Men’s perspectives on women’s empowerment and intimate partner violence in rural Bangladesh

Intimate partner violence (IPV) may increase as women in patriarchal societies become empowered, implicitly or explicitly challenging prevailing gender norms. Prior evidence suggests an inverse U-shaped relationship between women’s empowerment and IPV, in which violence against women first increases and then decreases as more egalitarian gender norms gradually gain acceptance. By means of focus-group discussions and in-depth interviews with men in 10 Bangladeshi villages, this study explored men’s evolving views of women, gender norms and the legitimacy of men’s perpetration of IPV in the context of a gender transition. It examines men’s often-contradictory narratives about women’s empowerment and concomitant changes in norms of masculinity, and identifies aspects of women’s empowerment that are most likely to provoke a male backlash. Findings suggest that men’s growing acceptance of egalitarian gender norms and their self-reported decreased engagement in IPV are driven largely by pragmatic self-interest: their desire to improve their economic status and fear of negative consequences of IPV.     

Cytokine networks in destructive periodontal disease

BACKGROUND Cytokines are important regulatory proteins, produced by activated cells, which act by binding high affinity cell surface receptors. They are involved in almost all aspects of cell biology and form interacting networks, with cascades of sequential cell activation. They often show overlapping activities ( redundancy ) or the same cytokine may have a variety of different effects (pleiotropy). In excess, certain cytokines are damaging and proinflammatory. Tumour necrosis factor a (TNFα) and interleukin-I (IL-I) are markedly proinflammatory, inducing bone resorption, collagenase and prostaglandin E₂ production.
OBJECTIVE: This paper focuses on the role of TNFa and IL-l in the cytokine networks of destructive chronic per-iodontitis; specifically their regulation by T cell cytokines, receptor antagonists and inhibitory soluble forms of the IL-l and TNF receptors.
CONCLUSION: A hypothesis is proposed that destructive periodontal disease may be due to disregulation of these inhibitors, rather than an overproduction of IL-l and TNFα per se.     

A Critical Analysis of the Role of Testosterone in Erectile Function: From Pathophysiology to Treatment—A Systematic Review

Context

Androgen modulation of erectile function (EF) is widely accepted. However, the use of testosterone replacement therapy (TRT) in men with erectile dysfunction (ED) has generated an unprecedented debate.

Objective

To summarize the relevant data on the incidence, diagnosis, and management of ED coexisting with hypogonadism and to develop a pathophysiology-based treatment algorithm.

Evidence acquisition

We reviewed the relevant medical literature, with a particular emphasis on original molecular studies, prospective observational data, and randomized controlled trials performed in the past 20 yr.

Evidence synthesis

Testosterone modulates nearly every component involved in EF, from pelvic ganglions to smooth muscle and the endothelial cells of the corpora cavernosa. It also regulates the timing of the erectile process as a function of sexual desire, coordinating penile erection with sex. Epidemiologic studies confirm the significant overlap of hypogonadism and ED; however, most guidelines do not consider the differential diagnosis of hypogonadism or the relevance of subclinical disease. Various clinical tools can help the physician to assess and restore androgen levels in men with ED. Special attention is given to fertility-sparing treatments, due to the increasing number of older men desiring fatherhood. The simultaneous use of phosphodiesterase type 5 inhibitors (PDE5-Is) and TRT has recently been questioned. Originally proposed as a salvage therapy for nonresponders to PDE5-Is, this approach has been inappropriately transformed into a combination therapy. Clinical data are consistent when reinterpreted in the proper framework, whereas molecular evidence remains controversial.

Conclusions

A body of molecular and clinical evidence supports the use of TRT in hypogonadal patients with ED, although the benefit–risk ratio is uncertain in advanced age. Critical appraisal of this evidence enabled the development of a pathophysiology-oriented algorithm designed to avoid inappropriate treatments and support whether to start with TRT, PDE5-I only, or both. Apparently divergent findings are reconciled when TRT is correctly indicated. An improved diagnosis and individualized management is desirable in light of the many available options.     

Commentary on “A novel treatment strategy for newly diagnosed high-grade T1 bladder cancer: Gemcitabine and cisplatin adjuvant chemotherapy—A single-institution experience.”

Background

Management of high-grade T1 (formerly T1G3) bladder cancer continues to be controversial. Should patients with T1G3 bladder cancer have an immediate radical cystectomy or should they receive intravesical bacillus Calmette-Guérin preserving bladder? Gemcitabine and cisplatin (GC) adjuvant chemotherapy may help to strike a balance between intravesical and early cystectomy. For purposes of this study, we continue to refer high-grade T1 lesion as “T1G3.”

Diabetes mellitus and late‐onset hypogonadism: the role of Glu298Asp endothelial nitric oxide synthase polymorphism

Nitric oxide has been associated with insulin resistance and type 2 diabetes mellitus (DM). An association has been suggested between a single nucleotide polymorphism (Glu298Asp variant) of the endothelial nitric oxide synthase (eNOS) gene and increased risk of DM. However, the role of this polymorphism in favouring DM has not been investigated in hypogonadism, in which low testosterone and obesity are believed to play the major role. We aimed to evaluate whether eNOS gene single nucleotide polymorphism (Glu298Asp variant) might give a relevant contribution also to the onset of hypogonadism‐associated DM. 110 men affected by late‐onset hypogonadism were retrospectively reviewed. Patients were clinically and biochemically evaluated. Detection of eNOS Glu298Asp polymorphism was performed. After splitting the sample according to the three genetic variants (i.e. eNOS_GG, eNOS_GT, eNOS_TT), no difference was evident in age, body mass index (BMI) and total testosterone. Conversely, DM prevalence, glycaemia and glycated haemoglobin were significantly higher in eNOS_TT than in eNOS_GT and eNOS_GG. Logistic regression analysis showed that, after adjustment for age, BMI and total testosterone, eNOS_TT was positively and significantly associated with DM. Our study suggests that Glu298Asp single nucleotide polymorphism of the eNOS gene may be an independent risk factor for hypogonadism‐associated type 2 DM.     

Nonenzymatic glycation of human platelet membrane proteins in vitro and in vivo

Human platelet membrane proteins (PMP), incubated in vitro in the presence of various concentrations of glucose, undergo nonenzymatic glycation, as evidenced by incorporation of [3-3H]glucose radioactivity into the acid-precipitable fraction. The time course of the reaction is linear for the first hours, and the rate of glycation depends on the glucose concentration in the medium: at a glucose concentration of 80 mmol/L, up to 60 nmol of glucose is bound per milligram of PMP. The ketoaminic nature of the glucose/protein linkages was demonstrated by the finding of 5-hydroxymethylfurfuraldehyde by liquid-chromatographic analysis of acid hydrolysates of PMP. We analyzed PMP from 13 subjects with type I poorly controlled diabetes and from 10 nondiabetics. Nonenzymatic glycation, evaluated as nanomoles of the aldehyde per milligram of protein, was much greater in diabetic patients than in nondiabetics: 1.58 +/- 0.70 vs 0.37 +/- 0.18 (mean +/- SD).     

Effects of experimental potassium depletion on renal function and urinary prostanoid excretion in normal women during moderate anti-diuresis

Summary. The hypothesis that potassium depletion (KD) might play a role in stimulating the renal synthesis of prostanoids, and that these materials can contribute to hypokalaemic renal dysfunction, has been tested. Healthy women were studied either in normal potassium balance (N, n= 14), or in experimental KD. KD was induced by low dietary potassium intake (10 mmol day^-1) and natriuretic treatment, associated with replacement of net NaCl and water loss. By using different depletive patterns, two groups with estimated cumulative potassium deficits of 160 ± 43 mmol (KD1, n= 8) and 198±22 mmol (KD2, n= 6), respectively, were obtained. Renal function by the clearance (cl.) method and urinary PGE₂, 6-keto-PGF_lä, TxB₂ concentrations by the RIA method were measured during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis induced by the infusion of low-dose lysine-8-vasopressin (LVP). Compared to the N group, only in the KD2 group do glomerular and tubular dysfunctions typical of hypokalaemia and reduced prostanoid excretions (significant for 6-keto-PGF_lä and TxB₂ but not for PGE₂) appear during polyuria besides the significant reductions of plasma potassium concentration, urinary potassium excretion and the significant increase in plasma renin activity. During LVP infusion the urinary prostanoid excretions were all significantly lower in absence of significant differences in urinary flow rate. Concerning its renal effects, LVP lost its ability to reduce the creatinine cl., while expressing a trend towards reduction in fractional chloride excretion. Indomethacin pretreatment restored the LVP effect on creatinine cl. and increased the antichloruretic LVP effect (although not significantly). To the extent that urinary prostanoid excretions reflect their intrarenal synthesis, our data demonstrate that KD inhibits this biosynthesis. A depressed production of prostanoids endowed with vasodilating and chloruretic activity probably played a role in attenuating the renal vascular hyporeactivity and the urinary chloride dispersion induced by KD.     

Aminergic tone correlates of migraine and tension-type headache: a study using the tridimensional personality questionnaire

BACKGROUND: Aminergic neurotransmitter activity has been studied in many neuropsychiatric diseases by means of a self-administered questionnaire proposed by Cloninger. Given that central aminergic modulation plays a major role in the pathophysiology of primary headaches, we investigated the personality dimensions related to aminergic neurotransmitter activity in patients with migraine and tension-type headache. METHODS: From a consecutive series of 230 patients, we selected those presenting with migraine and tension-type headache according to the International Headache Society criteria. All patients were assessed by means of the Cloninger 100-item self-report Tridimensional Personality Questionnaire and a depression scale. The four dimensions of personality are novelty seeking (dopaminergic), harm avoidance (serotonergic), reward dependence (noradrenergic), and persistence (glutaminergic). RESULTS: One hundred twenty-one patients presenting with migraine and 42 with tension-type headache were recruited. The results indicate significantly higher harm avoidance scores (P<.001) in both patients with migraine and those with tension-type headache than in controls. Furthermore, patients with migraine had a significantly low score in the novelty seeking dimension (P<.001). When we compared only the two groups of patients with headache, we found that the persistence dimension alone was significantly higher in patients with migraine than in those with tension-type headache (P<.05). No differences were observed either in the overall scores of the other personality dimensions or in the depression scale scores. CONCLUSIONS: The Tridimensional Personality Questionnaire results support a role of the serotonergic system in both migraine and tension-type headache pathophysiology. A dysfunction of dopaminergic and glutaminergic tone seems to be a specific feature of migraine.