ErbB4 deficiency exacerbates olfactory dysfunction in an early-stage Alzheimer's disease mouse model.

Olfactory dysfunction is increasingly recognized as an early indicator of Alzheimer's disease (AD). Aberrations in GABAergic function and the excitatory/inhibitory (E/I) balance within the olfactory bulb (OB) have been implicated in olfactory impairment during the initial stages of AD. While the neuregulin 1 (NRG1)/ErbB4 signaling pathway is known to regulate GABAergic transmission in the brain and is associated with various neuropsychiatric disorders, its specific role in early AD-related olfactory impairment remains incompletely understood. This study demonstrated that olfactory dysfunction preceded cognitive decline in young adult APP/PS1 mice and was characterized by reduced levels of NRG1 and ErbB4 in the OB. Further investigation revealed that deletion of ErbB4 in parvalbumin interneurons reduced GABAergic transmission and increased hyperexcitability in mitral and tufted cells (M/Ts) in the OB, thereby accelerating olfactory dysfunction in young adult APP/PS1 mice. Additionally, ErbB4 deficiency was associated with increased accumulation of Aß and BACE1-mediated cleavage of APP, along with enhanced CDK5 signaling in the OB. NRG1 infusion into the OB was found to enhance GABAergic transmission in M/Ts and alleviate olfactory dysfunction in young adult APP/PS1 mice. These findings underscore the critical role of NRG1/ErbB4 signaling in regulating GABAergic transmission and E/I balance within the OB, contributing to olfactory impairment in young adult APP/PS1 mice, and provide novel insights for early intervention strategies in AD. This work has shown that ErbB4 deficiency increased the burden of Aß, impaired GABAergic transmission, and disrupted the E/I balance of mitral and tufted cells (M/Ts) in the OB, ultimately resulting in olfactory dysfunction in young adult APP/PS1 mice. NRG1 could enhance GABAergic transmission, rescue E/I imbalance in M/Ts, and alleviate olfactory dysfunction in young adult APP/PS1 mice. OB: olfactory bulb, E/I: excitation/inhibition, Pr: probability of release, PV: parvalbumin interneurons, Aß: ß-amyloid, GABA: gamma-aminobutyric acid.

Antiferromagnetic Spin Fluctuations and Unconventional Superconductivity in Topological Superconductor Candidate YPtBi Revealed by

We report ^{195}Pt nuclear magnetic resonance (NMR) measurements on topological superconductor candidate YPtBi, which has broken inversion symmetry and topological nontrivial band structures due to the strong spin-orbit coupling. In the normal state, we find that Knight shift K is field- and temperature independent, suggesting that the contribution from the topological bands is very small at low temperatures. However, the spin-lattice relaxation rate 1/T_{1} divided by temperature (T), 1/T_{1}T, increases with decreasing T, implying the existence of antiferromagnetic spin fluctuations. In the superconducting state, no Hebel-Slichter coherence peak is seen below T_{c} and 1/T_{1} follows T^{3} variation, indicating the unconventional superconductivity. The finite spin susceptibility at zero-temperature limit and the anomalous increase of the NMR linewidth below T_{c} point to a mixed state of spin-singlet and spin-triplet (or spin-septet) pairing.

Modulation of α7nAchR by Melatonin Alleviates Ischemia and Reperfusion-Compromised Integrity of Blood-Brain Barrier Through Inhibiting HMGB1-Mediated Microglia Activation and CRTC1-Mediated Neuronal Loss.

The only food and drug administration (FDA)-approved drug currently available for the treatment of acute ischemic stroke is tissue plasminogen activator (tPA), yet the therapeutic benefits of this drug are partially outweighed by the increased risk of hemorrhagic transformation (HT). Analysis of the NIH trial has shown that cigarette smoking protected tPA-treated patients from HT; however, the underlying mechanism is not clear. Nicotinic acetylcholine receptors (nAChR) has shown anti-inflammatory effect and modulation nAChR could be a strategy to reduce ischemia/reperfusion-induced blood-brain barrier (BBB) damage. Since melatonin could regulate the expression of α7nAchR and melatonin's neuroprotective effect against ischemic injury is mediated via α7nAChR modulation, here, we aim to test the hypothesis that melatonin reduces ischemia and reperfusion (I/R)-induced BBB damage through modulation of α7nACh receptor (α7nAChR). Mice were subjected to 1.5 h ischemia and 24 h reperfusion and at the onset of reperfusion, mice received intraperitoneal administration (i.p.) of either drug or saline. Mice were randomly assigned into five groups: Saline; α7nAChR agonist PNU282987; Melatonin; Melatonin+Methyllycaconitine (MLA, α7nAChR antagonist), and MLA group. BBB permeability was assessed by detecting the extravasation of Evan's blue and IgG. Our results showed that I/R significantly increased BBB permeability accompanied by occludin degradation, microglia activation, and high mobility group box 1 (HMGB1) release from the neuron. In addition, I/R significantly induced neuronal loss accompanied by the decrease of CREB-regulated transcriptional coactivator 1 (CRTC1) and p-CREB expression. Melatonin treatment significantly inhibited the above changes through modulating α7nAChR. Taken together, these results demonstrate that melatonin provides a protective effect on ischemia/reperfusion-induced BBB damage, at least in part, depending on the modulation of α7nAChR.

Tuning the Distance to a Possible Ferromagnetic Quantum Critical Point in A_{2}Cr_{3}As_{3}.

Although superconductivity in the vicinity of an antiferromagnetic (AFM) instability has been extensively explored in the last three decades or so, superconductivity in compounds with a background of ferromagnetic (FM) spin fluctuations is still rare. We report ^{75}As nuclear quadrupole resonance measurements on the A_{2}Cr_{3}As_{3} family, which is the first group of Cr-based superconductors at ambient pressure, with A being alkali elements. From the temperature dependence of the spin-lattice relaxation rate (1/T_{1}), we find that by changing A in the order of A=Na, Na_{0.75}K_{0.25}, K, and Rb, the system is tuned to approach a possible FM quantum critical point (QCP). This may be ascribed to the Cr2-As2-Cr2 bond angle that decreases towards 90°, which enhances the FM interaction via the Cr2-As2-Cr2 path. Upon moving away from the QCP, the superconducting transition temperature T_{sc} increases progressively up to 8.0 K in Na_{2}Cr_{3}As_{3}, which is in sharp contrast to the AFM case where T_{sc} usually shows a maximum around a QCP. The 1/T_{1} decreases rapidly below T_{sc} with no Hebel-Slichter peak, and ubiquitously follows a T^{5} variation below a characteristic temperature T^{*}≈0.6 T_{sc}, which indicates the existence of point nodes in the superconducting gap function commonly in the family. These results suggest that the A_{2}Cr_{3}As_{3} family is a possible solid-state analog of superfluid ^{3}He.

Isorhynchophylline ameliorates cognitive impairment via modulating amyloid pathology, tau hyperphosphorylation and neuroinflammation: Studies in a transgenic mouse model of Alzheimer's disease.

Isorhynchophylline (IRN) has been demonstrated to have distinct anti-Alzheimer's disease (AD) activity in several animal models of AD. In this study, we aimed at evaluating the preventive effect of IRN on the cognitive deficits and amyloid pathology in TgCRND8 mice. Male TgCRND8 mice were administered with IRN (20 or 40 mg/kg) by oral gavage daily for 4 months, followed by assessing the spatial learning and memory functions with the Radial Arm Maze (RAM) test. Brain tissues were determined immunohistochemically or biochemically for changes in amyloid pathology, tau hyperphosphorylation and neuroinflammation. Our results revealed that IRN (40 mg/kg) significantly ameliorated cognitive deficits in TgCRND8 mice. In addition, IRN (40 mg/kg) markedly reduced the levels of Aß40, Aß42 and tumor necrosis factor (TNF-α), interleukin 6 (IL-6) and IL-1ß, and modulated the amyloid precursor protein (APP) processing and phosphorylation by altering the protein expressions of ß-site APP cleaving enzyme-1 (BACE-1), phosphorylated APP (Thr668), presenilin-1 (PS-1) and anterior pharynx-defective-1 (APH-1), as well as insulin degrading enzyme (IDE), a major Aß-degrading enzyme. IRN was also found to inhibit the phosphorylation of tau at the sites of Thr205 and Ser396. Immunofluorescence showed that IRN reduced the Aß deposition, and suppressed the activation of microglia (Iba-1) and astrocytes (GFAP) in the cerebral cortex and hippocampus of TgCRND8 mice. Furthermore, IRN was able to attenuate the ratios of p-c-Jun/c-Jun and p-JNK/JNK in the brains of TgCRND8 mice. IRN also showed marked inhibitory effect on JNK signaling pathway in the Aß-treated rat primary hippocampus neurons. We conclude that IRN improves cognitive impairment in TgCRND8 transgenic mice via reducing Aß generation and deposition, tau hyperphosphorylation and neuroinflammation through inhibiting the activation of JNK signaling pathway, and has good potential for further development into pharmacological treatment for AD.

Electron Mass Enhancement near a Nematic Quantum Critical Point in NaFe_{1-x}Co_{x}As.

A magnetic order can be completely suppressed at zero temperature (T), by doping carriers or applying pressure, at a quantum critical point, around which physical properties change drastically. However, the situation is unclear for an electronic nematic order that breaks rotation symmetry. Here, we report nuclear magnetic resonance studies on NaFe_{1-x}Co_{x}As where magnetic and nematic transitions are well separated. The nuclear magnetic resonance spectrum is sensitive to inhomogeneous magnetic fields in the vortex state, which is related to London penetration depth λ_{L} that measures the electron mass m^{*}. We discovered two peaks in the doping dependence of λ_{L}^{2}(T∼0), one at x_{M}=0.027 where the spin-lattice relaxation rate shows quantum critical behavior, and another at x_{c}=0.032 around which the nematic transition temperature extrapolates to zero and the electrical resistivity shows a T-linear variation. Our results indicate that a nematic quantum critical point lies beneath the superconducting dome at x_{c} where m^{*} is enhanced. The impact of the nematic fluctuations on superconductivity is discussed.

Preconditioning with recombinant high-mobility group box 1 induces ischemic tolerance in a rat model of focal cerebral ischemia-reperfusion.

Preconditioning with ligands of toll-like receptors (TLRs) is a powerful neuroprotective approach whereby a low dose of stimulus confers significant protection against subsequent substantial brain damage by reprogramming the ischemia-activated TLRs signaling. Herein, we aim to explore whether preconditioning with recombinant high-mobility group box 1 (rHMGB1), one of the TLRs ligands, decreases cerebral ischemia-reperfusion injury (IRI). Rats were intracerebroventricularly pretreated with rHMGB1, 1 or 3 days before induction of middle cerebral artery occlusion. Results showed that preconditioning with rHMGB1 1 day, but not 3 days, prior to ischemia dramatically reduced neurological deficits, infarct size, brain swelling, cell apoptosis, and blood-brain barrier permeability. Interleukin-1R-associated kinase-M (IRAK-M), a critical negative regulator of TLRs signaling, was robustly increased in response to brain IRI and was further elevated by rHMGB1 pretreatment, indicating its role associated with the rHMGB1 preconditioning-mediated ischemic tolerance. In vitro and in vivo assays indicated that the induced IRAK-M expression was localized in microglia. In addition, TLR4 specific inhibitor TAK-242 abolished the neuroprotective effects and the induction of IRAK-M offered by rHMGB1 preconditioning. Collectively, our study demonstrates that rHMGB1 preconditioning is neuroprotective during cerebral IRI, which is associated with activated TLR4/IRAK-M signaling in microglia. We found that high-mobility group box 1 (HMGB1) pretreatment conditioned the brain against subsequent ischemia-reperfusion injury. We propose the following mechanism for HMGB1 preconditioning-mediated ischemic tolerance: through toll-like receptor TLR4, HMGB1 preconditioning magnifies the up-regulation of interleukin-1R-associated kinase-M (IRAK-M) induced by ischemia-reperfusion in microglia, resulting in the decreased phosphorylation of IRAK-1. These findings are helpful in understanding the endogenous mechanisms that counteract ischemic insults.

Electroacupuncture Exerts Neuroprotection through Caveolin-1 Mediated Molecular Pathway in Intracerebral Hemorrhage of Rats.

Spontaneous intracerebral hemorrhage (ICH) is one of the most devastating types of stroke. Here, we aim to demonstrate that electroacupuncture on Baihui (GV20) exerts neuroprotection for acute ICH possibly via the caveolin-1/matrix metalloproteinase/blood-brain barrier permeability pathway. The model of ICH was established by using collagenase VII. Rats were randomly divided into three groups: Sham-operation group, Sham electroacupuncture group, and electroacupuncture group. Each group was further divided into 4 subgroups according to the time points of 6 h, 1 d, 3 d, and 7 d after ICH. The methods were used including examination of neurological deficit scores according to Longa's scale, measurement of blood-brain barrier permeability through Evans Blue content, in situ immunofluorescent detection of caveolin-1 in brains, western blot analysis of caveolin-1 in brains, and in situ zymography for measuring matrix metalloproteinase-2/9 activity in brains. Compared with Sham electroacupuncture group, electroacupuncture group has resulted in a significant improvement in neurological deficit scores and in a reduction in Evans Blue content, expression of caveolin-1, and activity of matrix metalloproteinase-2/9 at 6 h, 1 d, 3 d, and 7 d after ICH (P < 0.05). In conclusion, the present results suggested that electroacupuncture on GV20 can improve neurological deficit scores and reduce blood-brain barrier permeability after ICH, and the mechanism possibly targets caveolin-1/matrix metalloproteinase/blood-brain barrier permeability pathway.

The quality of reporting of randomized controlled trials of electroacupuncture for stroke.

BACKGROUND: Electroacupuncture (EA), as an extension technique of acupuncture based on traditional acupuncture combined with modern electrotherapy, is commonly used for stroke in clinical treatment and researches. However, there is still a lack of enough evidence to recommend the routine use of EA for stroke. This study is aimed at evaluating the quality of reporting of randomized controlled trials (RCTs) on EA for stroke. METHODS: RCTs on EA for stroke were evaluated by using CONSORT guidelines and STRICTA guidelines. Microsoft Excel 2010 and the R software were used for descriptive statistics analyses. RESULTS: Seventy studies involving 5468 stroke patients were identified. The CONSORT scores ranged from 16.2 to 67.6% and STRICTA scores from 29.4 to 82.4%. The central items in CONSORT as eligibility criterion, sample size calculation, primary outcome, method of randomization sequence generation, allocation concealment, implementation of randomization, description of blinding, and detailed statistical methods were reported in 100, 6, 68, 37, 14, 10, 16, and 97% of trials, respectively. The reporting of items in STRICTA as acupuncture rationale was 1a (91%), 1b (86%) and 1c 0%; needling details 2a (33%), 2b (97%), 2c (29%), 2d (64%), 2e (100%), 2f (55%) and 2 g (66%); treatment regimen 3a (69%) and 3b (100%); other components of treatment 4a (86%) and 4b (13%); practitioner background item 5 (16%); control intervention(s) 6a (93%) and 6b (10%). CONCLUSIONS: The quality of reporting of RCTs on EA for stroke was generally moderate. The reporting quality needs further improvement.

Activation of matrix metalloproteinase in dorsal hippocampus drives improvement in spatial working memory after intra-VTA nicotine infusion in rats.

The hippocampus receives dopaminergic projections from the ventral tegmental area (VTA) and substantia nigra. These inputs appear to provide a modulatory signal that influences hippocampus-dependent behaviors. Enhancements in working memory performance have been previously reported following acute smoking/nicotine exposure. However, the underlying mechanism remains unclear. This study investigated the effects of nicotine on spatial working memory (SWM) and the mechanisms involved. Delayed alternation T-maze task was used to assess SWM. In situ and gel gelatin zymography were used to detect matrix metalloproteinase-9 (MMP-9) in SWM. Systemic or local (intra-VTA) administration of nicotine significantly improves SWM, which was accompanied by increased MMP-9 activity in dorsal hippocampus (dHPC). Intra-dHPC administration of MMP inhibitor FN-439 abolished the memory enhancement induced by intra-VTA nicotine infusion. FN-439 had no effect on locomotor behavior. Our data suggest that intra-VTA nicotine infusion activates MMP-9 in dHPC to improve SWM in rats.

Ferromagnetic Spin Fluctuation and Unconventional Superconductivity in Rb2Cr3As3 Revealed by 75As NMR and NQR.

We report (75)As nuclear magnetic resonance (NMR) and nuclear quadrupole resonance (NQR) studies on the superconductor Rb(2)Cr(3)As(3) with a quasi-one-dimensional crystal structure. Below T∼100 K, the spin-lattice relaxation rate (1/T(1)) divided by temperature, 1/T(1)T, increases upon cooling down to T(c)=4.8 K, showing a Curie-Weiss-like temperature dependence. The Knight shift also increases with decreasing temperature. These results suggest ferromagnetic spin fluctuation. In the superconducting state, 1/T(1) decreases rapidly below T(c) without a Hebel-Slichter peak, and follows a T(5) variation below T∼3 K, which points to unconventional superconductivity with point nodes in the gap function.

Promoting blood circulation for removing blood stasis therapy for acute intracerebral hemorrhage: a systematic review and meta-analysis.

AIM: To conduct a systematic review and meta-analysis to assess the current evidence available regarding the promoting blood circulation and removing blood stasis (PBCRBS) therapy for Chinese patients with acute intracerebral hemorrhage (ICH). METHODS: Six databases were searched from their inception to November 2013. The studies assessed in ≥ 4 domains with 'yes' were selected for detailed assessment and meta-analysis. The herbal compositions for PBCRBS therapy for acute ICH patients were also assessed. RESULTS: From the 6 databases, 292 studies claimed randomized-controlled clinical trials (RCTs). Nine studies with 798 individuals were assessed in ≥ 4 domains with 'yes' by using the Cochrane RoB tool. Meta-analysis showed that PBCRBS monotherapy and adjuvant therapy for acute ICH could improve the neurological function deficit, reduce the volume of hematoma and perihematomal edema, and lower the mortality rate and dependency. Moreover, there were fewer adverse effects when compared with Western conventional medication controls. Xueshuantong Injection and Fufang Danshen Injection, Buyang Huanwu Decoction and Liangxue Tongyu formula, and three herbs (danshen root, sanqi and leech) were the most commonly used Chinese herbal patent injections, herbal prescriptions and single herbs, respectively. CONCLUSION: Despite the apparently positive findings, it is premature to conclude that there is sufficient efficacy and safety of PBCRBS for ICH because of the high clinical heterogeneity of the included studies and small number of trials in the meta-analysis. Further large sample-sizes and rigorously designed RCTs are needed.

[On the Conditionality of "Disease" in Treating Different Diseases with the Same Method].

Treating different diseases with the same method is a unique original thinking in Chinese medicine, which embodies the spirit of treatment based on syndrome differentiation. We briefly reviewed the origin and development of this concept. We also reviewed that thinking of combination of disease and syndrome is its premise and foundation. We put forward the conditionality of diseases in treating different diseases with the same method by cutting-in modern biological basic researches, that is to say, one kind specific diseases or disease of one specific system. We emphasized the importance of diseases conditionality in treating different diseases with the same method, which was of great significance in studies on combination of disease and syndrome, correspondence of prescription and syndrome, and modern biological basic researches of treating different diseases with the same method.

Strain-induced long-range charge-density wave order in the optimally doped Bi2Sr2-xLaxCuO6 superconductor.

The mechanism of high-temperature superconductivity in copper oxides (cuprate) remains elusive, with the pseudogap phase considered a potential factor. Recent attention has focused on a long-range symmetry-broken charge-density wave (CDW) order in the underdoped regime, induced by strong magnetic fields. Here by 63,65Cu-nuclear magnetic resonance, we report the discovery of a long-range CDW order in the optimally doped Bi2Sr2-xLaxCuO6 superconductor, induced by in-plane strain exceeding ∣ε∣ = 0.15 %, which deliberately breaks the crystal symmetry of the CuO2 plane. We find that compressive/tensile strains reduce superconductivity but enhance CDW, leaving superconductivity to coexist with CDW. The findings show that a long-range CDW order is an underlying hidden order in the pseudogap state, not limited to the underdoped regime, becoming apparent under strain. Our result sheds light on the intertwining of various orders in the cuprates.

Efficacy and safety of Suanzaoren decoction for primary insomnia: a systematic review of randomized controlled trials.

BACKGROUND: Insomnia is a widespread human health problem, but there currently are the limitations of conventional therapies available. Suanzaoren decoction (SZRD) is a well known classic Chinese herbal prescription for insomnia and has been treating people's insomnia for more than thousand years. The objective of this study was to evaluate the efficacy and safety of SZRD for insomnia. METHODS: A systematic literature search was performed for 6 databases up to July of 2012 to identify randomized control trials (RCTs) involving SZRD for insomniac patients. The methodological quality of RCTs was assessed independently using the Cochrane Handbook for Systematic Reviews of Interventions. RESULTS: Twelve RCTs with total of 1376 adult participants were identified. The methodological quality of all included trials are no more than 3/8 score. Majority of the RCTs concluded that SZRD was more significantly effective than benzodiazepines for treating insomnia. Despite these positive outcomes, there were many methodological shortcomings in the studies reviewed, including insufficient information about randomization generation and absence of allocation concealment, lack of blinding and no placebo control, absence of intention-to-treat analysis and lack of follow-ups, selective publishing and reporting, and small number of sample sizes. A number of clinical heterogeneity such as diagnosis, intervention, control, and outcome measures were also reviewed. Only 3 trials reported adverse events, whereas the other 9 trials did not provide the safety information. CONCLUSIONS: Despite the apparent reported positive findings, there is insufficient evidence to support efficacy of SZRD for insomnia due to the poor methodological quality and the small number of trials of the included studies. SZRD seems generally safe, but is insufficient evidence to make conclusions on the safety because fewer studies reported the adverse events. Further large sample-size and well-designed RCTs are needed.

Role of Crosstalk between Glial Cells and Immune Cells in Blood-Brain Barrier Damage and Protection after Acute Ischemic Stroke.

Blood-brain barrier (BBB) damage is the main pathological basis for acute ischemic stroke (AIS)-induced cerebral vasogenic edema and hemorrhagic transformation (HT). Glial cells, including microglia, astrocytes, and oligodendrocyte precursor cells (OPCs)/oligodendrocytes (OLs) play critical roles in BBB damage and protection. Recent evidence indicates that immune cells also have an important role in BBB damage, vasogenic edema and HT. Therefore, regulating the crosstalk between glial cells and immune cells would hold the promise to alleviate AIS-induced BBB damage. In this review, we first introduce the roles of glia cells, pericytes, and crosstalk between glial cells in the damage and protection of BBB after AIS, emphasizing the polarization, inflammatory response and crosstalk between microglia, astrocytes, and other glia cells. We then describe the role of glial cell-derived exosomes in the damage and protection of BBB after AIS. Next, we specifically discuss the crosstalk between glial cells and immune cells after AIS. Finally, we propose that glial cells could be a potential target for alleviating BBB damage after AIS and we discuss some molecular targets and potential strategies to alleviate BBB damage by regulating glial cells after AIS.

Antiferromagnetic spin fluctuations above the dome-shaped and full-gap superconducting states of LaFeAsO1-xFx revealed by (75)As-nuclear quadrupole resonance.

We report a systematic study by (75)As nuclear-quadrupole resonance in LaFeAsO(1-x)F(x). The antiferromagnetic spin fluctuation found above the magnetic ordering temperature T(N) = 58 K for x = 0.03 persists in the regime 0.04 ≤ x ≤ 0.08, where superconductivity sets in. A dome-shaped x dependence of the superconducting transition temperature T(c) is found, with the highest T(c) = 27 K at x = 0.06, which is realized under significant antiferromagnetic spin fluctuation. With increasing x further, the antiferromagnetic spin fluctuation decreases, and so does T(c). These features resemble closely the cuprates La(2-x)Sr(x)CuO(4). In x = 0.06, the spin-lattice relaxation rate (1/T(1)) below T(c) decreases exponentially down to 0.13T(c), which unambiguously indicates that the energy gaps are fully opened. The temperature variation of 1/T(1) below T(c) is rendered nonexponential for other x by impurity scattering.

History and mechanism for treatment of intracerebral hemorrhage with scalp acupuncture.

Intracerebral hemorrhage (ICH) is an important public health problem with high rates of mortality, morbidity, and disability, but no clinically proven treatment strategy is available to date. Scalp acupuncture (SA) refers to a therapy for treating diseases by needling and stimulating the specific areas of the scalp. The evidence from clinical studies suggested that SA therapy may produce significant benefits for patients with acute ICH. However, the therapeutic mechanisms are yet not well addressed. Therefore, in this paper, we provide a comprehensive overview on the history and mechanisms of SA therapy on acute ICH. Although SA has been practiced for thousands of years in China and could date back to 5 BC, SA therapy for acute ICH develops only in the recent 30 years. The possible mechanisms associated with the therapeutic effects of SA on ICH include the influence on hematoma, brain edema, and blood brain barrier, the products released from haematoma, the immune and inflammatory reaction, focal perihemorrhagic hypoperfusion and hemorheology, neuroelectrophysiology, and so on. At last, the existence of instant effect of SA on acute ICH and its possible mechanisms are presented.

Chinese herbal medicine paratherapy for Parkinson's disease: a meta-analysis of 19 randomized controlled trials.

Parkinson's disease (PD) is a common and debilitating neurodegenerative disorder that needs long-term levodopa administration and can result in progressive deterioration of body functions, daily activities and participation. The objective of this meta-analysis evaluates the clinical efficacy and safety of Chinese herbal medicine (CHM) as an adjunct therapy for PD patients. Methodological issues include a systematic literature search between 1950 and April 2011 to identify randomized trials involving CHM adjuvant therapy versus western conventional treatment. The outcome measures assessed were the reduction in scores of Unified Parkinson's Disease Rating Scale (UPDRS) and adverse effects. 19 trials involving 1371 participants were included in the meta-analysis. As compared to western conventional treatment, CHM adjuvant therapy resulted in greater improvement in UPDRS I, II, III, IV scores, and UPDRS I-IV total scores (P < 0.001). Adverse effects were reported in 9 studies. The side effects in CHM adjuvant therapy group were generally less than or lighter than the conventional treatment group. In conclusion, CHM adjuvant therapy may potentially alleviate symptoms of PD and generally appeared to be safe and well tolerated by PD patients. However, well-designed, randomized, placebo-controlled clinical trials are still needed due to the generally low methodological quality of the included studies.

Clinical efficacy and safety of buyang huanwu decoction for acute ischemic stroke: a systematic review and meta-analysis of 19 randomized controlled trials.

Buyang Huanwu Decoction (BHD) is a well-known traditional Chinese herbal prescription for treating stroke-induced disability. The objective of this study was to evaluate the efficacy and safety of BHD for acute ischemic stroke. A systematic literature search was performed in 6 databases until February 2012. Randomized controlled clinical trials (RCTs) that evaluate efficacy and safety of BHD for acute ischemic stroke were included. Nineteen RCTs with 1580 individuals were identified. The studies were generally of low methodological quality. Only one of the trial included death or dependency as a primary outcome measure. Only 4 trials reported adverse events. Meta-analysis showed the clinical effective rate of neurological deficit improvement favoring BHD when compared with western conventional medicines (WCM), P < 0.001. There is significant difference in the neurologic deficit score between the BHD treatment group and the WCM control group, P < 0.001. In Conclusion, BHD appears to improve neurological deficit and seems generally safe in patients with acute ischemic stroke. However, the current evidence is insufficient to support a routine use of BHD for acute ischemic stroke due to the poor methodological quality and lack of adequate safety data of the included studies. Further rigorously designed trials are required.