Feng Jz

The Mediterranean score of dietary habits in Chinese populations in four different geographical areas.

Objective: To compare the dietary intake of Chinese people living in Pan Yu, Hong Kong, San Francisco and Sydney with respect to cardiovascular health, using the Mediterranean diet score, examining the effects of age, gender, urbanization and acculturation on the diet score.Subjects: A total of 500 men and 510 women in Hong Kong were recruited as a territory-wide stratified random sample. Subjects were recruited in response to local advertisements for the other three sites: Pan Yu, 58 men, 95 women; San Francisco, 166 men, 192 women; Sydney, 95 men, 73 women.Method: Food-frequency questionnaire over a 7 week period. A high/healthy score was taken as ≥4 for men and ≥3 for women, representing a dietary pattern beneficial for cardiovascular health.Results: In Hong Kong, more women in the middle age group (35–54) had a high score than other age groups, and overall more women had high scores than men. In comparing the four geographical regions, Pan Yu had the highest number of subjects with high score, and Hong Kong had the lowest. With the exception of the younger population and men in Hong Kong, the percentage of the population with a high score in all sites is greater than among elderly Greeks consuming a more traditional heart-healthy Mediterranean diet.Conclusion: Considerable variations in Chinese dietary patterns exist with respect to age, gender and geographic location. Overall, the Chinese diet is comparable to the Mediterranean diet and may be expected to have similar health benefits that have been documented for the traditional Mediterranean diet.European Journal of Clinical Nutrition (2001) 55, 215–220

Minocycline promotes axonal regeneration through suppression of RGMa in rat MCAO/reperfusion model.

Minocycline has been recently implicated in protection against focal cerebral ischemia reperfusion (I/R), but the protective effects on neurobehavioral abnormalities remains contradictory. In the present study, we investigate whether minocycline improves axonal regeneration and neurological function recovery by inhibiting the expression of the repulsive guidance molecular A (RGMa) after focal cerebral ischemia reperfusion. Male Sprague‐Dawley (SD) rats were subjected to occlusion of the right middle cerebral artery (MCAO) for 2 h and 3 mg kg−1 minocycline was injected intravenously immediately after reperfusion twice a day for 14 days. The staircase test and modified neurological severity score (mNSS) were performed to evaluate functional outcome and blood‐brain barrier (BBB) permeability was assessed by Evans blue dye extravasation (EB) at the expected time point. The expression of RGMa in ischemic cortex was measured by immunohistochemical staining and Western blot 2 weeks after MCAO. Neurofilament protein 200 (NF‐200) immunohistochemical staining was used to assess axonal damage. Treatment with minocycline at a dose of 3 mg kg−1 via the caudal vein significantly reduced the extravasation of EB, elevated mNSS and improved forelimb motor function as assessed by the staircase test when compared to the I/R group (P < 0.05). Moreover, axonal regrowth was enhanced in the minocycline treatment group when compared to the I/R group (P < 0.05). In addition, minocycline significantly reduced the expression of RGMa protein 2 weeks after MCAO as assessed by both immunostaining and Western blot. Our studies suggest that early minocycline treatment promotes neurological functional recovery and axonal regeneration in rats after MCAO, which might be mediated by down‐regulating RGMa expression. Synapse, 2013.

Overexpression of Fibulin-5 Attenuates Ischemia/Reperfusion Injury After Middle Cerebral Artery Occlusion in Rats.

Ischemia/reperfusion (I/R) injury after middle cerebral artery occlusion (MCAO) induces detrimental processes such as oxidative stress, inflammation, and apoptosis. All parts of the neurovascular unit are involved in these pathological processes. Fibulin-5 is a 66-kD glycoprotein secreted by various vascular cells, including vascular smooth muscle cells (SMCs), fibroblasts, and endothelial cells. As an extracellular matrix protein involved in cell adhesion, fibulin-5 has been widely studied in tumor growth and invasion. However, the effects of fibulin-5 on brain injury following ischemia/reperfusion have not been reported. In this study, we examined the effect of overexpressed fibulin-5 on reactive oxygen species (ROS) production. Fibulin-5 overexpression attenuated ROS expression, which in turn decreased apoptosis and blood–brain barrier (BBB) permeability following MCAO and reperfusion. Fibulin-5 also improved neurological deficits but had no effect on infarction volume. T2-weighted MRI and electron microscopy further confirmed brain edema reduction and decreased BBB disruption in fibulin-5 overexpression recombinant adenovirus (Ad-FBLN) treated rats. In addition, tight junction protein occludin was significantly degraded and matrix metalloproteinase 9 (MMP-9) immunoreactivity was significantly increased. Fibulin-5-mediated ROS decrease was not due to increased total superoxide dismutase levels but was instead correlated with the activation of Rac-1 pathway. The findings highlight the importance of antioxidant mechanism underlying cerebral ischemia/reperfusion.

Curcumin Inhibits Mitochondrial Injury and Apoptosis from the Early Stage in EAE Mice

The exact pathophysiological change concerning mitochondrial injury and oligodendrocyte apoptosis in MS and EAE model is still unknown. Whether curcumin is able to inhibit mitochondrial injury and suppress the apoptosis in the early stages of MS/EAE is still unclear. We first explored mitochondrial injury and apoptosis at different time points p.i. in C57 BL/6 EAE mice. We then explored the effects of curcumin on mitochondria and apoptosis. Results showed that mitochondrial injury can be observed 3 days p.i. Apoptosis in the spinal cord occurred 3 days p.i. and the apoptotic cells were shown to be oligodendrocytes and neuronal cells. Curcumin significantly reduced the number of apoptotic cells and inhibited the upregulation of cyt-c, caspase-9, and caspase-3 at 7 days p.i. in the EAE mice. These observations demonstrate that mitochondrial injury and oligodendrocyte/neuronal apoptosis occur in the early stages of EAE. Curcumin can inhibit apoptosis in EAE mice which maybe act through protection of mitochondrial injury and inhibition of the intrinsic apoptotic pathway.

Systematic Review of Clinical Practice Guidelines Related to Multiple Sclerosis

Background High quality clinical practice guidelines (CPGs) can provide clinicians with explicit recommendations on how to manage health conditions and bridge the gap between research and clinical practice. Unfortunately, the quality of CPGs for multiple sclerosis (MS) has not been evaluated. Objective To evaluate the methodological quality of CPGs on MS using the AGREE II instrument. Methods According to the inclusion and exclusion criteria, we searched four databases and two websites related to CPGs, including the Cochrane library, PubMed, EMBASE, DynaMed, the National Guideline Clearinghouse (NGC), and Chinese Biomedical Literature database (CBM). The searches were performed on September 20th 2013. All CPGs on MS were evaluated by the AGREE II instrument. The software used for analysis was SPSS 17.0. Results A total of 27 CPGs on MS met inclusion criteria. The overall agreement among reviews was good or substantial (ICC was above 0.70). The mean scores for each of all six domains were presented as follows: scope and purpose (mean ± SD: 59.05±16.13), stakeholder involvement (mean ± SD: 29.53±17.67), rigor of development (mean ± SD: 31.52±21.50), clarity of presentation (mean ± SD: 60.39±13.73), applicability (mean ± SD: 27.08±17.66), editorial independence (mean ± SD: 28.70±22.03). Conclusions The methodological quality of CPGs for MS was acceptable for scope, purpose and clarity of presentation. The developers of CPGs need to pay more attention to editorial independence, applicability, rigor of development and stakeholder involvement during the development process. The AGREE II instrument should be adopted by guideline developers.

Serum Levels of IL-1β, IL-6, TGF-β, and MMP-9 in Patients Undergoing Carotid Artery Stenting and Regulation of MMP-9 in a New In Vitro Model of THP-1 Cells Activated by Stenting

Inflammation plays an important role in the pathophysiological process after carotid artery stenting (CAS). Monocyte is a significant source of inflammatory cytokines in vascular remodeling. Telmisartan could reduce inflammation. In our study, we first found that, after CAS, the serum IL-1β, IL-6, TGF-β, and MMP-9 levels were significantly increased, but only MMP-9 level was elevated no less than 3 months. Second, we established a new in vitro model, where THP-1 monocytes were treated with the supernatants of human umbilical vein endothelial cells (HUVECs) that were scratched by pipette tips, which mimics monocytes activated by mechanical injury of stenting. The treatment enhanced THP-1 cell adhesion, migration and invasion ability, and the phosphorylation of ERK1/2 and Elk-1 and MMP-9 expression were significantly increased. THP-1 cells pretreated with PD98095 (ERK1/2 inhibitor) attenuated the phosphorylation of ERK1/2 and Elk-1 and upregulation of MMP-9, while pretreatment with telmisartan merely decreased the phosphorylation of Elk-1 and MMP-9 expression. These results suggested that IL-1β, IL-6, TGF-β, and MMP-9 participate in the pathophysiological process after CAS. Our new in vitro model mimics monocytes activated by stenting. MMP-9 expression could be regulated through ERK1/2/Elk-1 pathway, and the protective effects of telmisartan after stenting are partly attributed to its MMP-9 inhibition effects via suppression of Elk-1.

Optimization of brain metabolism using metabolic-targeted therapeutic hypothermia can reduce mortality from traumatic brain injury

BACKGROUND Therapeutic hypothermia is widely used to treat traumatic brain injuries (TBIs). However, determining the best hypothermia therapy strategy remains a challenge. We hypothesized that reducing the metabolic rate, rather than reaching a fixed body temperature, would be an appropriate target because optimizing metabolic conditions especially the brain metabolic environment may enhance neurologic protection. A pilot single-blind randomized controlled trial was designed to test this hypothesis, and a nested metabolomics study was conducted to explore the mechanics thereof. METHODS Severe TBI patients (Glasgow Coma Scale score, 3–8) were randomly divided into the metabolic-targeted hypothermia treatment (MTHT) group, 50% to 60% rest metabolic ratio as the hypothermia therapy target, and the body temperature-targeted hypothermia treatment (BTHT) control group, hypothermia therapy target of 32°C to 35°C body temperature. Brain and circulatory metabolic pool blood samples were collected at baseline and on days 1, 3, and 7 during the hypothermia treatment, which were selected randomly from a subgroup of MTHT and BTHT groups. The primary outcome was mortality. Using 1H nuclear magnetic resonance technology, we tracked and located the disturbances of metabolic networks. RESULTS Eighty-eight severe TBI patients were recruited and analyzed from December 2013 to December 2014, 44 each were assigned in the MTHT and BTHT groups (median age, 42 years; 69.32% men; mean Glasgow Coma Scale score, 6.17 ± 1.02). The mortality was significantly lower in the MTHT than the BTHT group (15.91% vs. 34.09%; p = 0.049). From these, eight cases of MTHT and six cases from BTHT group were enrolled for metabolomics analysis, which showed a significant difference between the brain and circulatory metabolic patterns in MTHT group on day 7 based on the model parameters and scores plots. Finally, metabolites representing potential neuroprotective monitoring parameters for hypothermia treatment were identified through 1H nuclear magnetic resonance metabolomics. CONCLUSION MTHT can significantly reduce the mortality of severe TBI patients. Metabolomics research showed that this strategy could effectively improve brain metabolism, suggesting that reducing the metabolic rate to 50% to 60% should be set as the hypothermia therapy target. LEVEL OF EVIDENCE Therapeutic study, Level I.

The potential role of local voltage potentials in right ventricular outflow tract arrhythmias: 47 cases with ventricular arrhythmias originating from right ventricular outflow tract.

OBJECTIVE: The object of this study was to investigate the possible role of local voltage potentials (LVPs) in mapping the ventricular arrhythmias originating from right ventricular outflow (RVOT). METHODS: Forty-seven patients with RVOT VAs (ventricular arrhythmias), referred for radiofrequency catheter ablation to our hospital, were analysed retrospectively for the prevalence, characteristics and electrophysiological evaluation of the LVPs recorded in successful and unsuccessful ablation sites. RESULTS: Radiofrequency ablation was successful immediately in all the 47 cases. Catheter ablation was performed at a mean of 8 +/- 6 sites per patient. There were 58 effective ablation sites, 5 cases with changing morphology of ventricular arrhythmias (VAs), and 318 invalid ablation sites. Activation times at effective ablation sites were slightly earlierthan those at invalid ablation sites (-28 +/- 8 ms vs-24 +/- 7 ms, P < 0.05). The LVPs appeared during VAs in 47 sites of the 58 effective ablation sites (81.0%), far more than the 22 sites of the 318 invalid ablation sites (6.9%) (P < 0.01). In two cases VAs recurred during follow-up. They received a second catheter ablation. CONCLUSIONS: Local ventricular potentials can be recorded in most patients with idiopathic VAs originating from the right outflow tract.The local potentials may facilitate successful radiofrequency ablation.