No abstract

Introduction Penile prosthesis infections remain challenging despite advancements in surgical technique, device improvements, and adoption of antibiotic prophylaxis guidelines. Aim To investigate penile prosthesis infection microbiology to consider which changes in practice could decrease infection rates, to evaluate current antibiotic prophylaxis guidelines, and to develop a proposed algorithm for penile prosthesis infections. Methods This retrospective institutional review board–exempt multi-institutional study from 25 centers reviewed intraoperative cultures obtained at explantation or Mulcahy salvage of infected three-piece inflatable penile prostheses (IPPs). Antibiotic usage was recorded at implantation, admission for infection, and explantation or salvage surgery. Cultures were obtained from purulent material in the implant space and from the biofilm on the device. Main Outcome Measures Intraoperative culture data from infected IPPs. Results Two hundred twenty-seven intraoperative cultures (2002–2016) were obtained at salvage or explantation. No culture growth occurred in 33% of cases and gram-positive and gram-negative organisms were found in 73% and 39% of positive cultures, respectively. Candida species (11.1%), anaerobes (10.5%) and methicillin-resistant Staphylococcus aureus (9.2%) constituted nearly one third of 153 positive cultures. Multi-organism infections occurred in 25% of positive cultures. Antibiotic regimens at initial implantation were generally consistent with American Urological Association (AUA) and European Association of Urology (EAU) guidelines. However, the micro-organisms identified in this study were covered by these guidelines in only 62% to 86% of cases. Antibiotic selection at admissions for infection and salvage or explantation varied widely compared with those at IPP implantation. Conclusion This study documents a high incidence of anaerobic, Candida, and methicillin-resistant S aureus infections. In addition, approximately one third of infected penile prosthesis cases had negative cultures. Micro-organisms identified in this study were not covered by the AUA and EAU antibiotic guidelines in at least 14% to 38% of cases. These findings suggest broadening antibiotic prophylaxis guidelines and creating a management algorithm for IPP infections might lower infection rates and improve salvage success.

Secretogranin II (previously also called chromogranin C) is a member of the chromogranins/secretogranins which occur in secretory granules of a wide variety of peptidergic endocrine and neuronal cells (1). As a step towards elucidating the as yet unknown function of secretogranin II, we report here its complete primary structure deduced from.sequences of rat secreto$ranin II cDNA clones. These were isolated from a PC12 cell XgtlO library (indly donated by Dr. P. Seeburg) by using partial bovine and human secretogranin II cDNAs, obtained after oligonucleotide screening and identified on the basis of peptide sequence homologies (Gerdes et al., unpublished), as probes. Rat pre-secretogranin II is 619 amino acids long, very acidic and hydrophilic, contains nine potential dibasic cleavage sites (Figure, underlined letters) for the generation of smaller, perhaps biologically active peptides, and lacks the disulphide-bonded loop structure conserved in chromogranins A and B (2).

No abstract

A cosmid clone containing the gene for mouse chromogranin B (secretogranin I), a secretory protein found in secretory granules of most endocrine cells and neurons, was isolated and sequenced. The chromogranin B protein was found to be encoded by 5 exons which correspond to the cleaved signal peptide, the short N-terminal sequence preceding the disulfide-bonded loop structure, the disulfide-bonded loop structure itself, the large, variable region comprising -90% of the protein, and the conserved C-terminal sequence. The promoter region of the chromogranin B gene is very GC-rich and contains a CATAA motif, a CAMP-responsive element and an Spl binding site.

We tested the value of the activity (AI) and chronicity (CI) indices devised by Austin et al as predictors of outcome in lupus patients with diffuse proliferative glomerulonephritis (DPGN). Four renal pathologists independently scored the AI and CI on 84 renal biopsy specimens from patients with lupus DPGN followed for 109 +/- 74 weeks (mean +/- SD), and the mean score was compared to the development of renal failure and to adverse outcome (combined data for renal failure, death and predefined clinical stop points). Receiver operator characteristic curves were derived from a series of 2 x 2 tables in which one variable was renal failure or adverse outcome and the other variable was AI or CI dichotomized by a cut-off point. Over the entire range (0 to 10) of the CI there was no value that separated patients who developed renal failure from those who did not. The ROC curve analysis indicated that the sensitivity and specificity of the CI were too low to allow it to function as a good test. Once patients entering renal failure were identified, the mean CI approached but did not reach a significant difference when compared to the mean CI of those who did not go into renal failure (4.38 +/- 0.42, mean +/- SE vs. 3.19 +/- 0.23, P = 0.0620). The CI did not predict the adverse clinical outcomes. There was no cut-off value of the CI which separated patients who had an adverse outcome from those who did not, and this result was confirmed by ROC analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

The effects of conjugated equine estrogen and subsequent cyclical progestogen supplementation on lipoprotein and apolipoprotein A-I levels were investigated in three groups of postmenopausal women. Unopposed conjugated equine estrogen (0.625 mg) lowered total cholesterol 4-8% and low-density lipoprotein (LDL) cholesterol 12-19% below pre-treatment levels in all three groups. Levels of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I were increased 9-13 and 9-18%, respectively, with unopposed estrogen. The increase in HDL cholesterol was mainly due to increases in the high-density lipoprotein2 (HDL2) subfraction. Addition of medroxyprogesterone acetate, norethindrone acetate, or d,l-norgestrel at doses shown previously to provide protection against endometrial hyperplasia reversed some of the beneficial estrogen effects, reducing levels of HDL cholesterol 14-17%, HDL2 cholesterol 22-37%, and apolipoprotein A-I 11-15% from those obtained with unopposed estrogen. The LDL cholesterol levels fell 12-19% with unopposed estrogen but remained 7-12% below baseline when progestogens were added. These observations demonstrate that after 3 months of treatment, all three progestogens reversed some of the favorable effects of unopposed estrogen on lipoproteins but permitted a continued modest reduction in LDL cholesterol.