Objective To investigate the relationship between the endoscopic characteristics of chronic gastritis,duodenitis,peptic ulcer and their histopathologic findings in children,and explore the relationship between Helicobacter pylori(Hp) infection and the severity of histopathologic changes of gastroduodenal mucosa in children. Methods Three hundreds and sixty-six children with chronic upper gastrointestinal symptoms who were examined by gastroscopy were enrolled.The gastric and duodenal mucosal biopsy specimens of all the patients were studied histopathologically. ResultsTypes of chronic gastroduodenal diseases in all these patients were: chronic gastritis(n=206,56.3%),chronic gastritis combined with duodenitis(n=112,30.6%),chronic gastritis combined with peptic ulcer(n=48,13.1%).There was chronic inflammation in gastric mucosa and duodenal bulb mucosa in all the cases examined by histopathologic examination.Hp infection was found in 106 cases(28.96%).The gastric mucosal inflammation was more severe in those with Hp infection than those without(P0.05).The were significant differences in the incidences of inflammation activity,atrophia and nodulus lymphaticus of gastric mucosa between those with Hp infection and those without(P

Estimation of postmortem interval (PMI) is one of the difficult problems in forensic medicine. With the development of molecular biological techniques, DNA quantification methods were widely applied in estimating PMI. The postmortem degradation of DNA in different tissues and organs was discussed in this article and the recent DNA quantitative techniques being used for estimating PMI were reviewed. These techniques included single cell gel electrophoresis, Feulgen staining image analysis, flow cytometry.
Animals ; Cell Nucleus/metabolism* ; Comet Assay/methods* ; DNA/analysis* ; DNA Degradation, Necrotic ; Flow Cytometry ; Forensic Pathology ; Humans ; Image Processing, Computer-Assisted ; Kidney/pathology* ; Postmortem Changes ; Rosaniline Dyes ; Spleen/pathology* ; Temperature ; Time Factors

OBJECTIVETo study the relationship of the types of Helicobacter pylori (H. pylori) strains with the classification and the severity of chronic gastro-duodenal diseases in children.

METHODSOne hundred and fifteen children with chronic upper gastrointestinal symptoms who were diagnosed as H. pylori infection by gastroscopy were enrolled in this study. H. pylori strains were serotyped by immunoblot technique. The gastric biopsy specimens of all patients were studied histologically.

RESULTSType I H. pylori strains were confirmed in 84 cases (73.0%), intermediate type strains in 21 cases (18.3%), and type II strains in 10 cases (8.7%). Type I H. pylori strains infection caused a moderate gastric mucosal inflammation in 83 cases and a severe inflammation in 1 case. Intermediate type H. pylori strains infection caused a moderate gastric mucosal inflammation in 21 cases. Type II H. pylori strains infection caused a mild gastric mucosal inflammation in 2 cases and a moderate inflammation in 8 cases. Different types of H. pylori strains resulted in different severity of gastric mucosal inflammation (x2=15.444, P < 0.01). The gastric mucosal inflammation due to type I H. pylori strains was the most severe, while the inflammation due to type II H. pylori strains was relatively mild. The incidence of nodulus lymphaticus of gastric mucosa due to type I, type II and intermediate type H. pylori strains infection was 76.2%, 47.6% and 40.0%, respectively (x2=10.171, P < 0.01). The classification of chronic gastro-duodenal diseases was not associated with the types of H. pylori strains.

CONCLUSIONSType I strains were the leading cause of H. pylori infection in children. All of types of H. pylori strains can cause pathohistologic changes of gastric mucosa. Type I H. pylori strains infection can result in the most severe gastric mucosal inflammation and the highest incidence of nodulus lymphaticus. The immunoblot serotyping of H.pylori strains may be useless for the classification of chronic upper gastrointestinal diseases but it is helpful for the evaluation of the severity of the diseases in children.

Adolescent ; Antibodies, Bacterial ; blood ; Antigens, Bacterial ; genetics ; Bacterial Proteins ; genetics ; Child ; Child, Preschool ; Chronic Disease ; Female ; Gastric Mucosa ; pathology ; Gastrointestinal Diseases ; microbiology ; pathology ; Helicobacter Infections ; complications ; diagnosis ; Helicobacter pylori ; classification ; Humans ; Male

OBJECTIVESTo investigate the relationship between chromosome balanced translocation t(1;12) (q24;q24) and spermatogenesis in infertile twin brothers.

METHODSFor twin brothers, karotype were determined. The levels of testosterone, FSH and LH were detected. YRRM1, DAZ and DYS240 were analyzed. In younger brother a biopsy was taken from testis.

RESULTSChromosome analysis for both twin brothers revealed a karotype of 46, XY, t(1;12) (q24;q24). Sperm count was less than 1.0 x 10(6)/ml. There was no deletion for YRRM1, DAZ and DYS240 gene on Y chromosome. Photomicrograph of seminiferous tubules showed the arrest of spermatogenesis.

CONCLUSIONSChromosome balanced translocation t(1;12) (q24;q24) may be the cause of the spermatogenesis arrest in infertile twin brothers. Gene in the point of translocation may be related to spermatogenesis.

Adult ; Biopsy ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 12 ; Diseases in Twins ; genetics ; Humans ; Infertility, Male ; genetics ; Male ; Spermatogenesis ; genetics ; Testis ; pathology ; Translocation, Genetic ; genetics

This study was purposed to explore the correlation of CXCR4, CCR1, CCR2 expression with curative effect of multiple myeloma (MM). Flow cytometry was used to detect the expressions of CXCR4, CCR1, CCR2 on cell surface of bone marrow from 48 newly diagnosed MM patients. These patients were divided into two groups: one group with expression of chemokine receptor (group I) and another group without expression of chemokine receptor (group II). The group I was consisted of 34 patients, but 3 out of them could not be continuously followed up. The group II was consisted of 14 patients. The MM patients of 2 groups were treated with chemotherapeutic drugs for 3 and 6 months, the curative efficacy of 2 groups were compared. The results showed that after treating for 3 and 6 months the effective rates of group I and group II were 80.6% (25/31) vs 50% (7/14) and 83.9% (26/31) vs 50% (7/14) respectively, which suggested that curative efficacy of group I was better than that of group II (p < 0.05). It is concluded that CXCR4, CCR1, CCR2 may be used as indexes for evaluating curative effect of MM patients.
Adult ; Aged ; Aged, 80 and over ; Female ; Flow Cytometry ; Humans ; Male ; Middle Aged ; Multiple Myeloma ; drug therapy ; metabolism ; Receptors, CCR1 ; metabolism ; Receptors, CCR2 ; metabolism ; Receptors, CXCR4 ; metabolism ; Treatment Outcome

Mycoplasma infection is the most prevalent contamination in cell culture. Analysis of cell culture in laboratories from different countries shows that mycoplasma contamination ranges from 15% to 80% and, in some cases, even reaches 100% (Chernov et al., 2014). Whilst mycoplasma infection is not visible to the naked eye in cell culture, the consequences of mycoplasma contamination have been shown to induce a number of cellular changes, for example, increased resistance to chemotherapeutic drugs. Therefore, any results obtained from tissue culture studies, in the presence of mycoplasma contamination, potentially render the data invalid (Kim et al., 2015; Gedye et al., 2016). As such, mycoplasmas are not harmless bystanders and cannot be ignored in in vitro studies.
Arginine/pharmacology* ; HEK293 Cells ; Humans ; Mycoplasma/isolation & purification* ; Plasmids ; Transfection

The aim of this study was to investigate the effects of H3K27 methylation inhibitor EPZ005687 on the apoptosis, proliferation and cell cycle of U937 cells and normal CD34⁺ cells. The U937 cells and normal CD34⁺ cells were treated with different concentration of EPZ005687 at different time points. The apoptosis rate was determined by Annexin V/PI staining. The cell proliferation and cell cycle was determined using WST-1 assay and 7-AAD assay, respectively. The activity of H3K27 methylation was detected by chemiluminescent immunoassay. The results showed that the EPZ005687 induced an obvious apoptosis of U937 cells. The apoptotic rate was 3.96% ± 0.79%,5.74% ± 0.73%,13.34% ± 1.77% and 25.24% ± 2.55% in U937 cells treated with 0.5, 1, 5 and 10 µmol/L EPZ005687 for 48 hours, respectively. However, EPZ005687 had rare effect on normal bone marrow(NBM) CD34⁺ cells. The apoptotic rate was 3.64% ± 0.62%,4.28% ± 0.99%,6.18% ± 1.19% and 7.56% ± 1.34% after U937 cells were treated with 0.5, 1, 5 and 10 µmol/L EPZ005687 for 48 hours, respectively. EPZ005687 inhibited obviously the proliferation of U937 cells but had weak effect on the proliferation of NBMCD34⁺ cells. The inhibitory effect of EPZ005687 on U937 cells was time-dependent after treated with 0.5, 1, 5 and 10 µmol/L EPZ005687 from 12 to 96 hours. EPZ005687 induced G1 phase blocking (G1%, 64.18% ± 13.27% vs 49.43% ± 12.54%) and decreased the percentage of cells in S phase (9.67% ± 2.61% vs15.26% ± 5.58%) in U937 cells. However, EPZ005687 had no effect on the cell cycle of NBMCD34⁺ cells. In addition, EPZ005687 produced obviously depletion of H3K27 methylation in U937 cells (P < 0.05), but hardly had effect on the H3K27 methylation of NBMCD34⁺ cells. It is concluded that the EPZ005687 inhibites proliferation, induces apoptosis and cell cycle blocking in G1 phase in leukemia cells. This agent may have potential value in clinical application.
Antigens, CD34 ; metabolism ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Humans ; Indazoles ; pharmacology ; Methylation ; Pyridones ; pharmacology ; U937 Cells

OBJECTIVE: To investigate the dynamic changes of macrophage numbers and apoptosis during Schistosoma japonicum infection, and to investigate the possible mechanisms of macrophage apoptosis induced by S. japonicum soluble egg antigen (SEA). METHODS: C57BL/6 mice at ages of 6~8 weeks were randomly divided into 4 groups, including three experimental groups and a normal control group. Each mouse in the experimental groups was infected with (12 ± 1) cercariae of S. japonicum via the abdominal skin, and all mice in an experimental group were sacrificed 3, 5, 8 weeks post-infection, respectively, while mice in the control group were not infected with S. japonicum cercariae and sacrificed on the day of S. japonicum infection in the experimental group. Mouse liver specimens and peritoneal exudation cells were sampled in each group, and the dynamic changes of macrophage numbers and apoptosis were detected. Mouse peritoneal macrophages were isolated, purified and treated with S. japonicum SEA, PBS and ovalbumin (OVA) in vitro, and the macrophage apoptosis was detected using flow cytometry. The mRNA and protein expression of BCL-2 protein family members were determined in macrophages using real-time quantitative PCR (qP-CR) and Western blotting assays, and the activation of caspase 3 was determined using flow cytometry and Western blotting. In addition, macrophages were in vitro treated with S. japonicum SEA in presence of a caspase inhibitor, H₂O₂ or N-acetyl-L-cysteine, and the apoptosis of macrophages was detected using flow cytometry. RESULTS: The total macrophage numbers continued to increase in mouse liver [(0.873 ± 0.106) × 106, (2.737 ± 0.460) × 10⁶ and (3.107 ± 0.367) × 10⁶ cells, respectively; F = 81.900, P < 0.01] and peritoneal specimens [(5.282 ± 1.136) × 105, (7.500 ± 1.200) × 10⁵ and (12.800 ± 0.800) × 10⁵ cells, respectively; F = 55.720, P < 0.01] 3, 5 and 8 weeks post-infection with S. japonicum, and the numbers of apoptotic macrophages also continued to increase in mouse liver [(0.092 ± 0.018) × 10⁶, (0.186 ± 0.025) × 10⁶ and (0.173 ± 0.0270) × 10⁶ cells; F = 57.780, P < 0.01] and peritoneal specimens [(0.335 ± 0.022) × 10⁵, (0.771 ± 0.099) × 10⁵ and (1.094 ± 0.051) × 10⁵ cells; F = 49.460, P < 0.01] 3, 5 and 8 weeks post-infection with S. japonicum. The apoptotic rate of SEA-treated macrophages [(24.330 ± 0.784)%] was significantly higher than that of PBS-[(18.500 ± 1.077)%] and OVA-treated macrophages [(18.900 ± 1.350)%] (both P values < 0.01). There were no significant differences in the mRNA or protein expression of Bcl-2 [Bcl - 2 mRNA expression: (1.662 ± 0.943) vs. (1.000 ± 0.000), t = 1.215, P > 0.05; BCL protein expression: (0.068 ± 0.004) vs. (0.070 ± 0.005), t = 0.699, P > 0.05], Bax [Bax mRNA expression: (0.711 ± 0.200) vs. (1.000 ± 0.000), t = 2.507, P > 0.05; BAX protein expression: (0.089 ± 0.005) vs. (0.097 ± 0.003), t = 2.232, P > 0.05] and Bak [Bak mRNA expression: (1.255 ± 0.049) vs. (1.00 ± 0.00), t = 0.897, P > 0.05; BAK protein expression: (0.439 ± 0.048) vs. (0.571 ± 0.091), t = 2.231, P > 0.05] between in SEA- and PBS-treated macrophages. S. japonicum SEA induced macrophage apoptosis in the presence of a caspase inhibitor (F = 0.411, P > 0.05); however, SEA failed to induce macrophage apoptosis in the presence of H₂O₂ or NAC (F = 11.880 and 9.897, both P values < 0.05). CONCLUSIONS S. japonicum SEA may induce macrophage apoptosis through promoting reactive oxygen species expression during S. japonicum infections in mice.
Animals ; Apoptosis ; Caspases ; Hydrogen Peroxide ; Macrophages ; Mice ; Mice, Inbred C57BL ; RNA, Messenger ; Schistosoma japonicum ; Schistosomiasis japonica ; bcl-2-Associated X Protein