Kawasaki disease is a disease based on systemic vasculitis, which has become the most common disease in children with acquired heart disease, but its etiology and pathogenesis remain unclear.The homeostasis of the gut microbiota plays an important role in the maturation of the body′s immune system and immune regulation.The disorder of the gut microbiota is involved in a variety of inflammatory and immune diseases in children.Studies have found that there are changes in the composition of gut microbiota in children with Kawasaki disease.Gut microbiota disorders are related to the occurrence and development of Kawasaki disease, with the immune system function affected.Various mechanisms such as intestinal mucosal barrier dysfunction, immune inflammation, oxidative stress and metabolite effects promote the pathogenesis of Kawasaki disease.This article reviews the research on the relationship between gut microbiota and Kawasaki disease.

Objective To investigate the effect of intralesional lauromacrogol therapy on infantile hemangioma.Methods 30 cases all received intralesional injection of lauromacrogol.The changes of tumor size,texture and color were monitored and recorded.The adverse effects after medication were observed and managed accordingly.The adverse effects after medication were observed.The times of treatment were determined according to degree of reduction of tumor volume.To assess the efficacy,a 4 scales system was adopted.Results All patients had completed the treatment and followup.The overall response was scale Ⅰ in 2 cases (6.7 ％),scale Ⅱ efficacy in 4 patients (13.3 ％),scale Ⅲ efficacy in 5 cases (16.7 ％) and scale Ⅳ in 19 cases (63.3 ％).The smaller the tumor,the fewer the times of treatment,and the better the results.The effects of treatment were better if patient could be treated by intralesional lauromacrogol therapy in early stage.No severe adverse effects were observed during 6 months of follow-up.Conclusions Intralesional injection of lauromacrogol sclerotherapy is a safe and effective way to treat infantile hemangioma.

Air Pollutants ; toxicity ; Air Pollution, Indoor ; adverse effects ; Animals ; DNA Damage ; drug effects ; Female ; Interior Design and Furnishings ; Male ; Mice ; Mutagenicity Tests

This article introduces the independent experiment and social investigation activities in the course of medication analy- sis set up for strengthening students' comprehensive abilities.These activities create a good study atmosphere for enhancing stu- dents' ability to do research and their humanistic qualities.

Fingers ; Hand Dermatoses ; etiology ; Humans ; Infant ; Male ; Severe Combined Immunodeficiency ; complications ; Tuberculosis, Osteoarticular ; etiology

Background Heat shock proteins (HSPs) are highly conserved proteins that are induced in cells when confronted with a wide variety of proteotoxic stresses.HSP27 has a high degree of similarity with α-crystallin protein.The abnormality of HSP27 structure and expression are closely related to the formation of cataracts.Our previous study showed sodium salieylate has the protective effect on H2O2-induced lens damage.Objective This study was to investigate the roles of MAPK signal pathway in sodium salicylate-induced the expression of HSP27 in human lens epithelial cells (LECs) in vitro.Methods Human LECs were incubated in the fresh media containing sodium salicylate at different concentrations (0-55 mmol/L) for different times (1-5 hours) and allowed to be recovered in fresh medium without sodium salicylate for 1-24 hours with or without pretreatment with P38MAPK inhibitor (SB203580), ERK1/2 inhibitor (PD98059) and JNK/SAPK inhibitor ( SP600125). The expressions of P38MAPK, EBK1/2, JNK/SAPK, phosphorylated P38MAPK, phosphorylated ERK1/2, phosphorylated JNK/SAPK and HSP27 were detected by Western blot. HSP27 mRNA was detected by RT-PCR. The expression of HSP27 was also detected by immunohistochemistry. Results There was only weak expression of HSP27 in normal human LECs.After stimulation of 35-55 mmol/L sodium salicylate was removed and human LECs were cultured again for 6 hours,the expression of HSP27 in LECs were significantly increased ( F= 509. 953,P<0. 01). HSP27 was absent expressed in human LECs in 55 mmol/L sodium salicylate stimulation for 1-5 hours groups, but LECs were re-cultured for 3,6 hours after removed the stimulation, the expression of HSP27 was elevated (F = 452. 534, P<0. 01). Activation of P38 M APK occurred after sodium salicylate stimulation 30 minutes and 1 hour ( F = 865.68, P<0. 01). However, ERK 1/2 was expressed after sodium salicylate was eliminated for 1-6 hours ( F = 388.84, P<0. 01). JNK/SAPK was inactived by sodium salicylate. The expression of HSP27 could be down-regulated with the pretreatment of SB203580 and PD98059. Conclusion Sodium salicylatc can induce the expression of HSP27 in human (LECs) . The effects are mediated,at least in part ,through the activation of P38MAPK and ERK1/2 signaling pathway .

Objective To evaluate perioperative management of MEN 2A patients with medullary thyroid carcinoma after bilateral pheochromocytomas removal.Methods Seven cases of MEN 2A from three families were diagnosed as medullary thyroid carcinoma and adrenal pheochromocytoma by biochemical tests and imaging examinations.All had histories of operations due to medullary thyroid carcinoma and contralateral adrenal pheochromocytoma.Direct sequencing of entire exons was performed in all patients.Firstly they underwent laparoscopic surgery for pheochromocytoma, then after stetoids replacement they underwent total thyroidectomy and bilateral cervical lymph nodes dissection.Results One family had the combined C634Y/D707E mutations of RET mutation.The other two families had C634Y mutation and C634R mutation separately.All patients had histories of adrenal insufficiency because of bilateral laparoscopic adrenal pheochromocytomas removal.They suffered from medullary thyroid carcinoma at the same time and needed to do total thyroidectomy and bilateral cervical lymph node dissection.Under perioperative steroids treatment and closely monitoring, they successfully went through the surgery.No adrenal crisis or related complications happened.Conclusions MEN 2A patients in this study had RET mutations and D707E mutation is a newly discovered mutation.Patients of adrenal insufficiency face the risk of adrenal crisis after a major operation.Correct perioperative monitoring and management can avoid complications.

ABSTRACT:Objective To detect the expressions of thioredoxin (TRX1)and c-jun-activation-domain binding protein-1 (JAB1)in patients with acute myelogenous leukemia (AML)and healthy controls,and measure the TRX1 level in AML patients at different stages for evaluating its clinical significance.Methods The expressions of TRX1 and JAB1 in leukemia samples were analyzed by RT-PCR and Western blot at mRNA and protein levels, respectively.The correlation between TRX1 and JAB1,and the relationship between the gene expression and peripheral blood leukocytes count were also analyzed.Furthermore,serum TRX1 was measured by ELISA.Results TRX1 and JAB1 expressions at both mRNA and protein levels were obviously upregulated in leukemia patients (P<0.05). TRX1 was positively related to JAB1 in both newly diagnosed and recurrent AML patients.And high levels of TRX1 and JAB1 expressions were associated with white blood cell (WBC)counts in AML patients (P<0.05).Moreover, abundance of TRX1 in serum was significantly greater in AML patients,especially in the patients with recurrent AML,than in healthy donors (P<0.05).Conclusion There is a positive correlation between the expressions of TRX1 and JAB1 ,which is closely related to the occurrence and progression of AML.

AIM:To investigate the effect of microRNA-429 (miR-429) on the expression of occludin (Ocln) in intestinal epithelial cells ( IECs) and intestinal epithelial barrier function in diabetic mice.METHODS:Diabetes mel-litus mouse model was induced by intraperitoneal injection of streptozocin.The expression of miR-429 in IECs of diabetic mice was inhibited by antagomiRNA-429 injected via tail vein.The expression of miR-429 and mRNA expression of Ocln were detected by real-time PCR.The protein expression of Ocln was determined by Western blotting and immunohistochem-istry.The urinary lactulose/mannitol ratio was measured by gas chromatography.The plasma LPS concentrations in the mice were measured by chromogenic end-point TAL kit.RESULTS:The results of real-time PCR confirmed that the ex-pression of miR-429 in IECs of diabetic mice was remarkably inhibited by tail-vein administration of antagomiRNA-429, and resumed to similar level of normal mice on the 6th day after the administration.After suppressing the level of miR-429, the expression of Ocln in IECs of diabetic mice increased significantly (P<0.05), while the urinary lactulose/mannitol ra-tio and the plasma LPS concentration decreased obviously ( P<0.05 ) .CONCLUSION:AntagomiRNA-429 effectively suppresses miR-429 expression in IECs of diabetic mice, and then enhances the expression of Ocln and partially resumes the intestinal epithelial barrier function.

Objective To study the mechanism of oxidative stress involved in the pathogenesis and relapse of acute monocytic leukemia (M5 ).Methods We detected reactive oxide species (ROS)levels,conducted plasma analysis obtained from 76 M5 patients at diagnosis and at relapse,and observed the ultrastructure of mitochondria of mononuclear cells in peripheral blood by transmission electron microscope.Results Compared with that in the control group,the average fluorescence intensity of intracellular ROS was significantly increased in M5 groups, especially in the relapse patients (P < 0.05 ).Low total antioxidative capacity (T-AOC)and antioxidant enzyme activity were characteristic of M5 at both diagnosis and relapse. However, lactate dehydrogenase (LDH ), malondialdehyde (MDA)and 8-hydroxy-2’-deoxyguanine (8-OHdG)increased significantly at both diagnosis and relapse (P < 0.05 ).Prominent ultrastructural abnormalities (mitochondrial swelling,outer membrane blebs,and aberrant cristae disorder)were present in patients with primary M5,and they were obviously abnormal in relapsing M5 patients.Conclusion Oxidative stress is the initiating factor of M5.Mitochondria are the main intracellular location for ROS generation.To maintain the dynamic balance between ROS and antioxidant defence may be the critical factor for preventing relapse.