Microglia are the major immune cells in the central nervous system and play a key role in the normal function of the brain. Microglia exhibit functional diversity, and they control the inflammation in central nervous system through releasing inflammatory cytokine, clearing apoptotic cells via phagocytosis, regulating synaptic plasticity and the formation of neural network by synapse pruning. Recent studies have strongly indicated that the microglial dysfunction is associated with a variety of neuropsychiatric diseases such as depression, which have been termed as “microgliopathy”. The emergency of advanced technologies and tools has enabled us to comprehensively understand the role of microglia in physiology and pathology, and growing studies have targetted microglia to explore the treatment of neuropsychiatric diseases. Here, we describe the key progress of microglia research, and review the recent developments in the understanding of the role of microglia in physiology and etiology of depression.

N⁶-methyladenosine (m⁶A) is identified as the most widespread and abundant internal chemical modification of RNA in eukaryotes. A series of proteins including methyltransferases (also known as “writers”), demethylases (also known as “erasers”), and m⁶A-binding proteins (also known as “readers”) were indicated to participate in the m⁶A methylation. m⁶A has emerged as a regulator of various cellular, developmental, and disease processes. Notably, there is highest abundance of m⁶A methylation in brain than in other organs, which indicates that m⁶A plays an essential role in brain functions. Here, we describe the general features, mechanisms, and functions of m⁶A in the brain, and discuss the emerging roles of m⁶A in brain physiology and diseases.

Fluorescent nanoparticles have good chemical stability and photostability, controllable optical properties and larger stokes shift. In light of their designability and functionability, the fluorescent nanoparticles are widely used as the fluorescent probes for diverse applications. To enhance the sensitivity and selectivity, the combination of the fluorescent nanoparticles with the molecularly imprinted polymer, i.e. molecularly imprinted fluorescent nanoparticles (MIFN), was an effective way. The sensor based on MIFN (the MIFN sensor) could be more compatible with the complex sample matrix, which was especially widely adopted in medical and biological analysis. In this mini-review, the construction method, detective mechanism and types of MIFN sensors are elaborated. The current applications of MIFN sensors in pharmaceutical analysis, including pesticides/herbicide, veterinary drugs/drugs residues and human related proteins, are highlighted based on the literature in the recent three years. Finally, the research prospect and development trend of the MIFN sensor are forecasted.

Mitochondrial superoxide overproduction is believed to be responsible for the neurotoxicity associated with neurodegeneration. Mitochondria-targeted antioxidants, such as MitoQ, have emerged as potentially effective antioxidant therapies. Methionine sulfoxide reductase A (MsrA) is a key mitochondrial-localized endogenous antioxidative enzyme and it can scavenge oxidizing species by catalyzing the methionine (Met)-centered redox cycle (MCRC). In this study, we observed that the natural L-Met acted as a good scavenger for antimycin A-induced mitochondrial superoxide overproduction in PC12 cells. This antioxidation was largely dependent on the Met oxidase activity of MsrA. S-methyl-L-cysteine (SMLC), a natural analogue of Met that is abundantly found in garlic and cabbage, could activate the Met oxidase activity of MsrA to scavenge free radicals. Furthermore, SMLC protected against antimycin A-induced mitochondrial membrane depolarization and alleviated 1-methyl-4-phenylpyridinium (MPP⁺)-induced neurotoxicity. Thus, our data highlighted the possibility for SMLC supplement in the detoxication of mitochondrial damage by activating the Met oxidase activity of MsrA.

Progressive memory loss and cognitive impairment are the main clinical manifestations of Alzheimer’s disease (AD). Currently, there is no effective drug available for the treatment of AD. Previous studies have demonstrated that the cognitive impairment of AD is associated with oxidative stress and the inhibition of AKT and ERK phosphorylation. Grape seed proanthocyanidin extract (GSPE) has been shown to have strong antioxidant effect and can protect the nervous system from oxidative stress damage. This study aimed to investigate the protective effect of GSPE on the cognitive and synaptic impairments of AD using a sporadic AD rat model induced by intracerebroventricular (ICV) injection of streptozotocin (STZ) (ICV-STZ). Rats were treated with GSPE (50, 100, or 200 mg/kg every day) by intragastrical (ig.) administration for continuous 7 weeks, and ICV-STZ (3 mg/kg) was performed on the first day and third day of week 5. Learning and memory abilities were assessed by the Morris water maze (MWM) test at week 8. After behavioral test, hippocampal long-term potentiation (LTP) was recorded, and the levels of malondialdehyde (MDA), superoxide dismutases (SOD), glutathione (GSH) and the protein expression of AKT and ERK were measured in the hippocampus and cerebral cortex of rats. Our study revealed that ICV-STZ significantly impaired the working learning ability and hippocampal LTP of rats, significantly increased the levels of MDA, and decreased the activity of SOD and GSH in the hippocampus and cerebral cortex. In contrast, GSPE treatment prevented the impairment of cognitive function and hippocampal LTP induced by ICV-STZ, decreased the level of MDA, and increased the level of SOD and GSH. Furthermore, Western blot results showed that GSPE treatment could prevent the loss of AKT and ERK activities in the hippocampus and cerebral cortex induced by ICV-STZ. Our findings demonstrate that GSPE treatment could ameliorate the impairment of cognitive ability and hippocampal synaptic plasticity in a rat model of sporadic AD by inhibiting oxidative stress and preserving AKT and ERK activities. Therefore, GSPE may be an effective agent for the treatment of cognitive deficits associated with sporadic AD.

Pulmonary hypertension (PH) is a severe and progressive disease characterized by increased pulmonary vascular resistance leading to right heart failure and death. In PH, the cellular metabolisms including those of the three major nutrients (carbohydrate, lipid and protein) are aberrant in pulmonary vascular cells. Glucose uptake, glycolysis, insulin resistance, sphingolipid S1P, PGE₂, TXA₂, leukotrienes and glutaminolysis are upregulated, and phospholipid-prostacyclin and L-arginine-nitric oxide pathway are compromised in lung vascular cells. Fatty acid metabolism is disordered in lung endothelial cells and smooth muscle cells. These molecular mechanisms are integrated to promote PH-specific abnormal vascular cell proliferation and vascular remodeling. This review summarizes the recent advances in the metabolic reprogramming of glucose, fatty acid, and amino acid metabolism in pulmonary vascular remodeling in PH and the mechanisms for how these alterations affect vascular cell fate and impact the course of PH.

Benign paroxysmal positional vertigo (BPPV) represents the most common form of positional vertigo. It is caused by dislodged otoconia that freely float in the semicircular canals (canalolithiasis) or attach to the cupula (cupulolithiasis). A cupulolithiasis-type (or a heavy cupula-type) of BPPV implicating the lateral semicircular canal (LSCC) exhibits persistent ageotropic direction-changing positional nystagmus (DCPN) in a head-roll test. However, in some cases, unlike any type of BPPV, persistent geotropic DCPN cannot be explained by any mechanisms of BPPV, and don’t fit the current classifications. Recently, the notion of light cupula has been introduced to refer to the persistent geotropic DCPN. In this study, we looked at the clinical features of light cuplula and discussed the possible mechanisms and therapeutic strategies of the condition. The notion of light cupula is a helpful addition to the theory of peripheral positional vertigo and nystagmus.

Improvements in the diagnosis and treatment of cancer are urgently needed for use in nanotechnology. Nanoparticles (NPs) can reduce the side effects of traditional chemotherapy by sustained release of loaded drugs and increase therapeutic efficiency. NPs can also enhance endothelial permeation retention by size effect and its accumulation in tumor cells through passive targeting. Furthermore, it is critical to treat cancer with a controlled targeted drug which can be specifically delivered into tumor cells and released there, resulting in a targeted therapy to eradicate tumor cells while sparing normal cells. To this end, antibody-mediated targeting therapy has been developed, but imperfections in antibodies (Abs) limit this therapy. Therefore, the combination of NPs and Abs has been highly valued in recent years, because conjugating special Abs on the surface of NPs can increase targeting efficiency, enabling selective delivery of anti-cancer drugs to tumor cells. In this mini-review, we would like to enumerate the strategies for the conjugation of Abs to the surface of the NPs as well as the precise engineering of targeted NPs. The application of targeting antibody fragments in this drug delivery system will also be discussed.

Studies on the integration of cross-modal information with taste perception has been mostly limited to uni-modal level. The cross-modal sensory interaction and the neural network of information processing and its control were not fully explored and the mechanisms remain poorly understood. This mini review investigated the impact of uni-modal and multi-modal information on the taste perception, from the perspective of cognitive status, such as emotion, expectation and attention, and discussed the hypothesis that the cognitive status is the key step for visual sense to exert influence on taste. This work may help researchers better understand the mechanism of cross-modal information processing and further develop neutrally-based artificial intelligent (AI) system.

The efficient transmission of severe acute respiratory syndrome-2 coronavirus (SARS-CoV-2) from patients to health care workers or family members has been a worrisome and prominent feature of the ongoing outbreak. On the basis of clinical practice and in-vitro studies, we postulated that post-exposure prophylaxis (PEP) using Arbidol is associated with decreased infection among individuals exposed to confirmed cases of COVID-19 infection. We conducted a retrospective cohort study on family members and health care workers who were exposed to patients confirmed to have SARS-CoV-2 infection by real-time RT-PCR and chest computed tomography (CT) from January 1 to January 16, 2020. The last follow-up date was Feb. 26, 2020. The emergence of fever and/or respiratory symptoms after exposure to the primary case was collected. The correlations between post-exposure prophylaxis and infection in household contacts and health care workers were respectively analyzed. A total of 66 members in 27 families and 124 health care workers had evidence of close exposure to patients with confirmed COVID-19. The Cox regression based on the data of the family members and health care workers with Arbidol or not showed that Arbidol PEP was a protective factor against the development of COVID-19 (HR 0.025, 95% CI 0.003–0.209, P=0.0006 for family members and HR 0.056, 95% CI 0.005–0.662, P=0.0221 for health care workers). Our findings suggest Arbidol could reduce the infection risk of the novel coronavirus in hospital and family settings. This treatment should be promoted for PEP use and should be the subject of further investigation.

PRKAG2 cardiac syndrome (PS) is a rare inherited disease due to PRKAG2 gene mutation and characterized by Wolff-Parkinson-White syndrome (WPWs), conduction system lesions and myocardial hypertrophy. It can also lead to serious consequences, such as sudden death. But the genetic and clinical heterogeneity makes the early diagnosis of PS difficult. Here we studied a family with familial hypertrophic cardiomyopathy and other diverse manifestations. Gene analysis identified a missense mutation (Arg302Gln) in the five affected subjects of the family. The electrocardiograph performance of the five was composed of sinus bradycardia (SB), WPWs, right bundle branch block (RBBB), atrioventricular block (AVB), left bundle branch block (LBBB), supraventricular tachycardia (SVT) and atrial premature beat (APB). Among them, the youngest one began to show paroxysmal palpitation at the age of nine and was confirmed to have WPWs at 17 years old; two members progressed over time to serious conduction damage, and the proband received a pacemaker at the age of 27 due to AVB. Besides, according to cardiac magnetic resonance and echocardiography, the youngest one showed symmetric hypertrophy; three older members showed asymmetric myocardial hypertrophy characterized with a diffuse pattern of middle-anterior-lateral-inferior wall hypertrophy and especially interventricular septal hypertrophy; all five affected patients showed atrial enlargement regardless of myocardial hypertrophy at an earlier stage. In conclusion, the conduction system disorder, familial atrial enlargement and symmetric cardiac hypertrophy may occur in the early stage of PRKAG2 R302Q mutation.

Transferrin receptor 1 (TfR1), encoded by the TFRC gene, is the gatekeeper of cellular iron uptake for cells. A variety of molecular mechanisms are at work to tightly regulate TfR1 expression, and abnormal TfR1 expression has been associated with various diseases. In the current study, to determine the regulation pattern of TfR1, we cloned and overexpressed the human TFRC gene in HeLa cells. RNA-sequencing (RNA-seq) was used to analyze the global transcript levels in overexpressed (OE) and normal control (NC) samples. A total of 1669 differentially expressed genes (DEGs) were identified between OE and NC. Gene ontology (GO) analysis was carried out to explore the functions of the DEGs. It was found that multiple DEGs were associated with ion transport and immunity. Moreover, the regulatory network was constructed on basis of DEGs associated with ion transport and immunity, highlighting that TFRC was the node gene of the network. These results together suggested that precisely controlled TfR1 expression might be not only essential for iron homeostasis, but also globally important for cell physiology, including ion transport and immunity.

In order to demonstrate the relationship between methylation of fragile histidine triad (FHIT) and T-cadherin/H-cadherin (CDH13) genes and liver cancer, the methylation status of FHIT and CDH13 was detected in healthy individuals and in Mongolian and Han patients with liver cancer. The phenol-chloroform method was used to extract genomic DNA. The methylation specific polymerase chain reaction method was applied to detect the methylation status of FHIT and CDH13. The relationship between smoking and alcohol consumption and gene (FHIT and CDH13) methylation was analyzed. There was significant difference in methylation rate of FHIT (72.67%, 34.67%) and CDH13 (72.0%, 28.0%) between liver cancer patients and healthy individuals of Mongolian descent (P<0.05), as well as that of FHIT (68%, 30.67%) and CDH13 (64%, 26%) between liver cancer patients and healthy individuals of Han individuals (P<0.05). There was also a relationship between smoking and drinking and the methylation of FHIT and CDH13 (P<0.05). Thus, the methylation of FHIT and CDH13 had a relationship with liver cancer incidence. Smoking and alcohol ingestion may promote the methylation of FHIT and CDH13.

Women diagnosed with breast cancer may have serious psychological problems and will suffer from adjustment disorder (AjD). We investigated the prevalence of AjD in female breast cancer patients who were diagnosed within 1 year and examined the severe life events they experienced, and the most common symptoms of AjD. 342 newly diagnosed (<1 year) female breast cancer patients were recruited from Tongji Hospital and Hubei Cancer Hospital in Hubei, China, from July 2018 to May 2019. The patients completed the self-report questionnaire including demographic characteristics and the scale ADNM-20 for the diagnosis of AjD. SPSS20.0 was used for data analysis. As a result, the prevalence of AjD in breast cancer patients was 38.6%. Patients from rural areas and lacking of exercise were more likely to suffer from AjD (P<0.05). The prevalence of AjD in patients who did not regard breast cancer as the most severe life event was higher than that in patients who took breast cancer as the most severe life event (44.4% vs. 33.9%, P<0.05; OR=1.728, 95% CI=1.072-2.787). The symptom that scored highest was preoccupation (3.15). We found that the prevalence of AjD in women with breast cancer in this study is very high and warrants more attention. Patients from rural areas, lacking of exercise and subject to multiple stressors are more likely to suffer from AjD. The commonest and severe symptom is preoccupation.

Primary thyroid lymphoma (PTL) is an exceptionally rare and highly aggressive potentially curable malignant disease. We report three typical cases of PTL referred to our hospital. All three cases had long history of Hashimoto’s thyroiditis, and presented with progressively enlarging neck mass. The first two cases were confirmed by surgical biopsy to be diffuse large B cell lymphoma, and received radiotherapy combined with chemotherapy, or received only chemotherapy. The third case was confirmed by core needle biopsy to be mucosa-associated lymphoid tissue lymphoma, and received radiotherapy. In summary, confirmation of PTL diagnosis is essential for further clinical decisions. Core biopsy should be one of the most important methods to make the diagnosis of PTL, while the use of fine needle aspiration cytology alone is still limited in diagnosing PTL.

The association between glucose variability (GV) and adverse perioperative outcomes in type 2 diabetes mellitus (T2DM) patients undergoing orthopedic surgery was investigated. A retrospective cohort study was performed by analyzing data on T2DM patients receiving continuous blood glucose (BG) monitoring and continuous subcutaneous insulin infusion treatment due to poorly controlled preoperative BG prior to orthopedic surgery. GV was assessed with coefficient of variation (CV). Postoperative and perioperative CV, hypoglycemia cases, and other perioperative outcomes (diabetes preparation time [DPT], length of stay [LOS], and perioperative and infective complication cases) were analyzed. Results showed that a total of 168 patients were grouped into preoperative CV tertiles: 1st (n=56): 0–0.2921, 2nd (n=58): 0.2922–0.3779, and 3rd (n=54): 0.3780–0.5750. Fasting blood glucose (FBG), perioperative CV, rate of hypoglycemia cases (OR: 5.53, 95%CI: 2.43–12.59) (all P<0.001) and DPT (P=0.024) were higher in the 3rd than in the 1st tertile. After adjustments of covariates, regression analysis indicated that the 3rd tertile was associated with increased perioperative CV (adjusted coefficient=0.515, P<0.001), DPT (adjusted coefficient =0.169, P=0.073), rate of hypoglycemia cases (OR: 6.72, 95%CI: 2.69−16.82, P<0.001) and perioperative complication cases (OR: 2.50, 95%CI: 0.90−7.01, P=0.080). In conclusion, preoperative GV is associated with increased perioperative GV and adverse perioperative outcomes including longer DPT and higher rates of hypoglycemia and perioperative complications.

The effect and potential molecular mechanisms of berberine on gluconeogenesis in skeletal muscles and adipose tissues were investigated. After adaptive feeding for one week, 8 rats were randomly selected as the normal group and fed on a standard diet. The remaining 32 rats were fed on a high-fat diet and given an intravenous injection of streptozotocin (STZ) for 2 weeks to induce the diabetic models. The diabetic rat models were confirmed by oral glucose tolerance test (OGTT) and randomly divided into 4 groups (n=8 each), which were all fed on a high-fat diet. Berberine (3 g/kg per day) or metformin (183 mg/kg per day) was intragastrically administered to the diabetic rats for 12 weeks, serving as berberine group and metformin group respectively. 5-aminoimidazole-4-carboxamide1-β-D-ribofuranoside [AICAR, an agonist of AMP-activated protein kinase (AMPK), 0.5 mg/kg per day] was subcutaneously injected to the diabetic rats for 12 weeks, serving as AICAR group. The remaining 8 diabetic rats served as the model group, which was given a 0.5% carboxyl methylcellulose solution by oral gavage. Fasting serum insulin (FINS), OGTT as well as lipid parameters were tested by commercial kit. The protein levels of liver kinase B1 (LKB1), AMPK, phosphorylated AMP-activated protein kinase (p-AMPK), transducer of regulated CREB activity 2 (TORC2), phosphorylated transducer of regulated CREB activity 2 (p-TORC2), phosphoenolpyruvate carboxykinase (PEPCK), and glucose-6-phosphatase (G6Pase) in skeletal muscles and adipose tissues were examined by Western blotting. The results showed that berberine significantly decreased the body weight, plasma glucose, insulin levels, and homeostatic model assessment for insulin resistance (HOMA-IR) of diabetic rats compared with those in the model group. Meanwhile, the serum total triglyceride (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels were markedly decreased and high-density lipoprotein cholesterol (HDL-C) level was significantly increased after the treatment with berberine. In addition, we found that berberine significantly increased the expression of p-AMPK and LKB1, while decreasing the p-TORC2 levels in skeletal muscles and adipose tissues. Moreover, the expression of PEPCK and G6Pase was significantly down-regulated after the treatment with berberine compared to the model group. It was suggested that the mechanism by which berberine inhibited peripheral tissue gluconeogenesis may be attributed to the activation of the LKB1-AMPK-TORC2 signaling pathway.

Yu Gan Long (YGL) is a Chinese traditional herbal formula which has been reported to attenuate liver fibrosis for many years and we have explored its anti-fibrotic mechanism through blocking transforming growth factor (TGF-β) in the previous study. But the mechanisms associated with platelet-derived growth factor (PDGF)-BB remain obscure. In this study, we further investigated the mechanism of YGL reducing carbon tetrachloride (CCl₄)-induced liver fibrosis in rats. Our results showed that YGL suppressed CCl₄-induced upregulation of collagen IV (Col IV), type HI precollagen (PCHI), hyaluronuc acid (HA) and laminin (LN), which are implicated in liver fibrosis. Also, YGL reduced the α-smooth muscle actin (α-SMA) expression, which acts as the indicator of liver fibrosis. Furthermore, YGL decreased the serum levels of hepatic stellate cell (HSC) mitogen PDGF-BB and inflammation cytokines, including TNF-α, IL-1β, IL-6. Markers involved in liver fibrosis, such as Ras, p-Raf-1, p-ERK1/2, p-JNK, p-P38, p-PI3K, p-AKT, p-JAKl, p-STAT3 were downregulated significantly after treatment with YGL. Our results indicated that YGL ameliorated CCl₄-induced liver fibrosis by reducing inflammation cytokines production, and suppressing Ras/ERK, PI3K/AKT, and JAK1/STAT3 signaling pathways, which provided further evidence towards elucidation of the anti-fibrotic mechanism of YGL.

Large animal models are essential to pre-clinical trials of pulmonary transplantation and bronchial anastomosis poses a great technical challenge to the procedure. Presented here is a simplified continuous two-stitch suture technique into bronchial anastomosis during the course of left single lung transplantation in canine. Animals were divided into three groups with each group having 6 animals. Left single lung transplantation in canine was performed to assess the feasibility of using this technique for bronchial anastomosis. In the control groups, all anastomoses were done by using traditional technique. Allograft functions and hemodynamic parameters were monitored during a 3-h reperfusion period. Quality of bronchial healing and airway complications were assessed by bronchoscopic surveillance after transplantation. We successfully completed left lung transplantation in 18 dogs, and all the dogs survived the procedures. The new technique substantially simplified the procedures for bronchial anastomosis and greatly reduced the time for bronchial anastomosis (P<<0.01) and the ischemic time of the grafts (P<0.05) compared to the control group. The continuous two-stitch suture attenuated the tissue injury to allografts and led to better blood gas exchange function as compared to the control group (P<0.05). Good bronchial healing (Grade I) was observed in all the groups. A canine left single lung transplantation model is feasible by using the novel suture technique, and the new technique is as safe as the traditional method. The technique is easy to learn, particularly for less experienced operators. Simpler and time-saving, the technique has great potential to be widely employed in clinical lung transplantation.

To evaluate the potential effect of Ankaferd Blood Stopper (ABS) and oxytocin (OT) in an experimental endometriosis model, 18 female Sprague Dawley rats were used in this study. The animals were divided randomly into three groups after surgical induction of endometriosis: group 1: control group (isotonic NaCl, 1 mL/kg/day, intramuscular, n=6); group 2: OT group (OT, 80 U/kg/day, intramuscular, n=6); group 3: ABS group (ABS, 1.5 mL/kg/day, intraperitoneal, n=6). Each group was treated for four weeks (two times per week). Volumes of endometriotic explants were measured in biopsy samples for histopathological analysis. Vascular endothelial growth factor (VEGF), monocyte chemotactic protein-1 (MCP-1), and tumour necrosis factor (TNF-α) levels were measured in plasma and peritoneal fluid. Endometriotic explant volumes were significantly decreased after OT administration (P<0.0001). The epithelial score was significantly decreased in both treatment groups compared to the control group (P<0.05). TUNEL immunohistochemistry showed more apoptotic changes in the endometriosis foci (gland epithelium and surrounding tissue) in the OT group than in the control group (P<0.05). The levels of VEGF, MCP-1, and TNF-α were significantly reduced in the OT group (P<0.05), whereas no significant changes in protein levels were found in the ABS-applied group. The results indicate that OT has greater potential as a therapeutic agent in experimentally induced peritoneal endometriosis, where ABS, which is a VEGF modulator, appears to act through different mechanisms to show its palliative effects on a rat model of peritoneal endometriosis.

Accumulating evidence suggests that a disruption of early brain development, in which insulin-like growth factor-2 (IGF-2) has a crucial role, may underlie the pathophysiology of schizophrenia. Our previous study has shown that decreased serum IGF-2 was correlated with the severity of psychopathology in patients with schizophrenia. Here we conducted a prospective observation trial to investigate the effects of atypical antipsychotics on serum IGF-2 level and its relationship with clinical improvements in schizophrenia patients. Thirty-one schizophrenia patients with acute exacerbation and 30 healthy individuals were recruited in this study. Psychiatric symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS) and serum IGF-2 levels were determined using ELISA. We found that schizophrenia patients with acute exacerbation had lower serum IGF-2 levels than control individuals at baseline (P<0.05). After 2 months of atypical antipsychotic treatment, a significant improvement in each PANSS subscore and total score was observed in patients (all P<0.01), and the serum IGF-2 levels of patients were significantly increased compared with those at baseline (203.13±64.62 vs. 426.99±124.26 ng/mL; t =−5.044, P<0.001). Correlation analysis revealed that the changes of serum IGF-2 levels in patients were significantly correlated with the improvements of negative symptoms (r=−0.522, P=0.006). Collectively, our findings demonstrated changes of serum IGF-2 response to improvements of negative symptoms in schizophrenia patients treated with atypical antipsychotics, suggesting that serum IGF-2 might be a treatment biomarker for schizophrenia.

Cerebellar degeneration-related antigen 1 (CDR1) was described to be expressed in the nervous system and in different types of cancer tissues. In the present study, we demonstrate that CDR1 is in addition ubiquitously expressed in human epidermis, dermis and isolated skin cells. Both CDR1 mRNA and protein were detected in human skin-derived mast cells, melanocytes, fibroblasts and keratinocytes, suggesting that CDR1 does not have a neuron-specific function.

We previously reported that the increased expression of Dickkopf-related protein 1 (DKK1) is positively related to vascular endothelial growth factor in the synovial fluid from patients with temporomandibular joint disorders (TMDs). DKK1 is involved in angiogenic activities in the TMD synovium in vitro, but the expression of DKK1 after treatment of TMD-osteoarthritis (TMD-OA) with hyaluronic acid (HA) remains unknown. In this study, we assessed the expression of DKK1 in the synovial fluid of TMD-OA patients before and after treatment with HA via enzyme-linked immunosorbent assay. We also investigated the role of DKK1 in TMD-OA via immunohistochemical staining. The relationship between the expression of DKK1 and the clinicopathological characteristics was determined by Pearson analysis. The results showed that the expression of DKK1 was significantly decreased after treatment with HA. Correlation analyses indicated that the expression of DKK1 in the TMD-OA samples was closely correlated with mouth opening and pain. These findings suggest that DKK1 could play an important role in the pathogenesis and treatment of TMD. Reduction of the pain by HA treatment may be correlated with the decreased expression of DKK1.

Poor nutrition is the underlying cause of child death. However, comprehensive data showing the relationships between dietary-practices, food security, and nutritional status are scant. The present study aimed to examine the association of inappropriate feeding practices and household-hunger with anthropometric measures in children aged 6–23 months. A cross-sectional survey was conducted on randomly selected 525-households. Semi-structured interviewer-administered questionnaires were used to gather data on socio-demographic, child health, dietary-practices and household-hunger. Weight and height/length of the children were measured and analyzed using the new World Health Organization (WHO) Growth Standards. The prevalence of stunting, wasting and underweight as well as composite index of anthropometric failure (CIFA) were used to indicate under-nutrition. The overall prevalence of inappropriate feeding practices was 22.9%, rate of moderate households-hunger was 12.4%, and the prevalence of stunting, underweight and wasting was 16.2%, 6.9% and 6.3%, respectively, while the CIAF was 21.3%. The prevalence was significantly higher in young children aged 12–23 months than in infants aged 6–11 months. Children from households experiencing moderate hunger had significantly higher risk of being stunting (OR: 10.20; 95%CI: 2.00–51.50), underweight (OR:3.89; 95%CI: 1.40–10.90), wasting (OR: 1.97; 95%CI: 0.99–3.90), and CIAF (OR: 1.90; 95%CI: 1.05–3.45), than those residing in households experiencing no or mild hunger. Multi-disciplinary approaches are required to improve household food-security and child dietary practices, thus the nutritional status among young children.

This study aimed to construct a quality management model for phase I clinical drug trials. A cross-sectional survey was conducted and data were collected from 604 respondents at 69 institutions in China engaged in phase I clinical drug trials. Exploratory and confirmatory factor analyses were used to develop the survey tool. Structural equation modeling was used to construct a quality management model for phase I clinical drug trials. The results showed that the final survey tool had good reliability and validity (Cronbach’s α=0.938, root mean square error of approximation=0.074, comparative fit index=0.962, and Tucker—Lewis index=0.955). The model included five dimensions: government regulation, industry management, medical institution management, research team management, and contract research organization (CRO) management. In total, 22 measurement items were obtained. The structural equation model indicated government regulation, industry management, medical institution management, and CRO management significantly affected the quality of phase I clinical drug trials (β=0.195, β=0.331, β=0.279, and β=−0.267, respectively; P<0.05). Research team management had no effect on the quality of trials (β=0.041, P=0.610). In conclusion, the model is valuable for identifying factors influencing phase I clinical drug trials and guiding quality management practices.

The article “Kinetic Characterization of Tyrosinase-catalyzed Oxidation of Four Polyphenols”, written by Wan-yu LIU, Congming ZOU, Jian-hua HU, Zi-jun XU, Lu-qin SI, Jun-jun LIU, Jian-geng HUANG, was originally published electronically on the publisher’s internet portal on May 2020 without open access. With the author(s)’ decision to opt for Open Choice, the copyright of the article is changed to © The Author(s) 2020 and the article is forthwith distributed under a Creative Commons Attribution4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

The original article has been corrected.

The article “The Role of CARD9 in Metabolic Diseases”, written by Cheng TIAN, Ya-li TUO, Yi LU, Chuan-rui XU, Ming XIANG, was originally published electronically on the publisher’s internet portal on May 2020 without open access. With the author(s)’ decision to opt for Open Choice, the copyright of the article is changed to © The Author(s) 2020 and the article is forthwith distributed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

The original article has been corrected.

The article “Polysubstituted Phenyl Glucosides Produced by the Fungus Metarrhizium anisopliae”, written by Wen-jing WANG, Chong DAI, Jian-ping WANG, Hu-cheng ZHU, Chun-mei CHEN, Yong-hui ZHANG, was originally published electronically on the publisher’s internet portal on May 2020 without open access. With the author(s)’ decision to opt for Open Choice, the copyright of the article is changed to © The Author(s) 2020 and the article is forthwith distributed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made..

The original article has been corrected.