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Cholera, caused by Vibrio cholerae, is a severe diarrheal disease that necessitates prompt diagnosis and effective treatment. This review comprehensively examines various diagnostic methods, from traditional microscopy and culture to advanced nucleic acid testing like polymerase spiral reaction and rapid diagnostic tests, highlighting their advantages and limitations. Additionally, we explore evolving treatment strategies, with a focus on the challenges posed by antibiotic resistance due to the activation of the SOS response pathway in V. cholerae. We discuss promising alternative treatments, including low-pressure plasma sterilization, bacteriophages, and selenium nanoparticles. The paper emphasizes the importance of multidisciplinary approaches combining novel diagnostics and treatments in managing and preventing cholera, a persistent global health challenge. The current re-emergent 7th pandemic of cholera commenced in 1961 and shows no signs of abeyance. This is probably due to the changing genetic profile of V. cholerae concerning bacterial pathogenic toxins. Given this factor, we argue that the disease is effectively re-emergent, particularly in Eastern Mediterranean countries such as Lebanon, Syria, etc. This review considers the history of the current pandemic, the genetics of the causal agent, and current treatment regimes. In conclusion, cholera remains a significant global health challenge that requires prompt diagnosis and effective treatment. Understanding the history, genetics, and current treatments is crucial in effectively addressing this persistent and re-emergent disease., (© The Author(s) 2024. Published by Oxford University Press on behalf of Applied Microbiology International.)

Chitosan is an abundant organic polysaccharide, which can be relatively easily obtained by chemical modification of animal or fungal source materials. Chitosan and its derivatives have been shown to exhibit direct antiviral activity, to be useful vaccine adjuvants and to have potential anti-SARS-CoV-2 activity. This thorough and timely review looks at the recent history of investigations into the role of chitosan and its derivatives as an antiviral agent and proposes a future application in the treatment of endemic SARS-CoV-2., (© 2021 The Society for Applied Microbiology.)

This work is to investigate the levels of human xanthine oxidoreductase (HXOR), its antibodies, and microorganisms in synovial fluid of patients with untreated rheumatoid joint diseases. Synovial fluids were collected from sixty-four patients with rheumatoid joint diseases. Sixty-four age-matched individuals were included as control. Xanthine oxidoreductase (XOR) proteins level and anti-XOR antibodies were determined in the blood and synovial fluid, using human XOR as antigen, by enzyme-linked immunosorbent (ELISA) assay. Synovial fluids were cultured for bacteria and fungi. The titers of XOR protein in the synovial fluid of patients with rheumatoid arthritis were 90.43 ± 23.37 μg/ml (mean ± SD, n = 29) and up to 62.42 ± 8.74 μg/ml (mean ± SD, n = 35) in other joint inflammation. Anti-HXOR antibodies titers in patients were 167.72 ± 23.64 μg/ml, n = 64, which was significantly higher in rheumatoid arthritis patients. The results indicated that anti-HXOR antibodies in synovial fluids have a protective role as high concentrations against XOR were detected in inflammatory arthritis. These antibodies play a role in eliminating XOR from synovial fluids. However, immune complex formation could activate complement and participate in propagating the inflammatory cycle. Synovial aspirate ordinary microbial cultures were negative for any bacteria or fungi, but that does not exclude organisms of special culture requirements.

This study was conducted to determine whether changes in the levels of plasma apolipoproteins (apo) A-I, A-II, B, C-II, and C-III, along with cholesterol and triglycerides, could provide additional information on these parameters in relation to the control of glycemia. Plasma and lipoprotein lipids and apolipoprotein levels were measured in 123 insulin-dependent diabetic children (4- to 12-years-old), classified into good, fair, and poor diabetic control based on HbA1c and fructosamine levels, and in 62 comparable healthy controls. Total cholesterol, very low density lipoprotein cholesterol, and low density lipoprotein cholesterol, as well as total triglycerides, very low density lipoprotein, low density lipoprotein, and high density lipoprotein (HDL) triglycerides, and apo B and apo C-III were increased significantly in children with fair and poor diabetic control. While in diabetic children with good control, only very low density lipoprotein cholesterol was elevated significantly compared with healthy control subjects. Conversely, the levels of cholesterol in HDL, HDL2, HDL3, and apo A-I were decreased significantly in the three diabetic groups, but apo A-II and apo C-II did not change. We conclude that in children with insulin-dependent diabetes mellitus, abnormalities in plasma lipid, lipoprotein, and apolipoprotein levels occur, the extent of which depends on the degree (extent) of glycemic control (the poorer the control the more substantial the abnormality). We suggest that measurement of apo C-III level along with apo B and apo A-I in these patients may be a sensitive indicator to alterations in glycemic control.

Plasm levels of lipid, lipoprotein, and apolipoprotein (APO) A-I, A-II, C-II, C-III, and E were analyzed in 180 young survivors of myocardial infarction (MI) ages 28 to 45 years and in 200 sex-and age-matched normal healthy subjects to assess the importance of apolipoprotein concentrations in comparison with lipoproteins in MI patients. In comparison with control subjects, MI patients showed marked increases in the following parameters: total cholesterol (TC), low density lipoproteins (LDL) cholesterol, triglycerides (TG), very low density (VLDL) triglycerides, and cholesterol, and LDL-TG, apo B, apo C-III and apo E. There were no significant changes in levels of HDL3; cholesterol, apo A-II and apo C-II in these patients compared with their controls. Levels of high density lipoprotein (HDL), HDL2 cholesterol, and plasma apo A-I were markedly decreased in the young MI survivors' group demonstrated that the better discriminating lipoproteins and apolipoproteins in MI patients in descending order were HDL2 cholesterol, apo C-III, apo B, apo A-I, VLDL triglycerides and HDL cholesterol discriminated between patients and controls. Results indicate that measurement of apo C-III, B and A-I beside HDL2 cholesterol were shown to be of potential use in differentiating normal controls from patients with MI.

Plasma lipids, lipoproteins and apolipoproteins (apo) were analysed in 30 young Arab IDDM and 50 young insulin-requiring NIDDM women. The mean age of IDDM and NIDDM groups was 20.2 and 34.5 years, and mean duration of diabetes was 5.7 and 4.6 years, respectively. Two groups of 40 and 60 healthy women (matched for age and BMI) provided corresponding control groups. In comparison with control subjects, diabetics showed marked increases in the following parameters: total cholesterol (TC), low density lipoprotein (LDL) cholesterol, total triglycerides (TG), very low density lipoprotein (VLDL) triglycerides, phospholipids, apoB, LDL apoB, glucose and glycosylated hemoglobin (HbA1c) as well as the ratios of total cholesterol/high density lipoprotein (HDL) cholesterol, LDL-cholesterol/HDL-cholesterol, LDL cholesterol/high density lipoprotein (HDL) cholesterol, LDL-cholesterol/HDL-cholesterol, LDL cholesterol/high density lipoprotein 2 (HDL2) cholesterol and apoB/apoAI. Plasma LCAT activity, concentrations of HDL3 apoAI and apoAII in plasma and lipoprotein fractions were normal in both the diabetic groups. Levels of C-peptide, HDL, HDL2 and HDL3 cholesterol, plasma apoAI, HDL apoAI and HDL2 apoAI were markedly decreased in the diabetic groups as compared to their corresponding controls. There was no significant correlation between fasting glucose or HbA1c and any of the above parameters. Despite insulin therapy in both the diabetic groups studied, abnormalities in lipids, apoB and apoAI still persisted. Our data suggest a possible higher risk of atherosclerosis in these patients.

Glycerol 3-phosphate acyltransferase (GPAT) activity and triglyceride lipase (TGL) activity were measured in homogenates from hearts perfused with adrenergic agonists and antagonists. Perfusion with adrenalin or the beta-agonist isoprenaline produced an increase in TGL activity and a fall in GPAT activity. These changes could be imitated by incubation of heart homogenates with cAMP-dependent protein kinase. The alpha 2-agonist clondine produced the opposite effect, thus it increased GPAT activity and decreased TGL activity. Methoxamine, an alpha 1-agonist, had no effect on TGL activity but reduced GPAT activity. Continuous perfusion of the beta-antagonist atenolol reduced TGL activity to half that found in controls but also reduced GPAT activity. No change was seen on continuous perfusion of alpha 1- or alpha 2-antagonists. Changes in GPAT activity were localized mainly in the microsomal enzyme. These changes are consistent with both enzymes being regulated via a cyclic-AMP dependent protein kinase system and via alpha-adrenergic mechanisms.