Efficacy of Traditional Chinese Medicines in Preventing Oxaliplatin-induced Peripheral Neurotoxicity in Cancer Patients: A Network Meta-analysis

Objective Oxaliplatin-induced peripheral neurotoxicity(OIPN) is the main limitation for its continuation in cancer patients.Traditional Chinese medicines(TCMs) have been used to prevent OIPN in China and have been demonstrated to be effective.However,due to the lack of direct comparison among TCMs,it remains unclear that which TCM is the best for OIPN prevention.Consequently,the present study aimed to compare the relative efficacies of TCMs to find out the best TCM by applying a network meta-analysis.Methods Studies were identified by searching PubMed,EMbase,Cochrane Libraries,CNKI,WanFang,and WeiPu database from January 1990 to May2016.Randomized controlled trials(RCTs) that evaluated the efficacy of TCMs in preventing OIPN in cancer patients were included.Statistical analysis was performed with ADDIS 1.1 6.6.Results Twenty-five RCTs(1572 patients) involving five TCMs were included.The results of network meta-analyses showed that compared with oxaliplatin-based chemotherapy alone,the combination with Huangqi Injection(HQI),Shenmai Injection(SMI),Shenfu Injection(SFI),Buyang Huanwu Decoction(BHD),and Huangqi Guizhi Wuwu Decoction(HGWD) could decrease the overall OIPN incidence and the severe OIPN incidence in cancer patients.In addition,probability ranking results showed the order of efficacy in preventing overall OIPN incidence was HQI HGWD SFI =SMI BHD,while the order of efficacy in preventing severe OIPN incidence was HQI HGWD BHD SFI = SMI.Conclusion All five TCMs are effective neuroprotective agents against OIPN.Among these TCMs,HQI and HGWD were superior to others in clinical efficacy.Moreover,Astragalus membranaceus might be a more promising herb for the OIPN prevention.However,more direct head-to-head RCTs with high quality and large sample size are still needed to further confirm the conclusion.     

深刺久留针法结合火针治疗周围性面瘫体会

针灸治疗周围性面瘫是公认行之有效的方法,尤其采取分期多种方法联合治疗周围性面瘫效果会更加显著。急性期初起较轻,采用针刺配合刺血疗法;静止期采用火针点刺后再行刺血和毫针刺法;恢复期采用火针点刺,毫针深刺久留,同时配合刺血疗法。周围性面瘫采用针灸择期治疗能取得更好的治疗效果,从针刺治疗面瘫病的时机到穴位的选取都有其科学性和规律性。     

中西医治疗糖尿病周围神经病变研究进展

对于糖尿病周围神经病变的治疗,中医以"络以通为用"为治疗原则,在改善临床症状,阻止DPN进一步恶化,减少截肢率方面,都有很好的疗效。西医可以有效控制血糖、血压,弥补了中药不能快速降糖降压之不足,对防止DPN的发生和发展起了重要作用。中西医结合治疗具有一定互补优势,疗效确切,但其作用机制尚不明确,需进一步加强实验研究,明确中医药作用机理,提高临床疗效。     

药物涂层球囊治疗下肢动脉疾病研究进展

下肢动脉疾病(LEAD)是由动脉粥样硬化引起的下肢动脉管腔狭窄、闭塞,导致相应肢体出现缺血症状的一类疾病。腔内介入是治疗LEAD的主要方式,包括经皮腔内血管成型术(PTA)及支架植入术,但术后再狭窄率较高。药物涂层球囊(DCB)可在抑制血管内膜增生及炎症反应的同时避免腔内异物存留,对于原发病变及支架内再狭窄均有较好疗效。本文对DCB作用原理及其治疗LEAD应用现状和研究进展进行综述。     

The association between thrombotic and inflammatory biomarkers and lower‐extremity peripheral artery disease

Lower‐extremity peripheral artery disease (LEAD) is associated with increased rates of mortality and morbidity. The aim of this study was to evaluate the associations among inflammatory and thrombotic markers and lower‐extremity peripheral disease. A total of 280 patients were enrolled in this study. Of these patients, 152 patients had LEAD on peripheral angiography that was performed because of suspected lower‐extremity peripheral disease based on history, physical examination, and non‐invasive tests. The control group consisted of 128 patients without LEAD on peripheral angiography. Patients with LEAD were classified according to trans‐atlantic inter‐society consensus (TASC) II classification. Subsequently, patients in TASC A to B were defined as having mild to moderate peripheral artery disease, and those in TASC C to D were defined as having advanced peripheral artery disease. Thrombotic and inflammatory markers, such as the neutrophil‐to‐lymphocyte ratio (NLR), the high‐sensitivity C (hs‐C) reactive protein level, the monocyte‐to‐high‐density lipoprotein‐cholesterol ratio, the fibrinogen to albumin ratio (FAR), and whole‐blood viscosity at high shear rate (HSR) and low shear rate (LSR), were evaluated in this population. The NLR, the monocyte‐to‐high‐density lipoprotein‐cholesterol ratio, the FAR, and whole‐blood viscosity, both at a LSR and a HSR, were significantly higher in patients with lower‐extremity peripheral disease compared with patients without lower‐extremity peripheral disease. We determined that lower‐extremity peripheral disease severity was correlated with the NLR, monocyte‐to‐high‐density lipoprotein‐cholesterol ratio, FAR, whole‐blood viscosity at LSR, and whole‐blood viscosity at HSR (r = 0.719, P = .004; r = 0.25, P = .008; r = 0.691, P = .002; r = 0.546, P < .001; and r = 0.448, P = .001, respectively). However hs‐C reactive protein levels were similar between patients with or without LEAD (2.47 ± 1.32 1.61 ± 0.91 P = .685). In addition, there was no correlation between the severity of LEAD and hs‐C reactive levels. In this study, we determined that the levels of inflammatory and thrombotic biomarkers are elevated in peripheral artery disease, and these levels predict disease severity.     

PredyCLU: A prediction system for chronic leg ulcers based on fuzzy logic; part II—Exploring the arterial side

Peripheral arterial disease (PAD) and its most severe form, critical limb ischaemia (CLI), are very common clinical conditions related to atherosclerosis and represent the major causes of morbidity, mortality, disability, and reduced quality of life (QoL), especially for the onset of ischaemic chronic leg ulcers (ICLUs) and the subsequent need of amputation in affected patients. Early identification of patients at risk of developing ICLUs may represent the best form of prevention and appropriate management. In this study, we used a Prediction System for Chronic Leg Ulcers (PredyCLU) based on fuzzy logic applied to patients with PAD. The patient population consisted of 80 patients with PAD, of which 40 patients (30 males [75%] and 10 females [25%]; mean age 66.18 years; median age 67.50 years) had ICLUs and represented the case group. Forty patients (100%) (27 males [67.50%] and 13 females [32.50%]; mean age 66.43 years; median age 66.50 years) did not have ICLUs and represented the control group. In patients of the case group, the higher was the risk calculated with the PredyCLU the more severe were the clinical manifestations recorded. In this study, the PredyCLU algorithm was retrospectively applied on a multicentre population of 80 patients with PAD. The PredyCLU algorithm provided a reliable risk score for the risk of ICLUs in patients with PAD.     

In vitro marker gene expression analyses in human peripheral blood mononuclear cells: A tool to assess safety of influenza vaccines in humans

Vaccines are inoculated in healthy individuals from children to the elderly, and thus high levels of safety and consistency of vaccine quality in each lot must meet the required specifications by using preclinical and lot release testing. Because vaccines are inoculated into humans, recapitulation of biological reactions in humans should be considered for test methods. We have developed a new method to evaluate the safety of influenza vaccines using biomarker gene expression in mouse and rat models. Some biomarker genes are already known to be expressed in human lymphocytes, macrophages and dendritic cells; therefore, we considered some of these genes might be common biomarkers for human and mice to evaluate influenza vaccine safety. In this study, we used human peripheral blood mononuclear cells (PBMC) as a primary assessment tool to confirm the usefulness of potential marker genes in humans. Analysis of marker gene expression in PBMC revealed biomarker gene expressions were dose-relatedly increased in toxic reference influenza vaccine (RE)-stimulated PBMC. Although some marker genes showed increased expression in hemagglutinin split vaccine-stimulated PBMC, their expression levels were lower than that of RE in PBMC from two different donors. Many marker gene expressions correlated with chemokine production. Marker genes such as IRF7 were associated with other Type 1 interferon (IFN)-associated signals and were highly expressed in the CD304⁺ plasmacytoid dendritic cell (pDC) population. These results suggest PBMC and their marker genes may be useful for vaccine safety evaluation in humans.     

Combined therapies to treat complex diseases: The role of the gut microbiota in multiple sclerosis

The commensal microbiota has emerged as an environmental risk factor for multiple sclerosis (MS). Studies in experimental autoimmune encephalomyelitis (EAE) models have shown that the commensal microbiota is an essential player in triggering autoimmune demyelination. Likewise, the commensal microbiota modulates the host immune system, alters the integrity and function of biological barriers and has a direct effect on several types of central nervous system (CNS)-resident cells. Moreover, a characteristic gut dysbiosis has been recognized as a consistent feature during the clinical course of MS, and the MS-related microbiota is gradually being elucidated. This review highlights animal studies in which commensal microbiota modulation was tested in EAE, as well as the mechanisms of action and influence of the commensal microbiota not only in the local milieu but also in the innate and adaptive immune system and the CNS. Regarding human research, this review focuses on studies that show how the commensal microbiota might act as a pathogenic environmental risk factor by directing immune responses towards characteristic pathogenic profiles of MS. We speculate how specific microbiome signatures could be obtained and used as potential pathogenic events and biomarkers for the clinical course of MS. Finally, we review recently published and ongoing clinical trials in MS patients regarding the immunomodulatory properties exerted by some microorganisms. Because MS is a complex disease with a large variety of associated environmental risk factors, we suggest that current treatments combined with strategies that modulate the commensal microbiota would constitute a broader immunotherapeutic approach and improve the clinical outcome for MS patients.     

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome – Evidence for an autoimmune disease

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a frequent and severe chronic disease drastically impairing life quality. The underlying pathomechanism is incompletely understood yet but there is convincing evidence that in at least a subset of patients ME/CFS has an autoimmune etiology. In this review, we will discuss current autoimmune aspects for ME/CFS. Immune dysregulation in ME/CFS has been frequently described including changes in cytokine profiles and immunoglobulin levels, T- and B-cell phenotype and a decrease of natural killer cell cytotoxicity. Moreover, autoantibodies against various antigens including neurotransmitter receptors have been recently identified in ME/CFS individuals by several groups. Consistently, clinical trials from Norway have shown that B-cell depletion with rituximab results in clinical benefits in about half of ME/CFS patients. Furthermore, recent studies have provided evidence for severe metabolic disturbances presumably mediated by serum autoantibodies in ME/CFS. Therefore, further efforts are required to delineate the role of autoantibodies in the onset and pathomechanisms of ME/CFS in order to better understand and properly treat this disease.