Red cell and platelet‐derived microparticles are increased in G6PD‐deficient subjects

In response to oxidative stress and during apoptosis, cells often shed microparticles (MPs), submicron elements carrying phosphatidylserine and protein antigens. Glucose‐6‐phosphate dehydrogenase (G6PD)‐deficient cells are extremely sensitive to oxidative damage that may lead to the formation of MPs. To determine whether G6PD deficiency alters membrane phospholipid asymmetry and increases MPs production, we determined the concentrations and cellular origins of MPs in G6PD‐deficient individuals using flow cytometry. G6PD‐deficient individuals showed an increase in circulating MPs concentrations as compared with G6PD‐normal individuals [1051/μL (865–2532/μL) vs. 258/μL (235–575/μL), P < 0.01]. MPs concentrations were significantly increased with the severity of G6PD deficiency. Median MPs concentrations from individuals with severe G6PD deficiency, and individuals with moderate G6PD deficiency were 2567/μL (1216–2532/μL) and 984/μL (685–2107/μL), respectively (P < 0.01). Importantly, G6PD enzymatic activity was significantly correlated with MPs concentrations with r² = 0.731. MPs found in G6PD deficiency individuals were largely derived from red blood cells (RBCs) (45%) and platelets (30%). Additionally, Atomic Force Microscopy was used to study the morphology and measures the diameter of MPs found in G6PD‐deficient individuals. The mean (SD) width and height of RMPs were 0. 41 (0.18) and 2.04 (0.14) μm, respectively. Together, these results indicate that MP concentration is significantly correlated with G6PD enzymatic activity and is increased in G6PD‐deficient as compared with G6PD‐normal individuals. Our data also provide an evidence for an alteration in cell membrane associated with a decreased in G6PD activity. However, the significance of MPs in G6PD deficiency needs further clarification.     

Anatomical characterization of the neuropeptide S system in the mouse brain by in situ hybridization and immunohistochemistry

Neuropeptide S (NPS) is the endogenous ligand for GPR154, now referred to as neuropeptide S receptor (NPSR). Physiologically, NPS has been characterized as a modulator of arousal and has been shown to produce anxiolytic‐like effects in rodents. Neuroanatomical analysis in the rat revealed that the NPS precursor mRNA is strongly expressed in the brainstem in only three distinct regions: the locus coeruleus area, the principal sensory trigeminal nucleus, and the lateral parabrachial nucleus. NPSR mRNA expression in the rat is widely distributed, with the strongest expression in the olfactory nuclei, amygdala, subiculum, and some cortical structures, as well as various thalamic and hypothalamic regions. Here we report a comprehensive map of NPS precursor and receptor mRNA expression in the mouse brain. NPS precursor mRNA is only expressed in two regions in the mouse brainstem: the Kölliker‐Fuse nucleus and the pericoerulear area. Strong NPSR mRNA expression was found in the dorsal endopiriform nucleus, the intra‐midline thalamic and hypothalamic regions, the basolateral amgydala, the subiculum, and various cortical regions. In order to elucidate projections from NPS‐producing nuclei in the brainstem to NPSR‐expressing structures throughout the brain, we performed immunohistochemical analysis in the mouse brain by using two polyclonal anti‐NPS antisera. The distribution of NPS‐immunopositive fibers overlaps well with NPSR mRNA expression in thalamic and hypothalamic regions. Mismatches between NPSR expression and NPS‐immunoreactive fiber staining were observed in hippocampal, olfactory, and cortical regions. These data demonstrate that the distribution pattern of the central NPS system is only partially conserved between mice and rats. J. Comp. Neurol. 519:1867–1893, 2011. © 2011 Wiley‐Liss, Inc.     

Dietary intakes and antioxidant status in mind-body exercising pre- and postmenopausal women

Objective

The decline in antioxidant defenses due to both estrogen loss and frequent adoption of poor dietary choices exposes postmenopausal women to cardiovascular diseases. Adequate nutrition and physical exercise are two factors of health promotion. This study investigated whether regular practice of mind-body exercise (yoga and/or tai chi) alters dietary intake and antioxidant status and balances the menopause related increases in lipid peroxidation and cardiovascular risk.

Design

Cross-sectional study. Setting: The study was conducted in an urban community in Bangkok (Thailand) between May and August 2007.

Participants

Premenopausal (Pre M; 39±8 yrs; n=56) and postmenopausal (Post M; 54±5 yrs; n=39) women who had been practicing yoga (Y) and/or tai chi (TC) more than 3 hours/week for a year, or who had no regular physical activity practice (sedentary, S).

Measurements

All participants completed food frequency questionnaires and 4-day food and activity records. Blood was collected on day 5. Factorial ANOVA tests were performed according to menopause status, exercise, and hormone replacement therapy (HRT) groups.

Results

Post M had higher (p = 0.01) dietary fiber intake compared with Pre M. Yoga practitioners had lower BMI (p = 0.004) and lower fat intake (p = 0.02) compared with their S and TC counterparts. Plasma total antioxidant status was significantly and independently lower and higher in Y and Post M groups, respectively. However, no difference was shown after adjusting for BMI. Regardless of menopause status and HRT, the activity of erythrocyte glutathione peroxidase an aerobic training responsive enzyme was higher (p < 0.001 ) in TC practitioners compared with other groups. No effects were shown on erythrocyte superoxide dismutase activity, plasma lipid peroxidation (TEARS) or total homocysteine concentrations.

Conclusion

Yoga and tai chi exercises can be used as components of a strategy to promote healthy lifestyles (balanced diet and moderate intensity exercise) in vulnerable populations, such as menopausal women, in order to prevent aging induced oxidative stress diseases.     

Flow rate calibration to determine cell-derived microparticles and homogeneity of blood components

Background

Cell-derived microparticles (MPs) are currently of great interest to screening transfusion donors and blood components. However, the current approach to counting MPs is not affordable for routine laboratory use due to its high cost.

Effects of donor age,donor sex,blood-component processing,and storage on cell-derived microparticle concentrations in routine blood-component preparation

Background

A number of factors cause increases in the number of cell-derived microparticles (MPs) in blood components. However, the overall effects of these factors on the concentration of MPs during routine blood-component preparation have not fully been elucidated.

Circulating red cell-derived microparticles in human malaria

In patients with falciparum malaria, plasma concentrations of cell-derived microparticles correlate with disease severity. Using flow cytometry, we quantified red blood cell-derived microparticles (RMPs) in patients with malaria and identified the source and the factors associated with production. RMP concentrations were increased in patients with Plasmodium falciparum (n = 29; median, 457 RMPs/μL [range, 13-4,342 RMPs/μL]), Plasmodium vivax (n = 5; median, 409 RMPs/μL [range, 281-503/μL]), and Plasmodium malariae (n = 2; median, 163 RMPs/μL [range, 127-200 RMPs/μL]) compared with those in healthy subjects (n = 11; median, 8 RMPs/μL [range, 3-166 RMPs/μL]; P = .01). RMP concentrations were highest in patients with severe falciparum malaria (P = .01). Parasitized red cells produced >10 times more RMPs than did unparasitized cells, but the overall majority of RMPs still derived from uninfected red blood cells (URBCs). In cultures, RMP production increased as the parasites matured. Hemin and parasite products induced RMP production in URBCs, which was inhibited by N-acetylcysteine, suggesting heme-mediated oxidative stress as a pathway for the generation of RMPs.     

Urotensin II acts as a modulator of mesopontine cholinergic neurons

Urotensin II (UII) is a vasomodulatory peptide that was not predicted to elicit CNS activity. However, because we have recently shown that the urotensin II receptor (UII-R) is selectively expressed in rat mesopontine cholinergic (MPCh) neurons, we hypothesize that UII may have a central function. The present study demonstrates that the UII system is able to modulate MPCh neuron activity. Brain slice experiments demonstrate that UII excites MPCh neurons of the mouse laterodorsal tegmentum (LDTg) by activating a slow inward current. Furthermore, microinfusion of UII into the ventral tegmental area produces a sustained increase in dopamine efflux in the nucleus accumbens, as measured by in vivo chronoamperometry. In agreement with UII activation of MPCh neurons, intracerebroventricular injections of UII significantly modulate ambulatory movements in both rats and mice but do not significantly affect startle habituation or prepulse inhibition. The present study establishes that UII is a neuromodulator that may be exploited to target disorders involving MPCh dysfunction.     

Affective associations mediate the influence of cost–benefit beliefs on fruit and vegetable consumption

Consumption of fruits and vegetables is far lower than recommended. The behavioral affective associations model posits that affective associations influence behavior and mediate the influence of perceived benefits and barriers on behavioral choices. The purpose of this study was to test the model's predictions about the influence of affective associations and benefits/barriers on fruit and vegetable consumption. Community adults (N = 446) reported perceived benefits and barriers to fruit and vegetable consumption, affective associations with fruits and vegetables, and current fruit and vegetable intake. Affective associations predicted behavior and mediated the influence of benefits and barriers on behavior, supporting predictions made by the behavioral affective associations model. This highlights the need to incorporate affective factors in decision-making models and intervention strategies.     

Neuropeptide S Enhances Memory During the Consolidation Phase and Interacts with Noradrenergic Systems in the Brain

Neuropeptide S (NPS) has been shown to promote arousal and anxiolytic-like effects, as well as facilitation of fear extinction. In rodents, NPS receptors (NPSR) are prominently expressed in brain structures involved in learning and memory. Here, we investigate whether exogenous or endogenous NPS signaling can modulate acquisition, consolidation, or recall of emotional, spatial, and contextual memory traces, using two common behavioral paradigms, inhibitory avoidance (IA) and novel object recognition. In the IA paradigm, immediate and delayed post-training central NPS administration dose dependently enhanced memory retention in mice, indicating that NPS may act during the consolidation phase to enhance long-term memory. In contrast, pre-training or pre-test NPS injections were ineffective, suggesting that NPS had no effect on IA memory acquisition or recall. Peripheral administration of a synthetic NPSR antagonist attenuated NPS-induced IA memory enhancement, showing pharmacological specificity. NPS also enhanced hippocampal-dependent non-aversive memory in the novel object recognition task. In contrast, NPSR knockout mice displayed deficits in IA memory, novel object recognition, and novel place or context recognition, suggesting that activity of the endogenous NPS system is required for memory formation. Blockade of adrenergic signaling by propranolol attenuated NPS-induced memory enhancement in the IA task, indicating involvement of central noradrenergic systems. These results provide evidence for a facilitatory role of NPS in long-term memory, independent of memory content, possibly by acting as a salience signal or as an arousal-promoting factor.     

Mutational analysis of ras gene family in lung cancer in Thai

H-, K- and N-ras gene mutations were analyzed in lung cancer from Thai patients. Thirteen out of 58 cases (22%) harbored the mutations. Ten cases showed K-ras gene mutations at codon 12, 1 case presented a mutation at codon 13 and another case exhibited a mutation at codon 63. Silent mutations of N-ras gene in codons 57 and 62 were seen in one patient, whilst no H-ras mutation was found in these patients. Bases change in K-ras gene were G right curved arrow T transversion (62%), G right curved arrow A transition (15%) and G right curved arrow C transition (15%), whereas T right curved arrow G transversion and A right curved arrow G transition were detected in N-ras mutant gene.