miR-15b-5p targeting amyloid precursor protein is involved in the anti-amyloid eflect of curcumin in swAPP695-HEK293 cells.

Curcumin exerts a neuroprotective effect on Alzheimer's disease; however, it is not known whether microRNAs are involved in this protective effect. This study was conducted using swAPP695-HEK293 cells as an Alzheimer's disease cell model. swAPP695-HEK293 cells were treated with 0, 0.5, 1, 2, 5, and 10 µM curcumin for 24 hours. The changes in miR-15b-5p, miR-19a-3p, miR-195-5p, miR-101-3p, miR-216b-5p, miR-16-5p and miR-185-5p expression were assessed by real-time quantitative polymerase chain reaction. The mRNA and protein levels of amyloid precursor protein, amyloid-ß40 and amyloid-ß42 were evaluated by quantitative real-time polymerase chain reaction, western blot assays and enzyme-linked immunosorbent assays. swAPP695-HEK293 cells were transfected with miR-15b-5p mimic, or treated with 1 µM curcumin 24 hours before miR-15b-5p inhibitor transfection. The effects of curcumin on amyloid precursor protein, amyloid-ß40 and amyloid-ß42 levels were evaluated by western blot assays and enzyme-linked immunosorbent assay. Luciferase assays were used to analyze the interaction between miR-15b-5p and the 3'-untranslated region of amyloid precursor protein. The results show that amyloid precursor protein and amyloid-ß expression were enhanced in swAPP695-HEK293 cells compared with HEK293 parental cells. Curcumin suppressed the expression of amyloid precursor protein and amyloid-ß and up-regulated the expression of miR-15b-5p in swAPP695-HEK293 cells. In addition, we found a negative association of miR-15b-5p expression with amyloid precursor protein and amyloid-ß levels in the curcumin-treated cells. Luciferase assays revealed that miR-15b-5p impaired the luciferase activity of the plasmid harboring the 3'-untranslated region of amyloid precursor protein. These findings indicate that curcumin down-regulates the expression of amyloid precursor protein and amyloid-ß in swAPP695-HEK293 cells, which was partially mediated by miR-15b-5p via targeting of the 3'-untranslated region of amyloid precursor protein.

Inordinate glucose variation poststroke is associated with poor neurological improvement in patients without history of diabetes.

INTRODUCTION: Glucose variation is an important risk factor for the complications of diabetes mellitus. The plasma glucose level poststroke is in continuous fluctuation. However, whether the variation influences neurological improvement remains unknown. AIMS: This observational study aimed to investigate the association of glucose variation with neurological improvement poststroke. METHODS: We consecutively enrolled 216 ischemic stroke patients with no history of diabetes mellitus within 72 h of onset, with instant blood glucose <11.1 mmol/L at admission. The glucometabolic status was evaluated by an oral glucose tolerance test 1 day after admission and 14 days after stroke, respectively. The severity of neurological deficit was assessed with the National Institute of Health Stroke Scale (NIHSS). RESULTS: Fourteen days after stroke, 31% patients were found to have impaired glucose tolerance and 30.6% were newly diagnosed diabetes mellitus by oral glucose tolerance test. A higher level of instant blood glucose at admission or fasting plasma glucose (FPG) at 1 day correlated with a less neurological improvement. The number of patients with no <20% decrease in NIHSS was significantly decreased in patient group with higher than 30% variation of either FPG or 2-h postprandial glucose. Similar correlation between glucose variation and neurological improvement was also found in 117 patients with 2-h postprandial glucose ≥7.8 mmol/L at 1 day. CONCLUSIONS: Inordinate glucose variation correlated with less neurological improvement poststroke, giving the evidence that the fluctuation of glucose levels in stroke patients should be taken into consideration during glucose modulation.

A method of evaluating the lower limit of cerebral autoregulation and its correlation with blood pressure by transcranial Doppler in rats.

The aim of present study was to validate the assessment of lower limit of cerebral autoregulation (LLCA) as derived from mean artery blood pressure (MABP) and cerebral zero flow pressure (ZFP) by means of transcranial Doppler (TCD) and to determine the accurate relationship between LLCA and MABP in stroke-prone renovascular hypertensive rats (RHRSP). We studied two groups of rats: RHRSP and normal controls. Blood flow velocity of middle cerebral artery was monitored by TCD and arterial blood pressure was recorded in right femoral artery to compute the ZFP. The value of LLCA was determined as the difference between MABP and ZFP and validated by the value determined by blood withdrawal-induced cerebral autoregulation. In normal rats, the LLCA derived from the new method was 69.8 ± 8.7 mm Hg, from the change of blood velocity was 69.4 ± 9.8 mmHg and from blood volume flow after blood withdrawal was 68.8 ± 9.7 mmHg. In the RHRSP group, the corresponding values of LLCA were 109.1 ± 17.2 mm Hg, 110.0 ± 18.0 mm Hg and 109.0 ± 19.3 mm Hg, respectively. In each group, there was no statistically significant difference among the three values. LLCA in RHRSP began to increase 6 weeks after hypertension-induced operation, significantly higher than controls (p < 0.05), and stabilized at 110 mm Hg, 10 weeks after operation. The increase of LLCA was positively correlated with MABP, following an "S" curve, demonstrating that the change of LLCA was more obvious in the middle range of MABP in RHRSP (R(2) = 0.8848, p < 0.05). In conclusion, TCD is a valid and noninvasive method for determination of LLCA compared with the classic method in rats. Our data demonstrated that the change of LLCA may be correlated with MABP, following an "S" curve relationship.

[Energy response of Tb(3+)-doped silicate scintillating glass to hard X-ray].

Tb(3+)-doped silicate scintillating glass was made by high temperature melt-quenching method and the energy response to hard X-ray (from 5 to 80 keV) was measured. The response of photocurrent of silicate scintillating glass to X-ray (with various energy) is nonlinear. It was noted that the change in nonlinearity around 8 and 50 keV is obvious. This phenomenon is concerned with the production of abundant electrons when the scintillating glass absorbed X-ray and the energy response of scintillating glass to electrons.

[Analysis on data gathered from transcranial Doppler among 1500 normal adults community].

OBJECTIVE: To study the rates of receiving doppler signal, flow velocity of cerebral artery and the relationship between flow velocity,age and gender in normal adults in China. METHODS: A total of 1500 normal residents at the community level in Guangdong province were examined, using transcranial doppler. Data was gathered and analyzed. RESULTS: With the increase of age, the rate of receiving signal in cerebral artery gradually decreased. Difference between males and females was noticed. Mean velocity of cerebral artery decreased in both genders but the velocity was faster in females than in males and the pulsate index increased without difference. CONCLUSION: The rates of receiving signal and the flow velocity of cerebral artery were related to age and gender and the findings from this study offered criterion for clinical transcranial doppler.

[A study on shifts of cerebral autoregualtion following end-tidal CO2 by critical closing pressure].

OBJECTIVE: To investigate the shifts of cerebral autoregulation following end-tidal CO2, and set up a new clinical way to evaluate the lower limit of cerebral autoregulation. METHODS: The cerebral blood flow spectrum of middle cerebral artery, radial blood pressure and end-tidal CO2 (ETco(2)) were simultaneously monitored among 70 healthy volunteers, 38 males and 41 females, aged 21-77. The Lower limit of cerebral autoregulation (LLCA) was determined by critical closing pressure (CCP). We observed the shifts of LLCA of healthy subjects respectively between normocapnia and hyper- and hypocapnia. RESULTS: The LLCA of healthy subjects was 58 mm Hg +/- 10 mm Hg at normocapnia, increased at hypercapnia and decreased at hypocapnia significantly (69 mm Hg +/- 15 mm Hg and 44 mm Hg +/- 11 mm Hg, P < 0.05). The 95% CI of difference were 2.70 mmHg between hyper- and normocapnia and 2.18 mm Hg between hypo- and normocapnia. The shifting rates of LLCA correlated inversely to the rates of CCP at both hyper- and hypocapnia (r = -0.610 5, -0.555 1, both P < 0.05), and the relation between LLCA's and CCP's shifts displayed an "S" pattern curve at hypocapnia. The rate of mean velocity changing in middle cerebral artery was significantly correlative to the LLCA shifts' rate (r = 0.584 1, P < 0.05), and showing an "S" pattern curve. CONCLUSION: The lower limit of cerebral autoregulation can be determined by CCP exactly. The cerebral autoregulation can shift up or down following ETco(2), and its physiological basis is closely correlated with the cerebrovascular tone.