improve the functions of target cells. This review revealed that TNFAIP2 promotes the formation of TNTs and that MSCs rely on TNTs for mitochondrial transfer to ameliorate cell dysfunction.

Efficacy and safety of adalimumab in pediatric patients with Crohn's disease: A systematic review and meta-analysis.

PURPOSE: There is currently no curative treatment for childhood Crohn's disease (CD). This meta-analysis aimed to validate the efficacy and safety of adalimumab (ADA) in pediatric patients with CD. MATERIALS AND METHODS: We searched all relevant studies in the PubMed, Web of Science, Embase, and Cochrane Library databases. The primary outcomes were induction (≤ 12 weeks) and maintenance (up to 48 weeks) of remission and response. Secondary outcomes were severe adverse events and opportunistic infections to ADA. The Cochrane bias assessment tool was used to assess the risk of bias in randomized controlled trials. The methodological quality of the single-arm studies was assessed using the methodological index for non-randomized studies tool. RESULTS: Ten clinical trials involving a total of 885 patients were included. Results indicated that 59% (95% confidence interval [CI] 39-80%) of the subjects treated with ADA achieved induction of remission, and 60% (95% CI 35-86%) of the subjects treated with ADA achieved induction of response, 57% (95% CI 44-70%) achieved maintenance of remission, and 63% (95% CI 26-69%) achieved maintenance of response. CONCLUSION: Current evidence indicates that ADA is effective in children and adolescents with CD and that adverse events vary but are usually not severe. SYSTEMATIC REVIEW REGISTRATION: https://www.crd.york.ac.uk/prospero/ , identifier CRD42023402199.

Case report: A case of immune thrombocytopenia combined with Hashimoto's thyroiditis and Helicobacter pylori infection in a child.

Immune thrombocytopenia (ITP) is one of the most prevalent acquired bleeding disorders in children, which is primarily characterized by a decrease in platelet count. It can be classified into two subtypes: primary ITP and secondary ITP. The underlying mechanisms causing ITP are complex and not fully comprehended. Helicobacter pylori (H. pylori) infections can lead to ITP and potentially trigger various autoimmune diseases. Furthermore, there is evidence of a correlation between thyroid disease and ITP. In this case report, we describe the case of an 11-year-old patient who presented with ITP, Hashimoto's thyroiditis (HT), and H. pylori infection. Following anti-H. pylori treatment and thyroxine supplementation, the child's platelet count increased compared to the previous count. The limitation of this report is that the platelet count of this child returned to normal after anti-H. pylori and thyroxine supplementation, so we cannot distinguish the effect of anti-H. pylori and thyroxine supplementation on the platelet count in this child. Despite this limitation, we still believe that early screening for thyroid function and H. pylori, as well as prompt eradication of H. pylori, along with thyroxine supplementation, may be beneficial in treating and improving the prognosis of children diagnosed with ITP.

The role of RIM in neurotransmitter release: promotion of synaptic vesicle docking, priming, and fusion.

There are many special sites at the end of a synapse called active zones (AZs). Synaptic vesicles (SVs) fuse with presynaptic membranes at these sites, and this fusion is an important step in neurotransmitter release. The cytomatrix in the active zone (CAZ) is made up of proteins such as the regulating synaptic membrane exocytosis protein (RIM), RIM-binding proteins (RIM-BPs), ELKS/CAST, Bassoon/Piccolo, Liprin-α, and Munc13-1. RIM is a scaffold protein that interacts with CAZ proteins and presynaptic functional components to affect the docking, priming, and fusion of SVs. RIM is believed to play an important role in regulating the release of neurotransmitters (NTs). In addition, abnormal expression of RIM has been detected in many diseases, such as retinal diseases, Asperger's syndrome (AS), and degenerative scoliosis. Therefore, we believe that studying the molecular structure of RIM and its role in neurotransmitter release will help to clarify the molecular mechanism of neurotransmitter release and identify targets for the diagnosis and treatment of the aforementioned diseases.

Predictive value of neutrophil gelatinase-associated lipocalin in children with acute kidney injury: A systematic review and meta-analysis.

Purpose: Neutrophil gelatin lipase carrier protein (NGAL) has been used as an early biomarker to predict acute kidney injury (AKI). However, the predictive value of NGAL in urine and blood in children with acute kidney injury in different backgrounds remains unclear. Therefore, we conducted this systematic review and meta-analysis to explore the clinical value of NGAL in predicting AKI in children. Methods: Computerized databases were searched for relevant the studies published through August 4th, 2022, which included PUBMED, EMBASE, COCHRANE and Web of science. The risk of bias of the original included studies was assessed by using the Quality Assessment of Studies for Diagnostic Accuracy (QUADA-2). At the same time, subgroup analysis of these data was carried out. Results: Fifty-three studies were included in this meta-analysis, involving 5,049 patients, 1,861 of whom were AKI patients. The sensitivity and specificity of blood NGAL for predicting AKI were 0.79 (95% CI: 0.69-0.86) and 0.85 (95% CI: 0.75-0.91), respectively, and SROC was 0.89 (95% CI: 0.86-0.91). The sensitivity and specificity of urine NGAL for predicting AKI were 0.83 (95% CI: 0.78-0.87) and 0.81 (95% CI: 0.77-0.85), respectively, and SROC was 0.89 (95% CI: 0.86-0.91). Meanwhile, the sensitivity and specificity of overall NGAL (urine and blood NGAL) for predicting AKI in children were 0.82 (95% CI: 0.77-0.86) and 0.82 (95% CI: 0.78-0.86), respectively, and SROC was 0.89 (95% CI: 0.86-0.91). Conclusion: NGAL is a valuable predictor for AKI in children under different backgrounds. There is no significant difference in the prediction accuracy between urine NGAL and blood NGAL, and there is also no significant difference in different measurement methods of NGAL. Hence, NGAL is a non-invasive option in clinical practice. Based on the current evidence, the accuracy of NGAL measurement is the best at 2 h after cardiopulmonary bypass (CPB) and 24 h after birth in asphyxiated newborns. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier: CRD42022360157.

Activin A rescues preterm brain injury through a novel Noggin/BMP4/Id2 signaling pathway.

Activin A (Act A) has been reported to promote oligodendrocyte progenitor cell (OPC) differentiation in vitro and improve neurological outcomes in adult mice. However, the roles and mechanisms of action of Act A in preterm brain injury are unknown. In the present study, P5 rats were subjected to hypoxia­ischemia to establish a neonatal white matter injury (WMI) model and Act A was injected via the lateral ventricle. Pathological characteristics, OPC differentiation, myelination, and neurological performance were analyzed. Further, the involvement of the Noggin/BMP4/Id2 signaling pathway in the roles of Act A in WMI was explored. Act A attenuated pathological damage, promoted OPC differentiation, enhanced myelin sheath and myelinated axon formation, and improved neurological performance of WMI rats. Moreover, Act A enhanced noggin expression, which, in turn, inhibited the expression of bone morphogenetic protein 4 (BMP4) and inhibitor of DNA binding 2 (Id2). Furthermore, upregulation of Id2 completely abolished the rescue effects of Act A in WMI rats. In conclusion, the present findings suggested that Act A rescues preterm brain injury via targeting a novel Noggin/BMP4/Id2 signaling pathway.

Munc18-1 Contributes to Hippocampal Injury in Septic Rats Through Regulation of Syntanxin1A and Synaptophysin and Glutamate Levels.

Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction closely associated with mortality in the acute phase of sepsis. Abnormal neurotransmitters release, such as glutamate, plays a crucial role in the pathological mechanism of SAE. Munc18-1 is a key protein regulating neurotransmission. However, whether Munc18-1 plays a role in SAE by regulating glutamate transmission is still unclear. In this study, a septic rat model was established by the cecal ligation and perforation. We found an increase in the content of glutamate in the hippocampus of septic rat, the number of synaptic vesicles in the synaptic active area and the expression of the glutamate receptor NMDAR1. Meanwhile, it was found that the expressions of Munc18-1, Syntaxin1A and Synaptophysin increased, which are involved in neurotransmission. The expression levels of Syntaxin1A and Synaptophysin in hippocampus of septic rats decreased after interference using Munc18-1siRNA. We observed a decrease in the content of glutamate in the hippocampus of septic rats, the number of synaptic vesicles in the synaptic activity area and the expression of NMDAR1. Interestingly, it was also found that the down-regulation of Munc18-1 improved the vital signs of septic rats. This study shows that CLP induced the increased levels of glutamate in rat hippocampus, and Munc18-1 may participate in the process of hippocampal injury in septic rats by affecting the levels of glutamate via regulating Syntaxin1A and Synaptophysin. Munc18-1 may serve as a potential target for SAE therapy.

Knockdown of lncRNA MEG3 protects against sepsis-induced acute lung injury in mice through miR-93-5p-dependent inhibition of NF­κB signaling pathway.

Excessive inflammatory response is a prominent pathogenic hallmark of acute lung injury (ALI). Long noncoding RNA (lncRNA) has been recently reported to play a key role in the pathophysiology of many inflammatory disorders, including ALI. Herein, we attempted to explore the role and underlying mechanism of lncRNA MEG3 in the inflammation in ALI. Firstly, an ALI mouse model was generated via intra-tracheal instillation of lipopolysaccharide (LPS), and then, the impact of lncRNA MEG3 on lung tissue damage, pulmonary edema, lung microvascular permeability and pulmonary inflammatory response, as well as the ALI mice survival rate was investigated. LncRNA MEG3 was upregulated in lung tissues, and knockdown of lncRNA MEG3 protected mice from LPS-induced ALI, with significantly reduced lung pathological changes, decreased lung wet/dry (W/D) ratio and lung microvascular permeability, attenuated inflammatory response, along with increased ALI mice survival. Moreover, lncRNA MEG3 could sponge miR-93, negatively regulated its expression, and lncRNA MEG3 overexpression liberated the suppression of TLR4 expression caused by miR-93. Further, functional studies demonstrated that the protective effects of lncRNA MEG3 on excessive inflammatory response may be related to miR-93-mediated modulation of TLR4/MyD88/NF-κB pathway. Collectively, lncRNA MEG3 inhibition blocked TLR4/MyD88/NF-κB pathway to repress the progression of sepsis-induced lung injury via upregulating miR-93, implying that lncRNA MEG3 might be a viable therapeutic target for ALI.

The role of SCAMP5 in central nervous system diseases.

OBJECTIVE: Secretory carrier membrane proteins (SCAMPs) constitute a group of membrane transport proteins in plants, insects and mammals. The mammalian genome contains five types of SCAMP genes, namely, SCAMP1-SCAMP5. SCAMPs participate in the vesicle cycling fusion of vesicles and cell membranes and play roles in regulating exocytosis and endocytosis, activating synaptic function and transmitting nerve signals. Among these proteins, SCAMP5 is highly expressed in the brain and has direct or indirect effects on the function of the central nervous system. This paper may allow us to better understand the role of SCAMP5 in the central nervous system diseases. SCAMP5 regulates membrane transport, controls the exocytosis of SVs and is related to secretion carrier and membrane function. In addition, SCAMP5 plays a major role in the normal maintenance of the physiological functions of nerve cells. This article summarizes the effects of SCAMP5 on nerve cell exocytosis, endocytosis and synaptic function, as well as the relationship between SCAMP5 and various neurological diseases, to better understand the role of SCAMP5 in the pathogenesis of neurological diseases. METHODS: Through PubMed, this paper examined and analyzed the role of SCAMP5 in the central nervous system, as well as the relationship between SCAMP5 and various neurological diseases using the key terms "secretory carrier membrane proteins"," SCAMP5"," exocytosis"," endocytosis", "synaptic function", "central nervous system diseases" up to 01 March 2022. RESULTS: SCAMP5 regulates membrane transport, controls the exocytosis of SVs and is related to secretion carrier and membrane function. In addition, SCAMP5 plays a major role in the normal maintenance of the physiological functions of nerve cells. CONCLUSION: This article summarizes the effects of SCAMP5 on nerve cell exocytosis, endocytosis and synaptic function, as well as the relationship between SCAMP5 and various neurological diseases, to better understand the role of SCAMP5 in the pathogenesis of neurological diseases.

Comparison of the efficacy and safety of caplacizumab versus placebo in thrombotic thrombocytopenic purpura: a meta-analysis and systematic review based on randomized controlled trials.

Background: We conducted this meta-analysis to investigate the efficacy and safety of caplacizumab in patients with thrombotic thrombocytopenic purpura (TTP). TTP is a potentially fatal disorder characterized by systemic microvascular thrombosis. Methods: Randomized controlled trials (RCTs) were conducted from PubMed, Embase, Cochrane Library and Web of Science, China National Knowledge Infrastructure (CNKI), VIP and Wanfang databases. RCTs of caplacizumab treatment for TPP were mainly included. Data from eligible studies were extracted and analyzed using relative effect sizes versus placebo use. The Cochrane bias assessment tool was used to assess the risk of bias of included studies, and the assessment results were presented graphically in Revman5.3. Results: Four RCTs with a total of 416 patients were included, all of which were of high quality. Caplacizumab was associated with improvements in platelet counts normalization time [weighted mean difference (WMD) -1.18, 95% confidence interval (CI): -2.55 to 0.19, I2=69.9%, P=0.036], plasma exchange (PE) time (WMD -2.97, 95% CI: -4.44 to -1.50, I2=8.2%, P=0.163) and hospital stay (WMD -2.88, 95% CI: -4.56 to -1.21, I2=48.7%, P=0.036). In addition, the occurrence of adverse events was also investigated. The difference in mortality between the two groups was not statistically significant [relative risk (RR) 0.56, 95% CI: 0.18 to 1.72, I2=22.7%, P=0.275], relapse (RR 0.68, 95% CI: 0.13 to 3.49, I2=78.3%, P=0.01), or major thrombotic events (RR 1.01, 95% CI: 0.65 to 1.57, I2=43.4%, P=0.151). Conclusions: Caplacizumab shortens the platelet normalization time, PE time, and hospital stay in patients with TTP, and did not significantly increase the risk of adverse events. These results indicate that caplacizumab treatment provides significant benefits to patients with TTP. Even though this is evidence from RCTs, few original studies were included, so more multicenter RCTs are required.

The Role of Vti1a in Biological Functions and Its Possible Role in Nervous System Disorders.

Vesicle transport through interaction with t-SNAREs 1A (Vti1a), a member of the N-ethylmaleimide-sensitive factor attachment protein receptor protein family, is involved in cell signaling as a vesicular protein and mediates vesicle trafficking. Vti1a appears to have specific roles in neurons, primarily by regulating upstream neurosecretory events that mediate exocytotic proteins and the availability of secretory organelles, as well as regulating spontaneous synaptic transmission and postsynaptic efficacy to control neurosecretion. Vti1a also has essential roles in neural development, autophagy, and unconventional extracellular transport of neurons. Studies have shown that Vti1a dysfunction plays critical roles in pathological mechanisms of Hepatic encephalopathy by influencing spontaneous neurotransmission. It also may have an unknown role in amyotrophic lateral sclerosis. A VTI1A variant is associated with the risk of glioma, and the fusion product of the VTI1A gene and the adjacent TCF7L2 gene is involved in glioma development. This review summarizes Vti1a functions in neurons and highlights the role of Vti1a in the several nervous system disorders.

Inhibiting miR-466b-5p Attenuates Neonatal White Matter Injury by Targeting Lpar1.

miR-466b-5p is aberrantly upregulated in oligodendrocyte precursor cells (OPCs) after white matter injury (WMI). However, its roles in neonatal WMI pathogenesis are unknown. In this study, P3 rats were subjected to hypoxia-ischemia to establish a neonatal WMI model. A bioinformatic analysis was conducted to predict the possible target of miR-466b-5p as Lpar1. RT-PCR was performed to validate the expression of miR-466b-5p and Lpar1 mRNA. The miR-466b-5p antagomir was intracerebroventricularly administrated to inhibit miR-466b-5p; OPC differentiation, apoptosis, proliferation, and myelination were analyzed using immunofluorescence staining, western blotting, and electron microscopy. In addition, the behavioral performance of the rats was measured with the Morris water maze test. Sox10 expression and PLP trafficking were examined to elucidate the mechanism by which miR-466b-5p regulates WMI pathogenesis. We found that after inhibiting miR-466b-5p, the Edg2 protein was increased, OPC differentiation and myelinated axon formation were enhanced, and the rats' behavioral performance was improved, whereas OPC proliferation and apoptosis were not affected. Furthermore, the expression of Sox10 was promoted while PLP trafficking was attenuated after miR-466b-5p inhibition. We conclude that miR-466b-5p is involved in the regulation of WMI pathogenesis, partly through the Lpar1/Edg2/Sox10 and Lpar1/Edg2/PLP signaling pathways.

Behavioral tests for evaluating the characteristics of brain diseases in rodent models: Optimal choices for improved outcomes (Review).

Behavioral assessment is the dominant approach for evaluating whether animal models of brain diseases can successfully mimic the clinical characteristics of diseases. At present, most research regarding brain diseases involves the use of rodent models. While studies have reported numerous methods of behavioral assessments in rodent models of brain diseases, each with different principles, procedures, and assessment criteria, only few reviews have focused on characterizing and differentiating these methods based on applications for which they are most appropriate. Therefore, in the present review, the representative behavioral tests in rodent models of brain diseases were compared and differentiated, aiming to provide convenience for researchers in selecting the optimal methods for their studies.

m6A: An Emerging Role in Programmed Cell Death.

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.

The emerging roles of ferroptosis in cells of the central nervous system.

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.

Efficacy and safety of blinatumomab in children with relapsed/refractory B cell acute lymphoblastic leukemia: A systematic review and meta-analysis.

Objectives: Several clinical trials have been conducted to evaluate the effects of blinatumomab in childhood B cell acute lymphoblastic leukemia (B-ALL). We conducted this meta-analysis to validate the efficacy and safety of blinatumomab in pediatric patients with relapsed/refractory B-ALL (R/R B-ALL). Methods: We searched and investigated all relevant studies in the PubMed, Web of Science, Embase, and Cochrane Library databases. The primary outcomes were complete response (CR), overall survival (OS), event free survival (EFS), minimal residual disease (MRD) response, allogeneic hematopoietic stem cell transplantation (allo-HSCT) and were calculated separately for randomized controlled trials (RCTs) and single-arm studies. The secondary end points were adverse effects (AEs) and the relapse rate. The Cochrane, bias assessment tool, was used to assess the risk of bias in RCTs. The methodological quality of single-arm studies was assessed using the methodological index for non-randomized studies (MINORS) tool. Results: The meta-analysis included two RCTs and 10 single-arm studies, including 652 patients in total. Our study showed that in the single-arm studies, the combined CR rate was 0.56 (95% confidence interval (CI): 0.45 -0.68), the odds ratios (ORs) of OS was 0.43 (95% CI 0.32 -0.54), the EFS rate was 0.30 (95% CI: 0.20 -0.40), the MRD response was 0.51 (95% CI: 0.34 -0.68), allo-HSCT rate was 0.62 (95% CI: 0.50 -.74), the AE rate was 0.65 (95% CI: 0.54 -0.76) and the relapse rate was 0.32 (95% CI: 0.27 -0.38). In the RCTs, the blinatumomab-treated group compared with the chemotherapy group had a combined OS rate of 0.12 (95% CI: 0.05 -0.19) and an EFS rate of 2.16 (95% CI: 1.54 -3.03). The pooled MRD response rate was 4.71 (95% CI:2.84 -7.81), allo-HSCT was 3.24 (95% CI: 1.96 -5.35), the AE rate was 0.31 (95% CI: 0.16 -0.60), and the relapse rate was 0 .69 (95% CI: 0.43 -1.09). Conclusion: According to this meta-analysis, blinatumomab shows potent therapeutic efficacy and limited AEs in children with R/R B- ALL. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier CRD42022361914.

Cumulative evidence for association of rhinitis and depression.

BACKGROUND: Several primary studies evaluated the association between rhinitis and the incidence of depression and yielded inconsistent results. We conducted a meta-analysis of studies evaluating the association between rhinitis and depression. METHODS: We searched the EMBASE, PubMed and Cochrane Library databases for studies published in English before April 1, 2019. The studies were included if they reported any type of rhinitis in relation to depression. Two authors independently extracted the data. The odds ratios (ORs) were pooled using a random-effects model. Stratified analyses were conducted to evaluate the association. RESULTS: Among the 3472 initially identified studies, we included 14 studies involving a total of 19.36 ± 1.1 million participants according to predefined inclusion criteria. The associations between rhinitis (R), allergic rhinitis (AR), and nonallergic rhinitis (NAR) and depression were significant with ORs of 1.86 (95% CI 1.32 to 2.62, p < 0.05), 1.54 (95% CI 1.24 to 1.90, p < 0.05), and 2.15 (95% CI 1.49 to 3.09, p < 0.05), respectively. The results were consistent and statistically significant in all subgroup analyses. CONCLUSIONS: Rhinitis was associated with an increased risk of depression. Further prospective studies involving large sample sizes are required to confirm the results by considering more confounders and clarify the mechanisms.

CAPN3: A muscle­specific calpain with an important role in the pathogenesis of diseases (Review).

Calpains are a family of Ca2+­dependent cysteine proteases that participate in various cellular processes. Calpain 3 (CAPN3) is a classical calpain with unique N­terminus 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 muscle­specific 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 limb­girdle 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.