Objective To investigate the percentages of Th17 and CD4+CD25+FoxP3+ regulatory T(Tr) cells and the levels of related cytokines IL-6,IL-23,IL-17 and TGF-β in serum of patients with anlylosing spondylitis(AS).Methods Forty patients with AS and 37 age-matched healthy donors were studied.Flow cytometry Was used to analyze the percentages of blood Th17 and CD4+CD25+FoxP3+Tr cells.The levels of serum IL-6,IL-23,IL-17 and TGF-β were assayed by enzyme-linked immunosorbent assay ( ELISA).Results The proportion of Th17 cells in AS group was significantly higher than those in normal group [ (1.02±0.34)％ vs (0.68±0.29)％,P＜0.05) ],and the proportion of CD4+CD25+FoxP3+ cells was lower in AS group comparing with normal group [(3.77±0.81)％ vs (4.69±1.23)％,P＜0.05)].Meanwhile,serum levels of IL-6,IL-23 and IL-17 were significantly higher in AS group than those in normal group [ (6,15±2.71) ng/L vs (3.31±1.65) ng/L; (9.44±3.12) ng/ml vs (5.82±2.61) ng/ml;(10.53±4.97) ng/L vs (6.78±3.26) ng/L,all P＜0.01 ].In contrast,TGF-β level was decreased in AS group compares with the normal group [ ( 4.76±2.15) ng/ml vs (5.16±2.02) ng/ml,P＞0.05 ],but the difference was not significant.No associations of serum eytokine levels with clinical and laboratory parameters were found in AS.Conclusion The abnormality Th17 cells and Tr cells and their related cytokines IL-6,IL-23,IL-17 and TGF-β changes in patients with AS,which may be involved in immunological pathogenesis of AS.

Background Studies have determined that nucleotide binding oligomerization domain 2 (NOD2) plays a key role in innate immune response.However,whether NOD2 participates in the nature defense of fungal keratitis is unclear.Objective This study was to investigate the expression and significance of NOD2 on cornea in the initial of Aspergillus fumigatus keratitis (AFK) in rats.Methods Seventy-two adult clean Wistar rats were randomized into the normal control group,only corneal epithelial scraped group and AFK model group,and the AFK models were established by incubating Aspergillus fumigatus to cornea after corneal epithelium was scraped.All the operations were performed in the right eyes of rats.Reverse transcription PCR (RT-PCR) was carried out to detect the expression of NOD2 mRNA in corneal epithelium 4,8,16,24 hours after operation.Twenty-four hours after operation,the expression of NOD2 protein in rat corneas was examined by immunochemistry and immnunofluorescence technology.Also,the rat corneas were obtained for regular histopathological examination.The use and care of the animals complied with Institutional Animal Care and Use Committee Guidebook by NIH.Results All the models were made successfully.RT-PCR revealed that a fewer NOD2 mRNA were expressed on cornea in the normal control group,but the expressing levels of NOD2 mRNA were increased in the only corneal epithelial scraped group and AFK model group.Compared with only corneal epithelial scraped group,the elevated values of NOD2 mRNA expression in the AFK model group were statistically significant at 4,8,16 and 24 hours after operation (t =-0.409,-0.439,-0.534,-0.618,all at P=0.000).The histopathological examination displayed that the cornel tissue had intact structure in the normal control group,and partly corneal epithelial deficiency,slight corneal swelling and fewer neutrophil granulocytes were seen in the only corneal epithelial scraped group.However,corneal ulcer,severe corneal edema and a lot of neutrophil granulocytes were exhibited in the AFK model group.Immunochemistry and immnunofluorescence staining evidenced that weaker expression of NOD2 was visualized in the corneal epithelial and endothelial layers,and obviously enhanced staining was seen in the AFK model group.The expressing levels (absorbancy) were 0.045 ± 0.005,0.050 ± 0.005 and 0.092 ± 0.006 in the normal control group,only corneal epithelial scraped group and AFK model group,respectively,showing a significant increase in the AFK model group compared with the only corneal epithelial scraped group (t =0.042,P =0.000).Conclusions Expression of NOD2 is upregulated in the corneas with AFK,suggesting that NOD2 participates the natural defense in the initial of fungal keratitis.NOD2 may play an important role in the process of anti-fungal innate immune response in cornea.

Gastrectomy ; Humans ; Laparoscopy ; Stomach Neoplasms/surgery*

Acquired Immunodeficiency Syndrome ; complications ; pathology ; Antigens, CD34 ; metabolism ; Gastrectomy ; methods ; Humans ; Male ; Middle Aged ; Sarcoma, Kaposi ; metabolism ; pathology ; surgery ; virology ; Stomach ; pathology ; Stomach Neoplasms ; metabolism ; pathology ; surgery ; virology ; Vimentin ; metabolism

SARS-CoV is a newly discovery pathogen causing severe acute respiratory problems.It has been established that the S protein in this pathogen plays an important rule in the adsorption and penetration of SARS-CoV into the host cell by interaction with the ACE2 receptor.To determinant which functional motif of the S protein was involved in the interaction with ACE2,seven truncated S proteins deleted from the N or C terminal were obtained by an E.coli expression system and purified by column chromatography to homogeneity.Each truncated S protein was fixed on to the well of an ELISA plate and an interaction was initiated with the ACE2 protein.The adsorption were quantified by ELISA,and the results indicated that amino acids from 388 to 496 of the S protein was responsible for the interaction with the ACE2 receptor,and the interaction could be completely disrupted by an antibody specific to these amino acids.Deletions adjacent to this domain did not appear to have a significant impact on the interaction with ACE2,suggesting that the S protein of SARS-CoV could be developed as a vaccine to prevent the spread of SARS-CoV.

OBJECTIVETo investigate SiO2-induced EMT in human bronchial epithelial cells HBE in vitro.

METHODSHBE cells were cultured and then stimulated with indicated doses of SiO2 (0, 50, 100, 200, 300 µg/ml). The morphological changes were observed by microscope. In addition, Western blot was per-formed to detect the expression of E-cad, α-SMA and Vim. The changes of migration ability were examined by wound-healing assay in vitro.

RESULTS(1) After exposure to SiO2, HBE cells lost contact with their neighbor and displayed a spindle-shape, fibroblast-like morphology. (2) Compared with the control, the E-cad (300 µg/ml group) expression downregulated 2.98 fold (P < 0.05), and the Vim (300 µg/ml group) and α-SMA (200 µg/ml group) expression upregulated 4.46 fold and 3.55 fold (P < 0.05). There were significant differences between 100, 200, 300 µg/ml groups and the control group (P < 0.05). (3) In the test group, the percentage of wound-healing areas/wound areas were larger than those in control group (P < 0.05).

CONCLUSIONSSiO2 could induce EMT in human bronchial epithelial cells.

Bronchi ; cytology ; Cells, Cultured ; Epithelial Cells ; cytology ; drug effects ; Epithelial-Mesenchymal Transition ; drug effects ; Humans ; Silicon Dioxide ; adverse effects ; Stromal Cells ; cytology ; drug effects

The paper highlights the three key words:city, health and development.On the one hand, it is necessary to understand the city with systematic thinking, to focus on the health gap and health equity of different populations in the same city, and the continuous spectrum of health indicators or disease distribution in the same population.On the other hand, it is suggested to establish a "participatory governance" model in Healthy City development-government for health, to further promote the development of healthy cities.Finally, it briefly introduces the report of "Healthy City 2.0-Towards a Planet City" presented by Professor Hancock at the 23rd International Conference on Health Promotion of IUHPE, 2019 in New Zealand.

Objective To explore the changes of expression of uncoupling protein 2 (UCP2) in pressure overload induced failure myocardium in rats. Methods Male SD rats were randomized into 3 groups ( n = 15 each): abdominal aorta constriction ( AC) 20 weeks group ( H20w group) , sham operation group (SH20w group) and normal control group (N group). Twenty weeks later, myocardial function was evaluated by echocardiography and hemodynamic measurements. Mitochondria in ventricular tissue were isolated by centrifugation. Adenine nucleotide pools (ATP, ADP, AMP, PCr) in myocardium were measured by high performance liquid chromatography. The expression of UCP2 in mitochondria was detected by PT-PCR and Western blot analysis. Results Myocardial function was significantly decreased 20 weeks post-AC compared to SH20w group and N group. Myocardial ATP, ADP, AMP and PCr contents were also significantly decreased in H20w group than the other 2 control groups. The expression of UCP2 in myocardial mitochondria was significantly increased in H20w group and negatively correlated with ATP contents (r= -0.929,P<0. 01). Conclusions The expression of UCP2 was upregulated in pressure overload induced failure heart and might be responsible for decreased myocardial adenine nucleotide and energy metabolism disturbance in this model.

This article reports the results of tandem mass spectrometry and the mutation features of the ETFDH gene for an infant with multiple acyl-CoA dehydrogenase deficiency. The results of tandem mass spectrometry showed that C14 : 1, C8, C6, C10, and C12 increased. Exon sequencing was performed on this infant and his parents and revealed double heterozygous mutations in the ETFDH gene of the infant: c.992A>T and c.1450T>C. The former was inherited from his mother, and the latter was inherited from his father. c.1450T>C was shown to be the pathogenic mutation in the HGMD database. PolyPhen2, SIFT, and PROVEAN all predicted that the novel mutation c.992A>T might be pathogenic, and the mutant amino acids were highly conserved across various species. The findings expand the mutation spectrum of the ETFDH gene, and provide molecular evidence for the etiological diagnosis of the patient with multiple acyl-CoA dehydrogenase deficiency as well as for the genetic counseling and prenatal diagnosis in the family.
Base Sequence ; Electron-Transferring Flavoproteins ; genetics ; Exons ; Humans ; Infant, Newborn ; Iron-Sulfur Proteins ; genetics ; Male ; Multiple Acyl Coenzyme A Dehydrogenase Deficiency ; enzymology ; genetics ; Mutation ; Oxidoreductases Acting on CH-NH Group Donors ; genetics

Objective To clarify the impairment mechanisms of acute hyperglycemia in the first-phase insulin se-cretion in mice. Methods The mouse model of acute glucose toxicity was established by glucose infusion through jugular vein catheterization. The glucose and insulin levels were assessed by IPGTT and OGTT in the mice of acute hyperglycemia and control groups. The histology of pancreatic islets was observed using HE staining and the insulin granules and other cy-toplasmic organelles were observed by electron microscopy. Results The mouse model of acute hyperglycemia was suc-cessfully established. The IPGTT showed that the blood glucose level was decreased by 87% ( 10. 3 ± 0. 33 mmol/L vs. 19. 3 ± 1. 66 mmol/L) at 15 min in the acute hyperglycemia group compared with the control group. The OGTT showed that the blood glucose level was decreased by 85% (9. 8 ± 0. 31 mmol/L vs. 18. 16 ± 1. 01 mmol/L) at 30 min in the acute hy-perglycemia group compared with the control group. However, the peak values of insulin secretion were delayed in both IPGTT and OGTT. Insulin levels at 2. 8 and 16. 7 mmol/L glucose stimulation in the acute hyperglycemia group was de-clined by 46% and 67% than the control group, respectively (P<0. 05). Residual insulin content in isletβcells was de-clined by 49% at 2. 8 mmol/L and 94% at 16. 7 mmol/L glucose infusion than the control group (P<0. 05). The histolo-gy showed irregular structure of pancreatic islets in the acute hyperglycemia group. The electron microscopy revealed that the amount of insulin granules was decreased, and more cytoplasmic vacuoles and swollen mitochondria were observed. Conclusions Acute intravenous glucose load decreases insulin content of isletβcells, leading to decrease and delay of the first-phase insulin secretion.