Objective To investigate the status of infection of human herpes virus type-8 (HHV-8) in the mother and their infants of Wulumuqi and Aletai region. Methods BCBL-1 cell line was used as antigen and 406 matched sera samples were collected from mothers and their infants (cord blood) of different nationalities (Uighur, Kazak and Han nationality) from Wulumuqi and Aletai regions of Xinjiang A.R, tested for HHV-8 IgG and IgM antibody by immunofluorescence assay. Results HHV-8 IgG antibody positive rate of mothers and their infants of Uighur nationality was 22.9%(24/105), Han was 5.4%(8/149) ? 2=17.1,P

ObjectiveTo investigate the association between catechol-O-methyl transferase (COMT)gene polymorphism and Gilles de la Tourette' s syndrome(GTS).MethodsUsing Amplification Refractory Mutation System(ARMS) PCR genotyping assay method,a polymorphism (val158met) of COMT gene was genotyped in 112 of all GTS patients ( total GTS group) including 54 GTS-alone patients group,48 GTS + ADHD patients group among of them and 71 healthy controls.The correlation between positive association of polymorphism (val158met)of COMT gene in GTS and the age of onset in patients with GTS was also analyzed.ResultsCompared with healthy controls group,genotype of val158met did not differ in total GTS patients group or alone-GTS patients group (χ2 =0.56,P=0.756;χ2 =1.05,P=0.600 respectively).There was also no significant difference (P＞0.05)in allele distribution of val158met in total GTS patients group or alone-GTS patients group compared with controls group respectively (χ2 =0.18,P=0.669;χ2 =0.29,P=0.593 respectively).However,genotype distribution of val158met was significantly different between GTS + ADHD patients group and controls group( χ2 =6.35,P =0.041 ).The frequency of the val allele of this locus was significantly higher in GTS + ADHD patients group than those in controls group ( χ2 =5.49,P =0.019 ).The mean age of onset (6.80 ± 1.54 ) in 36 children within GTS + ADHD patients group with the val/val geantype of COMT gene val158met polymorphism was significantly earlier than the mean age of onset (8.04 ± 1.54)in 12 children in val/val genotype (P =0.016 ).ConclusionPolymorphism (val158met) of COMT gene may be associated with GTS children with comorbid ADHD,which may play an important role to make the age of onset in children with GTS become earlier.

Objective To analyze the clinical characteristics of children with Wilson's disease,and to improve the attention to Wil-son's disease in children.Methods The clinical data of 274 children with Wilson's disease admitted to the First Affiliated Hospital of Anhui University of Chinese Medicine from November 2020 to October 2022 were retrospectively analyzed.Results Among 274 children with Wilson's disease,aged 3 to 15 years,with a male/female ratio of 1.88∶1,the median age of onset was 5.6 years.Clinical classifica-tion:204 cases(74.5％)of liver type,19 cases(6.9％)of brain type,41 cases(15.0％)of mixed type,10 cases(3.6％)of other type.Age of onset:liver type＜other type＜mixed type＜brain type,the differences were statistically significant(P＜0.05).The main reasons for the initial diagnosis of 274 children were physical examination,family history and respiratory tract infection.Among them,135 cases(49.3％)with asymptomatic elevated transaminase.The abnormal rate of serum ceruloplasmin and 24-hour urine copper was 100％and 96.7％,respectively.The abnormal rates of hepatobiliary and spleen ultrasound,kidney ultrasound and craniocerebral mag-netic resonance imaging were 81.0％(204/218),15.6％(34/218)and 41.7％(48/115),respectively.The abnormal rate of hepato-biliary and spleen ultrasound and craniocerebral magnetic resonance examination increased with age,and the abnormal rate of renal ultra-sound and craniocerebral magnetic resonance examination was related to clinical classification.Conclusion The onset age of Wilson's disease in children is young,the initial symptoms are different,which is closely related to age and clinical classification,and has nothing to do with gender.For suspected children,relevant examinations should be improved to achieve the purpose of early diagnosis and treatment.

Objective:To investigate the intervention effect of topical shikonin on an imiquimod-induced psoriasis-like mouse model and its effect on expression of CCAAT enhancer binding protein δ (CEBPD) .Methods:Twenty specific pathogen-free BALB/c male mice were randomly and equally divided into model group, shikonin 1 group, shikonin 2 group and blank control group by using simple random sampling. Mice in the model group, shikonin 1 group and shikonin 2 group were topically treated with 50 mg of 5% imiquimod cream every day on the shaved back to establish the psoriasis-like mouse model. After 6-hour treatment, mice in the shikonin 1 group and shikonin 2 group were treated with 0.5 ml of shikonin at concentrations of 0.576 and 5.76 g/L respectively in the modeling area for 8 consecutive days; the blank control group received no treatment. Changes in the skin lesions of these mice were observed by naked eyes every day, and evaluated by using psoriasis area severity index (PASI) ; after 8-day treatment, the mice were sacrificed by cervical dislocation, the dorsal skin tissues were resected, and immunohistochemical study and Western blot analysis were performed to determine the expression of CEBPD in the mouse epidermis. Statistical analysis was carried out with SPSS 16.0 software by using one-way analysis of variance for comparisons of observation indices among different groups, as well as least significant difference- t test for multiple comparisons. Results:On day 8, the mice in the model group presented with obvious erythema, scales, and infiltrative and thickened skin lesions; compared with the model group, the skin lesions were markedly improved in the shikonin 1 group and shikonin 2 group, and the improvement was more obvious in the shikonin 2 group. On day 8, the PASI score significantly differed among the blank control group, model group, shikonin 1 group and shikonin 2 group (0, 11.0±1.22, 8.6±0.55, 5.8±1.30 points, respectively; F=128.21, P<0.01) , and there were significant differences between any two groups (all P < 0.01) . Immunohistochemical study showed a significant difference in the expression of CEBPD ( A value) among the model group, shikonin 1 group, shikonin 2 group and blank control group (0.072±0.026, 0.177±0.036, 0.290±0.062, 0.407±0.051, respectively; F=48.895, P < 0.01) , and there were also significant differences between any two groups (all P < 0.01) . Western blot analysis showed that the CEBPD expression in the mouse epidermis was highest in the blank control group, followed in descending order by the shikonin 2 group, shikonin 1 group and model group, and significantly differed among the above 4 groups ( F=10.237, P<0.05) ; moreover, there were significant differences in the CEBPD expression between the model group and blank control group, as well as between the shikonin 1 group and blank control group (both P<0.05) , while no significant difference was observed between the shikonin 2 group and the blank control group ( P > 0.05) . Conclusion:Topical shikonin could effectively interfere with the development of imiquimod-induced psoriasis-like mouse model; CEBPD expression decreased in the psoriasis-like mouse model, and could be markedly upregulated by topical application of shikonin.

ObjectiveTo investigate the potential mechanisms and pathways through which Gandouling （GDL） exerts its effects in the treatment of liver fibrosis in Wilson disease. MethodsSixty male SD rats were randomly divided into six groups： the normal group， the model group， the GDL low-， medium-， and high-dose groups （0.24， 0.48， 0.96 g·kg^-1）， and the penicillamine group （90 mg·kg^-1）， with 10 rats in each group. A copper-loaded Wilson disease rat model was established by gavage administration of 300 mg·kg^-1 copper sulfate pentahydrate to all groups except the normal group. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the pathomorphological changes in the liver. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of hyaluronic acid （HA）， laminin （LN）， procollagen type-Ⅲ peptide （PC-Ⅲ）， and collagen type-Ⅳ （C-Ⅳ）. Transmission electron microscopy was used to examine the ultrastructure of liver tissues. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the expression levels of liver tissues and serum exosomal long noncoding RNA H19 （LncRNA H19）， phosphatidylinositol 3-kinase （PI3K）， protein kinase B （Akt）， and mammalian target of rapamycin （mTOR）. Western blot analysis was performed to assess the expression levels of PI3K， Akt， mTOR， and their phosphorylated forms， as well as autophagy-related proteins Beclin1 and microtubule-associated protein 1 light chain 3B （LC3-Ⅱ/LC3-Ⅰ） in liver tissues. Beclin1 and LC3-Ⅱ fluorescence signal intensity was observed by immunofluorescence. ResultsCompared with the normal group， the model group exhibited inflammatory cell infiltration in hepatocytes， unclear nuclear boundaries with cell cleavage and necrosis， and collagen fiber deposition around confluent areas. The levels of HA， LN， PC-Ⅲ， and C-Ⅳ were significantly elevated （P<0.01）. Transmission electron microscopy revealed an increased number of autophagic vesicles， with autophagic lysosomes exhibiting a single-layer membrane structure following degradation of most envelopes. Expression levels of Beclin1 and LC3-Ⅱ/LC3-Ⅰ were significantly increased （P<0.01）， and fluorescence signals of Beclin1 and LC3-Ⅱ were markedly enhanced. The protein expression levels of PI3K， Akt， mTOR， p-PI3K， p-Akt， and p-mTOR were reduced （P<0.01）， while LncRNA H19 expression was increased （P<0.01）， and mRNA expression levels of PI3K， Akt， and mTOR were decreased （P<0.01）. After treatment with GDL， the degree of liver fibrosis was significantly improved， with decreased levels of HA， LN， PC-Ⅲ， and C-Ⅳ. The number of autophagic vesicles was significantly reduced， and expression levels of Beclin1 and LC3-Ⅱ/LC3-Ⅰ proteins were lower （P<0.01）. The fluorescence signals of Beclin1 and LC3-Ⅱ weakened dose-dependently. The protein levels of PI3K， Akt， mTOR， p-PI3K， p-Akt， and p-mTOR were elevated （P<0.01）， while the expression level of LncRNA H19 was reduced （P<0.01）. Furthermore， the mRNA expression levels of PI3K， Akt， and mTOR increased （P<0.05， P<0.01）. ConclusionGDL may alleviate liver fibrosis and reduce liver injury by regulating the PI3K/Akt/mTOR autophagy signaling pathway via LncRNA H19.

Objective:To summarize the clinical characteristics of patients with coronavirus disease 2019 (COVID-19) infected with Delta variant, so as to provide further references for clinical diagnosis and treatment.Methods:A real-world study was conducted to analyze the characteristics of 166 COVID-19 patients infected with Delta variant at Guangzhou Eighth People’s Hospital, Guangzhou Medical University.Results:The study enrolled 5 asymptomatic cases, 123 non-severe cases (mild and moderate type), and 38 severe cases (severe and critical type). Among these patients, 69 (41.6%) were male and 97 (58.4%) were female, with a mean age of 47.0±23.5 years. Thirty-nine cases (23.5%) had received 1 or 2 doses of inactivated vaccine. The incidence of severe COVID-19 cases was 7.7% in 2-doses vaccinated patients, which was lower than that of 11.5% in 1-dose and 26.8% in unvaccinated patients. The proportion of severe cases in 2 dose-vaccinated patients was 7.7%, which was lower than that of 11.5% in 1-dose vaccinated patients and 26.8% in unvaccinated patients, but the difference was not significant ( P>0.05). The most common clinical symptom was fever (134 cases, 83.2%), and 39.1% of cases presented with high-grade fever (≥39 °C); other symptoms were cough, sputum, fatigue, and xerostomia. The proportion of fever in severe cases was significantly higher than that of non-severe cases (97.4% vs. 76.4%, P<0.01). Similarly, the proportion of severe cases with high peak temperature (≥39 ℃) () was also higher than that of non-severe cases (65.8% vs. 30.9%, P<0.01). The median minimal Cycle threshold (Ct) values of viral nucleic acid N gene and ORFlab gene were 20.3 and 21.5, respectively, and the minimum Ct values were 11.9 and 13.5, respectively. Within 48 h of admission, 9.0% of cases presented with decreased white blood cell counts, and 52.4% with decreased lymphocyte counts. The proportions of increased C-reactive protein, serum amyloid A, interleukin 6, and interleukin 10 were 32.5%, 57.4%, 65.3%, and 35.7%, respectively. The proportions of elevated C-reactive protein, serum amyloid A and interleukin-6 in severe cases were significantly higher than those in non-severe cases ( P<0.01). Logistic regression analysis showed that older age and higher peak temperature were associated with a higher likelihood of severe cases ( OR>3, 95% CI: 2-7, P<0.01). In terms of treatment, traditional Chinese medicine (TCM) was used in 97.6% of non-severe cases and 100% in severe cases. Other treatments included respiratory and nutritional support, immunotherapy (such as neutralizing antibodies and plasma of recovered patients). The median times from admission to progression to severe cases, of fever clearance, and of nucleic acid conversion were 5 days, 6 days and 19 days, respectively. No deaths were reported within 28 days. Conclusions:The symptoms of Delta variant infection in Guangzhou are characterized by a high proportion of fever, high peak temperature, long duration of fever, high viral load, a long time to nucleic acid conversion, and a high incidence of severe cases. The severe cases exhibit a higher percentage of elderly patients, a longer duration of fever and have a higher fever rate and a higher hyperthermia rate than non-severe cases. Age and hyperthermia are independent risk factors for progression to severe disease. The combination of TCM and Western medicine can control the progression of the disease effectively.