Sexual desire, erectile dysfunction and the biomedicalization of sex in older heterosexual men

Aim To examine sexual desire in older age and the use of pharmaceuticals for sexual enhancement in the context of erectile dysfunction. Background The ability of the older person to fulfil sexual desire has not been well supported in Western society. Design The paper draws on themes that emerged during a phenomenological study of sexual desire in older age. Method Narratives were collected between 2008–2010 from in-depth interviews with six men and two women aged 65–84 years who were part of a larger Australian study of sexual desire in older age. Findings Emergent themes reveal that for some older people, the biomedicalization of sex can be a disappointing experience. Conclusion The findings illuminate the need for nurses who are at the front line of health care, health policy makers and educators, to consider sexual desire experienced in older age in the context of sexual health and healthy ageing. This study will contribute to a growing body of knowledge about sexual desire in older age

Drugs and local chemical mediators

10.1 Histamine and cytokines 10.1.1 Actions of histamine 10.1.2 Drugs that modify the actions of histamine 10.1.3 Cytokines 10.2 Eicosanoids 10.2.1 Cyclooxygenase (COX) and lipooxygenase system 10.2.2 Actions of eicosanoids 10.2.3 Drugs that modify the actions of eicosanoids 10.2.3.1 Inhibit phospholipase A2 10.2.3.2 Non-selective cyclooxygenase inhibitors 10.2.3.3 Selective COX-2 inhibitors 10.2.3.4 Agonists at prostaglandin receptors 10.2.3.5 Leukotriene receptor antagonists 10.3. 5-Hydroxtryptamine (serotonin), nitric oxide, and endothelin 10.3.1 5-HT and migraine 10.3.2 5-HT and the gastrointestinal tract 10.3.3 Nitric oxide and angina 10.3.4 Nitric oxide and erectile dysfunction 10.3.5 Endothelin and pulmonary hypertension

Male reproductive health disorders among Aboriginal and Torres Strait Islander men : a hidden problem?

OBJECTIVE: To better understand help-seeking behaviours and reproductive health disorders among Aboriginal and Torres Strait Islander men. DESIGN, SETTING AND PARTICIPANTS: A cross-sectional mixed-methods study conducted from 1 May 2004 to 30 April 2005 of 293 Aboriginal and Torres Strait Islander men aged 18 years and over from urban, rural and remote communities in the Northern Territory and Queensland. MAIN OUTCOME MEASURES: Subscale of the International Index of Erectile Function, self-reported help-seeking behaviours for erectile dysfunction (ED) and prostate disease, thematic analysis of semi-structured interviews and focus groups. RESULTS: The prevalence of moderate-to-severe ED increased across age groups, from about 10% in younger men (under 35 years) to 28% in men aged 55-74 years. Moderate-to-severe ED was strongly associated with reporting a chronic condition (odds ratio [OR], 3.67) and residing in a remote area (OR, 2.94). Aboriginal and Torres Strait Islander men aged 40-59 years showed similar low levels of help-seeking behaviours compared with non-Indigenous men from a comparable population-based study. About half of the men with ED saw a doctor or received treatment for ED in each population. While prostate cancer rates were low in both studies, testing for prostate problems was less frequent in Aboriginal and Torres Strait Islander men (11.4%) than in non-Indigenous men (34.1%, P < 0.001), despite similar levels of concern about prostate cancer. Barriers to help-seeking included shame, culturally inappropriate services and lack of awareness. CONCLUSION: This study, the first to investigate reproductive health of Aboriginal and Torres Strait Islander men, found low levels of help-seeking behaviours for reproductive health disorders, with implications for missing a predictor of chronic disease and late diagnosis of prostate disease.

Magnetic resonance spectroscopy and neurocognitive dysfunction in obstructive sleep apnea before and after CPAP treatment

STUDY OBJECTIVES: To determine whether cerebral metabolite changes may underlie abnormalities of neurocognitive function and respiratory control in OSA. DESIGN: Observational, before and after CPAP treatment. SETTING: Two tertiary hospital research institutes. PARTICIPANTS: 30 untreated severe OSA patients, and 25 age-matched healthy controls, all males free of comorbidities, and all having had detailed structural brain analysis using voxel-based morphometry (VBM). MEASUREMENTS AND RESULTS: Single voxel bilateral hippocampal and brainstem, and multivoxel frontal metabolite concentrations were measured using magnetic resonance spectroscopy (MRS) in a high resolution (3T) scanner. Subjects also completed a battery of neurocognitive tests. Patients had repeat testing after 6 months of CPAP. There were significant differences at baseline in frontal N-acetylaspartate/choline (NAA/Cho) ratios (patients [mean (SD)] 4.56 [0.41], controls 4.92 [0.44], P = 0.001), and in hippocampal choline/creatine (Cho/Cr) ratios (0.38 [0.04] vs 0.41 [0.04], P = 0.006), (both ANCOVA, with age and premorbid IQ as covariates). No longitudinal changes were seen with treatment (n = 27, paired t tests), however the hippocampal differences were no longer significant at 6 months, and frontal NAA/Cr ratios were now also significantly different (patients 1.55 [0.13] vs control 1.65 [0.18] P = 0.01). No significant correlations were found between spectroscopy results and neurocognitive test results, but significant negative correlations were seen between arousal index and frontal NAA/Cho (r = -0.39, corrected P = 0.033) and between % total sleep time at SpO(2) < 90% and hippocampal Cho/Cr (r = -0.40, corrected P = 0.01). CONCLUSIONS: OSA patients have brain metabolite changes detected by MRS, suggestive of decreased frontal lobe neuronal viability and integrity, and decreased hippocampal membrane turnover. These regions have previously been shown to have no gross structural lesions using VBM. Little change was seen with treatment with CPAP for 6 months. No correlation of metabolite concentrations was seen with results on neurocognitive tests, but there were significant negative correlations with OSA severity as measured by severity of nocturnal hypoxemia. CITATION: O'Donoghue FJ; Wellard RM; Rochford PD; Dawson A; Barnes M; Ruehland WR; Jackson ML; Howard ME; Pierce RJ; Jackson GD. Magnetic resonance spectroscopy and neurocognitive dysfunction in obstructive sleep apnea before and after CPAP treatment.

Serine protease inhibition and mitochondrial dysfunction associated with cisplatin resistance in human tumor cell lines : targets for therapy

Indicators of mitochondrial function were studied in two different cell culture models of cis-diamminedichloroplatinum-II (CDDP) resistance: the intrinsically resistant human ovarian cancer cell line CI-80-13S, and resistant clones (HeLa-S1a and HeLa-S1b) generated by stable expression of the serine protease inhibitor—plasminogen activator inhibitor type-2 (PAI-2), in the human cervical cancer cell line HeLa. In both models, CDDP resistance was associated with sensitivity to killing by adriamycin, etoposide, auranofin, bis[1,2-bis(diphenylphosphino)ethane]gold(I) chloride {[Au(DPPE)2]Cl}, CdCl2 and the mitochondrial inhibitors rhodamine-123 (Rhl23), dequalinium chloride (DeCH), tetraphenylphosphonium (TPP), and ethidium bromide (EtBr) and with lower constitutive levels of ATP. Unlike the HeLa clones, CI-80-13S cells were additionally sensitive to chloramphenicol, 1-methyl-4-phenylpyridinium ion (MPP+), rotenone, thenoyltrifluoroacetone (TTFA), and antimycin A, and showed poor reduction of 1-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT), suggesting a deficiency in NADH dehydrogenase and/or succinate dehydrogenase activities. Total platinum uptake and DNA-bound platinum were slightly lower in CI-80-13S than in sensitive cells. The HeLa-S1a and HeLa-S1b clones, on the other hand, showed poor reduction of triphenyltetrazolium chloride (TTC), indicative of low cytochrome c oxidase activity. Total platinum uptake by HeLa-S1a was similar to HeLa, but DNA-bound platinum was much lower than for the parent cell line. The mitochondria of CI-80-13S and HeLa-S1a showed altered morphology and were fewer in number than those of JAM and HeLa. In both models, CDDP resistance was associated with less platinum accumulation and with mitochondrial and membrane defects, brought about one case with expression of a protease inhibitor which is implicated in tumor progression. Such markers may identify tumors suitable for treatment with gold phosphine complexes or other mitochondrial inhibitors.

Serine protease inhibition and mitochondrial dysfunction associated with cisplatin resistance in human tumor cell lines: targets for therapy

Indicators of mitochondrial function were studied in two different cell culture models of cis-diamminedichloroplatinum-II (CDDP) resistance: the intrinsically resistant human ovarian cancer cell line CI-80-13S, and resistant clones (HeLa-S1a and HeLa-S1b) generated by stable expression of the serine protease inhibitor—plasminogen activator inhibitor type-2 (PAI-2), in the human cervical cancer cell line HeLa. In both models, CDDP resistance was associated with sensitivity to killing by adriamycin, etoposide, auranofin, bis[1,2-bis(diphenylphosphino)ethane]gold(I) chloride {[Au(DPPE)2]Cl}, CdCl2 and the mitochondrial inhibitors rhodamine-123 (Rhl23), dequalinium chloride (DeCH), tetraphenylphosphonium (TPP), and ethidium bromide (EtBr) and with lower constitutive levels of ATP. Unlike the HeLa clones, CI-80-13S cells were additionally sensitive to chloramphenicol, 1-methyl-4-phenylpyridinium ion (MPP+), rotenone, thenoyltrifluoroacetone (TTFA), and antimycin A, and showed poor reduction of 1-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT), suggesting a deficiency in NADH dehydrogenase and/or succinate dehydrogenase activities. Total platinum uptake and DNA-bound platinum were slightly lower in CI-80-13S than in sensitive cells. The HeLa-S1a and HeLa-S1b clones, on the other hand, showed poor reduction of triphenyltetrazolium chloride (TTC), indicative of low cytochrome c oxidase activity. Total platinum uptake by HeLa-S1a was similar to HeLa, but DNA-bound platinum was much lower than for the parent cell line. The mitochondria of CI-80-13S and HeLa-S1a showed altered morphology and were fewer in number than those of JAM and HeLa. In both models, CDDP resistance was associated with less platinum accumulation and with mitochondrial and membrane defects, brought about one case with expression of a protease inhibitor which is implicated in tumor progression. Such markers may identify tumors suitable for treatment with gold phosphine complexes or other mitochondrial inhibitors.

A possible role for mitochondrial dysfunction in migraine

Migraine is a common neurological disorder characterised by debilitating head pain and an assortment of additional symptoms which can include nausea, emesis, photophobia, phonophobia and occasionally visual sensory disturbances. Migraine is a complex disease caused by an interplay between predisposing genetic variants and environmental factors. It affects approximately 12 % of studied Caucasian populations with affected individuals being predominantly female. Genes involved in neurological, vascular or hormonal pathways have all been implicated in predisposition towards developing migraine. All of these are nuclear encoded genes, but given the role of mitochondria in a number of neurological disorders and in energy production it is possible that mitochondrial variants may play a role in the pathogenesis of this disease. Mitochondrial DNA has been a useful tool for studying population genetics and human genetic diseases due to the clear inheritance shown through successive generations. Given the clear gender bias found in migraine patients it may be important to investigate X-linked inheritance and mitochondrial-related variants in this disorder. This paper explores the possibility that mitochondrial DNA changes may play a role in migraine. Few variants in the mitochondrial genome have so far been investigated in migraine and new studies should be aimed towards investigating the role of mitochondrial DNA in this common disorder.

Metabolic dysfunction and laminitis

Objective: This review focuses on laminitis that develops as a result of metabolic dysfunction and aims to provide a concise assessment of the current state of knowledge on this form of the disease. Outline: The most prevalent form of laminitis is associated with metabolic or endocrinopathic diseases, such as Equine Metabolic Syndrome and pituitary pars intermedia dysfunction, and the feeding of high-energy diets, particularly those rich in non-structural carbohydrates. Insulin dysregulation is the key hormonal imbalance implicated in causing this form of laminitis and hyperinsulinaemia is an important risk factor for the disease. Hyperinsulinaemia can occur in association with insulin resistance, obesity, regionalised adiposity, dysregulated cortisol metabolism and may also be related to other factors, such as breed and genetic predisposition. Recognition of hyperinsulinaemia is best achieved by using a dynamic oral glucose test that can be performed relatively easily under field conditions. Insulin produces a unique pathological lesion in the lamellae and the features of this lesion have informed investigations on the pathogenesis of the disease. Research into the mechanism of disease is continuing so that more targeted therapies than are currently available can be developed. However, dietary restriction and exercise remain effective management strategies for metabolic disease. Conclusions: Although the pathogenic mechanism/s of metabolic and endocrinopathic forms of laminitis remain the subject of intense research, ample data on risk factors for the disease are available. Efforts focussed on preventing the disease should aim to identify metabolic disease and reduce obesity and insulin resistance in at-risk individuals.

The effectiveness of psychosocial interventions for cognitive dysfunction in cancer patients who have received chemotherapy : a systematic review

Background: Chemotherapy-related cognitive dysfunction (CRCD) refers to problems with memory,attention span, or concentration, experienced by patients with cancer who have had chemotherapy. CRCD can have a significant negative effect on a patient’s quality of life. The exact cause of CRCD is unknown but is presumed to be multifactorial. Objective: To conduct a systematic review of the effectiveness of psychosocial interventions designed to treat CRCD. Methods: Participants of interest to the review were over 18 years of age, diagnosed with cancer, and receiving chemotherapy or had received chemotherapy in the past. Interventions of interest were methods to improve cognitive function. Included study designs were randomized controlled trials, quasi-experimental trials, and quantitative observational studies. The primary outcome of interest was level of cognitive function. A three-step search strategy was utilized to identify studies published from 1985 to 2011 from a wide range of databases. Joanna Briggs Institute systematic review methods were used but findings were analyzed using the Cochrane Collaboration Review Manager 5.1 program.Weightedmean differences with 95% confidence intervals were calculated from the continuous data. Results: Searching identified 3,109 potentially relevant articles and 120 full-text articles were retrieved. Two further papers were sourced from reference lists of retrieved articles. From 122 papers, six were suitable for critical appraisal and six were included in the analysis. Meta-analysis was conducted on two cognitive behavioral therapy (CBT) trials for the outcome of inability to concentrate. Significant effect was seen for one CBT intervention at 20 weeks (p = .004). Significant effect from CBT on quality of life was seen at 6-month follow-up (p < .05). Conclusions: Despite some evidence of an effect, there is insufficient evidence at this stage to strongly recommend any of the interventions to assist in decreasing the effects of CRCD, except in terms of improving quality of life.

Long-term follow-up of flexor digitorum longus transfer and calcaneal osteotomy for stage II posterior tibial tendon dysfunction

Flexor digitorum longus transfer and medial displacement alcaneal osteotomy is a wellrecognised form of treatment or stage II posterior tibial tendon dysfunction. Although excellent short- and medium-term results have been reported, the long-term outcome is unknown. We reviewed the clinical outcome of 31 patients with a symptomatic flexible flatfoot deformity who underwent this procedure between 1994 and 1996. There were 21 women and ten men with a mean age of 54.3 years (42 to 70). The mean follow-up was 15.2 years (11.4 to 16.5). All scores improved significantly (p < 0.001). The mean American Orthopedic Foot and Ankle Society (AOFAS) score improved from 48.4 pre-operatively to 90.3 (54 to 100) at the final follow-up. The mean pain component improved from 12.3 to 35.2 (20 to 40). The mean function score improved from 35.2 to 45.6 (30 to 50). The mean visual analogue score for pain improved from 7.3 to 1.3 (0 to 6). The mean Short Form-36 physical component score was 40.6 (SD 8.9), and this showed a significant correlation with the mean AOFAS score (r = 0.68, p = 0.005). A total of 27 patients (87%) were pain free and functioning well at the final follow-up. We believe that flexor digitorum longus transfer and calcaneal osteotomy provides long-term pain relief and satisfactory function in the treatment of stage II posterior tibial tendon dysfunction.