Air pollution is a major concern of new civilized world, which has a serious toxicological impact on human health and the environment. It has a number of different emission sources, but motor vehicles and industrial processes contribute the major part of air pollution. According to the World Health Organization, six major air pollutants include particle pollution, ground-level ozone, carbon monoxide, sulfur oxides, nitrogen oxides, and lead. Long and short term exposure to air suspended toxicants has a different toxicological impact on human including respiratory and cardiovascular diseases, neuropsychiatric complications, the eyes irritation, skin diseases, and long-term chronic diseases such as cancer. Several reports have revealed the direct association between exposure to the poor air quality and increasing rate of morbidity and mortality mostly due to cardiovascular and respiratory diseases. Air pollution is considered as the major environmental risk factor in the incidence and progression of some diseases such as asthma, lung cancer, ventricular hypertrophy, Alzheimer's and Parkinson's diseases, psychological complications, autism, retinopathy, fetal growth, and low birth weight. In this review article, we aimed to discuss toxicology of major air pollutants, sources of emission, and their impact on human health. We have also proposed practical measures to reduce air pollution in Iran.

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At present, when a clinical diagnosis of Parkinson's disease (PD) is made, serious damage has already been done to nerve cells of the substantia nigra pars compacta. The diagnosis of PD in its earlier stages, before this irreversible damage, would be of enormous benefit for future treatment strategies designed to slow or halt the progression of this disease that possibly prevents accumulation of toxic aggregates. As a molecular biomarker for the detection of PD in its earlier stages, alpha-synuclein (α-syn), which is a key component of Lewy bodies, in which it is found in an aggregated and fibrillar form, has attracted considerable attention. Here, α-syn is reviewed in details.

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Autism is a developmental disability with age of onset in childhood (under 3 years old), which is characterized by definite impairments in social interactions, abnormalities in speech, and stereotyped pattern of behaviors. Due to the progress of autism in recent decades, a wide range of studies have been done to identify the etiological factors of autism. It has been found that genetic and environmental factors are both involved in autism pathogenesis. Hence, in this review article, a set of environmental factors involved in the occurrence of autism has been collected, and finally, some practical recommendations for reduction of the risk of this devastating disease in children are represented.

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Emergency departments (EDs) are the most challenging ward with respect to patient delay. The goal of this study is to present strategies that have proven to reduce delay and overcrowding in EDs. In this review article, initial electronic database search resulted in a total of 1006 articles. Thirty articles were included after reviewing full texts. Inclusion criteria were assessments of real patient flows and implementing strategies inside the hospitals. In this study, we discussed strategies of team triage, point-of-care testing, ideal ED patient journey models, streaming, and fast track. Patients might be directed to different streaming channels depending on clinical status and required practitioners. The most comprehensive strategy is ideal ED patient journey models, in which ten interrelated substrategies are provided. ED leaders should apply strategies that provide a continuous care process without deeply depending on external services.

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Mitochondrial dysfunction is one of the main causative factors in a wide variety of complications such as neurodegenerative disorders, ischemia/reperfusion, aging process, and septic shock. Decrease in respiratory complex activity, increase in free radical production, increase in mitochondrial synthase activity, increase in nitric oxide production, and impair in electron transport system and/or mitochondrial permeability are considered as the main factors responsible for mitochondrial dysfunction. Melatonin, the pineal gland hormone, is selectively taken up by mitochondria and acts as a powerful antioxidant, regulating the mitochondrial bioenergetic function. Melatonin increases the permeability of membranes and is the stimulator of antioxidant enzymes including superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase. It also acts as an inhibitor of lipoxygenase. Melatonin can cause resistance to oxidation damage by fixing the microsomal membranes. Melatonin has been shown to retard aging and inhibit neurodegenerative disorders, ischemia/reperfusion, septic shock, diabetes, cancer, and other complications related to oxidative stress. The purpose of the current study, other than introducing melatonin, was to present the recent findings on clinical effects in diseases related to mitochondrial dysfunction including diabetes, cancer, gastrointestinal diseases, and diseases related to brain function.

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Angiogenesis is critical for oxygen and nutrient delivery to proliferating tumor cells. Therefore, as angiogenesis is required and vital for the tumor growth and metastasis. Antiangiogenic therapy is considered to be beneficial for tumor growth prevention due to starvation of tumor of oxygen and nutrients, but in some cases, the benefits are not permanent. Tyrosine kinase inhibitors and many other agents often target angiogenesis through inhibition of the vascular endothelial growth factor (VEGF) pathway. Although preclinical studies showed satisfactory outcomes in tumor growth inhibition, antiangiogenic therapy in the clinical setting may not be effective.The resistance observed in several tumor types through alternative angiogenic “escape” pathways contributes to restoration of tumor growth and may induce progression, enhancement of invasion, and metastasis. Therefore, activation of major compensatory angiogenic pathways, sustaining tumor angiogenesis during VEGF blockade contributing to the recurrence of tumor growth overcome antiangiogenic strategies. In this review, we summarize the novel mechanisms involved in evasive resistance to antiangiogenic therapies and represent different cancer types which have the ability to adapt to VEGF inhibition achieving resistance to antiangiogenic therapy through these adaptive mechanisms.

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Aluminum (Al) is widely found in the nature. Although the relation between Al and neurodegenerative diseases is still controversial, Al is related with many brain diseases including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Al exposure occurs mainly through environment, occupational, and dietary factors for humans. Al exposure with diet can be through foods, food additives, water, and contamination of Al equipment/utensils. The aim of this review is to summarize various hypotheses, which link Al and neurodegeneration, and to determine the roles of Al exposure through different sources including diet, environment, and occupation. Future studies should be done in vulnerable subgroups of population including children, patients receiving antacid or Al-containing pharmeteucials on a daily basis, patients with reduced renal function, and patients on parenteral nutrition regimens that are likely to be affected by possible adverse health effects of Al. In addition, gender, age, and Al interactions need to be determined. One of the most important challanges in future epidemiological studies is to determine which variables should be controlled. In addition, experimental studies should be more focused and translational. In this context, exposure dose, dose–response effects, and time lapse between exposures and cognitive assessments are very important.

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Background: Osteonecrosis of the femoral head (ONFH) is a common disease with high disability rate. However, a few studies investigate the etiology and clinical characteristics of nontraumatic ONFH patients in China. Therefore, we conducted this cross-sectional study. Materials and Methods: Totally, information of 7268 nontraumatic ONFH patients treated between August 2005 and August 2015 was extracted from the medical records. The extracted information included the age, gender, diagnostic criteria, cause of nontraumatic ONFH, types of steroid use, and types of alcohol. Results: Among these included patients, there were 5126 (70.5%) male patients with average age of 44.5 years and 2142 (29.5%) female patients with average age of 47.6 years (P = 0.54). The number of steroid-, alcohol-, steroid/alcohol-, and idiopathic-induced nontraumatic ONFH men patients was 1684, 2310, 364, and 768, respectively, and nontraumatic ONFH women patients was 1058, 482, 140, and 462, respectively. Meanwhile, we found that both the levels of triglycerides (P = 0.03) and low-density lipoprotein (P = 0.02) were significantly changed in the idiopathic-induced nontraumatic ONFH patients. Conclusion: These results indicated the earlier onset of nontraumatic ONFH in male patients than in female patients, different main etiology for male (alcohol consumption) and female (steroid use) patients, and close relationship between the lipid metabolism and idiopathic-induced nontraumatic ONFH. Our findings could be helpful for researchers to investigate the pathogenesis of ONFH and aid the clinicians in the early prevention and diagnosis of nontraumatic ONFH.

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Breast cancer is the most common cancer in women around the world. So far, many attempts have been made to treat this disease, but few effective treatments have been discovered. In this work, we reviewed the related articles in the limited period of time, 2000–2016, through search in PubMed, Scopus database, Google Scholar, and psychology and psychiatry literature (PsycINFO). We selected the articles about the correlation of microRNAs (miRNAs) and breast cancer in the insight into therapeutic applicability from mentioned genetics research databases. The miRNAs as an effective therapy for breast cancer was at the center of our attention. Hormone therapy and chemotherapy are two major methods that are being used frequently in breast cancer treatment. In the search for an effective therapy for breast cancer, miRNAs suggest a promising method of treatment. miRNAs are small, noncoding RNAs that can turn genes on or off and can have critical roles in cancer treatment; therefore, in the near future, usage of these biological molecules in breast cancer treatment can be considered a weapon against most common cancer-related concerns in women. Here, we discuss miRNAs and their roles in various aspects of breast cancer treatment to help find an alternative and effective way to treat or even cure this preventable disease.

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Background: Depression is a common medical condition with a high prevalence leading to emotional abnormality. Despite some drawbacks, depression currently diagnosed using a combination of patient interviews and self-report questionnaires. Recently, there is emerging emphasis to establish biomarkers to diagnosis and clinical management of depression. This case–control study was designed to develop microRNA (miRNA)-based serum biomarker for depression. Materials and Methods: In this study, 39 patients with depression and 36 healthy controls were enrolled. Serum miRNAs gene expression was measured using real-time polymerase chain reaction (PCR) analysis; finally, the data represent as the 2^–ΔCt followed by further statistical analysis. Results: The serum level of miR-16 was significantly (P < 0.001) down-regulated (mean: 0.9123 and standard deviation [SD]: 0.06) in compared to normal individuals (mean: 1.6848 and SD: 0.09). The concentration of miR-135a was also catastrophically decreased (P < 0.001) in the patients (mean: 1.160 and SD: 0.07) in compared to control (mean: 1.819 and SD: 0.09). The relative miR-1202 expression levels were significantly lower (P < 0.001) in the patients (mean: 0.1755 and SD: 0.01) than in the healthy individuals (mean: 0.2939 and SD: 0.01). The receiver operating characteristic curve analysis indicated the obvious separation between patient and healthy control, with an AUC of 0.75 (95% confidence interval [CI] = 0.642–0.858, P < 0.001), 0.72 (95% CI = 0.607–0.834, P < 0.001), and 0.74 (95% CI = 0.630–0.861, P < 0.001) for miR-16, miR-135a, and miR-1202, respectively. The data suggest that these miRNAs have a potential to be used as a biomarker of depression with sensitivity 77.8% and specificity of 61.5% for miR-16, 94.4% and 41.0% for miR-135a as well as 86.1% and 61.5% for miR-1202, respectively (P < 0.001). Conclusion: Our findings showed that these miRNA can be used as a biomarker of depression diagnosis. MiR-135a and miR-1202 exhibited better sensitivity and specificity, respectively.

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Background: It is supposed that human colorectal cancer consists of a phenotypically distinct population of tumorigenic cancer cells known as cancer stem cells (CSCs) which play a pivotal role in cancer progression, maintenance, metastasis, and the relapse. The aim of this effort was to investigate and compare biological characterizations of CD133 ⁺ with CD133⁻ cell subsets isolated from both primary and metastatic human colorectal tumors. Materials and Methods: Using our optimized protocols, unfixed colorectal tumors were enzymatically and mechanically dissociated into single cells followed by evaluation of postdigestion viability. The obtained single cell suspensions were then subjected to cell sorting using magnetic beads according to CD133 marker. The resultant CD133 ⁺ and CD133⁻ cell subsets were cultured in specific cell culture medium followed by aldehyde dehydrogenases (ALDH) activity assessment and flow cytometric analyses. Results: The results demonstrate that CD133 ⁺ cells have smaller size and lower complexity of intracellular structure, sphere formation ability, and ALDH enzyme activity while CD133⁻ cells isolated from primary colon cancer samples were not able to form a sphere and did not show ALDH enzyme activity. Intriguingly, CD133⁻ cells isolated from metastatic colorectal cancer specimen were able to form a sphere and shown ALDH enzyme activity. The present study indicates that our results are in agreement with SC theory and possibility of the existence of cellular plasticity among cancer subpopulations should be portrayed. Conclusion: We also conclude that this cellular plasticity is greatly affected by tumor microenvironment cues and the role of CSCs niche in cancer therapeutic strategies should be precisely considered.

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Mycobacterium tuberculosis is a causative agent of tuberculosis that causes deaths across the world. The pathogen apart from causing disease manifestations can also enter into a phase of latency to re-emerge later. Among the various factors associated with the virulence of pathogen, the lipids composing the cell wall of the bacillus have drawn much interest among. The unique composition of the cell wall composed of mycolic acid, glycolipids such as diacyltrehaloses, polyacyltrehalose, lipomannan, lipoarabinomannan (LAM), mannose-capped-LAM, sulfolipids, and trehalose-6,6'-dimycolate, all have been implicated in providing the pathogen an advantage in the host. The pathogen also alters its metabolism of fatty acids to survive the conditions in the host that is reflected in an altered cell wall composition in terms of lipids. In addition, the lipid profile of the cell wall has been shown to modulate the immune responses launched by the host, especially in the suppression, or production of inflammatory factors, cytokines, and phagocytic cells, such as dendritic cells and macrophages. Apart from M. tuberculosis, the paper also briefly looks at the role of Mycobacterium bovis and its role in tuberculosis in humans along with its lipid profile of its cell wall. This review aims to summarize the various lipids of the cell wall of M. tuberculosis along with their roles in enabling the pathogen to maintain its virulence to infect further humans and its persistence inside the host.

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Chronic obstructive pulmonary disease (COPD) is known as a progressive lung disease and the fourth leading cause of death worldwide. Despite valuable efforts, there is still no accurate diagnostic and prognostic tool for COPD. Hence, it seems that finding new biomarkers could contribute to provide better therapeutic platforms for COPD patients. Among various biomarkers, microRNAs (miRNAs) have emerged as new biomarkers for the prognosis and diagnosis of patients with COPD. It has been shown that deregulation of miRNAs targeting a variety of cellular and molecular pathways such as Notch, Wnt, hypoxia-inducible factor-1α, transforming growth factor, Kras, and Smad could be involved in COPD pathogenesis. Multiple lines of evidence have indicated that extracellular vesicles such as exosomes could carry a variety of cargos (i.e., mRNAs, miRNAs, and proteins) which transfer various cellular and molecular signals to recipient cells. Here, we summarized various miRNAs which could be applied as diagnostic and prognostic biomarkers in the treatment of patients with COPD. Moreover, we highlighted the role of extracellular vesicles containing miRNAs as diagnostic and prognostic biomarkers in COPD patients.

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Background: Serum procalcitonin (PCT) levels differ in patients with bacterial or fungal infections and are significantly elevated in patients with Gram-negative bacteremia. We evaluated the diagnostic accuracy of different inflammatory markers to discriminate sepsis caused by different pathogens. Materials and Methods: We included 328 episodes of bacteremia from 292 patients with sepsis and 31 patients with suspected sepsis in this study. Medical records of patients who had bacteremia caused by Gram-negative bacteria (Gram-negative), Gram-positive bacteria (Gram-positive) or fungi were reviewed, and information about PCT and other inflammatory markers was recorded. The diagnostic performance of inflammatory markers was calculated via receiver operating characteristic (ROC) curves. Results: Serum PCT levels in Gram-negative, Gram-positive, and fungal sepsis were 7.47 (interquartile range [IQR]: 1.09–41.26) ng/mL, 0.48 (IQR: 0.15–2.16) ng/mL, and 0.60 (IQR: 0.14–2.06) ng/mL, respectively (P < 0.001). ROC analysis revealed an optimal cut-off value of 2.44 ng/mL for PCT in discriminating Gram-negative sepsis from Gram-positive sepsis, which yielded a sensitivity of 68.4% and a specificity of 77.1%. An optimal cut-off value of 3.11 ng/mL for PCT in discriminating Gram-negative sepsis from fungal sepsis, led to a sensitivity of 63.9% and specificity of 93.3%. Neither PCT nor other inflammatory markers could be used to distinguish between Gram-positive and fungal sepsis. Conclusion: Serum PCT levels were significantly higher in patients with Gram-negative sepsis than in those with Gram-positive or fungal sepsis. PCT is a potential sensitive biomarker for distinguishing Gram-negative sepsis from Gram-positive and fungal sepsis.

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Background: Myocardial infarction (MI) is one of the major causes of death and disability worldwide, which can reduces quality of life in patients. Some disabilities are depression and anxiety which delay returning to work. The aim of this study was to evaluate the effect of illness perception focused intervention on quality of life, anxiety, and depression in MI patients. Materials and Methods: A randomized controlled trial study of 48 recently hospitalized MI patients was conducted (24 in intervention group and 24 in control group). Intervention group was trained to understand the disease by a mental health counselor in three half-an-hour sessions for three consecutive days. Data were collected from three questionnaires: hospital anxiety and depression scale, the World Health Organization Quality of Life Questionnaire (short form), and Illness Perceptions Questionnaire Brief at admission, 1.5, and 3 months postdischarge. Data were analyzed with ANOVA repeated measure. Results: The mean duration of returning to work was 28.7 ± 8.1 days in intervention groups and 46 ± 7.6 days in control group which was statistically significant (P < 0.001). Moreover, anxiety, depression, and illness perceptions score were significantly decreased in intervention groups which were 8.3 ± 3.3, 6.8 ± 3.5, and 36.5 ± 5 in intervention groups and 15.8 ± 2.1(P < 0.001), 17.1 ± 2.3 (P < 0.001), and 41.9 ± 4 (P < 0.001) in control group, respectively. Mean of quality of life subscales scores just physical health subscale showed a significant reduction after 3 months in the control group. Conclusion: Training MI patients to understand the disease in three half-an-hour sessions for 3 consecutive days can decrease the duration of returning to work, anxiety and depression, and increase illness perceptions which can make a better outcome.

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Background: Vitamin D deficiency is common in pregnancy, leading to increase in the frequency of preeclampsia, cesarean delivery, neonatal bacterial vaginosis, and gestational diabetes. The current study was designed and implemented to investigate the effect of vitamin D during the first and second trimesters of pregnancy in reducing the risk of gestational diabetes mellitus (GDM) in women who are at high risk [history of GDM, birth macrosomia, family history, and high body mass index (BMI)]. Materials and Methods: In a randomized, double-blind, and placebo-controlled trial, 90 pregnant women who had at least one risk factor for GDM were randomized into intervention (46 participants) and control (44 participants) groups. Participants in the intervention group took 5000 units of vitamin D daily and the control group took placebo until the 26th week of pregnancy. Then the glucose challenge test (GCT) and the glucose tolerance test (GTT) were performed to evaluate GDM. Results: Mean ± standard deviation (SD) age was 31.28 ± 6.38 years and 29 ± 6.24 years for the intervention group and the placebo group, respectively, (P > 0.05). In addition, there were no significant differences between two groups in terms of vitamin D levels and GCT (P > 0.05), and the difference was not significant. The incidence of diabetes in the intervention groups was statistically lower than in control group (11.4% vs 34.8; P < 0.01). The results showed that abnormal GCT in the placebo group was statistically higher than in intervention group (35.9% vs 10.9 P < 0.005). Conclusion: The results of the current study showed that the prescription of vitamin D supplementation in the first and second trimesters of pregnancy was effective in reducing GDM and controlling GTT and GTC.

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Background: The aim of this study was to check the effectiveness of Vitamin D supplementation on the disease activity of Vitamin D-deficient systemic lupus erythematosus (SLE) patients. Materials and Methods: In this randomized, double-blind, placebo-controlled trial, 45 Vitamin D-deficient SLE patients were studied in two groups, namely interventional and placebo groups. The interventional group patients were treated with Vitamin D (50,000 unit/weekly Vitamin D for 12 weeks and then 50,000 unit/monthly for 3 months) and placebo group patients were only administered the placebo. The level of Vitamin D and the level of disease activity using SLE disease activity index (SLEDAI) were measured before and after intervention period in each group, and for intra- and between-groups comparison, we used t-test and repeated measure ANOVA. Results: A total of 90 patients were enrolled in this study. The mean of Vitamin D was increased significantly after therapy in interventional group (17.36 ± 4.26 ng/ml vs. 37.69 ± 5.92 ng/ml, P < 0.001). The mean of Vitamin D had no significant difference before and after intervention in placebo group (16.78 ± 4.39 ng/ml vs. 16.62 ± 4.61 ng/ml, P = 0.53). The mean of disease activity (SLEDAI) was not different significantly before and after Vitamin D administration in interventional group (3.09 vs. 1.62 ± 1.25, P = 0.39). The mean of disease activity (SLEDAI) was not different significantly before and after intervention in placebo group (3.09 vs. 1.98 ± 2.47, P = 0.42). Conclusion: According to our study, it is suggested that using Vitamin D in patients with SLE could not have better outcomes in this regard. However, there are many unknown environmental or biological factors which are associated with the disease activity of SLE and have not been identified yet.

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Atherosclerosis is one of the most important cardiovascular diseases that involve vessels through the development of fatty streaks and plaques. Plant-based compounds can help treat or prevent atherosclerosis through affecting the involved factors. The main purpose of this review article is to investigate and introduce medicinal plants and their potential activities regarding antioxidant properties, effective on lipids level and development of plaque, atherosclerosis, and progression of atherosclerosis as well as the development of cardiovascular disease and ischemia. To search for the relevant articles indexed in Information Sciences Institute, PubMed, Scientific Information Database, IranMedex, and Scopus between 1980 and 2013, with further emphasis on those indexed from 2004 to 2015, we used these search terms: atherosclerosis, antioxidant, cholesterol, inflammation, and the medicinal plants below. Then, the articles with inclusion criteria were used in the final analysis of the findings. Plant-based active compounds, including phenols, flavonoids, and antioxidants, can be effective on atherosclerosis predisposing factors and hence in preventing this disease and associated harmful complications, especially through reducing cholesterol, preventing increase in free radicals, and ultimately decreasing vascular plaque and vascular resistance. Hence, medicinal plants can contribute to treating atherosclerosis and preventing its progression through reducing cholesterolemia, free radicals, inflammation, vascular resistance, and certain enzymes. They, alone or in combination with hypocholesterolemic drugs, can therefore be useful for patients with hyperlipidemia and its complications.

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Neuromyelitis optica (NMO) is an autoimmune inflammatory disease of the central nervous system with preferential involvement in the optic nerve and spinal cord with a widespread spectrum of clinical features; multiple therapeutic agents have been used with different results. Recent evidence points to B-cell-mediated humoral immunity in the pathogenesis of NMO. Rituximab targets the CD20 antigen on B-cells. Treatment leads to profound B-cell depletion, principally over an antibody-dependent cell cytotoxicity mechanism. The aim of our study was to review clinical trials to elucidate the impact of rituximab on the relapse rate, Expanded Disability Status Scale (EDSS), and progression of disability in NMO. We performed a comprehensive review of all studies that evaluated clinical and paraclinical effects of rituximab on NMO. MEDLINE-PubMed, Web of Sciences, EMBASE, and Cochrane databases up to June 2016 included in our searches. In addition, reference lists from articles identified by search as well as a key review article to identify additional articles included in the study. Rituximab targets the CD20 antigen on B-cells and decreases attack frequency and severity in patients with NMO; however, it does not remove attacks, even when modifying treatment to achieve B-cell depletion. Most of the investigations revealed that EDSS significantly in all patients with rituximab treatment will be decreased after treatment with rituximab. No new or enlarged lesions or pathological gadolinium enhancement was observed in serial brain and spinal cord magnetic resonance imaging, except for those observed concomitantly with clinical relapses and the median length of spinal cord lesions was significantly reduced after therapy. Rituximab targets the CD20 antigen and decreases attack frequency and severity in patients with NMO.

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Background: Although several observational and experimental studies have examined the effects of low carbohydrate diets (LCDs) on nonalcoholic fatty liver disease (NAFLD), there are considerable inconsistencies among studies. We summarized the effect of LCDs on liver function tests, including intrahepatic lipid content (IHLC), alanine transaminase (ALT), aspartate aminotransferases (AST), and  gamma-glutamyl transferase (GGT) in patients with NAFLD. Materials and Methods: PubMed, ISI Web of Science, Scopus, and Google Scholar databases were searched for relevant publications until July 2014, resulting in ten relevant papers that were included in meta-analysis. Related articles were found by searching Medical Subject Heading terms of "NAFLD" in combination with "low carbohydrate." For this meta-analysis, we used mean differences and standard errors of liver function biomarkers. Summary effect and corresponding confidence interval (CI) were estimated using random effect models. Heterogeneity between studies was assessed using Cochran's Q- and I-squared tests. Results: Our search led to ten eligible papers that evaluated serum ALT levels (n = 238), nine reported serum AST levels (n = 216), five reported serum GGT concentrations (n = 91), and four assessed IHLC (n = 50). LCD decreased IHLC by −11.53% (95% CI: −18.10, −4.96; I² = 83.2%). However, the effect of LCD on liver enzymes was not significant. Mean differences for the effects of LCDs on ALT, AST, and GGT were −4.35 IU/L (95% CI: −12.91, 4.20; I² = 87.9%), −1.44 IU/L (95% CI: −4.98, 2.10; I² = 61.4%), and −7.85 IU/L (95% CI: −29.65, 13.96; I² = 99.4%), respectively. Conclusion: LCD consumption in subjects with NAFLD led to a significant reduction in IHLC, but did not significantly affect the concentration of liver enzymes.

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Diabetes mellitus (DM) is a common worldwide endocrine disorder characterized by hyperglycemia resulting from defects in insulin secretion and insulin action or both. A number of clinical studies have investigated diabetes and its causal relation with neoplasm. Several epidemiological studies have found that diabetic patients have an increased risk of different types of cancers, for example liver, pancreas, gastric (stomach), colorectum, kidney, and breast, and it is predicted that hyperglycemic state observed in diabetic milieu enhances the cancer risk in prediabetic and diabetic individuals. To explore the strength of evidence and biases in the claimed associations between type 2 DM (T2DM) and risk of developing cancer, an umbrella review of the evidence across published meta-analyses or systematic reviews is performed. The concurrence of T2DM with the growing burden of cancer globally has generated interest in defining the epidemiological and biological relationships between these medical conditions. Through this review, it was found that diabetes could be related to cancer. Yet, the results from most of the studies are obscure and conflicting and need a robust research so that the link between diabetes and cancer could be firmly and impeccably documented.

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Background: The prevalence of vitamin D deficiency is higher in end-stage renal disease (ESRD) patients compared to healthy populations. This deficiency could lead to several complications with different mechanisms and might result in reduced survival in patients. Leptin and adiponectin are messenger proteins with endocrine secretion from adipocytes and various effects in cellular mechanisms. The goal of this study was to find the effect of vitamin D administration on serum levels of leptin and adiponectin in ESRD patients. Materials and Methods: This double-blind randomized placebo-controlled clinical trial was carried out on 64 ESRD patients on hemodialysis in the Amin and Noor hospitals of Isfahan, Iran. Patients were categorized into two groups, on control and intervention; serum levels of vitamin D, leptin, and adiponectin were measured in both groups before and after the study. The intervention group was treated with vitamin D pearls, while the control group received placebo in the same manner. Results: The mean [standard deviation (SD)] ages of the patients were 62 (21) years and 60 (19) years in the control and treated groups, respectively. Conclusion: The change in serum level of vitamin D was statistically significant in the treatment group but not in the control group. The serum level of leptin was reduced in the treatment group, while the serum level of adiponectin increased significantly, but none of these changes were statistically significant in the control group. This study showed that vitamin D administration is associated with an increase in adiponectin and a decrease in leptin level in ESRD patients.

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Vitamin D has an important role in bone metabolism but recently has been recognized as an immunoregulator, and this has led to investigations on the effect of Vitamin D supplementation in various autoimmune diseases and its anti-inflammatory effects. There is some evidence that Vitamin D can regulate gastrointestinal inflammation. In addition, previous studies have shown that Vitamin D can affect the gut microbiome. The aim of this review is to evaluate the effect of Vitamin D on inflammatory processes, especially its relation to the inflammatory bowel disease (IBD) and gut microbiome. There is some evidence that Vitamin D can regulate gastrointestinal inflammation, with epidemiological studies showing that individuals with higher serum Vitamin D have a lower incidence of IBD, particularly Crohn's disease. Vitamin D changes transcription of cathelicidin and DEFB4 (defensin, beta 4) that can affect the gut microbiome. Several cell types of the immune system express Vitamin D receptor, and hence the use of Vitamin D in immune regulation has some potential. Furthermore, Vitamin D deficiency leads to dysbiosis of gut microbiome and reported to cause severe colitis. Vitamin D supplementation is low cost and available and can be a therapeutic option.

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As new research reveals, granulocyte colony-stimulating factor (G-CSF) plays an effective role in pregnancy success, considering that it not only affects the embryo implantation and ovarian function but also it promotes endometrial thickening and improves the pathophysiology of endometriosis, which all fundamentally lead to reducing pregnancy loss. In this review, we focus on the role of G-CSF in human reproduction. We summarized its role in ovulation, luteinized unruptured follicle syndrome, poor responders, improving repeated in vitro fertilization failure, endometrial receptivity and treatment of thin endometrium, and recurrent spontaneous abortion.

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The hyperimmunoglobulin E syndromes (HIESs) are very rare immunodeficiency syndromes with multisystem involvement, including immune system, skeleton, connective tissue, and dentition. HIES are characterized by the classic triad of high serum levels of immunoglobulin E (IgE), recurrent staphylococcal cold skin abscess, and recurrent pneumonia with pneumatocele formation. Most cases of HIES are sporadic although can be inherited as autosomal dominant and autosomal recessive traits. A fundamental immunologic defect in HIES is not clearly elucidated but abnormal neutrophil chemotaxis due to decreased production or secretion of interferon γ has main role in the immunopathogenesis of syndrome, also distorted Th1/Th2 cytokine profile toward a Th2 bias contributes to the impaired cellular immunity and a specific pattern of infection susceptibility as well as atopic-allergic constitution of syndrome. The ophthalmic manifestations of this disorder include conjunctivitis, keratitis, spontaneous corneal perforation, recurrent giant chalazia, extensive xanthelasma, tumors of the eyelid, strabismus, and bilateral keratoconus. The diagnosis of HIES is inconclusive, dependent on the evolution of a constellation of complex multisystemic symptoms and signs which develop over the years. Until time, no treatment modality is curative for basic defect in HIES, in terms of cytokines/chemokines derangement. Of note, bone marrow transplant and a monoclonal anti-IgE (omalizumab) are hoped to be successful treatment in future.

[ABSTRACT]  [FULL TEXT]  [PDF]  [Mobile Full text]  [EPub] [CITATIONS]  [PubMed]