Objective To observe the effect of Kechuanning Oral liquid on the expression of P13K in CD4+and CD8+T cells of asthma rats induced by respiratory syncytial virus (RSV), and explore its mechanism of preventing and treating asthma induced by virus. Methods SD rats were randomly divided into phosphate-buffered saline (PBS) control group, model group, dexamethasone and salbutamol group (positive drug group), and Kechuanning oral liquid group. Ovalbumin asthma rats model was built and induced by RSV. CD4+and CD8+T cells were separated by magnetic beads method. The expressive level of PI3K-110αin T cells was detected by immumofluorescence method with flow cytometry. Results Compared with PBS control group, positive drug group and Kechuanning oral liquid group, the CD4+and CD8+T cells percentage and the expression level of PI3K-110α in CD4+ and CD8+T cells of model group were significantly higher. The differences were statistically significant (P<0.01). The CD4+and CD8+T cells percentage was not associated with the expression level of PI3K-110α in CD4+ and CD8+T cells of each group by Pearson correlation analysis. Conclusion The CD4+ and CD8+T cells involve in the asthma immunity balanced modulation, and the level of PI3K expressed by CD4+ and CD8+T cells increase distinctly. Kechuanning oral liquid can restrain the expression of PI3K in CD4+ and CD8+T cells, which might be one of the immunologic mechanisms of treating asthma.

Objective To investigate the inhibitory effect of bardoxolone methyl(CDDO-Me)on activation of NLRP3 inflammasome and its mechanism for alleviating acute liver injury(ALI).Methods Mouse bone marrow-derived macrophages(BMDM)and THP-1 cells were pre-treated with CDDO-Me followed by treatment with Nigericin,ATP,MSU,intracellular LPS transfection for activation of NLRP3 inflammasomes,or poly A:T for activation of AIM2 inflammasomes.The levels of caspase-1 and IL-1β in the cell culture supernatant was determined with Western blotting and ELISA to assess the inhibitory effect of CDDO-Me on NLRP3 inflammasomes and its specificity.In the animal experiment,male C57BL/6J mouse models of acetaminophen-induced ALI were treated with low-dose(20 mg/kg)and high-dose(40 mg/kg)CDDO-Me,and the changes in serum levels of IL-1β,TNF-α,AST and ALT were measured by ELISA and liver tissue pathology was observed using HE staining.Results In mouse BMDM and THP-1 cells,CDDO-Me dose-dependently inhibited the activation of NLRP3 inflammasomes without significantly affecting the secretion of non-inflammasome-related inflammatory factors IL-6 and TNF-α or AIM2 inflammasome activation.In the mouse models of ALI,CDDO-Me treatment at both the low and high doses significantly reduced serum levels of IL-1β,AST and ALT,ameliorated histological changes and reduced inflammatory cell infiltration in the liver tissue,and the effects exhibited a distinct dose dependence.Conclusion CDDO-Me can specifically inhibit the activation of NLRP3 inflammasomes to alleviate acetaminophen-induced ALI in mice.

Objective:To explore the feasibility and technical tips of donor-site reconstruction of the latissimus dorsi myocutaneous flap using the perforator propeller flap technique.Methods:Between July 2012 and January 2019, a total of 24 patients, including 9 males and 15 females, underwent reconstructions of defects in various locations using the latissimus dorsi myocutaneous flap. The average patient age was 43.6 years (range, 4-81 years). Before surgery, perforators adjacent to the latissimus dorsi muscle were explored using an ultrasound Doppler probe and marked on the skin. A latissimus dorsi myocutaneous flap was elevated according to the resultant defect following the removal of the lesion and transferred to reconstruct the defect. The donor-site defects were reconstructed using one, dual, or even triple perforator propeller flap.Results:All the 24 myocutaneous flaps survived completely. The dimension and width of the myocutaneous flaps ranged from 16 cm × 11 cm to 33 cm × 17 cm and 9 cm to 20 cm, respectively. The donor-site defects of the myocutaneous flap were all closed by perforator propeller flaps including 22 pedicled flaps and 2 free flaps. The defect was reconstructed by one perforator propeller flap in 12 patients, two flaps in 11, and three flaps in the remaining one patient. There were 36 posterior intercostal artery perforator propeller flaps and one freestyle perforator propeller flap. The size, pedicle length, and rotation angle of the propeller flaps were 13 cm × 5 cm to 23 cm × 14 cm, 3 cm to 6 cm, and 90 to 180 degrees, respectively. All the donor sites of the perforator propeller flaps were closed primarily. Total necrosis of the propeller flap occurred in one patient and small-sized distal flap necrosis in another one. The remaining propeller flaps survived completely. All patients were followed up for one to 38 months and the mean follow-up time was 7 months. Tumor recurrence was noticed in four patients. All patients were satisfied with the final functional and aesthetic outcomes.Conclusions:Using the perforator propeller flaps could guarantee not only harvesting a wide latissimus dorsi myocutaneous flap, but also primary donor-site closure of the myocutaneous flap, and therefore greatly improve the versatility and capability of the latissimus dorsi myocutaneous in defect reconstruction.

Objective To investigate the inhibitory effect of bardoxolone methyl(CDDO-Me)on activation of NLRP3 inflammasome and its mechanism for alleviating acute liver injury(ALI).Methods Mouse bone marrow-derived macrophages(BMDM)and THP-1 cells were pre-treated with CDDO-Me followed by treatment with Nigericin,ATP,MSU,intracellular LPS transfection for activation of NLRP3 inflammasomes,or poly A:T for activation of AIM2 inflammasomes.The levels of caspase-1 and IL-1β in the cell culture supernatant was determined with Western blotting and ELISA to assess the inhibitory effect of CDDO-Me on NLRP3 inflammasomes and its specificity.In the animal experiment,male C57BL/6J mouse models of acetaminophen-induced ALI were treated with low-dose(20 mg/kg)and high-dose(40 mg/kg)CDDO-Me,and the changes in serum levels of IL-1β,TNF-α,AST and ALT were measured by ELISA and liver tissue pathology was observed using HE staining.Results In mouse BMDM and THP-1 cells,CDDO-Me dose-dependently inhibited the activation of NLRP3 inflammasomes without significantly affecting the secretion of non-inflammasome-related inflammatory factors IL-6 and TNF-α or AIM2 inflammasome activation.In the mouse models of ALI,CDDO-Me treatment at both the low and high doses significantly reduced serum levels of IL-1β,AST and ALT,ameliorated histological changes and reduced inflammatory cell infiltration in the liver tissue,and the effects exhibited a distinct dose dependence.Conclusion CDDO-Me can specifically inhibit the activation of NLRP3 inflammasomes to alleviate acetaminophen-induced ALI in mice.

Objective:To explore the feasibility and technical tips of donor-site reconstruction of the latissimus dorsi myocutaneous flap using the perforator propeller flap technique.Methods:Between July 2012 and January 2019, a total of 24 patients, including 9 males and 15 females, underwent reconstructions of defects in various locations using the latissimus dorsi myocutaneous flap. The average patient age was 43.6 years (range, 4-81 years). Before surgery, perforators adjacent to the latissimus dorsi muscle were explored using an ultrasound Doppler probe and marked on the skin. A latissimus dorsi myocutaneous flap was elevated according to the resultant defect following the removal of the lesion and transferred to reconstruct the defect. The donor-site defects were reconstructed using one, dual, or even triple perforator propeller flap.Results:All the 24 myocutaneous flaps survived completely. The dimension and width of the myocutaneous flaps ranged from 16 cm × 11 cm to 33 cm × 17 cm and 9 cm to 20 cm, respectively. The donor-site defects of the myocutaneous flap were all closed by perforator propeller flaps including 22 pedicled flaps and 2 free flaps. The defect was reconstructed by one perforator propeller flap in 12 patients, two flaps in 11, and three flaps in the remaining one patient. There were 36 posterior intercostal artery perforator propeller flaps and one freestyle perforator propeller flap. The size, pedicle length, and rotation angle of the propeller flaps were 13 cm × 5 cm to 23 cm × 14 cm, 3 cm to 6 cm, and 90 to 180 degrees, respectively. All the donor sites of the perforator propeller flaps were closed primarily. Total necrosis of the propeller flap occurred in one patient and small-sized distal flap necrosis in another one. The remaining propeller flaps survived completely. All patients were followed up for one to 38 months and the mean follow-up time was 7 months. Tumor recurrence was noticed in four patients. All patients were satisfied with the final functional and aesthetic outcomes.Conclusions:Using the perforator propeller flaps could guarantee not only harvesting a wide latissimus dorsi myocutaneous flap, but also primary donor-site closure of the myocutaneous flap, and therefore greatly improve the versatility and capability of the latissimus dorsi myocutaneous in defect reconstruction.

Following the principles of evidence-based medicine,in accordance with the structure and drafting rules of standardized documents,based on literature research,according to the characteristics of chronic cough in children and issues that need to form a consensus,the TCM Guidelines for Diagnosis and Treatment of Chronic Cough in Children was formulated based on the Delphi method,expert discussion meetings,and public solicitation of opinions.The guideline includes scope of application,terms and definitions,eti-ology and diagnosis,auxiliary examination,treatment,prevention and care.The aim is to clarify the optimal treatment plan of Chinese medicine in the diagnosis and treatment of this disease,and to provide guidance for improving the clinical diagnosis and treatment of chronic cough in children with Chinese medicine.

Objective To investigate the effect of interleukin-6 (IL-6) on the phagocytosis of MH-S alveolar macrophages and its related mechanisms. Methods A mouse acute lung injury (ALI) model was constructed by instilling lipopolysaccharide (LPS) into the airway. ELISA was used to detect the content of IL-6 in bronchoalveolar lavage fluid (BALF). In vitro cultured MH-S cells, in the presence or absence of signal transducer and activator 3 of transcription(STAT3) inhibitor Stattic (5 μmol/L), IL-6 (10 ng/mL~500 ng/mL) was added to stimulate for 6 hours, and then incubated with fluorescent microspheres for 2 hours. The phagocytosis of MH-S cells was detected by flow cytometry. Western blot analysis was used to detect the expression levels of phosphorylated Janus kinase 2 (p-JAK2), phosphorylated STAT3 (p-STAT3), actin-related protein 2 (Arp2) and filamentous actin (F-actin). Results The content of IL-6 in BALF was significantly increased after the mice were injected with LPS through the airway. With the increase of IL-6 stimulation concentration, the phagocytic function of MH-S cells was enhanced, and the expression levels of Arp2 and F-actin proteins in MH-S cells were increased. The expression levels of p-JAK2 and p-STAT3 proteins increased in MH-S cells stimulated with IL-6(100 ng/mL). After blocking STAT3 signaling, the effect of IL-6 in promoting phagocytosis of MH-S cells disappeared completely, and the increased expression of Arp2 and F-actin proteins in MH-S cells induced by IL-6 was also inhibited. Conclusion IL-6 promotes the expression of Arp2 and F-actin proteins by activating the JAK2/STAT3 signaling pathway, thereby enhancing the phagocytic function of MH-S cells.
Animals ; Mice ; Actins ; Disease Models, Animal ; Interleukin-6 ; Janus Kinase 2 ; Lipopolysaccharides ; Macrophages, Alveolar ; Signal Transduction