Molecular epidemiological characteristics of the virus in 96 children with acute diarrhea in Changdu of Tibet, China. / 西藏昌都地区96ä¾‹å„¿ç«¥æ€¥æ€§è ¹æ³»ç— æ¯’åˆ†å­æµè¡Œç— å­¦åˆ†æž.

OBJECTIVES: To study the molecular epidemiological characteristics of the virus in children with acute viral diarrhea in Changdu of Tibet, China. METHODS: Fecal specimens were collected from 96 children with acute diarrhea who visited the People's Hospital of Changdu, Tibet, from November 2018 to November 2020 and were tested for adenovirus, norovirus, astrovirus, sapovirus, and rotavirus. Gene sequencing was performed for the genotypes of these viruses. RESULTS: The overall positive rate of the five viruses was 39% (37/96), among which astrovirus had the highest positive rate of 17%, followed by norovirus (9%), rotavirus (8%), adenovirus (7%), and sapovirus (5%). There was no significant difference in the positive rate of the five viruses among different age groups (P>0.05). Only the positive rate of astrovirus was significantly different among the four seasons (P<0.05). For adenovirus, 6 children had F41 type and 1 had C2 type; for norovirus, 6 had GⅠ.3 type, 1 had GⅠ.7 type, 1 had GⅡ.3 type, and 2 had GⅡ.4 Sydney_2012 type; HAstrV-1 type was observed in all children with astrovirus infection; for sapovirus, 1 child each had sporadic GⅠ.2, GⅠ.6, and GⅡ.1 sapovirus and 2 children had unknown type; 6 children had rotavirus G9[P8]. CONCLUSIONS: Astrovirus and norovirus are important pathogens in children with acute diarrhea in Changdu, Tibet. The positive rate of adenovirus, norovirus, astrovirus, sapovirus, and rotavirus is not associated with age, and only the positive rate of astrovirus has obvious seasonality. F41 type is the dominant genotype of adenovirus; GⅠ.3 is the dominant genotype of norovirus; HAstrV-1 is the dominant genotype of astrovirus; sporadic GⅠ.2, GⅠ.6, and GⅡ.1 are the dominant genotypes of sapovirus; G9[P8] is the dominant genotype of rotavirus.

A renal cell carcinoma with EWSR1-TFE3 fusion gene.

Both EWSR1 and TFE3 are well-known oncogenes. EWSR1 encodes an RNA-binding protein involved in multiple soft tissue tumors, including Ewing's sarcoma/peripheral neuroectodermal tumor, desmoplastic small round cell tumor, soft tissue clear cell sarcoma (malignant melanoma of soft parts), extraskeletal myxoid chondrosarcoma, and myxoid liposarcomas. TFE3 regulates both Golgi and lysosomal homeostasis and is rearranged in renal cell carcinoma (RCC), alveolar soft part sarcoma, epithelioid hemangioendothelioma, and perivascular epitheloid cell tumors (PEComas). In this report, we found a rare case of RCC with a fusion between 5' EWSR1 and 3' TFE3. The fusion product retained most functional motifs of TFE3. The oncogenic mechanism likely involves TFE3 overexpression through its juxtaposition with the regulatory elements of EWSR1 and its translocation to the nucleus, resulting in the deregulation of Golgi and lysosomal homeostasis. This is a second case of RCC containing EWSR1-TFE3 fusion.

Effect of open heart surgery with cardiopulmonary bypass on peripheral blood lymphocyte apoptosis in children.

Children undergoing cardiopulmonary bypass (CPB) operations have an increased risk for the development of immunosuppression and severe infection. Lymphocyte apoptosis plays an important role in regulating immune responses. This study aimed to investigate the effect of open heart surgery with CPB on peripheral blood lymphocyte (PBL) apoptosis and the possible mechanism of lymphocyte apoptosis in infants and young children. This study enrolled 20 consecutive infants and children as a CPB group and 20 age-matched children who underwent patent arterial duct closure without CPB as control subjects. Samples were taken from peripheral blood after induction of anesthesia (preoperatively) and again 24 h after the operations. The degree of apoptosis and the expression level of Fas (CD95) on PBL were measured using flow cytometry. The percentage of lymphocyte apoptosis significantly increased after surgery in both groups, but it was much higher in the children with CPB than in those without CPB (14.46%+/-4.83% vs. 7.33%+/-1.43%; p<0.01). The expression level of Fas in the individuals with CPB was significantly higher than in those without CPB (52.80%+/-8.80% vs. 37.82%+/-6.32%; p<0.01). As shown by the study findings, both surgical stress and CPB can induce PBL apoptosis, which may lead to lymphopenia after open heart surgery with CPB for infants and young children.

Comparison of effects of epigallocatechin-3-gallate on hypoxia injury to human umbilical vein, RF/6A, and ECV304 cells induced by Na(2)S(2)O(4).

Hypoxia is related to the etiology of numerous pathological disease states, such as the formation of tumors or diverse retinopathies. Epigallocatechin-3-gallate (EGCG), a potent polyphenolic antioxidant and antiangiogenic compound found in green tea, has been shown to suppress the growth of blood vessels necessary for the growth of tumors and the induction of retinopathies. However, only a few studies have been carried focusing on the protective effects of EGCG on hypoxia-induced injury of cultured endothelial cells. The present study investigated the effects of EGCG on Na(2)S(2)O(4)-induced hypoxic injury in three types of cultured endothelial cells, primary isolates of normal human umbilical vein endothelial cells (HUVECs), and two transformed endothelial cells lines, RF/6A and ECV304. Our results indicated that Na(2)S(2)O(4) inhibited the growth of HUVE, RF/6A, and ECV304 cells in a dose-dependent manner; EGCG also exerted inhibitory effects on the growth of the three cell types, but the toxicity of EGCG to HUVECs was less than to RF/6A and ECV304 cells. The viability of HUVE, RF/6A, and ECV304 cells treated with EGGC were the lowest at 24, 24, and 36 h, respectively, and the IC(50) of EGCG were 420 +/- 8.0, 125 +/- 7.1, and 75 +/- 5.1 microM, respectively. Furthermore, EGCG, an efficient nontoxic agent, protected all three cell types from Na(2)S(2)O(4)-induced hypoxia injury, providing partial protection from hypoxia-induced injury in normal endothelial cells at 100, 30, and 10 microM for HUVE, RF/6A, and ECV304 cells, respectively.

Interleukin 10.G microsatellite in the promoter region of the interleukin-10 gene in severe sepsis.

BACKGROUND: The highly polymorphic interleukin 10.G (IL10.G) microsatellite located in the promoter region of the interleukin-10 (IL-10) gene exerts a positive transcriptional regulatory effect on IL-10 gene expression and correlates with the in vitro IL-10 secretion. This study was conducted to investigate whether IL10.G microsatellite is associated with the incidence and/or the outcome of severe sepsis. METHODS: One hundred and fifteen patients with severe sepsis who had been treated at the intensive care unit of the university hospital were studied. One hundred and forty-one healthy individuals served as controls. IL10.G microsatellite genotyping was performed with the following two methods: fluorescent based polymerase chain reaction (PCR) techniques and silver staining of the amplified DNA fragment in polyacrylamide gel. Alleles were defined according to the size of the amplified DNA product. RESULTS: Ten alleles and 36 genotypes were detected both in the patients with severe sepsis and in the healthy controls. Allele IL10.G9 and allele IL10.G13 were the commonest alleles with the frequencies of 32.6% and 21.3% respectively in the patients with severe sepsis, and 34% and 27% respectively in the healthy controls. The allele frequencies of IL10.G microsatellite were neither different between the patients with severe sepsis and the healthy controls (P > 0.05), nor between survivors and non-survivors (P > 0.05). However, the frequency of one common allele IL10.G13 was slightly lower in the patients with severe sepsis than in the healthy controls (21.3% vs 27%, P > 0.05), and the frequency of allele IL10.G9 was slightly higher in the non-survivors than in the survivors (37.1% vs 28.1%, P > 0.05). CONCLUSION: IL10.G microsatellite may neither contribute to the susceptibility to severe sepsis nor to the fatal outcome of severe sepsis.