Adult ; Aorta, Thoracic ; abnormalities ; surgery ; Heart Arrest, Induced ; Humans ; Male

To retrospectively analyze the clinical data of a child with congenital broncho-bile duct fistula(CBBF) in Guiyang Children′s Hospital in June 2019.A female, aged 7 years and 6 months old, patient presented cough with a large amount of yellow green mucus.The main clinical manifestation was recurrent pulmonary infection after birth.After the fistula was found by electronic bronchoscope, doctors cooperated with imaging department, anesthe-siology department and pediatric surgery department.After treatment, the child recovered and discharged.There are few reports on CBBF.This study suggested that, in view of the refractory pneumonia with recurrent pulmonary infection and yellow green sputum after birth, and that the effect of anti-infection treatment was poor, clinicians should pay attention to the CBBF, take bronchoscopy as soon as possible, and make early diagnosis by combining with imaging technology, thus formulating a reasonable diagnosis and treatment plan under multidisciplinary cooperation, so as to improve the diagnosis and treatment of this rare disease clinical diagnosis and treatment level, and reduce missed diagnosis and misdiagnosis as well.

This paper aimed to study phenylpropanoids of Tripterygium hypoglaucum. Twenty-four compounds were isolated from the 70% EtOH extracts of T. hypoglaucum by silica gel column chromatography, reversed phase column chromatography, gel column chromatography, preparative thin layer chromatography, and semi-preparative high performance liquid chromatography. Compounds 1-3 were three new phenylpropionds. Their structures were identified by ultraviolet spectrum, infrared spectroscopy, high resolution electrospray ionization mass spectrometry, and nuclear magnetic resonance data as: threo-2-(4-hydroxy-3-methoxyphenoxy)-3-(4-hydroxy-3-methoxyphenyl)-1,3-propanedol (1), erythro-2-(4-hydroxy-3-methoxyphenoxy)-3-(4-hydroxy-3-methoxyphenyl)-1,3-propanediol (2), erythro-3-(4-hydroxy-3,5-dimethoxyphenyl)-3-ethoxypropane-1,2-propanediol (3). Compounds 4-6, 9, 14, 15, 18, 19, and 21-24 were obtained from Tripterygium genus for the first time. The cytotoxicity assay of cancer cells suggested that compound 20 displayed cytotoxicity on the breast cancer 4T1 cells whose 50% inhibitory concentration was 125.60 μmol·L^-1.

OBJECTIVETo observe the expression of urotensin II (UII) on the lung of patients with pulmonary hypertension (PH) with congenital heart disease and investigate the meaning of this phenomenon.

METHODThirty eight patients with CHD were divided into three groups according to pulmonary arterial systolic pressure (PASP) measured in cardiac catheterization and surgery: normal pulmonary pressure group (N group, PASP < 30 mm Hg, n = 10), mild PH group (M group, PASP ≥ 30 mm Hg, n = 15), severe or moderate PH group (S group, PASP ≥ 50 mm Hg, n = 13). The expression of UII protein and UII mRNA in pulmonary arterioles were measured separately by immunohistochemical (IHC) analysis and in situ hybridization (ISH) analysis.

RESULT(1) The results of UIIIHC staining: The UII protein expression of group M was higher than that of group N (20.22 ± 3.58 vs. 14.34 ± 2.18, P < 0.01), but less than group S (20.22 ± 3.58 vs. 28.92 ± 3.22, P < 0.05). (2) The results of UIIISH mRNA staining were similar to IHC staining, the A value of group M was higher than group N (12.51 ± 2.02 vs. 8.85 ± 1.41, P < 0.05), less than that of group S(12.51 ± 2.02 vs. 25.35 ± 4.33, P < 0.01). (3) Correlation study: there was a positive correlation between the A values of UIIIHC and pulmonary hypertension (r = 0.64, P < 0.01, n = 38), a positive correlation between the A values of UIIISH and pulmonary hypertension (r = 0.58, P < 0.01, n = 38).

CONCLUSIONThere was the expression of Urotensin II protein and mRNA in the lung of pulmonary hypertension patients with congenital heart disease, and these expression may involve the formation of pulmonary hypertension of congenital heart disease.

Adolescent ; Blood Pressure ; Case-Control Studies ; Child ; Child, Preschool ; Female ; Heart Defects, Congenital ; complications ; metabolism ; physiopathology ; Humans ; Hypertension, Pulmonary ; etiology ; metabolism ; physiopathology ; Immunohistochemistry ; In Situ Hybridization ; Infant ; Lung ; metabolism ; physiopathology ; Male ; Pulmonary Artery ; metabolism ; physiopathology ; RNA, Messenger ; genetics ; metabolism ; Severity of Illness Index ; Urotensins ; genetics ; metabolism

12E7 Antigen ; Adolescent ; Adult ; Antigens, CD ; metabolism ; Biomarkers, Tumor ; metabolism ; Brain Neoplasms ; secondary ; Cell Adhesion Molecules ; metabolism ; Child ; Child, Preschool ; Diagnosis, Differential ; Extremities ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Infant ; Ki-67 Antigen ; metabolism ; Male ; Neuroectodermal Tumors, Primitive ; metabolism ; pathology ; Oncogene Proteins, Fusion ; metabolism ; Repressor Proteins ; metabolism ; Sarcoma, Ewing ; metabolism ; pathology ; Sarcoma, Synovial ; diagnosis ; metabolism ; pathology ; surgery ; Soft Tissue Neoplasms ; diagnosis ; metabolism ; pathology ; surgery ; Vimentin ; metabolism ; Young Adult

Objective: To observe the impact of cardiac contractility modulation (CCM) on myocardial remodeling in rabbit model of chronic heart failure (CHF) with its possible mechanism. Methods: Rabbit HF model was established by ascending aortic root ligation; the animals were divided into 3 groups: Sham group, the animals received thoracotomy without aortic ligation, HF group and HF+CCM group, the HF animals received CCM treatment for 4 weeks. n=10 in each group. Cardiac function was measured by echocardiography at 12 and 16 weeks in each group respectively; myocardial tissue fibrosis and pathological changes were examined by Masson staining; plasma BNP level was assessed by ELISA; protein expressions of collagen I, collagen II, MMP2,MMP9, TIMP1 and galectin-3 in myocardial tissue were determined by Western blot analysis. Results: ① By echocardiography: with 12 weeks treatment, compared with Sham group, HF group and HF+CCM group had increased LVESD, LVEDD and decreased LVFS, LVEF, all P<0.05; with 16 weeks treatment, compared with HF group, HF+CCM group had improved LVESD, LVEDD, LVEF and LVFS, all P<0.05. ② Pathological changes:compared with Sham group, HF group showed increased collagen content in myocardial tissue, P<0.05; CCM treatment could partially decrease collagen accumulation, P<0.05. ③ After 12 weeks treatment, compared with Sham group, HF group and HF+CCM group presented elevated plasma BNP level, P<0.05; after 16 weeks treatment, compared with HF group, HF+CCM group presented reduced plasma BNP, while it was still higher than that in Sham group, P<0.05. ④ By Western blot analysis: compared with Sham group, HF group demonstrated increased protein expressions of collagen I, collagen II, MMP2, MMP9, TIMP1 and galectin-3 in myocardial tissue; the above indexes were much lower in HF+CCM group while still higher than those in Sham group, all P<0.05. Conclusion: CCM could improve myocardial remodeling in rabbit model of CHF which might be related to down-regulated protein expressions of collagen I, collagen III, MMP2, MMP9, TIMP1 and galectin3 in myocardial tissue.

Objective To investigate the effect of BDNF on cell injuries, cell apoptosis especially, induced by 25-35 segment of β-amyloid protein (Aβ25-35) at condensed state in PC12 cells.Methods The viability of PC12 cells, the apoptosis of PC12 cells and the expressions of Bax and Bcl-2 were detected by MTT, Annexin V-PI staining and Western blotting, respectively. Trk B receptor inhibitor K252a (200 nmol/l) was employed to observe the mechanism of 50 ng/ml BDNF on Aβ25-35 (20 μmol/L)-induced cell injury. Results BDNF (50 ng/ml) could significantly prevent the decrease of cell viability and cell apoptosis, and the increase of Bax expression and the decrease of Bcl-2 expression induced by 20 μmol/L Aβ25-35, and prevent the increase of up-regulation of Bax/Bcl-2 ratio; and these effects were blocked by K252a (200 nmol/1). Conclusion BDNF can prevent Aβ25-35-induced cell injury, cell apoptosis especially, by binding to its specific receptor Trk B.

OBJECTIVEPrevious studies have shown that hydrogen sulfide (H2S) plays key roles in a number of biological processes, including vasorelaxation, inflammation, apoptosis, ischemia/reperfusion and oxidative stress, which are involved in the pathogenesis of myocarditis. This study aimed to examine the expression of cystathionine-γ-lyase(CSE)/H2S pathway in mice with viral myocarditis.

METHODSSix-week-old inbred male mice were randomly assigned to control (n=25) and myocarditis group (n=30). The myocarditis and the control groups were inoculated intraperitoneally with 0.1 mL 10-5.69TCID50/mL CVB3 or vehicle (PBS) alone respectively. Ten mice were sacrificed 4 and 10 days after injection. Blood and heart specimens were harvested for measuring the content of serum H2S and the H2S production rates in cardiac tissues. Heart sections were stained with hematoxylin and eosin. Immunohistochemisty was used to detect the CSE protein expression in the heart.

RESULTSIn the myocarditis group, the serum H2S content and H2S production rates in cardiac tissues were significantly higher than those in the control group 4 and 10 days after injection (P<0.05). The expression of CSE protein in the heart in the myocarditis group was also significantly higher than that in the control group (P<0.05).

CONCLUSIONSCSE and its downstream production H2S increase in mice with acute viral myocarditis. The increased expression of CSE/H2S pathway might be involved in the pathogenesis of viral myocarditis.

Animals ; Coxsackievirus Infections ; etiology ; Cystathionine gamma-Lyase ; analysis ; Enterovirus B, Human ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Hydrogen Sulfide ; metabolism ; Killer Cells, Natural ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Myocarditis ; etiology

OBJECTIVETo find a way to having higher bond strength on mottled enamel.

METHODSSixty mottled enamel first bicuspid teeth extracted from fifteen patients needing orthodontic force were prepared and divided into four groups. Group A was routine acid etched, group B was air abraded, group C was etched by clearfil liner self-etching primer, group D was air abraded and then etched by clearfil liner self-etching primer. Next the bond and resin were used. The shear bond strength was observed and compared. The data were analysed by SPSS 11.5 statistical package.

RESULTSThe shear bonding strength of group A was (2.247 +/- 0.261) MPa, group B was (5.374 +/- 0.469) MPa, group C was (4.345 +/- 0.401) MPa, group D was (5.791 +/- 0.636) MPa. The strengths of four groups were significantly different (P < 0.01). The adhesive remnant index (ARI) scores of the four groups had no significant difference.

CONCLUSIONIn clinic, using air abrasion surface preparation technique is an acceptable way to enhancing the shear bond strength before sticking the orthodontic bonding on dental fluorosis.

Acid Etching, Dental ; Dental Bonding ; Dental Stress Analysis ; Fluorosis, Dental ; Humans ; Orthodontic Brackets ; Resin Cements ; Shear Strength

The purpose of this study was to investigate the molecular genetic basis of A2 subgroup and identify the novel alleles at ABO locus in Chinese Han population. All seven exons and their flanking sequences, enhancer and promoter in the ABO gene of five samples from individuals with serological discrepancies were amplified by polymerase chain reaction (PCR); the PCR products were screened by directly sequencing; the haplotypes of exon 6 and 7 were analyzed by TOPO cloning sequencing. The results showed that five samples were identified as A2 or A2B subgroup by serological technology. The A201 and A205 alleles were confirmed in one A2B individual and one A2 individual, respectively. A novel A2 variant allele was identified in three A2B individuals. The two nucleotide acid alterations (467C > T and 539G > C) at the exon 7 resulting in two amino acid substitutions (P156L and R180P) in this novel allele were observed, when compared with A101 allele. It is concluded that the polymorphism of A2 allele is found to be relatively variable in Chinese population, and a novel A208 allele responsible for A2 subgroup is firstly reported.
ABO Blood-Group System ; genetics ; Alleles ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; China ; ethnology ; Female ; Fucosyl Galactose alpha-N-Acetylgalactosaminyltransferase ; genetics ; Genotype ; Humans ; Male ; Molecular Sequence Data ; Point Mutation