Background: With the outbreak of Coronavirus disease 2019 (COVID-19), many studies’ attention to this world’s complexity increased dramatically. Different views on sports and physical activities have been presented, which have addressed the advantages and disadvantages of sports activities in this period differently. The purpose of this review was to investigate the physiological and psychological effects of physical activity during the COVID-19 pandemic.
Methods: Using PubMed, Science Direct, Medline, and Web of Science electronic databases, this review summarizes the current knowledge of direct and indirect effects of physical activity during the COVID-19 pandemic, evaluating the advantages and drawbacks of specific exercise physiology conditions. All types of studies were assessed, including systematic reviews, case-studies, and clinical guidelines. The literature search identified 40 articles that discussed COVID-19, immune system, the relation between immune system and exercise or diet, and psychological impacts of physical activity.
Results: Forty articles review showed that the immune system depends on the type, frequency, intensity, and duration of the exercise.
Intense or prolonged exercise with short recovery periods can progressively weaken the immune system and increase the risk of COVID-19. One of the acute responses after moderate-intensity training is improved immune function and a decrease in inflammatory cytokines. Paying attention to dietary intakes of micro-and macronutrients in conjunction with exercise can strengthen the condition to fight against coronavirus. Exercise can also affect the psychological dimensions of the COVID-19 pandemic, including depression, anxiety, and stress, which improve community mental health during the quarantine.
Conclusion: Setting appropriate physical activity based on individuals’ properties and proper diet plan may enhance the physiological and psychological body’s condition to fight against coronavirus.
Introduction: Systemic lupus is a disseminated inflammation of the conjunctive tissue. Cardiovascular lesions are the first cause of morbidity and mortality in the course of that disease. These lesions are prevalent in 30 to 62% of cases, depending on whether the diagnostic tool is clinical, echocardiographic, or autopsic. Any part of the heart can be affected, yielding manifestations of pericarditis, endocarditis, coronary heart disease, conduction disorders, and rarely myocarditis.
Objective: Describe cardiac manifestations during the follow up of patients diagnosed with systemic lupus.
Patients and Methods: We conducted a transversal descriptive study over a period of 27 months, in the departments of Internal Medicine, Dermatology, and Cardiology of Yalgado Ouedraogo University Hospital of Ouagadougou. All patients diagnosed with systemic lupus according to the American College of Rheumatology criteria, and having done an EKG, a Holter EKG, or a transthoracic echocardiography, were included in the study. Data were collected from inpatient medical records, outpatient follow up registry and booklets.
Results: Cardiovascular lesions were prevalent in 7 cases (43.75%) out of 16 patients diagnosed with systemic lupus. Mean age of patients was 36 years, with extremes of 23 and 51 years. Only female patients were affected in our study. Cardiac manifestations were mainly benign pericarditis, heart failure, and conduction disorders.
Conclusions: Cardiovascular manifestations are frequent during the course of systemic lupus, and occur after few years of disease progression. Transthoracic echocardiography and EKG remain useful non-invasive explorations for the assessment of cardiovascular lesions, despite minor shortcomings.
Background: An increasing body of evidence indicates that inflammatory activation profoundly impacts the electrophysiological properties of cardiomyocytes. A marker of systemic inflammation such as C-reactive protein(CRP), is associated with all parameters of the Mtabolic syndrome(MetS) and that may result in adverse cardiac events via multiple effects, ultimately resulting in a prolongation of Action Potential duration (APD), and thereby of the QTC (QT corrected) interval on ECG.
Objective: We sought to investigate the influence of CRP levels on the prevalence of prolonged QT-dispersion and prolonged Tpeak-Tend –dispersion in the patients with MetS.
Methods: We conducted a multicenter observational cross-sectional study. The study population consisted of 200 patients with MetS, stratified in two groups:103 participants (50 females and 53 males) with level of CRP>3mg/l, and 97 participants (47 females and 50 males) with level of CRP<3mg/l), who attended outpatient visits at general cardiology Health Care Clinics during 1 calendar year. For the analysis of the ECG, we performed a manual measurement of the values using a digital caliper with measuring range of 0-150 mm, 0.01 mm resolution, and 0-100 ± 0.02 mm accuracy. QT interval dispersion was obtained by the difference between the maximum and the minimum QT intervals found in the 12-lead electrocardiogram. The Tpeak-Tend interval was obtained from the difference between QT interval and QTpeak interval.
Results: Prolonged QTC. dispersion, was found in 51.4% of participants with level of CRP>3mg/l and in 32.9% of with level of CRP<3mg/l, the differences were statistically significant. (p=0.004). The results showed that 51.4% participants with level of CRP>3mg/l had a prolonged Tpeak-Tend interval, and 32.9% of participants with level of CRP<3mg/l had prolonged Tpeak-Tend interval. Difference were statistically significant.( p=0.04). There were significant association of increased levels of CRP and QTC-dispersion (OR = 2.486, 95% CI 1.389-4.446).There were significant association of increased levels of CRP with Tpeak-Tend Dispersion (OR=2.239,95%CI 1.262-3.976). Prolonged QTC max. Interval OR=2.236,%CI 1.246-4.014),Prolonged Tp-Te-interval. (OR=2.367, 95%CI 1.327-4.222), also there were significant association of increased levels of CRP with BMI. (OR=1.154, 95%CI 1.095-1.227) and significant association of increased levels of CRP with presence of uncontrolled glicemia.(OR=1.779, 95%CI 1.014-3.12).
Conclusion: We think we proved the hypothesis that patients with MetS and high level of CRP have higher prevalence of QT- dispersion and Tpeak-Tend dispersion than patients with MetS and lower level of CRP. These findings have both epidemiological and clinical relevance, also these findings might lend further insight into potential mechanisms by which MetS is associated with adverse cardiac events.
Background: There is an important shortage of blood in the greatest blood banks worldwide to meet up with requirements for numerous medical interventions. Limited studies have associated regular blood donation to the lowering of lipid function parameters. Assessing the lipid function is a classical method of evaluating an individual’s risk for coronary heart disease.
Objective: The general goal of the study is to determine lipid and hematological profile among blood donors in European Gaza Hospital, Palestine.
Materials and Methods: This study was a case-control study that involved 120 male, 40 of whom were regular blood donors (study group), 40 first time donors and 40 non- donors (control group) aged between 18-60 years. A volume of 5ml venous blood was drawn from each fasting participant into a dry biochemistry screw-capped tube. This was allowed to clot and the serum was used to determine total cholesterol (TC), triglycerides, High-density lipoprotein cholesterol (HDL-C), Low-density lipoprotein cholesterol (HDL-C), while HDL-C/LDL-C and TC/LDL ratio were calculated by using the following formula. Anthropometric parameters (weight, height) of donors were measured using standard protocol. The height (in meter), weight (in kilogram) were used to calculate the body mass index (BMI) using the following formula. BMI= weight (kg)/ (height in meter)² and blood was collected from each participant in EDTA (for hematocrit, ESR). Three groups were matched for age and BMI. Data were analyzed using SPSS version 23. Chi-square (χ²) was used to compare the relationship between categorical variables, ANOVA was used to measure the difference between means. Data were summarized using tables, pie charts, histograms. A P-value < 0.05 was considered to be statistically significant for all tests conducted.
Results: The mean total cholesterol (169±10.85 mg/dl), triglycerides (116±9.73 mg/dl), HDL (54±2.5 mg/dl ), LDL (92±11.4mg/dl), LDL/HDL ratio (1.73±0.25) and TC/HDL ratio (3.16±0.26) were lower in the regular blood donors than the first time donors(198±10.13, 179±5.82, 42.33±1.6, 120±11.2, 2.85±0.36, 4.7±0.40) and non- donors (202±10.19, 180±12.68, 41.75±1.4, 125±11.7, 2.99±0.33, 4.86±0.32) respectively and statistically significant (P < 0.05).The mean ESR (6.63±0.87mm/hr) was lower statistically significant in the regular blood donors than the first time donors (7.40±1.17) and non- donors (7.60±1.48) respectively (P < 0.05). The mean HCT (42.98±0.86%) was lower statistically significant in the regular blood donors than the first time donors (44.63±0.90) and non- donors (44.75±0.74, P < 0.05).
Conclusion: Regular donors have reduced risk of developing coronary heart disease as reflected by the low total cholesterol, triglycerides, LDL-c, LDL-c/HDL-c ratio, TC/HDL-c ratio and HCT and high HDL. BMI in regular donor was less than the donor for the first time and did not donate, but did not reach the statistical significance. Also in our study regular donors have reduced risk of developing inflammation as reflected by low ESR.
Background: Current guidelines for diagnosis and management of heart failure (HF) rely on clinical findings and natriuretic peptide values, but evidence suggests that recently identified cardiac biomarkers may aid in early detection of HF and improve risk stratification. The aim of this study was to assess the diagnostic and prognostic utility of multiple biomarkers in patients with HF and left ventricular systolic dysfunction (LVSD).
Methods: High-sensitivity cardiac troponin I (cTnI), N-terminal pro b-type natriuretic peptide (NT-proBNP), interleukin-6 (IL-6), endothelin-1 (ET-1), pro-matrix metalloproteinase-9 (pMMP-9), and tumor necrosis factor-alpha (TNF-α) were measured using single-molecule counting technology in 200 patients with varying stages of HF. Plasma detection with cross-sectional associations of biomarkers across all HF stages, and advanced-therapy and transplant-free survival were assessed using multivariate analysis and Cox regression analyses, respectively.
Results: NTproBNP, pMMP-9, IL-6 were elevated in early, asymptomatic stages of HF, and increased with HF severity. Higher circulating levels of combined IL-6, NTproBNP, and cTnI predicted significantly worse survival at 1500-day follow-up. Cox regression analysis adjusted for ACC/AHA HF stages demonstrated that a higher concentration of IL-6 and cTnI conferred greater risks in terms of time to death, implantation of left ventricular assist device (LVAD), or heart transplantation.
Conclusion: Biomarkers of inflammation, LV remodeling, and myocardial injury were elevated in HF and increased with HF severity. Patients had a significantly higher risk of serious cardiac events if multiple biomarkers were elevated. These findings support measuring NTproBNP, cTnI and IL-6 among patients with HF and LVSD for diagnostic and prognostic purposes.
Background: Inflammation is associated with enhanced cardiovascular risk profile and increased cardiovascular mortality in end-stage kidney disease patients undergoing hemodialysis. Mechanisms of activated acute phase reaction in patients on chronic hemodialysis remain to be identified. As successful treatment of the inflammatory condition in these patients may improve long-term survival, we studied potential changes in different inflammatory biomarkers of cardiovascular risk in end-stage kidney disease patients after a mid-week hemodialysis session.
Methods: Inflammatory biomarkers of cardiovascular risk (cystatin-C, homocysteine, C-reactive protein, procalcitonin, pentraxin-3, serum amyloid-A) and atherogenic plasma lipoproteins (Lipoprotein(a), cholesterol low and high density lipoproteins) were studied in 21 end-stage kidney disease patients previously and after a mid-week hemodialysis session.
Results: We found a significant reduction in serum levels of low molecular weight molecules: cystatin-C (5.56 to 1.85 mg/L, 66.73%, p < 0.001), homocysteine (22.85 to 13.25 µmol/L, 42.01%, p < 0.001) and procalcitonin (0.788 to 0.457 ng/mL, 42.01%, p < 0.001). Large molecules as C-reactive protein (9.70 to 9.90 mg/L, 2.06%, p = 0.022) and pentraxin-3 (1.67 to 4.28 ng/mL, 156%, p < 0.001) increased, but serum amyloid-A decreased (15.90 to 12.70 mg/L, 20.13%, p < 0.05). There was no change in Lipoprotein (a) levels.
Conclusion: Pentraxin-3 was a more specific inflammatory vascular marker than C-reactive protein, and the best inflammatory marker associated with hemodialysis. Homocysteine, procalcitonin and the other small proteins could be released and removed during hemodialysis session. Further studies are needed to understand the behavior and significance of these markers after successive hemodialysis.
Atherosclerosis is an important promoter of cardiovascular disease potentiating myocardial infarction or stroke. Current demand in biomedical imaging necessitates noninvasive characterization of arterial changes responsible for transition of stable plaque into rupture-prone vulnerable plaque. in vivo contrast enhanced magnetic resonance (MR) imaging (MRI) allows quantitative and functional monitoring of pathomorphological changes through signal differences induced by the contrast agent uptake in the diseased vessel wall, therefore it is the ideal modality toward this goal. However, studies have so far focused on the cellular targets of persisting inflammation, leaving extracellular matrix (ECM) far behind. In this review, we portray ECM remodeling during atherosclerotic plaque progression by summarizing the state of the-art in MRI and current imaging targets. Finally, we aim to discuss glycosaminoglycans (GAGs) and their functional interactions, which might offer potential toward development of novel imaging probes for in vivo contrast-enhanced MRI of atherosclerosis.
Intraperitoneal vancomycin absorption is higher when there is peritoneal inflammation, but the absorption decreases with recovery from peritonitis. Consequently, intraperitoneal maintenance doses are ineffective, reducing the rate of cure.
Aim:To evaluate the outcome of Gram-positive peritonitis treated with intraperitoneal and subsequent intravenous vancomycin.
Methods: In April 1996, we initiated a protocol for treating peritonitis caused by Gram-positive organisms using a 2-g intraperitoneal loading dose of vancomycin followed by intravenous vancomycin at 1 g twice in 5 days for coagulase-negative Staphylococcus and at 1 g three times in 5 days for Staphylococcus aureus. We analyzed episodes of Gram-positive peritonitis (coagulase-negative and S. aureus) and the efficiency of the treatment protocol in 113 patients undergoing peritoneal dialysis between 1 April, 1996 and 3 August, 2016. There were 6090 patient-months and the mean treatment lasted 54±44 months. The outcomes were evaluated as (1) complete cure, (2) relapsing peritonitis, (3) catheter removal for refractory peritonitis, and (4) death.
Results: A total of 51 cases of coagulase-negative Staphylococcus peritonitis and 37 of S. aureus were seen in 46 of the 113 patients (40.7%). Of these, coagulase-negative Staphylococcus (92.15%) and 34 S. aureus peritonitis (91.89%) resolved.
Conclusion:The response to treatment was very satisfactory.
Aims: Histological diagnostic criteria are used for the assessment of the degree of dysplasia and hence the risk of cancer progression for premalignant lesions. Clonal changes in the form of hyperorthokeratosis and hyperchromasia that are sharply demarcated from adjacent areas are not currently part of the criterion for dysplasia diagnosis. The objective of this study was to determine whether such clonal change should be regarded as a diagnostic feature for dysplasia. The following histological conditions were used to define such change: (1) hyperorthokeratosis; (2) hyperchromatism but no other features of dysplasia; (3) sharp margin demarcation from adjacent area by both the hyperorthokeratosis and hyperchromasia (clonal change), and (4) no prominent rete ridges, marked acanthosis or heavy inflammation. Lesions fitting these criteria were termed orthokeratotic lesions with no dysplasia.
Methods: Patients from a population-based longitudinal study with more than 10 years of follow up were analyzed. Of the 214 patients with primary oral premalignant lesions, 194 had mild or moderate dysplasia (dysplasia group) and 20 fit the criteria for orthokeratotic lesions without dysplasia (orthokeratotic with no dysplasia group). The two groups were compared for their cancer risks using clinical (site and toluidine blue), histological (nuclear phenotype score), and molecular criteria (loss of heterozygosity) and by outcome (progression).
Results and conclusions: The lesions from orthokeratotic with no dysplasia group showed a similar cancer risk (clinical, histological and molecular risk) and time to progression as the dysplastic lesions. We recommend that the clonal change should be included as a criterion for dysplasia diagnosis
Background: Despite remarkable progress in surgical, cardiopulmonary bypass (CPB) and anesthetic tecniques, neurocognitive damage still remains an important cause of postoperative morbidity in cardiac surgery. The aetiology of neurocognitive damage is likely to be multifocal; including macro and microemboli, cerebral hypoperfusion, inflammation and nonpulsatile flow. N-methyl-D-asparticAcid (NMDA) receptors play an important role during neurocognitive damage. Ketamine is a non-competitive antagonist to the phencyclidine site of NMDA receptor for glutamate and directly suppresses proinflammatory cytokine production. The aim of the present study was to evaluate whether ketamine has neuroprotective effects during open-heart surgery through the use of neurocognitive tests.
Methods: We considered all patients aged between 58-76 years who were referred to a single cardiothoracic surgical team for elective, primary coronary revascularization. Patients were excluded from the study for the following reasons: a history of neurological, psychiatric, gastrointestinal, hepatic, renal, hematologic and clotting systems disorder and repeat procedures. Undergoing CPB were randomized 2 groups: Group1 (ketamine)(n=25) or Group2 (propofol)(n= Patients 25) In the propofol group, anesthesia was induced with 3mg/kg propofol, 1µg/kg remifentanyl, 0.1mg/kg vecuronium. Remifentanyl 0.5-1μg/kg/min was infused intravenously throughout the whole procedure. In the ketamine group, anesthesia was induced with 1-2mg/kg propofol, 1-2mg ketamin, 0.1mg/kg vecuronium. Ketamin 1mg/kg/hour was infused intravenously. Pressors, inotropic agents and antiarrhythmics were used as needed. The Mini-Mental State Examination(MMSE) was administered the day before surgery and three days later. The change in scores for MMSE was calculated for each patient and all the group. The results were compared statistically with paired simple t-test.
Results: The mean age, CBP duration, lowest temperature was not statistically significant (Table1). Peroperative and postoperative blood pressures and pulse rates showed differences between groups. There were no preoperative differences between the groups on any of the mean MMSE score (Table2). The ECG monitoring revealed that most patients remained in sinus rhythm, with no difference between groups.
Conclusions: We could not demonstrate that intraoperatively administered ketamine resulted in greater neuroprotective effects compared with propofol. Ketamine in combination with propofol during cardiac surgery is associated with a stable hemodynamic profile. Propofol may reduce the delivery of microemboli to the cerebral circulation by decreasing the cerebral blood flow. Propofol has a direct neuroprotective effect in vitro, although Roach et al. could not demonstrate a protective effect of propofol during open-heart surgery. Propofol enhances the antiinflammatory response to surgery by several mechanisms. This might have masked a neuroprotective effect of ketamine because propofol was administered in both groups in our study.
Background: Dysmenorrhea is menstrual disorder that affects about 40% - 90% of women worldwide, it is associated with oxidative stress. The current treatment of this condition is administration of non-steroidal anti-inflammatory drugs, which when frequently used, may affect organs.
Objective: Assess the hepatotoxicity and nephrotoxicity side effects related to dysmenorrhea and its treatment
Materials and methods: A survey (questionnaire) was designed and implemented on 689 female students of the University of Dschang. After this, and following the inclusion criteria, 191 blood samples were collected for assay of hepatotoxicity markers (transaminases, albumin), nephrotoxicity indicators (creatinine, urea, total protein) and the inflammation associated indicators. The measurements were performed on fully automated Olympus AU 400 Analyzer, using standard reagent kits.
Results: Subjects with untreated dymenorrhea lasting more than five years had a significantly high level (p < 0.05) of ALT (39.47 ± 15.74 IU/L) and AST (44.37 ± 13.74 IU/L). Transaminases levels were significantly associate (p < 0.01) and positively correlate (0.251 for ALT and 0. 223 for AST) with the disease duration. Dysmenorrheic individuals on medication for more than 9 years had significantly higher ALT (25.14 ± 7.85 IU/L) and AST (35.26 ± 0.70 IU/L) levels (p < 0.05) compared to those under treatment for less than 5 years (19.37 ± 8.27 UI/L and 27.68 ± 8.56 UI/L). The use of analgesics, regardless of the duration of treatment, had normal creatinine clearance (107.44 ± 30.86 ml/min), compared to those treated with either anti-inflammatory drugs (71.56 ± 26.44 ml/min), or a combination of analgesics and anti-inflammatory drugs (81.34 ± 31.97 ml/min), which was significantly reduced (p < 0.05).
Conclusion: Dysmenorrhea duration, type and duration of treatment potentially expose participants to liver and kidney disorders.
Endothelial dysfunction and inflammation play a key role in the pathophysiology of diabetic nephropathy; Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthase, when BH4 is reduced to dihydrobiopterin (BH2), endothelial dysfunction is induced.
Purpose: The aim of this study is to evaluate the relationship between the levels of biopterins with albuminuria in type-2 diabetic hypertensive patients.
Methods: We studied 30 hypertensive type-2 diabetic patients in whom biopterins levels were measured by reverse phase high performance liquid chromatography with fluorescence detection. Additionally, 24 h urinary albumin excretion was also measured (nephelometry). The levels of biopterins and albuminuria were correlated with the Pearson correlation coefficient.
Results: We did not find a significantly correlation between biopterins levels and albuminuria, However, we found a significantly inverse correlation (R= -0.498, p<0.005) between the BH4/BH2 ratio and albuminuria.
Conclusion: Our results suggest that the BH4/BH2 ratio instead of biopterins levels may be a marker of nephropathy in hypertensive type-2 diabetic patients.
Haemophagocytosis is a dysregulated immune condition characterised by both inflammation and uncontrolled activation of macrophages and T-cells, which causes aberrant cytokine release, leading to cytokine storm  it can be primary or secondary, depending upon the etiology.
Infectious bursal disease (IBD) considered as one of the major viral diseases threatening the poultry industry worldwide. The causative agent of the IBD is Infectious bursal disease virus (IBDV) which replicates in developing B lymphocytes in the bursa of Fabricius leading to its destruction and bursal inflammation. In this study, we investigated a technology to produce therapeutic recombinant antibodies against IBDV in bacteria by constructing a bacterial displayed recombinant scFv library from immunized chickens, followed by screening the scFv library by fluorescence activated cell sorting (FACS) with FITC-labeled VP2. Twelve VP2-binding scFv clones with unique sequences were obtained, with overall amino acid homology of 81.53%. The complementarity determining region (CDR) 3 in the heavy chain displayed the lowest homology, while the amino acid sequences in framework regions and CDR2 of both chains and CDR1 of the heavy chain are relatively conserved. Twelve VP2-binding scFv clones were expressed in E.coli and purified through denaturation and denaturation of inclusion bodies. Our ELISA results showed that all scFvs exhibited binding ability and specificity to VP2 and various IBDV strains. In addition, two scFvs showed significant neutralizing activity to IBDV (B-87 strain) as these scFvs inhibited cytopathic effect of chicken embryo fibroblast (DF1) caused by IBDV. In conclusion, our study provides a lead candidate for further development of therapeutic antibodies for IBDV infection.
Age related macular degeneration is a severe disease of mainly elderly people and leads to central vision loss because of the degeneration of the retinal pigment epithelium . Genetic and environmental factors are responsible for the accumulation of extracellular material and deposit formation near the retinal pigment epithelial (RPE) layer, which leads to loss of photoreceptors and induction of chronic inflammation. The deposits are composed of lipids and proteins including many complement proteins, indicating the involvement of the complement system in the degenerative process and chronic inflammation . So far there is no treatment for the dry form of AMD, except nutritional supplementation with antioxidants and vitamins . Combined with a prolonged lifetime expectation in developed countries, AMD is developing to a social and economic burden. Therefore, there is an urgent need for a treatment of AMD that can delay disease manifestation and progression for several years.
We present below a mechanistic molecular approach for development of Anti-Inflammatory biomarkers of Probiotic Bacteria in Fermented Foods. Probiotics are live microorganisms that promote human health by counteracting the noxious toxic gut microflora in human intestine, by modulating of the tight junctions, and by increasing mucin production, enforcing intestinal epithelial cell barrier function, modifying microbial community within the gut intestinal disorders, and improving immune responses associated with chronic inflammation in experimental animal models, collectively enhancing human health. Cytokine secretion by intestinal epithelial cells and macrophages are regulated by probiotics through key signaling pathways such as nuclear factor-κB and mitogen-activated kinases, resulting in alleviation of several disorders such as allergies, diabetes, obesity, heart diseases and cancer. MicroRNAs are small non-coding RNA molecules involved in transcriptional and post-translational regulation of gene expression by inhibiting gene translation. Using in vitro and in vivo approaches in cell lines and mice models to study effects of probiotic conditional media and heat-killed bacterial strains with anti-inflammatory effect to elucidate the mechanisms by which probiotics affect signaling pathways, and by using global cytokine and microRNA gene expression analyses arrroaches to develop biomarkers for studying different pro- and anti-inflammatory activities, and using statistical approaches to analyse the data, we show that cytokines and miRNAs have an essential role in regulation of cancerous and inflammatory bathways. This mechanistic approach will result in developing specific disease biomarkers for the early diagnosis of certain pathogenic states, as well as evaluating the effect of different dietary componenents on developed biomarkers in health states that will promote and enhance human health. Comparing the concordance of the in vitro to the in vivo research findings will confirm the correspondence of both approaches to each other. Moreover, this study will have a major public health relevance in elucidating the role of miRNAs and their targets in inflammation, paving the way to diagnosing and treating of pathogenic human disease stages.
Lung cancer is the leading cause of cancer-related deaths worldwide, and almost accounts for 20% of these deaths, however, the cure rate is less than 10% . Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all cases of lung cancer , but fewer than 15% of individuals diagnosed with NSCLC can survive for more than 5 years, which poses a great threat to the patient’s life and health . Recently, the incidence of lung cancer keeps dynamically growing, but more than 75% of patients at diagnosis has appeared local development or metastasis, missing the best period of surgery. Moreover, despite surgical treatment is the optimal choice for early-stage NSCLC patients, 30%-40% of patients with NSCLC develop tumor recurrence in a short time. Therefore, improving the prognosis of patients with lung cancer and predicting the long-term survival of patients is of particular importance . At present, tumor and node metastasis (TNM) staging system, clinicopathological characteristics, visceral pleural invasion and marginal status are used to predict the disease progression and overall survival of NSCLC patients. There is no index which is stable, effective, reliable and less harmful to assess prognosis, predict recurrence risk and overall survival.
There is growing evidence that gastroesophageal disease is influenced by the esophageal microbiome, and that commensal bacteria of the oropharynx, stomach, and colon are thought to have a role in modulatiing pathogenesis. These emerging hypotheses are based on observed changes in the composition of the esophageal ﬂora, notably, repeated observations: 1. There is an abundance of gram-positive bBacteria in the healthy esophagus. are more gram positive prevalent 2. The esophageal bacterial population becomes increasingly gram negative with disease progression. Associated with this shift to a more gram negative prevalence is an increase in the potential for the presence of antigenic lipopolysaccharide (LPS). The immunoreactivity of LPS endotoxin thought to promote susceptibility to inflammation and disease.
The pathogenesis of the more common diseases of the esophagus e.g. gastroesophageal reflux disease (GERD), esophageal dysmotility (achalasia), eosinophilic esophagitis (EoE), Barrett’s esophagus (BE), and esophageal cancer, are well-established. Emerging data suggest however, that these are all characterized by an immune-mediated inflammatory cascade, propogated by a dysbiotic state. Thereby, the ability of the healthy “normative state” to protect against foreign bacteria is compromised. This dysbiosis thereby can create adverse inflammatory or immunoregulatory responses with progression of disease.
In the normal healthy state, the esophageal microbiome is constituted in-part, by a multitude of gram positive bacteria, many of which produce antibacterial peptides called bacteriocins. Bacteriocins are selective and used to maintain population integrity by killing off foreign bacteria. When the “normative biome” is interrupted (e.g. antibiotics, medications, diet, environmental factors), the constitutional changes may allow a more hospitable imbalance favoring the proliferation of opportunistic pathogens. Therefore it seems rational that defining, perhaps that defining, perhaps cultivating, a protective bacterial community that could help prevent or mitigate inflammatory diseases of the esophagus. Furthermore, in conjunction with evidence demonstrating that some bacteriocins are cytotoxic or antiproliferative toward cancer cell lines, further exploration might provide a rich source of effective peptide-based drug targets.
Therapeutic options targeting the microbiome, including prebiotics, probiotics, antibiotics and bacteriocins, have been studied, albeit the attributable effects on the esophagus for the most part, have been unrecognized by clinicians. This review focuses on the current knowledge of the involvement of the microbiome in esophageal diseases (most notably GERD/Barrett’s esophagus/esophageal cancer) and identifies emerging new concepts for treatment.
Acute pancreatitis is inflammation of the pancreas that may be accompanied by a systemic inflammatory response which results in impairment of the functioning of various organs, systems. Pancreatitis associated vascular complications very often cause morbidity and mortality. There are various cardiovascular complications like shock, hypovolemia, pericardial effusion, and sometimes ST–T changes in the electrocardiogram (ECG) presenting as acute myocardial infarction (AMI). Acute myocardial infarction complicating acute pancreatitis has rarely been studied and the exact process of myocardial injury still remains unclear. We here report a case of Acute Pancreatitis associated with acute myocardial Infarction.
Introduction: Forty-six per cent children have allergic rhinoconjunctivitis (Allergologica 2005).
Working hypothesis: Ocular topical cyclosporine improves the quality of life for these patients.
Material, methods, design: 2-year prospective study (2015-16), 40 patients with topical corticosteroids without improvement, followed 20 and 20 switched to corticosteroids cyclosporine 0.05%. Interview with Quality of Life Questionnaire in Children with rhinoconjunctivitis (PRQLQ) before and at the end of treatment. Mean age of 10.3 years with 60% male-40% female. Treatments were applied from January to March. There were 15 questions divided into two blocks. Children responded using a card with responses rated from zero (not bothered at all) to 6 (quite upset).
Results: Before the 100% reported that, the itching was very bothersome. In the group of 40 children, 80% showed symptoms of epiphora and 60% showed symptoms of ocular inflammation. 100% complained of significant discomfort in rubbing their eyes, 30% did not like to take medications. Headaches affected 20%. 100% stated that they cannot play normally. 80% showed decreased concentration in class.
Continuing with corticosteroids did not show statistically significant changes.
Patients with cyclosporine improved the results by 3 points, with decreased itching, tearing, swelling, pain, eye rubbing, medication and headaches. In the 2nd questionnaire there was limited variation in the results related to fatigue, malaise, and irritability but with substantially improved balance of sleep, insomnia and concentration at school.
Conclusion: Cyclosporine A is a cyclic polypeptide calcineurin inhibitor developed from the fungus Tolypocladium inflatum. The first dilution was 2% but it is currently used at a dilution of 0.05% and recent publications suggest nanosuspensions. Our study showed improvement in parameters related to symptoms, especially itching and lower improvement of psychological aspects, this achieves a better quality of life for children and more willingness to adhere to the treatment.
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