Predictors of Male Sexual Dysfunction in Urologic Chronic Pelvic Pain Syndrome (UCPPS), Other Chronic Pain Syndromes, and Healthy Controls in the Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network.

Background: Sexual dysfunction (SD), including erectile (ED) and ejaculatory dysfunction, is associated with diminished quality of life (QoL) in men with UCPPS (chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and/or interstitial cystitis/bladder pain syndrome (IC/BPS)).

Aim: We sought to compare SD among male patients with UCPPS, other chronic pain conditions (positive controls, PC), and healthy controls (HC) without chronic pain, and to evaluate the association of comorbidities, psychosocial factors, and urologic factors of SD in all 3 groups.

Methods: Baseline data from male UCPPS participants, PC (irritable bowel syndrome, chronic fatigue syndrome, fibromyalgia) and HC enrolled in the Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network Epidemiology and Phenotyping Study were included in the analysis.

Representation of Minority Groups in Key Pelvic Floor Disorder Trials.

Background: Multicenter randomized clinical trials on pelvic floor disorders (PFDs) support evidence-based care. However, many of these studies include homogenous study populations lacking diversity. Heterogeneous sampling allows for greater generalizability while increasing knowledge regarding specific subgroups.

Does Obtaining a Diagnosis of Interstitial Cystitis/Bladder Pain Syndrome Improve Symptoms or Quality of Life? A Cross-sectional Questionnaire-Based Study.

Objectives: The aim of this study was to investigate whether receiving a clinical diagnosis of interstitial cystitis (IC) or bladder pain syndrome (BPS) improves patients' symptoms, health-related quality of life (HRQOL), or ability to cope with their symptoms.

Methods: In this cross-sectional study, participants with self-reported IC/BPS completed an online questionnaire recalling their perceived change in symptoms after diagnosis and treatment. The questionnaire included demographic information, overall HRQOL measured on a visual analog scale (VAS), O'Leary-Sant Interstitial Cystitis Problem Index, the Urinary Impact Questionnaire, and questions regarding patient beliefs about diagnosis.

Vaginal Angiomyofibroblastoma: A Case Report and Review of Diagnostic Imaging.

Background: Angiomyofibroblastoma (AMFB) is a benign mesenchymal tumor most commonly found in the female genital tract of premenopausal women. Although rare, AMFB is an important consideration in the differential diagnosis of vulvar and vaginal masses, as it must be distinguished from aggressive angiomyxoma (AA), a locally recurrent, invasive, and damaging tumor with similar clinical and pathologic findings.

Case: We describe a patient with a 4 cm vaginal AMFB and the relevant preoperative radiographic imaging findings.

Oxidative Stress and its Implications for Future Treatments and Management of Alzheimer Disease.

Oxidative imbalance is one of the earliest manifestations of Alzheimer disease (AD) actually preceding the classic pathology of amyloid β deposits and neurofibrillary tangles. Clinical trials examining antioxidant modulation by a number of global interventions show efficacy, while simple supplementation has limited benefit suggesting complexity of multiple contributing factors. In this review, we highlight new insights regarding novel approaches to understanding and treating AD based on holistic views of oxidative balance including diet.

Physician knowledge of and adherence to the revised breast cancer screening guidelines by the United States Preventive Services Task Force.

Objective: We sought to assess knowledge and adherence to the revised US Preventive Services Task Force breast cancer screening guidelines among gynecologic care providers.

Study Design: This was a cross-sectional descriptive study based on a survey conducted among gynecologic care providers.

Results: Forty providers completed the survey (80%).

Sublethal RNA oxidation as a mechanism for neurodegenerative disease.

Although cellular RNA is subjected to the same oxidative insults as DNA and other cellular macromolecules, oxidative damage to RNA has not been a major focus in investigations of the biological consequences of free radical damage. In fact, because it is largely single-stranded and its bases lack the protection of hydrogen bonding and binding by specific proteins, RNA may be more susceptible to oxidative insults than is DNA. Oxidative damage to protein-coding RNA or non-coding RNA will, in turn, potentially cause errors in proteins and/or dysregulation of gene expression.

Iron: A Pathological Mediator of Alzheimer Disease?

Metal-catalyzed oxidation and free radical formation are potent mediators of cellular injury to every category of macromolecule found in vulnerable neuronal populations and are thought to play an early and central role in Alzheimer disease (AD) pathogenesis. While metal-binding sites are present in proteins that accumulate in AD, metal-associated redox activity is primarily noted with nucleic acids, specifically with cytoplasmic RNA. Iron dyshomeostasis in AD is thought to arise from haem breakdown and mitochondrial turnover, and a reduction in microtubule density in vulnerable neurons increases redox-active metals, initiating a cascade of events culminating in characteristic pathologic features.

Treatment advances in Alzheimer's disease based on the oxidative stress model.

Effective therapy for Alzheimer's disease (AD), up to this point, has been hampered by our inability to diagnose the disease in its early stages, before the occurrence of significant neurodegeneration and clinical symptoms. Because AD historically has been defined by neuropathologic criteria, treatment strategies have been aimed at diminishing the pathologic end result of the disease process, namely neurodegenerative changes associated with extracellular amyloid-beta-containing plaques, as well as intracellular neurofibrillary tangles of the hyper-phosphorylated microtubule protein, tau. While these avenues continue to be pursued, results thus far have been disappointing.

Evidence for the novel expression of human kallikrein-related peptidase 3, prostate-specific antigen, in the brain.

Human kallikrein-related peptidase 3 (hK3), also known as prostate-specific antigen (PSA), is a 33 kDa single chain glycoprotein belonging to the kallikrein family of serine proteases. With chymotrypsin-like enzymatic activity, hK3 is directly and indirectly involved in a number of diverse biological functions including male fertility, the regulation of cell proliferation, and the inhibition of angiogenesis. The gene encoding hK3, hKLK3, is located on chromosome 19 and its expression has been shown to be regulated by steroid hormones through androgen receptor-mediated transcription.

Menopause, estrogen, and gonadotropins in Alzheimer's disease.

For decades, Alzheimer's disease (AD) has been linked to aging, gender, and menopause. Not surprisingly, this led most investigators to focus on the role of estrogen. While undoubtedly important, estrogen is unlikely the key determinant of disease pathogenesis.

Prevention and treatment of Alzheimer disease and aging: antioxidants.

There is considerable evidence showing that oxidative damage is one of the earliest neuronal and pathological changes of Alzheimer disease and many, if not all, of the etiological and pathological causes of the disease are related, directly or indirectly, to free radical production and oxidative damage. Here we summarize the current body of knowledge suggestive that oxidative damage is, if not the key factor, certainly a major factor in Alzheimer disease. As such, therapeutic modalities encompassing antioxidants may be an effective approach to the treatment of neurodegenerative diseases and delay the aging process.

Nanoparticle iron chelators: a new therapeutic approach in Alzheimer disease and other neurologic disorders associated with trace metal imbalance.

Accumulating evidence suggests that oxidative stress may be a major etiologic factor in initiating and promoting neurodegeneration in Alzheimer disease. Contributing to this, there is a dyshomeostasis of metal ions in Alzheimer disease with abnormally high levels of redox-active metals, particularly iron, in affected areas of the brain. Although it is unclear whether metal excesses are the sole cause of oxidative stress and neurodegeneration or a by-product of neuronal loss, the finding that metal chelators can partially solubilize amyloid-beta deposits in Alzheimer disease suggests a promising therapeutic role for chelating agents.

Microdissection genotyping of archival fixative treated tissue for Gaucher disease.

The genetic diagnosis of Gaucher disease by molecular methods is complicated by the existence of a highly homologous transcribed pseudogene (96% identity) that is found in close proximity to the true gene on chromosome 1q21. In addition, the pseudogene sequence can mimic disease-causing mutations in the true gene. Selective polymerase chain reaction (PCR) amplification of the true gene can be accomplished in extracted DNA from fresh-frozen samples by designing oligonucleotide primers to hybridize to defined regions that are not present in the pseudogene.

New cytogenetic variant, insertion (15;17)(q22;q12q21), in an adolescent with acute promyelocytic leukemia.

We present the case of a 15-year-old female with acute promyelocytic leukemia and a new variant chromosome rearrangement identified as ins(15;17)(q22;q12q21) by conventional cytogenetic analysis. This finding was confirmed by fluorescence in situ hybridization using the PML-RARA DNA probe and whole chromosome paints 15 and 17. A typical PML-RARA fusion transcript consistent with a breakpoint in intron 3 of the PML gene and intron 2 of the RARA gene was identified by reverse transcription polymerase chain reaction.

Genetic testing in acute and chronic pancreatitis.

Hereditary pancreatitis (HP) is clinically indistinguishable from pancreatitis with other causes. Patients with HP have an increased chance of developing pancreatitis. Mutations in the cationic trypsinogen gene appear to cause most HP, although there is evidence for mild genetic heterogeneity with defects in other genes.

Does primary salt wasting occur in 11-beta-hydroxylase deficiency?

Renal salt wasting secondary to 11-beta-hydroxylase deficiency (11-beta-OHD) has been described in a few patients. This report describes an infant with 11-beta-OHD initially thought to be in adrenal crisis with renal salt wasting. Subsequently the sodium loss was found to be due to a secretory diarrhea, and this prompted us to critically review the literature of the previous case reports.

Intravenous calcitonin gene-related peptide stimulates net water secretion in rat colon in vivo.

We have studied the effect of exogenous calcitonin gene-related peptide on net fluxes of water and electrolytes in the rat small and large intestine. In ligated intestinal loops, intravenous calcitonin gene-related peptide (CGRP) induced colonic fluid secretion but had no effect on the small intestine. Subsequently, using a single-pass perfusion technique, we observed an immediate dose-dependent secretion of water by the rat colon upon intravenous administration of CGRP.