Plasma vitamin C status plays a role in PHN, and intravenous ascorbate helps relieve spontaneous pain in PHN.

The purpose of this study is to extend the literature by examining the effects of an acute bout of moderate to vigorous intensity aerobic exercise on the executive functions of planning and problem solving assessed using a Tower of London Task (TOL Task). Forty-two participants were randomly assigned into either exercise or control group, and performed the TOL Task, before and immediately following exercise or a control treatment. The exercise group performed 30 min of exercise on a stationary cycle at moderate to vigorous intensity while the control group read for the same length of time. Results indicated that the exercise group achieved improvements in TOL Task scores reflecting the quality of planning and problem solving, but not in those reflecting rule adherence and performance speed. These findings indicate that an acute bout of aerobic exercise has facilitative effects on the executive functions of planning and problem solving.

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Bone morphogenetic protein (BMP)-7 protects sepsis-induced acute kidney injury (AKI). Dexmedetomidine (DEX), an α(2)-adrenoceptor (α(2)-AR) agonist, has anti-inflammatory effects. We investigated the protective effects of DEX on sepsis-induced AKI and the expression of BMP-7 and histone deacetylases (HDACs). In vitro, the effects of DEX or trichostatin A (TSA, an HDAC inhibitor) on TNF-α, monocyte chemotactic protein (MCP-1), BMP-7, and HDAC mRNA expression in LPS-stimulated rat renal tubular epithelial NRK52E cells, was determined using real-time PCR. In vivo, mice were intraperitoneally injected with DEX (25 μg/kg) or saline immediately and 12 h after cecal ligation and puncture (CLP) surgery. Twenty-four hours after CLP, we examined kidney injury and renal TNF-α, MCP-1, BMP-7, and HDAC expression. Survival was monitored for 120 h. LPS increased HDAC2, HDAC5, TNF-α, and MCP-1 expression, but decreased BMP-7 expression in NRK52E cells. DEX treatment decreased the HDAC2, HDAC5, TNF-α, and MCP-1 expression, but increased BMP-7 and acetyl histone H3 expression, whose effects were blocked by yohimbine, an α(2)-AR antagonist. With DEX treatment, the LPS-induced TNF-α expression and cell death were attenuated in scRNAi-NRK52E but not BMP-7 RNAi-NRK52E cells. In CLP mice, DEX treatment increased survival and attenuated AKI. The expression of HDAC2, HDAC5, TNF-α, and MCP-1 mRNA in the kidneys of CLP mice was increased, but BMP-7 was decreased. However, DEX treatment reduced those changes. DEX reduces sepsis-induced AKI by decreasing TNF-α and MCP-1 and increasing BMP-7, which is associated with decreasing HDAC2 and HDAC5, as well as increasing acetyl histone H3.

Propofol reduces apoptosis in LPS-stimulated lung epithelial cells by decreasing HIF-1α, BNIP3, and cytokine production. Using propofol to inhibit HIF-1α expression may protect against the acute lung injury caused by LPS-induced sepsis.

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Postherpetic neuralgia (PHN) is the most common complication of herpes zoster (HZ). The aim of the present study was to compare the nutritional status of PHN patients with that of healthy controls, and then to identify risk factors for PHN using multivariate multiple logistic regressions. In the present cross-sectional study, we prospectively enrolled fifty PHN patients for at least 3 months and fifty healthy controls. We selected nine circulating nutrients including ionised Ca, Zn, retinol, folic acid, vitamin B 12 , vitamin C, a-tocopherol, g-tocopherol and lycopene associated with both immunity and the modulation of neuropathic pain, and measured their concentrations in plasma/serum. Concentrations of ionised Ca, Zn, vitamin C and vitamin B 12 were significantly lower in PHN patients than in controls after excluding those patients receiving supplements since the outbreak of HZ. The prevalence of either mild/marginal or severe deficiencies for any of the nine selected circulating nutrients in PHN patients (92 %) was much higher than that in controls (46 %) (P, 0·001). Lower concentrations of vitamin C (#45·0 mmol/l), ionised Ca (#1·05 mmol/l) and Zn (#0·91 g/l) were found to increase independently the risk of PHN using binary variable (dichotomy) analyses with both PHN patients and controls in a multivariate logistic regression analysis. No significant correlations existed between the risks of PHN and the concentrations of retinol, folic acid, vitamin B 12 , lycopene or a:g-tocopherol ratios. Thus, lower concentrations of circulating nutrients, namely vitamin C, ionised Ca or Zn, are probably a risk factor in Taiwanese patients with PHN.Key words: Nutritional status: Herpes zoster: Postherpetic neuralgia: Nutrient deficiencies: Risk factors Postherpetic neuralgia (PHN), a peripheral neuropathic pain syndrome, is the most common complication of herpes zoster (HZ) (1) . PHN can lead to long-term psychological distress, physical disability and tremendous use of health care resources (2) . Therefore, to identify risk factors for PHN and to effectively improve preventive strategies are clinically meaningful. Although old age, female sex, presence of a prodrome, greater acute pain severity, presence of severe rash (3) and immunocompromised patients (1) have been identified as independent predictors of PHN, discovering additional risk factors is still needed to prevent developing PHN with respect to HZ management (3) .An outbreak of HZ caused by a reactivation of latent varicella zoster virus (VZV) is primarily attributed to a reduction in host cellular immunity (1) . Additionally, two non-mutually exclusive theories of PHN are an alteration in the excitability of central neurons and a chronic active VZV ganglionitis caused by ongoing viral activity in patients developing PHN compared with HZ patients who do not (1,4) . Thus, reduced cellular immunity plays a critical factor in both zoster risk and the persistence of PHN (1,4) . Diminished cellular immunity has been advocated to be closely associated with def...

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