Laparoscopic partial cystectomy for a vesical leiomyoma

A 47-year-old woman presented with gross hematuria and urinary frequency for 6 months. The tumor located at the dome of bladder was resected by transurethral resectoscope. The pathology revealed leiomyoma; however, her symptoms did not improve after the endoscopic procedure. We performed transurethral mucosal incision for circumscribing the margin of tumor and transperitoneoscopic partial cystectomy to treat the patient successfully.     

Impact of diabetes mellitus, hypertension, and coronary artery disease on tooth extraction after nonsurgical endodontic treatment

Introduction

Limited prospective data are available on the long-term prognosis of teeth receiving nonsurgical root canal treatment (NSRCT) in patients with systemic diseases including diabetes mellitus (DM), hypertension (HT), and coronary artery disease (CAD). This prospective study aimed to elucidate the impact of systemic diseases on the risk of tooth extraction after NSRCT.

Methods

A total of 49,334 NSRCT teeth were randomly selected from databank in October 2003 and were followed for 2 years for tooth extraction after NSRCT. Cox proportional hazards model was used to estimate the risk of tooth extraction after NSRCT.

Results

Of the 49,334 teeth, 1592 (3.2%) were extracted during the 2-year follow-up period, yielding a 2-year tooth retention rate of 96.8%. We found that DM (hazard ratio [HR], 1.79), HT (HR, 1.75), and CAD (HR, 1.70) were significant risk factors for tooth extraction after NSRCT (all P values <.0001) in univariate Cox proportional analyses. After adjustment for age, gender, and tooth type in multivariate analyses, DM (HR, 1.29) and HT (HR, 1.18) remained as independent risk factors (both P values <.05). Simultaneous possession of 2 diseases of DM, HT, and CAD was a significant and robust predictor for an increased long-term risk of tooth extraction after NSRCT (P for trend <.001).

Conclusions

An increased risk of tooth extraction after NSRCT is significantly associated with DM, HT, and CAD individually. Moreover, the constellation of systemic disease burden also manifests the importance in addition to other potential confounders.     

Influenza A(H6N1) Virus in Dogs,Taiwan

We determined the prevalence of influenza A virus in dogs in Taiwan and isolated A/canine/Taiwan/E01/2014. Molecular analysis indicated that this isolate was closely related to influenza A(H6N1) viruses circulating in Taiwan and harbored the E627K substitution in the polymerase basic 2 protein, which indicated its ability to replicate in mammalian species.     

Verification of Design Spaces Developed at Subscale

Recent concerns about the applicability of design space boundaries developed on small scale to commercial manufacturing processes have been raised by regulators worldwide. These concerns center around the scalability of unit operations and their corresponding process parameters, and the impact this has on the desired attributes of the drug substance or product. Requests have been made to verify design space boundaries with data generated at commercial scale. Because it is not always feasible to manufacture large-scale batches, alternative approaches to verification are necessary. The following article discusses various science-based strategies that could be used to verify design space boundaries. These approaches balance the requirements to address regulatory concerns and ensure that quality standards are maintained for both drug substances and products, within the operating constraints currently facing the pharmaceutical industry.     

Capsaicin inhibits preferentially the NADH oxidase and growth of transformed cells in culture.

A hormone- and growth factor-stimulated NADH oxidase of the mammalian plasma membrane, constitutively activated in transformed cells, was inhibited preferentially in HeLa, ovarian carcinoma, mammary adenocarcinoma, and HL-60 cells, all of human origin, by the naturally occurring quinone analog capsaicin (8-methyl-N-vanillyl-6-noneamide), compared with plasma membranes from human mammary epithelial, rat liver, normal rat kidney cells, or HL-60 cells induced to differentiate with dimethyl sulfoxide. With cells in culture, capsaicin preferentially inhibited growth of HeLa, ovarian carcinoma, mammary adenocarcinoma, and HL-60 cells but was largely without effect on the mammary epithelial cells, rat kidney cells, or HL-60 cells induced to differentiate with dimethyl sulfoxide. Inhibited cells became smaller and cell death was accompanied by a condensed and fragmented appearance of the nuclear DNA, as revealed by fluorescence microscopy with 4',6-diamidino-2-phenylindole, suggestive of apoptosis. The findings correlate capsaicin inhibition of cell surface NADH oxidase activity and inhibition of growth that correlate with capsaicin-induced apoptosis.     

Concordance of a point mutation 5' to the G gamma globin gene with G gamma beta +. Hereditary persistence of fetal hemoglobin in the black population

Hereditary persistence of fetal hemoglobin (HPFH) is a genetically heterogeneous and clinically benign condition characterized by persistent expression of fetal hemoglobin (Hb F) into adulthood. In the G gamma beta + type, no major deletions in the globin gene cluster occur; adult heterozygotes produce approximately 20% Hb F, which results from overproduction of G gamma chains, with no apparent increase in production from the adjacent A gamma gene. We have recently described a point mutation 202 base pairs 5' to the cap site of the G gamma gene in an individual with G gamma beta + HPFH. This mutation abolishes a normal ApaI restriction endonuclease site, and thus can be detected by blotting of genomic DNA. We present here further data on the ApaI mutation: (1) It occurs in six of seven families with G gamma beta + HPFH. (2) In three families, detailed haplotype analysis using 11 polymorphic restriction sites in the beta globin cluster has been done. The two that carry the missing ApaI site are identical but the third, which has a normal ApaI pattern, differs from the other two in at least two sites, one of which is a new polymorphic Nco I site between the delta and beta globin genes. This suggests the possibility of a different HPFH mutation in the third family. (3) The haplotype of the G gamma beta + HPFH chromosome carrying the ApaI mutation is different from that of 108 beta A chromosomes of black individuals that have been tested. (4) The G gamma ApaI site is normal in 61 beta A and 109 beta S alleles from non-HPFH black individuals, including 22 who share the same haplotype for the intragenic G gamma, A gamma HindIII polymorphisms. These data add support to the possibility that the -202 mutation is actually causative of the G gamma beta + HPFH phenotype.