Mean platelet volume and platelet distribution width in vascular dementia and Alzheimer's disease.

Activated platelets play a substantial role in Alzheimer's disease (AD) and atherothrombosis. Mean platelet volume (MPV) is an early marker of platelet activation, which is linked to a variety of pro-thrombotic and pro-inflammatory diseases. This study is to examine the association between platelet indices and vascular dementia (VaD) and AD. In this cross-sectional study, we investigated the levels of platelet count, MPV, and platelet distribution width (PDW) in 150 VaD patients, 110 AD patients, and 150 non-demented controls. MPV and PDW were significantly lower in patients with VaD and AD as compared with controls. The decrease in PDW for AD patients as compared with VaD patients was also significant (p < 0.001). In addition, there was a positive correlation between Mini-Mental State Examination (MMSE) and MPV and PDW, after adjusting confounding factors (r = 0.532 for MPV and r = 0.425 for PDW, p < 0.001 for both). Multivariate regression analysis showed that MPV and PDW were significantly associated with MMSE (ß = 0.366 for MPV and ß = 0.273 for PDW, p < 0.001 for both). In conclusion, MPV and PDW were both decreased in VaD and AD. PDW levels were significantly lower in AD as compared to those in VaD. Our findings suggest that PDW in combination with MMSE scores could be potential indicators for distinguishing VaD from AD.

[A case-control study on the duration of sleeping and cerebral infarction].

OBJECTIVE: To explore the relationship between duration of sleeping and cerebral infarction. METHODS: A case-control study involved 1037 cerebral infarction patients admitted by the Second Affiliated Hospital of Harbin Medical University,December 2011-December 2012 as cases. Another 1205 adults free from cerebro-vascular diseases who had undergone physical examination in the hospital at the same period, were served as controls. All the subjects were interviewed with unified questionnaire. Chi-square test, u-test and multivariate logistic regression analysis were performed. RESULTS: After adjustment for potential confounding factors including age, sex, body mass index, wrist-hip ratio, smoking, alcohol intake, hypertension, diabetes mellitus, coronary artery disease and lipid parameters, data from the multivariate logistic regression analysis showed that the risk of cerebral infarction was greater in people who slept less than 6 hours per night than those who slept between 6 hours and 8 hours per night, with an odds ratio (95% CI)as 2.81 (95% CI:1.68-4.70). There was no significant association between factor as 'sleeping longer than 8 hours/pre day' and cerebral infarction. Through the subgroup analysis, data showed that the association between 'shorter than 6 hour sleep/night' and cerebral infarction consistently existed, across the categories of sex, and the degree of association was greater in women than in men, with the odds ratio as 5.58 (95% CI: 1.78-17.52) and 2.00 (95% CI:1.10-3.64) respectively. CONCLUSION: Short sleeping duration might increase the risk of developing cerebral infarction.

Decreased mean platelet volume and platelet distribution width are associated with mild cognitive impairment and Alzheimer's disease.

Neuroinflammation is a critical driving force underlying mild cognitive impairment (MCI) and Alzheimer's disease (AD) pathologies. Activated platelets play an important role in neuroinflammation and have been implicated in AD pathogenic mechanisms. Mean platelet volume (MPV), a marker of platelet activation, is involved in the pathophysiology of a variety of pro-inflammatory diseases. However, little research has been conducted to investigate the relationship between platelet indices and MCI and AD pathogenesis. In this cross-sectional study, we investigated the levels of platelet count, MPV and platelet distribution width (PDW) in 120 AD patients, 120 MCI patients, and 120 non-demented controls. Our study showed that MPV and PDW were significantly lower in patients with AD as compared with either MCI or controls. Moreover, MCI patients had lower MPV and PDW values compared with the controls (P < 0.001). In addition, there is a positive correlation between mini-mental state examination (MMSE) and MPV and PDW, after adjusting age, gender, and body mass index (r = 0.576, P < 0.001 for MPV; r = 0.465, P < 0.001 for PDW, respectively). Multivariate analysis showed that MPV and PDW were significantly associated with MMSE (ß = 0.462; P < 0.001 for MPV; ß = 0.245; P < 0.001 for PDW; respectively). In conclusion, MPV and PDW were decreased in MCI and AD patients. Further prospective research is warranted to determine the potential clinical application of MPV and PDW as biomarkers in the early diagnosis of AD.

Bis{µ-[4-(1,3-benzothia-zol-2-yl)phen-yl]methane-thiol-ato-κS,S':S,S'}bis-[tricarbonyl-iron(I)](Fe-Fe).

The title compound, [Fe(2)(C(14)H(10)NS(2))(2)(CO)(6)], was synthesized as a structural and biochemical model for the active site of [FeFe]-hydrogenase. The bond lengths (Fe-Fe, Fe-S and Fe-C) and angles (C-Fe-Fe and Fe-S-Fe) are within expected ranges. The S⋯S distance [2.9069 (12) Å] and the dihedral angle between two Fe-S-Fe planes [78.5 (3)°] of the butterfly-shaped Fe(2)S(2) core are enlarged compared with related bridged dithiol-ate diiron analogues. The calculated 4-benzothia-zolebenzyl best planes are almost parallel [dihedral angle = 3.7 (7)°].

[Culture and characterization of and lentiviral vectors mediated glial cell derived neurotrophic factor expression in mesenchymal stem cells from human umbilical cord blood].

OBJECTIVE: To isolate and culture mesenchymal stem cells from umbilical cord blood (UCB-MSCs), study its biological characterization in vitro, transfect UCB-MSCs using lentiviral vectors encoding glial cell derived neurotrophic factor (GDNF) gene, evaluate the biological function change of UCB-MSCs, and detect GDNF expression level in vitro. METHODS: We isolated monocyte by Ficoll density gradient, separated two kinds of adherent cells through different trypsin digestion time, and detected the cells surface markers by fluorescence activated cell sorting when it was proliferated for P7 passages. At the same time, we sub-cloned GDNF gene into lentiviral vectors and packaged lentiviral supernatant through three plasmids co-transfection method, then transfected the UCB-MSCs using lentiviral vectors encoding GDNF at different multiplicity of infection, and evaluated the change of biological function by observing the ability of proliferation and differentiation, morphology, and the cells surface markers. We detected the GDNF mRNA and protein expression level by using real-time polymerase chain reaction (real-time PCR) and enzyme-link immunosorbent assay (ELISA). RESULTS: The UCB-MSCs were successfully isolated and cultured in vitro, and induced it to differentiate into fat cells. FACS results showed that the UCB-MSCs expressed CD90, CD73, and CD105 positively, and CD14, CD34, CD45, CD19, HLA-DR, Stro-1, and CD106 negatively. Real-time PCR and ELISA showed that the expressions of GDNF protein and mRNA were correlated with the copy number of transfected cells: high copy number of transfected cells were associated with high GDNF expression. The biological characterization of UCB-MSCs did not obviously change after sub-cloning with GDNF. CONCLUSIONS: UCB-MSCs was successfully isolated and cultured in vitro. By transfecting UCB-MSCs with GDNF gene-containing lentiviral vectors, the secretion of GDNF protein and mRNA expression level can be controlled by the copy number of transfected cells, and thus make it constantly express GDNF at high level.

Cholecystokinin-8 antagonizes electroacupuncture analgesia through its B receptor in the caudate nucleus.

OBJECTIVES: The analgesic effect of electroacupuncture (EA) stimulation has been proved. However, its mechanism of action is not clear. It has been well-known that cholecystokinin-8 (CCK-8) is a neuropeptide which is mainly related to the mediation of pain. The caudate nucleus was selected to determine if the release of CCK and the neural activity in this nucleus were involved in producing EA analgesia. MATERIALS AND METHODS: Radiant heat focused on the rat-tail was used as the noxious stimulus. The pain threshold of rats was measured by tail-flick latency (TFL). EA stimulation at the bilateral Zusanli (ST 36) acupoints of rats was used to investigate the effects of EA analgesia. The electrical activities of pain-excited neurons (PEN) and pain-inhibited neurons (PIN) in the caudate nucleus were recorded with a glass microelectrode. The present study examined the antagonistic effects of the intracerebral ventricular injection of CCK-8 on EA analgesia and reversing effects of CCK-B receptor antagonist (L-365,260) injection into the caudate nucleus on CCK-8. RESULTS: The radiant heat focused on the tail of rats caused an increase in the evoked discharge of PEN and a reduction in the evoked discharge of PIN. EA stimulation at the bilateral ST 36 acupoints of rats resulted in the inhibition of PEN, the potentiation of PIN, and prolongation of TFL. The analgesic effect of EA was antagonized when CCK-8 was injected into the intracerebral ventricle of rats. The antagonistic effect of CCK-8 on EA analgesia was reversed by injection of CCK-B receptor antagonist (L-365,260) into the caudate nucleus of rats. CONCLUSIONS: Our results suggest that CCK-8 antagonize EA analgesia through its B receptor.

1-Ethyl-6-fluoro-7-(4-methyl-piperazin-4-ium-1-yl)-4-oxo-1,4-dihydroquinoline-3-carboxylate hexa-hydrate.

In the title compound, C(17)H(20)FN(3)O(3)·6H(2)O, the pefloxacin (pef) neutral zwitterion is accompanied by six water mol-ecules of hydration. An extensive network of O-H⋯O and N-H⋯O hydrogen bonds help to establish the crystal packing.