Ahmed Negida

An updated review of Zika virus

The current outbreak of Zika virus (ZIKV) in South America is one of the most serious public health emergencies since the Ebola outbreak of West Africa [2014]. ZIKV belongs to the flaviviridae family and has two lineages (Asian and African). The virus was first discovered in Uganda [1947] and the first human infection was identified in Nigeria [1952]. The current epidemic is the third of its type after that of Yap Island, Micronesia [2007] and French Polynesia [2013]. Phylogenetic studies revealed that the current strain shares about 99.7% of nucleotides and 99.9% of amino acids with the strain of French Polynesia epidemic [2013], suggesting that it has spread across the Pacific Ocean to invade South America. Aedes Aegypti mosquito is the main vector for ZIKV and there are some reports describing possible sexual and maternal to fetal transmission. ZIKV infection is known to be self-limited. However, recent reports suggested that it can be associated with neurological manifestations as Guillan-Barrè Syndrome and microcephaly in the newborn population. Currently, vector control seems to be the most effective available preventive measure against ZIKV spread. The development of broad spectrum antivirals and ZIKV vaccines should be a priority of future research.

Neuroprotective mechanisms of plant extracts against MPTP induced neurotoxicity: Future applications in Parkinson’s disease

Parkinsons disease (PD) is the second most common neurodegenerative disease after Alzheimers disease, affecting about seven to 10 million patients worldwide. The major pathological features of PD are loss of dopaminergic neurons in the nigrostriatal pathway and accumulation of alpha-synuclein molecules, forming Lewy bodies. Until now, there is no effective cure for PD, and investigators are searching for neuroprotective strategies to stop or slow the disease progression. The MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) induced neurotoxicity of the nigrostriatal pathway has been used to initiate PD in animal models. Multiple experimental studies showed the ability of several plant extracts to protect against MPTP induced neurotoxicity through activation of catalase, superoxide dismutase, and glutathione reductase enzymes, which reduce the cellular concentration of free radicals, preventing intracellular Ca++ release and subsequent apoptosis signaling. Other neuroprotective mechanisms of plant extracts include promoting autophagy of alpha-synuclein molecules and exerting an antiapoptotic activity via inhibition of proteolytic poly (ADP-ribose) polymerase and preventing caspase cleavage. The variety of neuroprotective mechanisms of natural plant extracts may allow researchers to target PD progression in different pathological stages and may be through multiple pathways. Further investigations are required to translate these neuroprotective mechanisms into safe and effective treatments for PD.

Parkinson’s disease and pesticides: A meta-analysis of disease connection and genetic alterations

Parkinsons disease (PD) is a globally prevalent, multifactorial disorder that occurs due to interactions between genetic and environmental factors. Observational studies have shown a link between exposure to pesticides and the risk of PD. We performed this study to systemically review published case-control studies and estimate quantitatively the association between pesticide exposure and PD. We searched Medline (through PubMed) for eligible case-control studies. The association between pesticide exposure and PD risk or occurrence of certain genetic alterations, related to the pathogenesis of PD was presented as odds ratios (OR) and pooled under the random effects model, using the statistical add-in (MetaXL, version 5.0). The pooled result showed that exposure to pesticides is linked to PD (OR 1.46, 95% CI [1.21, 1.77]), but there was a significant heterogeneity among included studies. Exposure to pesticides increased the risk of alterations in different PD pathogenesis-related genes, such as GST (OR 1.97, 95% CI [1.41, 2.76]), PON-1 (OR 1.32, 95% CI [1.09, 1.6]), MDR1 (OR 2.06, 95% CI [1.58, 2.68]), and SNCA genes (OR 1.28, 95% CI [1.02, 1.37]). There was no statistically significant association between exposure to pesticides and alteration of CYP2D6 (OR 1.19, 95% CI [0.91, 1.54]), SLC6A3 (OR 0.74, 95% CI [0.55, 1]), MnSOD (OR 1.45, 95% CI [0.97, 2.16]), NQO1 (OR 1.35, 95% CI [0.91, 2.01]), and PON-2 genes (OR 0.88, 95% CI [0.53, 1.45]). In conclusion, this meta-analysis provides evidence that pesticide exposure is significantly associated with the risk of PD and alterations in genes involved in PD pathogenesis. However, the underlying mechanism of this association and the effect of the duration of exposure or the type of pesticides should be addressed by future research.

The Role of Caffeine in Pain Management: A Brief Literature Review

Context: Caffeine is the most commonly used psychoactive legal drug in the world. Caffeine’s role in controlling pain has received less attention in the past, yet is being increasingly considered. This article briefly reviewed the literature to clarify the role of caffeine as a drug for pain control and attract investigators to this topic. Evidence Acquisition: The data on Caffeine as an adjuvant therapy or as a main component for pain modulation has been narratively reviewed. Results: Caffeine plays an important role in pain modulation through their action on adenosine receptors which are involved in nociception. The use of caffeine as adjuvant treatment was well-established in the literature and caffeine is currently available in some over the counter medications. Studies showed controversial results about the interaction between caffeine and morphine for pain relief in patients with terminal stage cancer. As a main component for pain modulation, Caffeine can be used for hypnic headache and postdural puncture headache. Conclusions: Caffeine has a potential role for pain modulation. Current evidence on caffeine use for migraine and terminal stage cancer is not well-established. Future studies should address the use of caffeine alone for different types of pain with dose escalation and standardization of outcome measurement.

Coenzyme Q10 for Patients with Parkinson's Disease: A Systematic Review and Meta-Analysis

INTRODUCTION Coenzyme Q10 (CoQ10) is an antioxidant that enhances the activity of complex I and II in the Electron Transport Chain. Many preclinical and clinical studies evaluated CoQ10 for neuroprotection against Parkinsons disease (PD). The aim of this study is to synthesize evidence from published randomized controlled trials (RCTs) about the benefit of CoQ10 supplementation for patients with Parkinsons disease. METHODS We followed the PRISMA statement guidelines during the preparation of this systematic review and metaanalysis. A computer literature search for (PubMed, EBSCO, Web of science and Ovid Midline) was carried out. We included RCTs comparing CoQ10 with placebo in terms of motor functions and quality of life. Outcomes of total Unified Parkinsons Disease Rating Scale (UPDRS), UPDRS I, UPDRS II, UPDRS III and Schwab and England scores were pooled as standardized mean difference (SMD) between two groups from baseline to the endpoint. RESULTS Five RCTs (981 patients) were included in this study. The overall effect did not favor either of the two groups in terms of: total UPDRS score (SMD -0.05, 95%CI [-0.10, 0.15]), UPDRS I (SMD -0.03, 95% CI [-0.23, 0.17]), UPDRS II (SMD -0.10, 95%CI [-0.35, 0.15]), UPDRS III (SMD -0.05, 95%CI [-0.07, 0.17]) or Schwab and England score (SMD 0.08, 95%CI [-0.13, 0.29]). CONCLUSION CoQ10 supplementation does not slow functional decline nor provide any symptomatic benefit for patients with Parkinsons disease.

Comparing the Interpretation of Traumatic Chest X-Ray by Emergency Medicine Specialists and Radiologists

Background: Discrepancy between X-ray readings of emergency physicians (EPs) versus radiologists was reported between 0.95% and 16.8% in different studies. The discordance was even higher when specific studies such as chest X-rays (CXR) were probed. Objectives: This prospective study was conducted to assess the discrepancies between emergency and radiology departments with respect to interpretation of the traumatic chest X-rays. Patients and Methods: This prospective study was conducted in Shohadaye Tajrish Hospital, Tehran, Iran, from March to April 2014. Based on Advanced Trauma Life Support (ATLS) guidelines, plain chest radiography (CXR) was ordered for all patients in two standard views of posterior-anterior and lateral. All CXRs were interpreted by a corresponding emergency medicine specialist and a radiologist blind to the clinical findings of the patients. Finally, the results of two interpretations were compared. Accuracy, sensitivity, specificity, and predictive values of traumatic CXR interpretation were calculated by EPs with 95% of confidence interval (CI). Results: The evaluation of EPs was identical to that of the radiologists in 89.5% of the cases. Ninety-eight percent (98%) indicated total agreement and 1.5 percent total disagreement. Conclusions: There is a high agreement between EPs and radiologists in CXR interpretations in Shohadaye Tajrish Hospital. Thus, EPs can substitute radiologists in the emergency department. More improvements are recommended to achieve the standard level of agreement.

Bee venom for the treatment of Parkinson’s disease: How far is it possible?

Parkinsons disease (PD) is the second most common neurodegenerative disease, characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta leading to depletion of striatal dopamine and motor symptoms as bradykinesia, resting tremors, rigidity, and postural instability. Current therapeutic strategies for PD are mainly symptomatic and may cause motor complications, such as motor fluctuations and dyskinesia. Therefore, alternative medicine may offer an effective adjuvant treatment for PD. Bee venom therapy (BVT) has long been used as a traditional therapy for several conditions, such as rheumatoid arthritis, asthma, and skin diseases. Experimental and clinical studies showed that BVT could be an effective adjuvant treatment for PD. Several mechanisms were suggested for these findings including the ability of BVT to attenuate neuroinflammation, inhibit apoptosis of dopaminergic neurons, protect against glutamate-induced neurotoxicity, and restore normal dopamine levels in the nigrostriatal pathway. In this article, we reviewed and summarized the literature regarding the potential of BVT for the treatment of PD.

Safety and efficacy of sofosbuvir plus ledipasvir with and without ribavirin for chronic HCV genotype-1 infection: a systematic review and meta-analysis.

BACKGROUND Ledipasvir and sofosbuvir are new direct-acting antiviral agents for patients with HCV infection. Ledipasvir inhibits the HCV non-structural 5A protein, while sofosbuvir is a nucleotide polymerase inhibitor. Many studies have evaluated the safety and efficacy of ledipasvir and sofosbuvir combination with and without ribavirin for patients with chronic HCV genotype-1. METHODS A computer literature search of PubMed, SCOPUS, Web of Knowledge and Cochrane CENTRAL has been conducted. Studies were screened for eligibility and data were extracted. Sustained virological response (SVR) rate and commonly reported adverse events were pooled as risk ratio (RR) using Review Manager version 5.3 for windows and OpenMeta (Analyst) software. RESULTS Eight randomized controlled trials (n=1,892) were pooled in the final analysis. A 12-week ledipasvir and sofosbuvir regimen achieved SVR in 97.5% and 89% of non-cirrhotic and cirrhotic patients, respectively. A 24-week ledipasvir and sofosbuvir regimen achieved SVR in 99.6% and 92.6% in non-cirrhotic and cirrhotic patients, respectively. When ribavirin was added to the treatment regiment, the SVR did not differ significantly in either of the treatment regimens (12-week SVR: 93.9% versus 96.7%, RR=0.97, P=0.19 and 24-week SVR: 94.8% versus 97.2%, RR=0.98, P=0.24). CONCLUSIONS The combination of sofosbuvir and ledipasvir achieved high SVR rates (>90%) in both cirrhotic and non-cirrhotic patients with HCV genotype-1. The addition of ribavirin to this regimen did not significantly increase the SVR rates.

Self-gripping versus sutured mesh fixation methods for open inguinal hernia repair: A systematic review of clinical trials and observational studies.

Background. We performed this systematic review and meta‐analysis to compare the outcomes of Lichenstein hernia repair using either self‐gripping mesh or techniques of sutured mesh fixation. Methods. We searched PubMed, Cochrane CENTRAL, Scopus, Embase, and Web of Science for all clinical trials and observational studies that compared self‐gripping mesh versus sutured mesh fixation in Lichtenstein hernia repair. Combined outcomes were pooled as odds ratios or mean differences in a fixed‐effect model, using Comprehensive Meta‐Analysis software for Windows. Results. Twelve randomized, controlled trials and 5 cohort studies (n = 3,722 patients) were included in the final analysis. The two groups, using self‐gripping mesh or sutured mesh fixation, did not differ significantly in terms of recurrence rate (odds ratio = 0.66, 95% confidence interval 0.18–2.44; P = .54) or postoperative chronic groin pain (odds ratio = 0.75, 95% confidence interval 0.54–1.05; P = .09). The operative time was less in the self‐gripping mesh group (mean difference = −7.85, 95% confidence interval −9.94 to −5.76; P < .0001). For safety analysis, there were comparable risks between self‐gripping mesh and sutured mesh fixation groups in terms of postoperative infection (odds ratio = 0.81, 95% confidence interval 0.53–1.23; P = .32), postoperative hematoma (odds ratio = 0.97, 95% confidence interval 0.7–1.36; P = .9), and urinary retention (odds ratio = 0.66, 95% confidence interval 0.18–2.44; P = .54). Conclusion. Data from our analysis did not favor either of the two fixation techniques over the other in terms of recurrence or postoperative chronic groin pain. Decreased operative time in the self‐gripping mesh group cannot justify a recommendation for its routine use. Longer follow‐up studies are needed to compare the risk of long‐term recurrence for both meshes.

Evidence for association between hepatitis C virus and Parkinson’s disease

Parkinson’s disease (PD) is a globally prevalent neurodegenerative disorder, characterized by progressive neuronal loss in the substantia nigra and formation of Lewy bodies. These pathological characteristics are clinically translated into motor symptoms, such as bradykinesia, rigidity, resting tremors, and postural instability. Emerging data from epidemiological studies suggest a possible association between PD and hepatitis C virus (HCV) infection, which affects up to 71 million individuals worldwide. Preclinical studies have shown that HCV can penetrate and replicate within the brain macrophages and microglial cells, increasing their production of pro-inflammatory cytokines that can directly cause neuronal toxicity. Other studies reported that interferon, previously used to treat HCV infection, can increase the risk of PD through inhibition of the nigrostriatal dopaminergic transmission or induction of neuroinflammation. In this article, we provide a comprehensive review on the possible association between HCV infection and PD and highlight recommendations for further research and practice in this regard.