Shock caused by spontaneous rupture uterine vessels during puerperal period: a case report and literature review.

Hemoperitoneum caused by spontaneous rupture of uterine vessels during delivery is relatively rare in obstetric hemorrhage, and even rarer during the puerperal period. It can be life-threatening without timely diagnosis and treatment; therefore, the literature on this topic is very scarce. To explore its etiology and identify its diagnosis and treatment principle, we are reporting a case of shock caused by spontaneous rupture of uterine vessels admitted in our hospital. Its etiology is still unknown, its presenting symptoms are commonly unspecific, and its diagnosis is often made during the surgery. The rupture of uterine vessels during pregnancy should be differentiated from placental abruption, uterine rupture, placenta implantation through the uterus, and abdominal organ rupture. Active and timely operative intervention can prevent the mortality. This case stresses the need for careful post-delivery monitoring for revealed postpartum hemorrhage. We will discuss possible etiologies of uterine vessels rupture during pregnancy, associated imaging findings, and management options.

[Clinical characteristics of human adenovirus type 7 pneumonia and genetic characteristics of human adenovirus type 7].

Objective: To better understand the clinical features of human adenovirus type 7 (hAdV7) pneumonia and to identify whether there is a variation in the genome of the strain (CHN/BeiJing/2018) isolated during the small-scale epidemic. Method: Forty-two patients were diagnosed with hAdV7 pneumonia between October 27th, 2017 and February 28th, 2018. They were all males with an average age of (21±2) years. Demographic and clinical data were reviewed and analyzed in detail. The nucleic acid of the epidemic strain was extracted from a bronchoalveolar lavage fluid sample. Whole genome sequencing (WGS) was then performed and sequences were compared with other hAdV7 strains distributed globally. Phylogenetic tree analysis was conducted based on whole genome sequences of the epidemic strain. Results: Thirty-eight cases with hAdV7 pneumonia presented with influenza-like symptoms (90.5%) at the onset and 36 cases developed fever (85.7%), followed by cough (97.6%), expectoration (90.5%) and chest pain (28.6%). Five cases presented with tonsillitis(11.9%) and 4 had transient hemoptysis (9.5%), while 3 patients reported dyspnea (7.1%). Moist rales were only heard in 3 patients (7.1%). Notably elevated creatine kinase (CK) concentrations were observed in 8 patients (19.1%), but all returned to normal after treatment. Four cases developed hypoxemia (9.5%), but none of them progressed to respiratory failure or acute respiratory distress syndrome (ARDS). Chest CT imaging showed bilateral patchy parenchymal opacities with a random distribution with or without consolidation. Ten patients were co-infected with influenza virus (23.8%), while 32 patients developed atypical pneumonia (76.2%). Genomic analysis revealed that the strain isolated during this epidemic was 99% similar to the known hAdV7 strains (19BOVLB/Volgograd/Rus/2014 and 0901HZ/ShX/CHN/2009). Phylogenetic tree analysis suggested that the strain was closely related to the hAdV7 strain isolated in Jingmen China in 2012. Conclusions: Cases with hAdV7 pneumonia were generally mild. Symptomatic treatment was sufficient for a favorable prognosis. A good genome stability of the hAdV7 strain was observed, indicating that hAdV7 could remain stable for a long period and cause continuing sporadic cases and clusters.

The novel KIR3DS1*085 allele identified in a southern Chinese Han individual.

KIR3DS1*085 allele differs from the closest allele KIR3DS1*01301 at nucleotide 934 C>T in exon 5.

The full length genomic sequence of a novel HLA-A*24 allele, HLA-A*24:353, identified in a patient with hepatitis B infection.

HLA-A*24:353 differs from HLA-A*24:02:01 by an amino acid exchange glutamine to glutamate at position 316.

A novel HLA-A*24 allele, HLA-A*24:325, identified in a Chinese individual.

HLA-A*24:325 differs from A*24:02:01:01 by two nucleotide substitutions at position 411 and 412.

Identification and characterization of polymorphic microsatellite loci in the red-crowned crane.

We isolated and characterized microsatellite loci for the red-crowned crane (Grus japonensis) from a microsatellite-enriched database, which was obtained using high-throughput sequencing technology. We designed primer sets for 445 microsatellite loci and after initial screening, 34 loci were genotyped in 31 red-crowned cranes. The number of observed alleles ranged from 3 to 10. Observed and expected heterozygosities ranged from 0.197 to 0.935 and 0.453 to 0.887, respectively; the mean polymorphic information content was 0.663. Loci Lia10943, Lia60455, Lia48514, Lia62171, Lia1059, and Lia5286 deviated from expectation of the Hardy-Weinberg equilibrium; however, significant linkage disequilibrium was not observed among the 34 loci. Using these 34 markers, we successfully completed parental identification for 19 cranes. The probability of exclusion for 7 selected loci (Lia271333, Lia3745, Lia11091, Lia45761, Lia16468, Lia21909, and Lia22355) was >0.9977 and analyses with more loci increased the combination efficiency. These 34 markers were also proven to be efficient for individual identification. We recommend that this marker system be used in the systematic control of pedigree management and future genetic variation studies of red-crowned cranes.

Evaluation of remedial options for a benzene-contaminated site through a simulation-based fuzzy-MCDA approach.

A simulation-based fuzzy multi-criteria decision analysis (SFMCDA) method is developed for supporting the selection of remediation strategies for petroleum contaminated sites. SFMCDA integrates process modeling (using BIOPLUME III) and fuzzy ranking (based on fuzzy TOPSIS) into a general management framework, and can compare various remediation alternatives, in light of both cost-risk tradeoffs and uncertainty impacts. The proposed method is applied to a hypothetical contaminated site suffering from a benzene leakage problem. Six remediation alternatives are taken into consideration, including natural attenuation (NA), pump-and-treat (PAT), enhanced natural attenuation (ENA), and a number of their combinations. Six fuzzy criteria, including both cost and risk information, are used to compare different alternatives through fuzzy TOPSIS. The results demonstrates that the proposed method can help systematically analyze fuzzy inputs from contaminant transport modeling, cost implications and stakeholders' preferences, and provide useful ranking information covering a variety of decision-relevant remediation options for decision makers.

Determination of InN/Diamond Heterojunction Band Offset by X-ray Photoelectron Spectroscopy.

Diamond is not only a free standing highly transparent window but also a promising carrier confinement layer for InN based devices, yet little is known of the band offsets in InN/diamond system. X-ray photoelectron spectroscopy was used to measure the energy discontinuity in the valence band offset (VBO) of InN/diamond heterostructure. The value of VBO was determined to be 0.39 ± 0.08 eV and a type-I heterojunction with a conduction band offset (CBO) of 4.42 ± 0.08 eV was obtained. The accurate determination of VBO and CBO is important for the application of III-N alloys based electronic devices.

Altered insulin-mediated and insulin-like growth factor-1-mediated vasorelaxation in aortas of obese Zucker rats.

OBJECTIVE: Insulin and insulin-like growth factor-1 (IGF-1) have vasorelaxant effects in vivo, which is dependent on nitric oxide (NO) production. The aim of this study was to investigate the vasorelaxant responses mediated by insulin and/or IGF-1 in aortas of obese Zucker rats. METHODS: The thoracic aortas of eight lean and eight obese Zucker rats (6 months old) were isolated for vasorelaxation analysis. Insulin-induced and IGF-1-induced vasorelaxant responses were evaluated by the isometric tension of aortic rings in the organ bathes. The roles of phosphatidylinositol 3-kinase (PI3K) and nitric oxide synthase (NOS) in vasorelaxant responses were examined by treating selective inhibitors, such as wortmannin (an inhibitor of PI3K) and N (omega)-nitro-L-arginine methyl ester (L-NAME, a NOS inhibitor). In addition, the vascular responses to sodium nitroprusside (SNP), a direct vasodilator of vascular smooth muscle, were examined. RESULTS: The insulin-induced vasorelaxation in aortas of obese rats was significantly decreased, whereas the IGF-1-induced vasorelaxation was significantly increased, compared with that in lean rats. After the pre-administration of wortmannin or L-NAME, the altered insulin-induced or IGF-1-induced vasorelaxation was abolished. There was no significant difference in the SNP-induced vasorelaxation between lean and obese rats. CONCLUSION: Our findings suggested that the decreased insulin-mediated vasorelaxation in obese rats appeared to be counteracted by the increased IGF-1-mediated vasorelaxation. Furthermore, the NO-dependent pathway was involved in the altered vasorelaxant responses. However, the SNP-induced vasorelaxation was not changed in obese rats.

A promoter function of the CCCGGG Sma I recognition sequence and its specific role in determining p53 status and identifying DNA damaging agents.

The tumour suppressor p53 protein regulates many genes involved in cellular responses to DNA damage. To date, a common transcriptionally active DNA-binding site for p53 in vivo has not been identified. The pGL3-Basic vector contains a modified fire-fly luciferase cDNA designated luc+ and is designed for studying putative regulatory sequences as it lacks any known eukaryotic promoter sequences. We report here that the CCCGGG sequence, a Sma I site, in the cloning region of the pGL3-Basic vector can promote p53-dependent transcription of the luc+ gene. We have demonstrated, by electrophoretic mobility shift assay (EMSA), that human p53 is able to bind to the CCCGGG sequence in vitro. These data provide the first demonstration that the CCCGGG sequence is a transcriptionally active DNA-binding site for p53. Thus, the pGL3-Basic vector could be used as an indicator of p53 transcriptional activity, to determine the p53 status of cell lines and to identify DNA damaging agents that initiate the activation of p53. The CCCGGG sequence has been found to be present in a number of promoter regions of p53-regulated genes. This and the present study suggest that the CCCGGG sequence may be a consensus sequence recognized by p53 in vivo and may be used to identify genes whose expression may be controlled by p53.

Clinical application of NMP22 and urinary cytology in patients with hematuria or a history of urothelial carcinoma.

For evaluation of the clinical application of immunoassay for nuclear matrix protein 22 (NMP22 immunoassay) and urinary cytology for early diagnosis and detection of bladder cancer in patients with hematuria and/or a previous history of bladder cancer, 209 urine samples obtained from 137 patients presenting episodes of hematuria or a history of bladder cancer were assayed for NMP22 levels and/or prepared for cytology examination. Biopsy was performed when any visible tumor was identified during cystoscopy examination. The median NMP22 concentrations measured in samples taken from patients with active bladder cancer, from patients with a history of bladder cancer but no active disease, from patients with hematuria, and from healthy volunteers were 18.95, 5.45, 6.39, and 3.75 U/ml, respectively. The urinary NMP22 level recorded for patients with urothelial carcinoma was significantly higher than that noted for individuals without active disease. The sensitivity of the NMP22 assay and of urinary cytology in diagnosing bladder cancer was 69% and 67%, respectively. In contrast, the specificity of these two diagnostic modalities reached 72% and 93%, respectively. The NMP22 assay is slightly more sensitive but less specific than urinary cytology in detecting bladder cancer. This study indicates that determination of urinary NMP22 levels is a useful and noninvasive tool for the detection of bladder cancer because of its high sensitivity. The urinary NMP22 assay may be used as a first-line routine screening method; however, it cannot replace the use of urinary cytology because of its lower specificity.

Low levels of p53 are associated with resistance to tetrachlorodibenzo-p-dioxin toxicity in DBA/2 mice.

We show here that DBA/2 strain mice have a complex mutation/polymorphism in the promoter region of the Trp53 locus (the mouse p53 locus). This region has previously been shown to be essential for p53 expression. We further show that the DBA/2 mutation is associated with approximately fourfold lower p53 levels in thymocytes treated with the DNA-damaging agent etoposide in-vitro, and with relative resistance of these thymocytes to apoptosis induced by the DNA-damaging agent etoposide compared with C57BL/6 mice. When part of the promoter containing this mutation was inserted into a plasmid containing a luciferase reporter gene but lacking eukaryote promoter sequences and transfected into MCF-7 human breast cell line cells, the mean luciferase activity was slightly less with the DBA/2 than with the C57BL/6 promoter-reporter construct (p < 0.01). We found that DBA/2xC57BL/6 F2 hybrid mice with the DBA/2 genotype at the Trp53 locus were relatively resistant to tetrachlorodibenzo-p-dioxin toxicity, and this resistance was additive with resistance associated with the Ahr locus. DBA/2 mice are long-lived and do not have particularly high levels of cancer, suggesting either that they carry other compensatory tumour resistance alleles (such as Ahr(d)), or that, while there may be a p53 protein dosage effect for acute toxicity, lower than normal levels of p53 may still be sufficient to protect against cancer. In evolutionary terms, it may be better to maintain low levels of p53 in order to avoid death from acute toxicity, even at the expense of a higher incidence of cancer in later life.

The repair of large DNA adducts in mammalian cells.

This paper describes experiments involving the measurement of DNA damage and repair after treatment with 4-nitroquinoline 1-oxide (4NQO) or aflatoxin B1 (AFB1) epoxide in a number of mammalian cell cultures primarily associated with defects in the excision repair of UV-induced DNA damage. The results with transformed derivatives of XP cells belonging to different complementation groups showed that the extent of repair of 4NQO adducts at the N2 or C8 of guanosine did not correlate to the extent of repair reported by others after UV-irradiation. An examination of 4NQO repair in rodent UV-sensitive cell lines from different ERCC groups indicated that again there was little correlation between the extent of 4NQO and UV repair. However, regardless of complementation group those mutants that were defective in the repair of pyrimidine dimers and 6,4-photoproducts did exhibit a reduced ability to repair the 4NQO N2 guanosine adduct, whereas those mutants defective in pyrimidine dimer repair alone were able to repair this lesion as normal. In all of these cell lines there was a normal capacity to repair the 4NQO C8 guanosine adduct. Less extensive experiments involving AFB1 epoxide showed an XPC-transformed cell line was able to repair 40% of lesions after 6 h, whereas only 20% of repair is seen after UV. The rodent mutant V-C4 which belongs to the same ionising radiation group as irs2, was partially defective in repairing AFB1-induced damage. These experiments highlight the fact that although there are many commonalities between the repair of UV damages and lesions classed as large DNA adducts differences clearly exist, the most striking example here being the repair of the C8 guanosine 4NQO adduct which rarely correlates with a defect in UV repair.

The repair of 4-nitroquinoline-1-oxide induced DNA adducts in hypersensitive Chinese hamster mutants: lack of repair of UV induced (6-4) photoproduct correlates with reduced repair of adducts at the N2 of guanosine.

UV sensitive Chinese hamster mutants belonging to ERCC groups 1, 2 and 6 together with one cross-link- and one X-ray-sensitive mutant have been examined for sensitivity to 4-nitroquinoline-1-oxide (4NQO) and the ability to repair 4NQO adducts at the N2 and C8 of guanosine. Despite the fact that all of the mutants examined were hyper-sensitive to 4NQO there was little difference between the mutants V-H1, V-H4, V-C4 and UV61 and the parental cell lines as regards the ability to remove these lesions from bulk DNA. The UV5 and UV20 mutants were both defective in the ability to remove N2 guanosine adducts yet repaired the C8 guanine adduct as normal. The fact that the mutants V-H1, V-H4, V-C4 and UV61 are 4NQO sensitive but repair the above adducts suggests that either some other lesion(s) is responsible for increased toxicity in these mutants, or that some regions of the genome may not be repaired as effectively as bulk DNA in these mutants, or that the quality of the repair is less than in the parental cells. Clearly the inability to remove UV induced pyrimidine dimers and the (6-4) photoproduct associated with the UV5 and UV20 mutants correlates with the inability to repair 4NQO-N2 guanosine adducts. However, mutants capable of (6-4) photoproduct repair but not dimer repair (VH-1 and UV61) can repair this lesion. Hence it is possible that the same domains in these repair proteins are required for the recognition of (6-4) photoproduct repair and 4NQO-N2 guanosine adducts.(ABSTRACT TRUNCATED AT 250 WORDS)

[Relationship between HBcAg in the liver and mechanisms of chronic type B hepatitis HBVM in serum].

We detected the presence and distribution of HBcAg in the liver by immunohistochemistry (ABC method) and the presence of HBV-DNA in serum (spot hybridization) and anti-HBe in serum (ELISA) from 59 cases of hepatitis B hospitalized in our hospital, including 47 cases of CAH, 5 cases of CPH, and 7 cases of subacute fulminant hepatitis. 1. HBcAg in the liver was detected in 25 out of 47 cases (53%) of CAH, in 2 out of 5 cases of CPH and in 4 out of 7 cases of subacute fulminant hepatitis. The total percentage was 53% (31/59). 2. There was no positive correlation between HBV replication activity and liver disease activity (P greater than 0.05). Our results did not support the hypothesis that suggests a direct cytopathic effect of HBV. Oppositely, the fact was that the presence, the amount and the patterns of HBcAg in the liver, and the presence of HBV-DNA in serum were predominant in mild CAH compared with those in severe CAH, predominant in CAH without cirrhosis compared with those in CAH with cirrhosis. There was a tendency of inverse correlation between HBV replication activity and liver disease activity. The results above were in line with the concept that HBcAg expressed on the surface of infected hepatocytes may be relevant target for T lymphocyte cytotoxicity. The results have suggested that an immune response to HBV is present, leading to the destruction of most infected cells. 3. There was a positive correlation between HBV-DNA in serum and HBcAg in the liver (P less than 0.005), indicating that HBV-DNA in serum can represent HBV replication.(ABSTRACT TRUNCATED AT 250 WORDS)