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.

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.

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.

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.