Objective To investigate the empathic abilities and the association between empathic abilities and executive function in schizophrenic patients. Methods Empathy with the Interpersonal Reactivity Index-C (IRI-C) and executive function with Wisconsin Card Sorting Test (WCST) , Stroop Color-Word Task (Stroop), Spatial n-back Task (n-back) were applied to 74 schizophrenic patients and 69 healthy controls. Results Compared with healthy controls, schizophrenic patients showed significantly lower total scores ((46. 8 ± 10. 0) vs (51.5 ±9.7), P<0.01),and subscores in Perspective Taking ((9.5 ±4.2) vs (12.2 ±3.9) , P<0. 01), Fantasy ((12.5 ±4.2) vs (15.5 ±3.8), P<0.01) and Empathic Concern((15. 9 ±4.2) vs (17. 3 ±3.4), P< 0.05) ,but higher subscore((8.8 ±5. 1) vs (6.5 ±3.7), P<0.01) in personal distress of IRI-C. A significant difference(P<0.01) were fund on the scores of WCST, Stroop task and n-back task between schizophrenic patients and healthy controls. Pearson correlation analysis showed that the total scores of IRI-C was negatively correlated with the response administered (Ra), the number of responses errors (Re) and non-perseverative errors (nRpe) of WCST (r= -0.293, r= -0.253, r= -0.272, P<0.05) respectively, that empathic concern sub-score of IRI-C was negatively correlated with Ra, Re, perseverative responses (Rp) and perseverative errors (Rpe) of WCST (r= -0.326, r= -0.300, r= -0.294, r= -0.287, P<0.01 -0.05) respectively , but positively correlated with Rfp. of WCST (r=0.279, P<0.05), and that the fantasy subscore of IRI-C was negatively correlated with the reaction time of B part(r= -0.299, P<0.01) and C part (r= -0.322, P<0.01) of the Stroop task. Conclusion Schizophrenics have a general impairment of empathy and executive function,and affective empathy is related to the executive function, suggesting that the impairment of executive function maybe the one of pathological mechanism for the empathic deficit of patients with schizophrenia.

Objective: To explore the clinical features and molecular basis for a child featuring infantile epilepsy and developmental disorders. Methods: Clinical data and peripheral blood samples of the child and his parents were collected. The coding regions of genes associated with nervous system development were subjected to target region capture sequencing. Results: The child developed generalized spasm at 3 months and was diagnosed with epilepsy at 6 months of age. He was treated with Depakin but was diagnosed with mental retardation and developmental retardation at 3 years of age. A novel heterozygous c. 3842T>G variant of the SYNE1 gene was detected. His father was found to carry the same variant and had a history of convulsions in infancy but with no mental or developmental anomalies. Conclusion A novel variant of SYNE1 gene was identified in this child, and the prognosis may be poor.

OBJECTIVE: To explore the genetic basis for a child featuring delayed intellectual development. METHODS: The child and his parents were subjected to conventional G-banding karyotyping and single nucleotide polymorphism array (SNP-array) analysis. Suspected copy number variations (CNVs) were verified in both parents. RESULTS: No karyotypic abnormality was found with the child and his parents. SNP-array results for both parents were normal. The child was found to harbor a de novo 172 kb deletion at 18q21.2 with a physical position of 52 957 042-53 129 237. The deletion only involved one OMIM gene, namely TCF4, resulting in removal of its exons 6 to 8. CONCLUSION The SNP-array assay has facilitated with the diagnosis of this child. Deletion of 18q21.2 region probably accounts for the Pitt-Hopkins syndrome (PTHS) in this patient.
Child ; Chromosome Deletion ; Chromosomes, Human, Pair 18 ; genetics ; DNA Copy Number Variations ; Developmental Disabilities ; genetics ; Facies ; Humans ; Hyperventilation ; genetics ; Intellectual Disability ; genetics ; Phenotype ; Transcription Factor 4 ; genetics

Objective Through analyzing the surveillance data on typhoid fever and paratyphoid fever in 2015 to understand the related epidemiological features and most possible clustering areas of high incidence.Methods Individual data was collected from the passive surveillance program and analyzed by descriptive statistic method.Characteristics on seasonal,regional and distribution of the diseases were described.Spatial-temporal clustering characteristics were estimated,under the retrospective space-time method.Results A total of 8 850 typhoid fever cases were reported from the surveillance system,with incidence rate as 0.65/100 000.The number of paratyphoid fever cases was 2 794,with incidence rate as 0.21/100 000.Both cases of typhoid fever and paratyphoid fever occurred all year round,with high epidemic season from May to October.Most cases involved farmers (39.68％),children (15.89％) and students (12.01％).Children under 5 years showed the highest incidence rate.Retrospective space-time analysis for provinces with high incidence rates would include Yurnan,Guangxi,Guizhou,Hunan and Guangdong,indicating the first and second class clusters were mainly distributed near the bordering adjacent districts and counties among the provinces.Conclusion In 2015,the prevalence rates of typhoid fever and paratyphoid fever were low,however with regional high prevalence areas.Cross regional transmission existed among provinces with high incidence rates which might be responsible for the clusters to appear in these areas.

The obstacle to successful remyelination in demyelinating diseases, such as multiple sclerosis, mainly lies in the inability of oligodendrocyte precursor cells (OPCs) to differentiate, since OPCs and oligodendrocyte-lineage cells that are unable to fully differentiate are found in the areas of demyelination. Thus, promoting the differentiation of OPCs is vital for the treatment of demyelinating diseases. Shikimic acid (SA) is mainly derived from star anise, and is reported to have anti-influenza, anti-oxidation, and anti-tumor effects. In the present study, we found that SA significantly promoted the differentiation of cultured rat OPCs without affecting their proliferation and apoptosis. In mice, SA exerted therapeutic effects on experimental autoimmune encephalomyelitis (EAE), such as alleviating clinical EAE scores, inhibiting inflammation, and reducing demyelination in the CNS. SA also promoted the differentiation of OPCs as well as their remyelination after lysolecithin-induced demyelination. Furthermore, we showed that the promotion effect of SA on OPC differentiation was associated with the up-regulation of phosphorylated mTOR. Taken together, our results demonstrated that SA could act as a potential drug candidate for the treatment of demyelinating diseases.
Animals ; Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Demyelinating Diseases ; prevention & control ; Encephalitis ; prevention & control ; Encephalomyelitis, Autoimmune, Experimental ; prevention & control ; Female ; Mice, Inbred C57BL ; Myelin Basic Protein ; metabolism ; Neuroprotective Agents ; administration & dosage ; Oligodendrocyte Precursor Cells ; drug effects ; metabolism ; Rats ; Remyelination ; drug effects ; Shikimic Acid ; administration & dosage ; TOR Serine-Threonine Kinases ; metabolism

The aim of the study was to determine the feasibility of the Vitellaria paradoxa nutshell as a new medicinal resource for treating diabetes. A total of forty-one compounds were identified by HPLC-DAD-Q-TOF-MS and phytochemical methods in V. paradoxa nutshell methanol extract. Based on HPLC fingerprints, four characteristic constituents were quantified and the origin of twenty-eight V. paradoxa nutshells from seven sub-Saharan countries was compared, which were classified into three groups with chemometric method. Twenty-eight samples contained high total phenolic content, and exhibited moderate-higher antioxidant activity and strong α-glucosidase inhibitory activity. Furthermore, all fractions and isolated compounds were evaluated for their antioxidant and α-glucosidase inhibitory activities, and α-glucosidase inhibitory action mechanism of four characteristic constituents including protocatechuic acid, 3, 5, 7-trihydroxycoumarin, (2R, 3R)-(+)-taxifolin and quercetin was investigated via molecular docking method, which were all stabilized by hydrogen bonds with α-glucosidase. The study provided an effective approach to waste utilization of V. paradoxa nutshell, which would help to resolve waste environmental pollution and provide a basis for developing potential herbal resource for treating diabetes.
Africa South of the Sahara ; Chromatography, High Pressure Liquid ; Diabetes Mellitus ; drug therapy ; enzymology ; Glycoside Hydrolase Inhibitors ; chemistry ; pharmacology ; Humans ; Hypoglycemic Agents ; chemistry ; pharmacology ; Molecular Docking Simulation ; Plant Extracts ; chemistry ; pharmacology ; Plants, Medicinal ; chemistry ; Sapotaceae ; chemistry ; alpha-Glucosidases ; metabolism

The differentiation and maturation of oligodendrocyte precursor cells (OPCs) is essential for myelination and remyelination in the CNS. The failure of OPCs to achieve terminal differentiation in demyelinating lesions often results in unsuccessful remyelination in a variety of human demyelinating diseases. However, the molecular mechanisms controlling OPC differentiation under pathological conditions remain largely unknown. Myt1L (myelin transcription factor 1-like), mainly expressed in neurons, has been associated with intellectual disability, schizophrenia, and depression. In the present study, we found that Myt1L was expressed in oligodendrocyte lineage cells during myelination and remyelination. The expression level of Myt1L in neuron/glia antigen 2-positive (NG2) OPCs was significantly higher than that in mature CC1 oligodendrocytes. In primary cultured OPCs, overexpression of Myt1L promoted, while knockdown inhibited OPC differentiation. Moreover, Myt1L was potently involved in promoting remyelination after lysolecithin-induced demyelination in vivo. ChIP assays showed that Myt1L bound to the promoter of Olig1 and transcriptionally regulated Olig1 expression. Taken together, our findings demonstrate that Myt1L is an essential regulator of OPC differentiation, thereby supporting Myt1L as a potential therapeutic target for demyelinating diseases.
Animals ; Cell Differentiation ; physiology ; Demyelinating Diseases ; chemically induced ; Lysophosphatidylcholines ; toxicity ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins ; metabolism ; Oligodendrocyte Precursor Cells ; cytology ; metabolism ; Oligodendroglia ; cytology ; metabolism ; Remyelination ; physiology ; Transcription Factors ; metabolism