[Show abstract][Hide abstract] ABSTRACT: Parkinson's disease (PD) is a common and debilitating neurodegenerative disorder without a known neuroprotective cure. Currently, an increasing number of patients with PD resort to complementary and alternative medicine (CAM). This study aimed to determine the epidemiology of CAM use for PD worldwide. Methodological issues included the definition of CAM, running a search strategy using five databases, and citation tracking. Six studies estimated the prevalence of CAM use for PD to be between 25.7% and 76%. The response rates in these surveys varied from 81% to 100%. Frequently utilized forms of therapy were acupuncture, massage, herbs, and vitamins/health supplements, and these therapies were mainly used to improve the associated motor symptoms of PD. However, only 11% to 20% of these patients were referred to use CAM by a healthcare professional. Of the sociodemographic and disease-specific factors, CAM use was correlated with female sex, age, age at onset of PD, longer duration of PD, degree of education, higher income, rural location, comorbidity for indications, levodopa load, and severe motor symptoms. These results suggested that CAM use is widespread among patients with PD worldwide, but the largely unexamined use of CAM requires more attention. Moreover, there is a lack of communication between physicians and patients, increasing the risks associated with CAM use and the potential for adverse events.
Journal of Clinical Neuroscience 06/2013; DOI:10.1016/j.jocn.2012.10.022 · 1.38 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Wilson's disease is an autosomal recessive disorder of copper metabolism. Despite being treatable, there is no universally accepted treatment regimen. Currently, various Chinese herbal medicines (CHMs) are widely used in the treatment of Wilson's disease in China, but there is a lack of reliable scientific evidence for the effectiveness of such therapies. The objective of this systematic review is to assess the clinical efficacy and safety of CHM as an alternative or/and adjuvant therapy for Wilson's disease. A systematic literature search in different medical databases was performed to identify randomized controlled trials comparing CHM as monotherapy or CHM as adjuvant therapy with western conventional medical therapy in the treatment of Wilson's disease. A total of 687 participants were included in nine eligible studies. The main findings are that CHM as monotherapy or adjuvant therapy for Wilson's disease may be able to improve the clinical symptoms, to promote the urinary copper excretion, to ameliorate liver function and/or liver cirrhosis, and has fewer adverse effects in comparison with western conventional medication. Furthermore, CHM generally appeared to be safe and well tolerated in patients with Wilson's disease. However, the evidence presented in this review are insufficient to warrant a clinical recommendation due to the generally low methodological quality of the included studies. In conclusion, CHM seems to be beneficial and safe for Wilson's disease, but high-quality evidences are still needed to further evaluate this therapy. Therefore, additional well-designed, randomized, placebo-controlled clinical trials are needed.
Complementary therapies in medicine 06/2012; 20(3):143-54. DOI:10.1016/j.ctim.2011.12.004 · 1.55 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Studies with multiple sclerosis patients and animal models of experimental autoimmune encephalomyelitis (EAE) implicate adenosine and adenosine receptors in modulation of neuroinflammation and brain injury. Although the involvement of the A(1) receptor has been recently demonstrated, the role of the adenosine A(2A) receptor (A(2A) R) in development of EAE pathology is largely unknown. Using mice with genetic inactivation of the A(2A) receptor, we provide direct evidence that loss of the A(2A) R exacerbates EAE pathology in mice. Compared with wild-type mice, A(2A) R knockout mice injected with myelin oligodendroglia glycoprotein peptide had a higher incidence of EAE and exhibited higher neurological deficit scores and greater decrease in body weight. A(2A) R knockout mice displayed increased inflammatory cell infiltration and enhanced microglial cell activation in cortex, brainstem, and spinal cord. In addition, demyelination and axonal damage in brainstem were exacerbated, levels of Th1 cytokines increased, and Th2 cytokines decreased. Collectively, these findings suggest that extracellular adenosine acting at A(2A) Rs triggers an important neuroprotective mechanism. Thus, the A(2A) receptor is a potential target for therapeutic approaches to multiple sclerosis.
Journal of Neurochemistry 05/2012; 123(1):100-12. DOI:10.1111/j.1471-4159.2012.07807.x · 4.28 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Ginseng, the root of Panax ginseng C.A. Meyer, is one of the most commonly used healing herbs for stroke and chronic debilitating conditions in China. Ginsenosides are the main active principles for ginseng's efficacy, but the mechanisms have not been fully clarified.
To test the hypothesis whether or not the administration of Ginseng total saponins (GTS) can enhance neurogenesis after focal cerebral ischemia, and thereby improve neurological deficits.
Male Wistar rats received intraperitoneal injections of GTS dissolved at a dose of 25 mg kg(-1) d(-1) or normal saline (NS) of same volume 3 days before the permanent middle cerebral artery occlusion (MCAO) model establishment until the animals were killed at the time points of 1d, 3d, 7d and 14d. The neurological function was assessed blindly. BrdU immunostaining and double staining were performed by following the 3-steps method.
(A) GTS-treated rats have better neurological scores compared with those in NS group at 14d time point (p<0.05); (B) the number of BrdU(+) cells and BrdU(+)/NeuN(+) cells in GTS group were significantly higher than those in NS group in the ipsilateral subventricular zone and in the ipsilateral infarct area after MCAO, respectively (p<0.05 or p<0.01); (C) the increase of the number of BrdU(+)/NeuN(+) cells highly correlated with the decrease of neurological scores. Coefficient correlation r=-0.828 (p<0.01).
GTS can improve neurological deficits after focal cerebral ischemia by inducing endogenous neural stem cells activation and thereby enhance adult central nervous system regeneration.
Journal of ethnopharmacology 11/2010; 133(2):724-8. DOI:10.1016/j.jep.2010.01.064 · 3.00 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To assess neovascularization within human carotid atherosclerotic soft plaques in patients with ischemic stroke.
Eighty-one patients with ischemic stroke and 95 patients without stroke who had soft atherosclerotic plaques in the internal carotid artery were studied. The thickest soft plaque in each patient was examined using contrast-enhanced ultrasound. Time-intensity curves were collected from 5 s to 3 min after contrast injection. The neovascularization within the plaques in the internal carotid artery was evaluated using the ACQ software built into the scanner by 2 of the experienced investigators who were blinded to the clinical history of the patients.
Ischemic stroke was present in 7 of 33 patients (21%) with grade I plaque, in 14 of 51 patients (28%) with grade II plaque, in 26 of 43 patients (61%) with grade III plaque, and in 34 of 49 patients (69%) with grade IV plaque (P < 0.001 comparing grade IV plaque with grade I plaque and with grade II plaque and P = 0.001 comparing grade III plaque with grade I plaque and with grade II plaque). Analysis of the time intensity curves revealed that patients with ischemic stroke had a significantly higher intensity of enhancement (IE) than those without ischemic stroke (P < 0.01). The wash-in time (WT) of plaque was significantly shorter in stroke patients (P < 0.05). The sensitivity and specificity for IE in the plaque were 82% and 80%, respectively, and for WT were 68% and 74%, respectively. There was no significant difference in the peak intensity or time to peak between the 2 groups.
This study shows that the higher the grade of plaque enhancement, the higher the risk of ischemic stroke. The data suggest that the presence of neovascularization is a marker for unstable plaque.
World Journal of Cardiology (WJC) 04/2010; 2(4):89-97. DOI:10.4330/wjc.v2.i4.89 · 2.06 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Stroke is associated with high mortality and major disability burdens worldwide, but there are few effective and widely available therapies. Tau plays an important role in promoting microtubule assembly and stabilizing microtubule networks with phosphorylation regulating these functions. Based on the "ischemia-reperfusion theory" of Alzheimer's disease, some previous studies have focused on the relationship of tau and Alzheimer lesions in experimental brain ischemia. Thus, we hypothesize that the alterations in phosphorylation of tau are critical to microtubule dynamics and metabolism, and contribute to the pathophysiologic mechanisms during brain ischemia and/or reperfusion processes. We infer that regulation of phosphorylation of tau may be considered as a potential new therapeutic target in ischemic stroke.
[Show abstract][Hide abstract] ABSTRACT: There is evidence that adenosine acting at A(2A) receptors (A(2A)R) can influence striatal plasticity and cognitive functions. We examined spatial working memory in wild-type (WT) and A(2A) receptor knock-out (KO) mice using two assessments: the eight arm radial maze and a repeated trial Morris water maze (MWM) paradigm. Compared to WT littermates, A(2A)R KO mice displayed enhanced working memory as evidenced by a decrease in escape latency in trial 2 compared to trial 1 in the repeated trial MWM, and by a reduction in working memory errors in the radial arm maze. Both MWM and radial maze results indicated that this enhancement of working memory in A(2A)R KO mice was selective for this specific short-term memory. The decrease in escape latency in MWM was detected with an inter-trial interval of 15 s but not with intervals of 10 or 60 min. In the radial maze, spatial reference memory and memory retention after prolonged training (15 days but not 6 days) were not affected by the A(2A)R KO. These results demonstrate preferential improvement in spatial working memory by genetic inactivation of the A(2A)R and support a modulatory role of the A(2A)R in spatial working memory in mice.
Brain research 09/2009; 1303:74-83. DOI:10.1016/j.brainres.2009.09.082 · 2.84 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Thrombin plays an important role in brain injuries associated with intracerebral hemorrhage (ICH). The protease-activated receptor (PAR)-1 is responsible for the vast majority of the thrombin's cellular activation functions. We tested the hypothesis that thrombin-induced brain damage after ICH, at least in part, is mediated by PAR-1. We report that there are significant differences between PAR-1 positive cell number and PAR-1 mRNA absorbance ratio between ICH model group (at 6h, 24h, 3 d, 7 d and 14 d) and normal group (P<0.05). These results suggest that the long-time course of PAR-1 expression may be partly involved in the mechanism of thrombin-induced brain damage after ICH.
[Show abstract][Hide abstract] ABSTRACT: Coronary heart disease is the major cause of death worldwide and is affecting millions of people in both developed and developing countries. Patients with myocardial ischemia typically experience chest pain (angina pectoris). Traditional viewpoint of ischemic cardiac pain might be related to "mechanical hypothesis" in early time and "chemical hypothesis" in modern time. However, perception of cardiac ischemic pain is still not well understood. The previous studies suggested that neurogenic mechanisms including neurogenic inflammation and neurogenic activity might participate in the pathophysiological processes following myocardial ischemia. Therefore, we raise "neurogenic hypothesis", that is, neurogenic mechanisms might play a pivotal role in myocardial ischemic injury. Analgesia intervention, rivalry of neurogenic inflammatory reactions and electrostimulatory therapy, etc. could not only relieve the pain symptoms, but also block nociception of body and neurogenic reaction induced by ischemia. Thereby ischemic myocardial injury would be extenuated and myocardial protection be produced. Attempts to confirm this hypothesis may lead to new theory of pathophysiologic mechanisms and provide potential intervention strategy for cardiac ischemic pain.
Medical Hypotheses 02/2009; 72(4):402-4. DOI:10.1016/j.mehy.2008.12.001 · 1.07 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To study the expression and effect of TLR4 and NFkappaB protein in hippocampus neuron in rats exposed to chronic hypoxic hypercapnia.
The disorder of learning-memory in pulmonary hypertension rat model was reproduced by chronic hypoxic hypercapnia. Thirty rats were randomly divided into three groups: normal control group, hypoxic hypercapnia 2-week and 4-week group. The number of apoptosis neurons in hippocampus CA1/3 was counted by TUNEL method. Activity of TLR4 and NFkappaB in hippocampus CA1/3 was detected by using SP immunocytochemical technique.
The expression of TLR4 protein in hippocampus CA1/3 in group 2HH( CA1: 0.1275 +/- 0.0242, CA3: 0.1156 +/- 0.0376) and 4HH (CA1: 0.1522 +/- 0.0187, CA3: 0.1427 +/- 0.0453) were significantly higher than those in the NC group (P < 0.05, P < 0.01). The positive expression of NFkappaB were showed in cell nucleus in group 2HH (CA1: 0.1326 +/- 0.0324, CA3: 0.1301 +/- 0.0112) and group 4HH (CA1: 0.1612 +/- 0.0428, CA3: 0.1578 +/- 0.0365), and significantly higher than those in the NC group (P < 0.05, P < 0.01). The apoptosis of neural cells in hippocampus CA1/3 gradually increased with the time of exposure, and reached peak at 4 weeks (P < 0.01 vs NC group).
The activation of TLR4 and NFkappaB may play an important role in the apoptosis of hippocampus neural cells in rat exposed to chronic hypoxic hypercapnia.
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 02/2009; 25(1):27-30.
[Show abstract][Hide abstract] ABSTRACT: Parkinson's disease (PD) is one of the most common neurodegenerative disorders and still remains incurable. New targets for potential pharmacological intervention should be explored and evaluated in order to slow down, delay or reverse the progress of this disease, and/or to avoid the serious side effects of levodopa praeparatum. Potassium (K+) channels widely express in basal ganglia and play crucial roles in the pathophysiology of PD, thereby raising their therapeutic application. Based on data from some pilot studies, we propose that K+ channels may provide possible new therapeutic targets for slowing down the progressive loss of dopamine neurons in PD. The most promising targets of K+ channels, including Kv, KATP, Kir, SK, and K2P channels, etc. deserve further pursuit for making comprehensive use of their novel therapeutic potential. Attempts to confirm this hypothesis may lead to new therapeutic strategy of PD.
Medical Hypotheses 10/2008; 71(4):546-50. DOI:10.1016/j.mehy.2008.05.021 · 1.07 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To evaluate neovascularization within carotid atherosclerotic plaques with contrast-enhanced sonography.
We used contrast-enhanced sonography to examine 63 patients with carotid atherosclerotic plaques. The features of neovascularization within the plaques were analyzed and correlated with plaque size and echogenicity.
There were 81 atherosclerotic plaques, 62 of which (43 soft and 19 mixed) enhanced after injection of a contrast agent. The enhancement occurred from the carotid wall to the center of the plaque with a short-line pattern in 36 plaques, whereas 26 plaques enhanced from both the carotid wall and the carotid lumen, with a sparse spot pattern. The arrival time of contrast was shorter (p < 0.001) and time to peak was longer (p < 0.001) in the plaques than in the carotid lumen. Time to peak was shorter, whereas enhanced intensity was greater in soft plaques than in mixed plaques (p < 0.01 and p < 0.05, respectively). Among the 19 unenhanced plaques, 6 were hard, 3 were calcified, 3 were soft, and 7 were mixed. The thickness of the unenhanced plaques was <2.4 mm.
Contrast-enhanced sonography allows the noninvasive, dynamic evaluation of neovascularization within carotid plaques, and the presence of neovascularization may correlate with plaque morphology.
[Show abstract][Hide abstract] ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a slowly progressive lung disease that results in several complications, including cognitive dysfunction. Some evidences support that cognitive impairment is common and clinically important in COPD, but the exact mechanism is still unclear. It has been confirmed that chronic hypoxia-hypercapnia contributes a lot to the development in pathophysiology of COPD. Data from some pilot studies indicated that chronic hypoxia-hypercapnia influences cognitive functions both in patients and in animals, which includes some distinctive pattern of cognitive dysfunction in human being or impairment of spatial learning-memory in rat. Therefore, we propose that cognitive impairment is strongly related to combination of chronic hypoxia and hypercapnia, and chronic hypoxia-hypercapnia-induced animal models may mimic the cognitive dysfunction of COPD. Attempts to confirm this hypothesis may lead to new model of cognitive dysfunction in COPD.
Medical Hypotheses 02/2008; 71(1):111-3. DOI:10.1016/j.mehy.2008.01.025 · 1.07 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To explore the effect of chronic hypoxic hypercapnia on learning-memory and the possible mechanisms involved.
Fifty-eight male SD rats were randomly divided into three groups: Normal control group (NC, n=18), 2-week (2HH, n=18), and 4-week hypoxic hypercapnia (4HH, n=20) group. The rats, spatial learning-memory tasks were assessed by the Morris water maze. The expression of NMDAR1mRNA was determined by hybridization in situ.
Compared with NC group, rats exposed to chronic hypoxic hypercapnia displayed significant impairment in their performance assessed by two measures: mean escape latencies (2HH: 38.59 +/- 8.35 s, 4HH: 60.59 +/- 17.28 s) and swim path distances(2HH: 9893.45 +/- 1958.16 mm, 4HH: 18077.57 +/- 6878.85 mm). The expression level of NMDAR1mRNA in the hippocampus and cortex were lower than those in the NC group, especially, the NMDAR1mRNA expression of hippocampus CA1 in 4HH decreased by 21.4% (P < 0.01).
Chronic hypoxic hypercapnia could impair the rat spatial learning-memory and the decrease in expression of NMDAR1mRNA might be involved in.
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 11/2007; 23(4):434-7.
[Show abstract][Hide abstract] ABSTRACT: To study the dynamic and long-lasting expression of thrombin receptor after acute intracerebral hemorrhage (ICH) in rats.
36 rats were randomly divided into 6 groups (n = 6): Normal group and ICH model groups at 6 hours, 24 hours, 3 days, 7 days and 14 days. ICH models were produced with the induction of collagenase type VII-S. Immunohistochemical method was used to detect PAR-1 protein and RT-PCR technique was used to detect PAR-1mRNA in brain tissue around the haematoma in different groups.
PAR-1 protein and mRNA were mild positive in normal group. In model groups, intensity of PAR-1 expression started to enhance at 6 hours, and enhanced more at 24 hours. PAR-1 expression reached the peak at 3 days and began to descend. At 7 days the descent was obvious and there was further descent at 14 days. At each time point, the PAR-1 protein positive cell number and PAR-1mRNA absorbance ratio in ICH model groups were significantly higher than those in normal group (P < 0.05 or P < 0.01). In addition, PAR-1 proteins were obviously expressed in vivo in brain capillary endothelial cell.
Functional PAR-1 exists in brain capillary endothelial cells. Activation of PAR-1 after ICH due to the stimulation of thrombin is not only the initiating agent of cerebral edema after ICH, but also participates the development of cerebral edema.
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 08/2007; 23(3):328-32.
[Show abstract][Hide abstract] ABSTRACT: Xuan Fu (sweat pore) theory was derived from Huangdi Nei Jing (Canon of Internal Medicine), formulated by Liu Wan-su in his Su Wen Xuan Ji Yuan Bing Shi (Pattern of Mysterious Mechanism of Pathogenesis in Plain Questions) in the Jin Dynasty, and perfected by doctors later. The article introduces the establishment and development of Xuan Fu (sweat pore) theory from its concept and function, pathology for its stasis, therapeutical principles and treatment for opening Xuan Fu, its special theory and modern exploration in its essence.
Zhonghua yi shi za zhi (Beijing, China: 1980) 11/2005; 35(4):209-13.