Relationship Between the Bee Venom Therapy and Tumor Necrosis Factor-308 Variation in the Management of Rheumatoid Arthritis, a Prospective Study

Bee venom (BV) was traditionally used to treat various inflammatory disorders including rheumatoid arthritis (RA). The current study aims to assess the anti-arthritic effect of BV and the relation between tumor necrosis factor (TNF)-308 polymorphism and BV treatment response in RA. Methods: 50 RA patients received BV injection for 6 months, with an evaluation of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), visual analog scale (VAS), disease activity score (DAS28-ESR), TNF-α, at baseline and after 6ms. Genotyping assay for TNF-α G308A rs1800629 gene polymorphism. Results: The mean age was 36.0 (29.0 -40.0) years; 90% were females and 10% were males with a mean disease duration 8 (5-10 years). Most of the studied patients (64%) had high disease activity and 37% had moderate disease activity with a mean 5.5 (4.7 -6.8) at baseline. Treatment with BV was associated with a significant improvement in ESR, CRP, VAS, and significant decline in the DAS28-ESR score with p-value \u3c0.005. Most of cases achieved moderate and good EULAR response and a significant reduction of (TNFα) Level. TNF-α-308 genetic variant showed that the GG genotype (32 patients, 64 %) was more prevalent followed by AA genotypes (14 patients, 28 %). There was no difference between TNF-α G308 genotypes regarding the post-treatment response. Conclusion: Treatment with Bee venom can improve joint pain, disease activity, reduce ESR, CRP, and TNFα levels in RA patients. No difference between TNF-α G308 genotypes regarding treatment response

Arabic gum acacia improves diabetic peripheral neuropathy in rats: a biochemical and histopathological evidence

Background: Diabetic peripheral neuropathy (DPN) is a frequent complication of diabetes mellitus and unfortunately, its present therapeutic alternatives are exceptionally poor. Objectives of this study was to assess the antidiabetic, antioxidant and hypolipidemic action of Gum Arabic (GA) and its role in promoting the functional recovery from diabetic neuropathy developed in in an experimental model of diabetic neuropathy.Methods: Sixty adult male Sprague-Dawley rats were utilized and randomly assigned into six groups (n= 10); control, Arabic gum-treated, untreated diabetic, diabetic received metformin, diabetic received metformin and B12 vitamin and diabetic received metformin, B12 vitamin and AG. Locomotor activity and hyperalgesia were assed at the end of the study. Fasting and two hours post-prandial blood glucose, serum insulin levels, lipid Profile, oxidants/antioxidants parameters were assessed in the blood. Sciatic nerve was assessed histopathologically.Results: The locomotor activity of the untreated diabetic rats was significantly (p<0.001) reduced compared to the control group while it was significantly increased in all treated groups. The lipid profile and Malondialdehyde were significantly improved in all treated groups. Levels of CAT, GSH, SOD, GPx were significantly decreased in untreated diabetic group compared to the control while they were significantly increased in all treated groups compared to the untreated diabetic group. Sciatic nerve fibers of untreated diabetic rats showed degenerated axons with dilated myelin sheaths and degenerated Schwann cells. The nerve had significantly fewer fiber compared to the control. These changes were alleviated in all the treated groups specifically that received metformin, vitamin B12 and GA.Conclusions: It could be concluded that Arabic gum had hypoglycemic, antioxidant and hypolipidemic activity and had a protective effect on diabetic neuropathy. Based on this it is recommended that human clinical trials are necessary to prove this therapeutic effect

MHD natural convection in an inclined cavity filled with a fluid saturated porous medium with heat source in the solid phase

A numerical investigation of unsteady magnetohydrodynamic free convection&nbsp;in an inclined square cavity filled with a fluid-saturated porous medium and with internal&nbsp;heat generation has been performed. A uniform magnetic field inclined with the same&nbsp;angle of the inclination of the cavity is applied. The governing equations are formulated&nbsp;and solved by a direct explicit finite-difference method subject to appropriate initial and&nbsp;boundary conditions. Two cases were considered, the first case when all the cavity walls&nbsp;are cooled and the second case when the cavity vertical walls are kept adiabatic. A parametric study illustrating the influence of the Hartmann number, Rayliegh number, the&nbsp;inclination angle of the cavity and the dimensionless time parameter on the flow and&nbsp;heat transfer characteristics such as the streamlines, isotherms and the average Nusselt&nbsp;number is performed. The velocity components at mid section of the cavity as well as the&nbsp;temperature profiles are reported graphically. The values of average Nusselt number for&nbsp;various parametric conditions are presented in tabular form

Symptomatic Uncomplicated Diverticular Disease (SUDD): Practical Guidance and Challenges for Clinical Management

Symptomatic Uncomplicated Diverticular Disease (SUDD) is a syndrome within the diverticular disease spectrum, characterized by local abdominal pain with bowel movement changes but without systemic inflammation. This narrative review reports current knowledge, delivers practical guidance, and reveals challenges for the clinical management of SUDD. A broad and common consensus on the definition of SUDD is still needed. However, it is mainly considered a chronic condition that impairs quality of life (QoL) and is characterized by persistent left lower quadrant abdominal pain with bowel movement changes (eg, diarrhea) and low-grade inflammation (eg, elevated calprotectin) but without systemic inflammation. Age, genetic predisposition, obesity, physical inactivity, low-fiber diet, and smoking are considered risk factors. The pathogenesis of SUDD is not entirely clarified. It seems to result from an interaction between fecal microbiota alterations, neuro-immune enteric interactions, and muscular system dysfunction associated with a low-grade and local inflammatory state. At diagnosis, it is essential to assess baseline clinical and Quality of Life (QoL) scores to evaluate treatment efficacy and, ideally, to enroll patients in cohort studies, clinical trials, or registries. SUDD treatments aim to improve symptoms and QoL, prevent recurrence, and avoid disease progression and complications. An overall healthy lifestyle – physical activity and a high-fiber diet, with a focus on whole grains, fruits, and vegetables – is encouraged. Probiotics could effectively reduce symptoms in patients with SUDD, but their utility is missing adequate evidence. Using Rifaximin plus fiber and Mesalazine offers potential in controlling symptoms in patients with SUDD and might prevent acute diverticulitis. Surgery could be considered in patients with medical treatment failure and persistently impaired QoL. Still, studies with well-defined diagnostic criteria for SUDD that evaluate the safety, QoL, effectiveness, and cost-effectiveness of these interventions using standard scores and comparable outcomes are needed

BJS commission on surgery and perioperative care post-COVID-19

Background: Coronavirus disease 2019 (COVID-19) was declared a pandemic by the WHO on 11 March 2020 and global surgical practice was compromised. This Commission aimed to document and reflect on the changes seen in the surgical environment during the pandemic, by reviewing colleagues' experiences and published evidence. Methods: In late 2020, BJS contacted colleagues across the global surgical community and asked them to describe how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) had affected their practice. In addition to this, the Commission undertook a literature review on the impact of COVID-19 on surgery and perioperative care. A thematic analysis was performed to identify the issues most frequently encountered by the correspondents, as well as the solutions and ideas suggested to address them. Results: BJS received communications for this Commission from leading clinicians and academics across a variety of surgical specialties in every inhabited continent. The responses from all over the world provided insights into multiple facets of surgical practice from a governmental level to individual clinical practice and training. Conclusion: The COVID-19 pandemic has uncovered a variety of problems in healthcare systems, including negative impacts on surgical practice. Global surgical multidisciplinary teams are working collaboratively to address research questions about the future of surgery in the post-COVID-19 era. The COVID-19 pandemic is severely damaging surgical training. The establishment of a multidisciplinary ethics committee should be encouraged at all surgical oncology centres. Innovative leadership and collaboration is vital in the post-COVID-19 era

Identification of a novel homozygous nonsense mutation in EYS in a Chinese family with autosomal recessive retinitis pigmentosa

<p>Abstract</p> <p>Background</p> <p>Retinitis pigmentosa is the most important hereditary retinal degenerative disease, which has a high degree of clinical and genetic heterogeneity. More than half of all cases of retinitis pigmentosa are autosomal recessive (arRP), but the gene(s) causing arRP in most families has yet to be identified. The purpose of this study is to identify the genetic basis of severe arRP in a consanguineous Chinese family.</p> <p>Methods</p> <p>Linkage and haplotype analyses were used to define the chromosomal location of the pathogenic gene in the Chinese arRP family. Direct DNA sequence analysis of the entire coding region and exon-intron boundaries of <it>EYS </it>was used to determine the disease-causing mutation, and to demonstrate that the mutation co-segregates with the disease in the family.</p> <p>Results</p> <p>A single nucleotide substitution of G to T at nucleotide 5506 of EYS was identified in the Chinese arRP family. This change caused a substitution of a glutamic acid residue at codon 1,836 by a stop codon TAA (p.E1836X), and resulted in a premature truncated EYS protein with 1,835 amino acids. Three affected siblings in the family were homozygous for the p.E1836X mutation, while the other unaffected family members carried one mutant allele and one normal EYS allele. The nonsense mutation p.E1836X was not detected in 200 unrelated normal controls.</p> <p>Conclusions</p> <p>The <it>EYS </it>gene is a recently identified disease-causing gene for retinitis pigmentosa, and encodes the orthologue of <it>Drosophila </it>spacemaker. To date, there are only eight mutations in <it>EYS </it>that have been identified to cause arRP. Here we report one novel homozygous nonsense mutation of <it>EYS </it>in a consanguineous Chinese arRP family. Our study represents the first independent confirmation that mutations in <it>EYS </it>cause arRP. Additionally, this is the first <it>EYS </it>mutation identified in the Chinese population.</p

Biallelic mutation of Protocadherin-21 (PCDH21) causes retinal degeneration in humans

PurposeTo describe the clinical findings and mutations in affected members of two families with an autosomal recessive retinal dystrophy associated with mutations in the protocadherin-21 (PCDH21) gene.MethodsA full genome scan of members of two consanguineous families segregating an autosomal recessive retinal dystrophy was performed and regions identical by descent identified. Positional candidate genes were identified and sequenced. All patients had a detailed ophthalmic examination, including electroretinography and retinal imaging.ResultsAffected members of both families showed identical homozygosity for an overlapping region of chromosome 10q. Sequencing of a candidate gene, PCDH21, showed two separate homozygous single-base deletions, c.337delG (p.G113AfsX1) and c.1459delG (p.G487GfsX20), which were not detected in 282 control chromosomes. Affected members of the two families first reported nyctalopia in late teenage years and retained good central vision until their late 30s. No color vision was detected in any proband. The fundus appearance included the later development of characteristic circular patches of pigment epithelial atrophy at the macula and in the peripheral retina.ConclusionsBiallelic mutations in the photoreceptor-specific gene PCDH21 cause recessive retinal degeneration in humans