Evidence-Based Framework to Manage Cyanobacteria and Cyanotoxins in Water and Sludge from Drinking Water Treatment Plants

Freshwater bodies and, consequently, drinking water treatment plants (DWTPs) sources are increasingly facing toxic cyanobacterial blooms. Even though conventional treatment processes including coagulation, flocculation, sedimentation, and filtration can control cyanobacteria and cell-bound cyanotoxins, these processes may encounter challenges such as inefficient removal of dissolved metabolites and cyanobacterial cell breakthrough. Furthermore, conventional treatment processes may lead to the accumulation of cyanobacteria cells and cyanotoxins in sludge. Pre-oxidation can enhance coagulation efficiency as it provides the first barrier against cyanobacteria and cyanotoxins and it decreases cell accumulation in DWTP sludge. This critical review aims to: (i) evaluate the state of the science of cyanobacteria and cyanotoxin management throughout DWTPs, as well as their associated sludge, and (ii) develop a decision framework to manage cyanobacteria and cyanotoxins in DWTPs and sludge. The review identified that lab-cultured-based pre-oxidation studies may not represent the real bloom pre-oxidation efficacy. Moreover, the application of a common exposure unit CT (residual concentration × contact time) provides a proper understanding of cyanobacteria pre-oxidation efficiency. Recently, reported challenges on cyanobacterial survival and growth in sludge alongside the cell lysis and cyanotoxin release raised health and technical concerns with regards to sludge storage and sludge supernatant recycling to the head of DWTPs. According to the review, oxidation has not been identified as a feasible option to handle cyanobacterial-laden sludge due to low cell and cyanotoxin removal efficacy. Based on the reviewed literature, a decision framework is proposed to manage cyanobacteria and cyanotoxins and their associated sludge in DWTPs.     

Angiogenesis and blood vessel stability in inflammatory arthritis

Objective

To assess blood vessel stability in inflammatory synovial tissue (ST) and to examine neural cell adhesion molecule (NCAM), oxidative DNA damage, and hypoxia in vivo.

Methods

Macroscopic vascularity and ST oxygen levels were determined in vivo in patients with inflammatory arthritis who were undergoing arthroscopy. Vessel maturity/stability was quantified in matched ST samples by dual immunofluorescence staining for factor VIII (FVIII)/α‐smooth muscle actin (α‐SMA). NCAM and 8‐oxo‐7,8‐dihydro‐2′‐deoxyguanosine (8‐oxodG) were examined by immunohistochemistry. Angiogenesis was assessed in vitro, using human dermal endothelial cells (HDECs) in a Matrigel tube formation assay.

Results

A significant number of immature vessels (showing no pericyte recruitment) was observed in tissue from patients with inflammatory arthritis (P < 0.001), in contrast to osteoarthritic and normal tissue, which showed complete recruitment of pericytes. Low in vivo PO ₂ levels in the inflamed joint (median [range] 22.8 [3.2–54.1] mm Hg) were inversely related to increased macroscopic vascularity (P < 0.04) and increased microscopic expression of FVIII and α‐SMA (P < 0.04 and P < 0.03, respectively). A significant proportion of vessels showed focal expression of NCAM and strong nuclear 8‐oxodG expression, implicating a loss of EC–pericyte contact and increased DNA damage, levels of which were inversely associated with low in vivo PO ₂ (P = 0.04 for each comparison). Circulating cells were completely negative for 8‐oxodG. Exposure of HDEC to 3% O₂ (reflecting mean ST in vivo measurements) significantly increased EC tube formation (P < 0.05).

Conclusion

Our findings indicate the presence of unstable vessels in inflamed joints associated with hypoxia, incomplete EC–pericyte interactions, and increased DNA damage. These changes may further contribute to persistent hypoxia in the inflamed joint to further drive this unstable microenvironment.

     

Real-Time PCR Quantification of Methanobrevibacter oralis in Periodontitis

A real-time PCR assay developed to quantify Methanobrevibacter oralis indicated that its inoculum significantly correlated with periodontitis severity (P = 0.003), despite a nonsignificant difference in prevalence between controls (3/10) and patients (12/22) (P = 0.2, Fisher test). The M. oralis load can be used as a biomarker for periodontitis.     

Rapid detection of beta-Thalassemia alleles in Egypt using naturally or amplified created restriction sites and direct sequencing: a step in disease control

beta-Thalassemia (thal), the most common genetic disorder in Egypt, is a major health problem with an estimated carrier rate of 9-10%. This study, aimed at describing the beta-globin gene mutations in the Suez Canal area, an important Egyptian region, to provide a foundation for a disease control program. We studied 44 beta-thalassemic patients (and their relatives) from 35 families living in this region. The commonest mutations were genetically diagnosed using naturally or amplified created restriction sites. Less frequent mutations were characterized by denaturing gradient gel electrophoresis (DGGE) and direct sequencing. Twelve different mutations were identified in 51 unrelated chromosomes. The three most frequent mutations were IVS-I-110 (G-->A), IVS-I-1 (G-->A) and IVS-I-6 (T-->C). The spectrum of rarer mutations was heterogeneous and differed from that reported in other areas of Egypt. We also identified the first homozygous case of a rare mutation, codon 24 (-G; +CAC), displaying a thalassemia major phenotype. Parental consanguinity was high (60.6%) with 35.7% of the compound heterozygous patients having consanguineous parents. These data provide insights for the distribution of beta-thal alleles in this region, and could be used as a basis for genetic counseling and prenatal diagnosis.     

Intravenous glutamine decreases lung and distal organ injury in an experimental model of abdominal sepsis

Introduction

The protective effect of glutamine, as a pharmacological agent against lung injury, has been reported in experimental sepsis; however, its efficacy at improving oxygenation and lung mechanics, attenuating diaphragm and distal organ injury has to be better elucidated. In the present study, we tested the hypothesis that a single early intravenous dose of glutamine was associated not only with the improvement of lung morpho-function, but also the reduction of the inflammatory process and epithelial cell apoptosis in kidney, liver, and intestine villi.

Methods

Seventy-two Wistar rats were randomly assigned into four groups. Sepsis was induced by cecal ligation and puncture surgery (CLP), while a sham operated group was used as control (C). One hour after surgery, C and CLP groups were further randomized into subgroups receiving intravenous saline (1 ml, SAL) or glutamine (0.75 g/kg, Gln). At 48 hours, animals were anesthetized, and the following parameters were measured: arterial oxygenation, pulmonary mechanics, and diaphragm, lung, kidney, liver, and small intestine villi histology. At 18 and 48 hours, Cytokine-Induced Neutrophil Chemoattractant (CINC)-1, interleukin (IL)-6 and 10 were quantified in bronchoalveolar and peritoneal lavage fluids (BALF and PLF, respectively).

Results

CLP induced: a) deterioration of lung mechanics and gas exchange; b) ultrastructural changes of lung parenchyma and diaphragm; and c) lung and distal organ epithelial cell apoptosis. Glutamine improved survival rate, oxygenation and lung mechanics, minimized pulmonary and diaphragmatic changes, attenuating lung and distal organ epithelial cell apoptosis. Glutamine increased IL-10 in peritoneal lavage fluid at 18 hours and bronchoalveolar lavage fluid at 48 hours, but decreased CINC-1 and IL-6 in BALF and PLF only at 18 hours.

Conclusions

In an experimental model of abdominal sepsis, a single intravenous dose of glutamine administered after sepsis induction may modulate the inflammatory process reducing not only the risk of lung injury, but also distal organ impairment. These results suggest that intravenous glutamine may be a potentially beneficial therapy for abdominal sepsis.     

One year cardiac follow up of young world cup football team compared to nonathletes

IntroductionSudden cardiac death among professional young athletes has become a significant concern mainly attributed to structural heart changes and ECG abnormalities.ObjectivesWe aimed primarily to compare echocardiographic and electrocardiographic changes in young professional athletes versus a control group of sedentary lifestyled nonathletic individuals of the same age group. Secondly, we aimed to follow up echocardiographic and electrocardiographic changes in young professional athletes after one year.MethodsWe conducted the study from May 2008 to May 2009 by clinical examination, transthoraxic echocardiography and 12 lead ECG. Our study group was the national football team candidates for the youth world cup occurring in Cairo 2009. This study group was compared to a control group of randomly picked nonathletic third year medical students after exclusion of anyone with a known medical illness. The study group was classified into Athletes I representing athletes at the beginning of the study and Athletes II representing athletes after one year follow up.ResultsThe Study group comprised 34 males, mean age 18.82 ± 1.56 years while the Control group comprised 28 males, age mean 19.64 ± 2.31 years. There was not a significant difference between the two groups regarding number, age, height or weight (P > 0.05).Athletes I vs controlClinical parameters showed significantly lower Systolic Blood Pressure SBP (athletes 117.79 ± 6.536, control 126.43 ± 17.043, P = 0.008) and Heart Rate HR (athletes 68.88 ± 5.044, control 77.43 ± 6.033, P = 0.001). ECG parameters showed a significantly longer RR interval (athletes 0.88 ± 0.065, control 0.76 ± 0.078, P = 0.001), while Corrected QTc interval was not significantly different (athletes 0.41 ± 0.029, control 0.42 ± 0.022, P > 0.05). Echo parameters showed a significant increase in Ejection fraction EF (athletes 60.94 ± 3.084 vs control 54.14 ± 13.063, P = 0.005) and Left atrial dimension LA (athletes 3.28 ± 0.392 vs control 2.58 ± 1.321, P = 0.005). On the other hand Septal wall in diastole SWD, Right ventricle dimension RV, Left ventricular end systolic dimension LVESD, Left Ventricular End Diastolic Dimension LVEDD, Aortic Root AO, and Posterior wall in diastole PWD were not significantly different (P > 0.05).Athletes II vs controlQTc became significantly longer (athletes 0.43 ± 0.028 vs control 0.42 ± 0.022, P = 0.05). SWD was significantly thicker (athletes 1.21 ± 0.23 vs control 1.07 ± 0.17, P = 0.04). SBP, HR remained significantly lower and RR, EF, LA remained significantly greater (P < 0.05), while RV, LVESD, LVEDD, AO, PWD remained not significantly different both at the beginning and also after 1 year (P > 0.05).Athletes I vs athletes IIECG parameters showed a significant increase in QTc (0.41 ± 0.029 vs 0.43 ± 0.028, P = 0.005) and RR interval (0.81 ± 0.167 vs 0.88 ± 0.065, P = 0.046). Echo parameters showed a significant increase in SWD (1.21 ± 0.232 vs 0.93 ± 0.124, P < 0.001), LA (3.62 ± 0.423 vs 3.28 ± 0.392, P = 0.001), RV (2.37 ± 0.565 vs 2.09 ± 0.234, P = 0.011), PWD (1.00 ± 0.200 vs 0.90 ± 0.200, P = 0.008), and a significant decrease in LVESD (3.19 ± 0.679 vs 3.48 ± 0.190, P = 0.016). Other parameters were not statistically significant (P > 0.05).ConclusionsProfessional football playing in young males results in significant changes compared to their control of sedentary nonathletic medical students of similar age. Clinical parameters showed a significant decrease in systolic blood pressure SBP and heart rate HR, ECG parameters showed significant increase in RR interval and QTc interval, and Echocardiographic parameters showed a significant increase in Left atrium diameter LA, Septal wall in diastole SWD, and ejection fraction EF. One year of professional football playing in young males causes a continuing significant increase in ECG parameters QTc, RR interval, and echocardiographic parameters SWD, LA, Right ventricle dimension RV, Posterior wall in diastole PWD and decrease in Left ventricular end systolic diameter LVESD compared to themselves one year earlier. The international concern of Sudden cardiac death among professional young athletes may be attributed to Structural heart changes and ECG abnormalities acquired with professional training.