BACKGROUND:The mechanical environment of skin tissue and spreading state of epithelial cels are closely related with the wound healing and scar formation process. OBJECTIVE:To analyze the effect of extracelular mechanical stimulation on cel spreading, to test the cel proliferation in order to analyze the effect of spreading form on cel proliferation and other physiological activities. METHODS: Cyclic sine wave mechanical stretching was exerted on immortalized human keratinocyte by using FX-4000 flexible substrate loading system, on the condition of 0.2 Hz and at frequency of 10% amplitudes. The spreading form was compared at 0, 24 and 48 hours, the cel proliferation was analyzed with flow cytometry, and the distribution of vinculin was analyzed with immunofluorescence staining. RESULTS AND CONCLUSION: human keratinocyte would keep the spreading state and could induce more cel proliferation by 24 hours mechanical stretching stimulation. Conversely, after stimulated for 48 hours, the morphology of the human keratinocyte was significantly changed, and the number of human keratinocyte in the division stage was larger than that in the static control group; under tensile stress, the distribution of vinculin was transformed from the surrounding nucleus membrane area to the cel edge. The results indicate that proper mechanical stimulate can increase cel proliferation with keeping cel spreading and adhesion state; the stimulating time of continuous cyclic stretching is the major factor to determine cel spreading morphology and adhesion regions of immortalized human keratinocyte.

Objective To compare the efficacy of uniform multi-drug therapy (UMDT) versus routine multi-drug therapy (RMDT) for the treatment of multi-bacillary (MB) leprosy patients based on bacterial index changes and frequencies of leprosy reaction.Methods This study recruited newly diagnosed leprosy patients after taking informed consent in three districts of Guizhou province as well as in one district of Yunnan province from November 2003 to June 2005.The patients received 6-month UMDT or 2-year RMDT.Clinical follow up and bacterial reexamination were carried out once a year.Changes of bacterial index (BI) and frequencies of leprosy reaction were compared between the patients receiving RMDT and UMDT.Results A total of 166 patients received UMDT and 170 received RMDT in this study.Among the UMDT-treated patients,114 were skin smear positive,and 83 had been followed up for 42 months; of the RMDT-treated patients,149 underwent all the bacterial examinations during a 48-month follow up.The mean bacterial index decreased from 2.84 before treatment to 0.33 at the end of the 42-month follow up in the 83 patients,and from 2.55 to 0.26 at the end of the 48-month follow up in the 149 patients,with no significant difference in the changes of bacterial index between the two groups (t =0.77,P ＞ 0.05).Bacterial index became negative in 73.5％ (61/83) of the UMDT-treated patients and in 77.2％ (115/149) of the RMDT-treated patients (x2 =0.40,P＞ 0.05)at the end of follow up.During the follow up peroid,the incidence of type Ⅰ leprosy reaction was 14.6％ (13/89) in the UMDT group,significantly higher than that in the RMDT group (3.4％ (5/149),x2 =10.08,P＜ 0.01 ).Conclusions There is no significant difference in mean bacterial index changes and bacterial clearance rate during the follow up peroid between UMDT- and RMDT-treated patients.The incidence of type Ⅰ leprosy reaction is higher in the UMDT group than in the RMDT group,and further investigation is needed to clarify the mechanisms underlying the phenomenon.

Objective To detect gene mutations associated with dapsone-,rifampicin-and ofloxacinresistance in lesions of patients with recurring or treatment-resistant leprosy collected from 2010 to 2011.Methods Clinical data and lesional specimens were collected during 2010-2011 from patients with recurring or treatment-resistant leprosy who were diagnosed and reported by provincial centers for leprosy control.Mycobacterium leprae DNA was extracted from the specimens and subjected to PCR for the amplification of folP1,rpoB and gyrA genes.The PCR products were directly sequenced and BLAST program was used to compare the sequence of isolated strains with the reference sequence in GenBank.Results Twenty-four patients were enrolled in this study,including 13 with recurring leprosy and 11 with treatment-resistant leprosy.Twenty-one patients showed positive PCR results in all the three regions.Of these PCR-positive specimens,3 from 1 patient with recurring and 2 patients with resistant leprosy harbored a point mutation,acc (threonine)→gcc (alanine),at codon 53 in the floP1 gene,1 from a patient with recurring leprosy harbored a missense mutation,gat (aspartic acid) → aac (asparagine),at codon 441 in the rpoB gene.Conclusions Mutations are detected in the folP1 and rpoB genes,which are associated with the resistance to dapsone and rifampicin respectively,but not in the ofloxacin resistance-associated gyrA gene,in Mycobacterium leprae isolates from patients with recurring or treatment-resistant leprosy.

Objective: To investigate the determinants affecting the heart rate deceleration capacity (DC) in patients with dilated cardiomyopathy (DCM). Methods: One hundred patients with DCM (DCM group) and 202 healthy subjects (control group) were respectively enrolled. Echocardiography and 24 hours electrocardiogram were performed in all subjects. DC value was compared between the two groups. Multiple regression analysis was made to evaluate the related determinants of DC ((age, sex, echocardiographic parameters including the left atrial diameter (LAD) and left ventricular ejection fraction (LVEF)). Results: (1) DC value was significantly lower in DCM group than in control group( (4.40±2.03) ms vs. (7.30±1.81) ms, P<0.01), prevalence of DC value≤4.5 ms was significantly higher in DCM group than in control group (62% vs. 6%, P<0.01). (2) DC value in the DCM group decreased in proportion to increasing LAD dimension, DC value was (5.60±2.04) ms, (4.50±2.07) ms and (3.60±1.62) ms (P<0.05) in DCM patients with LAD≤40 mm, 40 mm50 mm, respectively. (3) DC value in the DCM group was negatively related to the LAD (r=-0.366, P<0.01), positively related to the LVEF (r= 0.241, P<0.01), but not related with age and sex. Multiple factors regression analysis showed that increased LAD was related to the reduced DC values independtly. Conclusion DC value of the patients in the DCM group is decreased, which indicate the decrease of the vagus nerve tension, and increased LAD is related to the reduced DC value independtly in DCM patients.

Objective To explore the efficacy and safety of traditional Chinese medicine(TCM) combined with chemotherapy in the prevention and treatment of postoperative recurrence and metastasis of locally advanced gastric cancer (LAGC) by meta-analysis. Moreover, we evaluated the efficacy of TCM on the quality of life, immune indexes, and toxic and side effects during adjuvant chemotherapy. Methods The CNKI, Wanfang, PubMed, and other databases were searched by computer. Randomized controlled trials (RCTs) were searched. After literature screening and data extraction, Review Manager 5.3 software provided by Cochrane was used for meta-analysis. Results A total of 18 RCTs were included. Compared with chemotherapy alone, TCM combined with chemotherapy could improve the KPS score and CD3⁺ and CD4⁺/CD8⁺ index levels. The incidence rates of postoperative leucopenia, hemoglobin reduction, thrombocytopenia, nausea and vomiting, diarrhea, and neurotoxicity were reduced. In terms of postoperative QLQ-C30 score, abnormal liver function, and abnormal renal function, the incidence of TCM combined chemotherapy was similar to that of chemotherapy alone, with no statistical difference. Compared with chemotherapy alone, TCM combined chemotherapy could reduce the 1-, 2-, 3-, and 5-year cumulative recurrence and metastasis rates and prolong the disease-free survival time. Conclusion Compared with chemotherapy alone in adjuvant chemotherapy, TCM combined chemotherapy could improve the immune level and KPS score of LACC patients after surgery, reduce the incidence of adverse reactions, as well as reduce the recurrence and metastasis rate of LAGC after surgery and DFS could be improved.

OBJECTIVE: To carry out genetic testing for a patient with 45,X/46,XY mosaicism and autism spectrum disorder (ASD). METHODS: Peripheral blood samples of the patient and his parents were collected for the extraction of genomic DNA. Trio-based whole exome sequencing and Sanger sequencing were carried out thereafter. RESULTS: The proband and his father were found to harbor a heterozygous c.4781G>A (p.Arg1594Gln) variant of the CACNA1I gene. In addition, the proband was also found to harbor a de novo c.268C>T (p.Arg90Trp) missense variant of the MTRR gene. Based on guidelines of the American College of Medical Genetics and Genomics (ACMG), the c.4781G>A (p.Arg1594Gln) variant of the CACNA1I gene was predicted to be pathogenic (PVS1, PM1, PM2, PP3), while the c.268C>T (p.Arg90Trp) variant of the MTRR gene was predicted to be of uncertain significance. CONCLUSION Variants of the CACNA1I and MTRR genes, together with the chromosomal mosaicism, may have predisposed to the susceptibility to the ASD in this patient.
Autism Spectrum Disorder/genetics* ; Genomics ; Heterozygote ; Humans ; Mosaicism ; Whole Exome Sequencing

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.