We performed a case-control study of diarrhoea to determine its causes in children less than 1 year old in Guangzhou, People's Republic of China, in April to September 1989. Stools were cultured for Salmonella, Shigella, Campylobacter and vibrios by standard techniques; rotavirus (RV) was identified by polyacrylamide gel electrophoresis; and specific deoxyribonucleic acid probes were used to identify Escherichia coli containing genes coding for Shiga-like toxin I and II, enteropathogenic E. coli adherence factor, and enteroinvasive E. coli (EIEC). E. coli isolates were tested for heat-labile toxin (LT) and heat-stable toxin (ST) production and mannose-resistant adherence to HeLa cells. Rotavirus was identified in 13 of 174 children with diarrhoea (cases) and in 2% of 174 age-matched children without diarrhoea (controls), P less than 0.001. C. jejuni was identified in 10% of cases and 2% of controls, P = 0.003. Giardia lamblia was identified in 4 cases, LT and ST enterotoxigenic E. coli (ETEC) in 2, and S. flexneri in 1 case; they were not found in controls. ETEC that produced LT only was isolated from 5 cases and 3 controls, P = 0.721; E. coli that adhered to HeLa cells in a diffuse pattern was isolated from 30 cases and 40 controls, P = 0.229; and E. coli that adhered in an aggregative pattern was isolated from 20 cases and 18 controls, P = 0.863. EIEC was not isolated from cases or controls. Nine cases (5%) developed persistent diarrhoea (greater than 14 d duration). C. jejuni and aggregative E. coli were isolated from different children with persistent diarrhoea.(ABSTRACT TRUNCATED AT 250 WORDS)

: ST8Sia II (STX) is a highly homologous mammalian polysialyltransferase (polyST), which is a validated tumor-target in the treatment of cancer metastasis reliant on tumor cell polysialylation. PolyST catalyzes the synthesis of α2,8-polysialic acid (polySia) glycans by carrying out the activated CMP-Neu5Ac (Sia) to N- and O-linked oligosaccharide chains on acceptor glycoproteins. In this review article, we summarized the recent studies about intrinsic correlation of two polybasic domains, Polysialyltransferase domain (PSTD) and Polybasic region (PBR) within ST8Sia II molecule, and suggested that the critical amino acid residues within the PSTD and PBR motifs of ST8Sia II for polysialylation of Neural cell adhesion molecules (NCAM) are related to ST8Sia II activity. In addition, the conformational changes of the PSTD domain due to point mutations in the PBR or PSTD domain verified an intramolecular interaction between the PBR and the PSTD. These findings have been incorporated into Zhou’s NCAM polysialylation/cell migration model, which will provide new perspectives on drug research and development related to the tumor-target ST8Sia II.

The microbial spectrum in patients with urinary stones had a complex pattern. The uropathogens showed marked multidrug resistance and a large proportion of the uropathogens were able to produce β-lactamase.

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Acute graft-versus-host disease (GVHD) is an uncommon but often fatal complication following liver transplant. We describe a GVHD case in which a female patient with primary biliary cirrhosis underwent a living-related liver transplant from her son. The human leukocyte antigen typing of the donor was homozygous at all loci. The recipient's human leukocyte antigen type was haplo-identical to that of the donor. A bone marrow aspirate performed for pancytopenia revealed a severely hypoplastic marrow. Fluorescent in situ hybridization (FISH) using X-and Y-chromosome probes demonstrated that 80% of marrow cells were of donor origin. Comparison of Giemsa-stained cell morphology and FISH showed that the erythroid precursor cells were predominantly of male pattern (XY). This report is one of only a few studies that prove the migration of a donor's hematopoietic stem cells to a recipient's bone marrow. We demonstrated that FISH analysis using sex chromosome probes is useful to confirm a diagnosis of GVHD following organ transplantation from a donor of the opposite sex. We also showed that donor hematopoietic stem cells in a liver graft can migrate to the recipient's bone marrow. We suggest that FISH is a rapid and reliable test for confirming the diagnosis of GVHD in a peripheral blood or skin biopsy sample. (J Mol

Numerous differentially expressed circular RNAs (circRNAs) have been identified; however, their roles have not been fully elucidated. Since dysregulated circRNAs may have clinical applications, it is vital to study their expression characteristics, function, and mechanism in prostate cancer cells. The role, regulatory mechanism, and expression of hsa_circ_0075542 were analyzed using quantitative reverse transcription polymerase chain reaction. The results indicated that the expression of hsa_circ_0075542 was downregulated in prostate tumor tissues. The functions of prostate cancer cell lines LNCaP and PC3 cells were assessed using cell counting kit-8 and transwell assays and flow cytometry analysis. The results of the functional experiments showed that overexpression of hsa_circ_0075542 suppressed cell proliferation, reduced migration and invasiveness capabilities, and promoted apoptosis. Moreover, hsa_circ_0075542 targeted the microRNA-1197 (miR-1197) homeobox C11 (HOXC11) axis by sponging miR-1197. Overexpression of miR-1197 played a tumor-promoting role. Overexpression of hsa_circ_0075542 alleviated the tumor-promoting effect of miR-1197 overexpression In conclusion, hsa_circ_0075542 suppressed malignant characteristics and promoted apoptosis in LNCaP and PC3 cells by acting as a competing endogenous RNA of miR-1197. The hsa_circ_0075542/miR-1197 axis might play a role via HOXC11.

PurposeThis study aims to characterize the wild-type staphylococcal enterotoxin A (SEA)-producing Staphylococcus aureus.Materials and methodsWe identified 29 wild-type sea-positive S. aureus isolates from dairy and meat samples, as well as from patients, measured the amount of SEA produced under favorable cultivation conditions using enzyme-linked immunosorbent assay and sea mRNA transcriptional level and investigated the phage type as well as genetic diversity by means of pulsed-field gel electrophoresis and multilocus sequence typing.ResultsAmong 29 sea-positive isolates, 22 were from food sources (including one outbreak case) and seven from clinical patients. Five enterotoxin gene profiles, namely, sea (14 isolates), sea+sec (9 isolates), sea+seb (4 isolates), sea+seb+sec (1 isolate) and sea+seb+sed (1 isolate), were identified. Multilocus sequence typing generated sequence type (ST)1 (13 isolates), ST6 (5 isolates), ST59 (3 isolates), ST239 (3 isolates), ST5 (2 isolates), ST188 (2 isolate) and ST15 (1 isolate). The amount of SEA per 108 colony-forming unit (CFU) after 24 h of incubation was 1.1–33.5 (mean, 8.74; SD, 7.7) ng/108 CFU. The amount of SEA per hour incubation in the log growth phase was 0.1–12.0 (mean, 2.37; SD, 3.06) ng/108 CFU. Overall, 54.2% of SEA was produced in the log growth phase. Both the transcriptional level of sea mRNA and the amount of SEA in the log growth phase correlated well with the amount of SEA after 24 h of cultivation. Four isolates, namely, SA-212, SA-217, SA-340 and SA-341, were categorized to be of high SEA production (877–1,109 ng/mL, 24 h). The total amount of SEA was mainly based on the amount of SEA in 108 CFU, not the relatively fixed bacterial cell counts (21.1–43×108 CFU/mL). Seven isolates from patients all carried the ФMu3A phage, whereas 21 of the 22 isolates from the environmental sources all carried the ФSa3ms phage.ConclusionThe present study exhibits varied SEA production capacity of the wild sea-positive S. aureus strains. An apparent boundary in phage types between strains from the clinical samples and strains from the environment was also identified.

MYC-driven medulloblastomas are highly aggressive childhood brain tumors, however, the genetic events triggering MYC amplification and malignant transformation remain elusive. Here we report that mutations in CTDNEP1, a CTD nuclear-envelope-phosphatase, are the most significantly enriched recurrent alterations in MYC-driven medulloblastomas, and define high-risk subsets with poorer prognosis. CTDNEP1 ablation transforms murine cerebellar progenitors into MYC-amplified medulloblastomas, resembling their human counterparts. CTDNEP1 deficiency stabilizes MYC protein by elevating MYC serine-62 phosphorylation, and triggers genomic instability with eventual MYC amplification and p53 loss. Further, phosphoproteomics reveals that CTDNEP1 post-translationally modulates the activities of key regulators for proper chromosome segregation and mitotic checkpoints including topoisomerase TOP2A and checkpoint kinase CHEK1. Co-targeting CHEK1 and MYC activities synergistically inhibits CTDNEP1-deficient MYC-amplified tumor growth and prolongs animal survival. Together, our studies identify CTDNEP1 acting as a tumor suppressor in highly aggressive medulloblastomas by maintaining homeostatic MYC levels and genomic stability, highlighting a CTDNEP1-dependent therapeutic vulnerability.