Painful diabetic neuropathy (PDN) is one of the most common complications of diabetes mellitus. Recently it has become clear that nitric oxide (NO) and proinflammatory cytokines play an important role in the pathogenesis of PDN. We investigated whether the cytokine tumor necrosis factor alpha (TNF-α) and NO play a role in PDN pathogenesis by performing a cross-sectional and a case–control study in 110 type 2 diabetic patients. Of 110 subjects, 59 patients suffered from PDN (cases) and the remaining were painless DN (controls). Cross-sectionally, plasma TNF-α levels and immunoreactivity for inducible NO synthase (iNOS) and TNF-α were higher in patients with more severe pain on the visual analog scale. There were statistically significant differences between mild and severe pain for TNF-α levels, iNOS immunoreactivity, and TNF-α immunoreactivity. There were statistically significant differences between mild and severe pain for TNF-α levels (mean 15.24 pg/mL ± 5.42 vs 20.44 ± 10.34), iNOS immunoreactivity (9.76% ± 8.60% vs 15.48% ± 11.56%), and TNF-α immunoreactivity (13.0% ± 9.48% vs 20.44% ± 11.75%). The case–control study showed that TNF-α had an odds ratio of 5.053 (P < 0.001), TNF-α immunoreactivity of 4.125 (P < 0.001), and iNOS immunoreactivity of 3.546 (P = 0.002). DN patients with high TNF-α levels, and high iNOS and TNF-α expression in macrophages are at risk of suffering from pain. The higher the TNF-α level, and iNOS and TNF-α immunoreactivity, the more severe the pain. These findings could form the basis of further research into better management of PDN.

Alzheimer's disease (AD) is one of the most debilitating neurodegenerative diseases and is predicted to affect 1 in 85 people by 2050. Despite much effort to discover a therapeutic strategy to prevent progression or to cure AD, to date no effective disease-modifying agent is available that can prevent, halt, or reverse the cognitive and functional decline of patients with AD. Several underlying etiologies to this failure are proposed. First, accumulating evidence from past trials suggests a preventive as opposed to therapeutic paradigm, and the precise temporal and mechanistic relationship of β-amyloid (Aβ) and tau protein should be elucidated to confirm this hypothesis. Second, we are in urgent need of revised diagnostic criteria to support future trials. Third, various technical and methodological improvements are required, based on the lessons learned from previous failed trials.

BACKGROUND: Stroke is a serious health condition and the leading cause of disability, including erectile dysfunction (ED). The mechanisms and factors that predict ED in stroke are not fully elucidated. Several studies have shown a relationship between the location of the lesion in stroke with the onset of ED. The left hemispheric lesion was believed to disrupt the parasympathetic nervous system which is responsible for the regulation of erection. Stroke attack in this region therefore can be the underlying reason for ED. However, there are still contradictory findings in this area, and very few studies attempted to look at this problem, particularly among Asian male. AIM: We would like to evaluate the association between left hemisphere lesion after ischemic stroke and the subsequent risk of developing ED. METHODS: The study was conducted in the neurology polyclinic of Sanglah and Wangaya Hospital from February to August 2013. Subjects are all post-stroke patients who visited the neurology polyclinic of Sanglah and Wangaya Hospital that met inclusion and exclusion criteria. RESULTS: There is a significant positive correlation (p < 0.05) between left hemisphere lesions and ED in stroke patients with a correlation coefficient (r) = 0.361 which means weak correlation and p = 0.032. CONCLUSION: Left hemisphere lesions positively correlated with ED in stroke patients. Further longitudinal research is needed to see whether left hemisphere lesion in post-stroke patients is a risk factor for ED.

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