Aquatic ecosystem health and trophic status classification of the Bitter Lakes along the main connecting link between the Red Sea and the Mediterranean

The Bitter Lakes are the most significant water bodies of the Suez Canal, comprising 85% of the water volume, but spreading over only 24% of the length of the canal. The present study aims at investigation of the trophic status of the Bitter Lakes employing various trophic state indices, biotic and abiotic parameters, thus reporting the health of the Lake ecosystem according to the internationally accepted classification criteria’s. The composition and abundance of phytoplankton with a dominance of diatoms and a decreased population density of 4315–7376?ind. l^?1 reflect the oligotrophic nature of this water body. The intense growth of diatoms in the Bitter Lakes depends on silicate availability, in addition to nitrate and phosphate. If the trophic state index (TSI) is applied to the lakes under study it records that the Bitter Lakes have an index under 40. Moreover, in the total chlorophyll-a measurements of 0.35–0.96?µg?l^?1 there are more indicative of little algal biomass and lower biological productivity. At 0.76–2.3?µg?l^?1, meanwhile, the low quantity of Phosphorus is a further measure of low biological productivity. In the Bitter Lakes, TN/TP ratios are high and recorded 147.4, and 184.7 for minimum and maximum ratios, respectively. These values indicate that in Bitter lakes, the limiting nutrient is phosphorus and confirm the oligotrophic status of the Bitter Lakes. The latter conclusion is supported by Secchi disc water clarity measurements, showing that light can penetrate, and thus algae can photosynthesize, as deep as >13?m. This study, therefore, showed that the Bitter Lakes of the Suez Canal exhibit oligotrophic conditions with clear water, low productivity and with no algal blooming.     

Multiplicity of strand incision at G:T base mismatches in DNA by human cell extracts

Cell extract from the HT29 human colon carcinoma cell line (lacking mutator phenotype) was used to study the ATP-dependent G:T mismatch repair. We found that when a 45-bp (model) DNA with a single CpG/TpG mispair was incubated with the cell extract and ATP, it was incised immediately 5' and 3' to the mismatched T, and we noted that the actual 5'- and 3'-labeled fragments were similar to the cleaved products of thymine DNA glycosylase (TDG). This TDG-like cleavage product was enhanced (5-fold) with stimulation of several novel fragments, as inferred from the effect on incision at CpG/TpG site of the addition of G:U competitor DNA and ATP to the HT29 extract. The novel fragments were compatible with a strand incision on both sides of the mismatch (the third phosphodiester bond 5' and the second phosphodiester bond 3' to the mismatched T) and an incision 3' to the mismatched T, respectively. This suggests that while the ATP-dependent (TDG-like) incision activity, contrary to expectation, shows a lack of substrate competition, its catalytic property is likely modified by an interaction with G:U mispair. These multiple ATP-dependent incision events were not detected when extracts of the mismatch repair (MMR) defective HCT15 or HCT116 cell line were augmented with ATP and G:U. We postulate that these multiple ATP-dependent incision events possibly require the same MMR factors, and together they constitute a modified single ATP-dependent G:T incision activity. This activity toward the CpG/TpG was competitively inhibited by a 45-bp DNA with an ApG/TpT mispair; incision at a single site 5' to the latter mismatch compares with one of the multiple sites incised 5' to the former mismatch. These results suggest that one of several mismatch-incision factors is required by the human ATP-dependent G:T incision activity, in addition to MMR factors and ATP.     

Apigenin protects from hepatorenal damage caused by lead acetate in rats

Exposure to lead (Pb) is associated with serious health problems including hepatorenal toxicity. Apigenin is a natural-sourced flavonoid with promising antioxidant and anti-inflammatory effects. In this research, we investigated the potential protective role of apigenin against lead acetate (PbAc)-induced hepatorenal damage. Thus, this experiment studied the exposure of male Wistar Albino rats to apigenin and/or PbAc and their effects in comparison to the control rats. Apigenin administration decreased the levels of Pb and prevented the histopathological deformations in liver and kidney tissues following PbAc exposure. This was confirmed by the normalized levels of liver and kidney function markers. Additionally, apigenin inhibited significantly oxidative reactions through upregulating Nrf2 and HO-1, and activating their downstreamed antioxidants accompanied by a marked depletion of pro-oxidants. Moreover, apigenin decreased the elevated pro-inflammatory cytokines and inhibited cell loss in liver and kidney tissues in response to PbAc intoxication in both tissues. The obtained results demonstrated that apigenin could be used to attenuate the molecular, biochemical, and histological alterations associated with Pb exposure due to its potent antioxidant, anti-inflammatory, and antiapoptotic effects.     

Comparative plastome data analysis of Dendrosicyos socotranus and Corallocarpus boehmii

Comparison of the Dendrosicyos socotranus and Corallocarpus boehmii (tribe Coniandreae, family Cucurbitaceae) plastome data was of interest. Data on RNA, tRNA, GC%, plastome size, CDS and pseudogene were tabulated for the two species. The total length of 1,57,380 bp and 1,58,744 bp which includes LSC, SSC, IRa, and IRb, while their GC content was 37.1% and 37% respectively. The variation in the length of genes e.g. ndhD, ndhI, rpl22, rpoC2, rps16, rps19, rps8, ycf1and ycf2 noted. Data help to document the genetic differences between usual (climber) with those of tree cucurbits.     

Outcomes in patients with and without disability admitted to hospital with COVID-19: a retrospective cohort study

Background:Disability-related considerations have largely been absent from the COVID-19 response, despite evidence that people with disabilities are at elevated risk for acquiring COVID-19. We evaluated clinical outcomes in patients who were admitted to hospital with COVID-19 with a disability compared with patients without a disability.Methods:We conducted a retrospective cohort study that included adults with COVID-19 who were admitted to hospital and discharged between Jan. 1, 2020, and Nov. 30, 2020, at 7 hospitals in Ontario, Canada. We compared in-hospital death, admission to the intensive care unit (ICU), hospital length of stay and unplanned 30-day readmission among patients with and without a physical disability, hearing or vision impairment, traumatic brain injury, or intellectual or developmental disability, overall and stratified by age (≤ 64 and ≥ 65 yr) using multivariable regression, controlling for sex, residence in a long-term care facility and comorbidity.Results:Among 1279 admissions to hospital for COVID-19, 22.3% had a disability. We found that patients with a disability were more likely to die than those without a disability (28.1% v. 17.6%), had longer hospital stays (median 13.9 v. 7.8 d) and more readmissions (17.6% v. 7.9%), but had lower ICU admission rates (22.5% v. 28.3%). After adjustment, there were no statistically significant differences between those with and without disabilities for in-hospital death or admission to ICU. After adjustment, patients with a disability had longer hospital stays (rate ratio 1.36, 95% confidence interval [CI] 1.19–1.56) and greater risk of readmission (relative risk 1.77, 95% CI 1.14–2.75). In age-stratified analyses, we observed longer hospital stays among patients with a disability than in those without, in both younger and older subgroups; readmission risk was driven by younger patients with a disability.Interpretation:Patients with a disability who were admitted to hospital with COVID-19 had longer stays and elevated readmission risk than those without disabilities. Disability-related needs should be addressed to support these patients in hospital and after discharge.

A successful public health response to the COVID-19 pandemic requires accurate and timely identification of, and support for, high-risk groups. There is increasing recognition that marginalized groups, including congregate care residents, racial and ethnic minorities, and people experiencing poverty, have elevated incidence of COVID-19.^1,2 Older age and comorbidities such as diabetes are also risk factors for severe COVID-19 outcomes.^3,4 One potential high-risk group that has received relatively little attention is people with disabilities.The World Health Organization estimates there are 1 billion people with disabilities globally.⁵ In North America, the prevalence of disability is 20%, with one-third of people older than 65 years having a disability.⁶ Disabilities include physical disabilities, hearing and vision impairments, traumatic brain injury and intellectual or developmental disabilities.^5,6 Although activity limitations experienced by people with disabilities are heterogeneous,^5,6 people with disabilities share high rates of risk factors for acquiring COVID-19, including poverty, residence in congregate care and being members of racialized communities.^7–9 People with disabilities may be more reliant on close contact with others to meet their daily needs, and some people with disabilities, especially intellectual developmental disabilities, may have difficulty following public health rules. Once they acquire SARS-CoV-2 infection, people with disabilities may be at risk for severe outcomes because they have elevated rates of comorbidities.¹⁰ Some disabilities (e.g., spinal cord injuries and neurologic disabilities) result in physiologic changes that increase vulnerability to respiratory diseases and may mask symptoms of acute respiratory disease, which may delay diagnosis.^11–13 There have also been reports of barriers to high-quality hospital care for patients with disabilities who have COVID-19, including communication issues caused by the use of masks and restricted access to support persons.^14–17Some studies have suggested that patients with disabilities and COVID-19 are at elevated risk for severe disease and death, with most evaluating intellectual or developmental disability.^13,18–26 Yet, consideration of disability-related needs has largely been absent from the COVID-19 response, with vaccine eligibility driven primarily by age and medical comorbidity, limited accommodations made for patients with disabilities who are in hospital, and disability data often not being captured in surveillance programs.^14–17 To inform equitable pandemic supports, there is a need for data on patients with a broad range of disabilities who have COVID-19. We sought to evaluate standard clinical outcomes in patients admitted to hospital with COVID-19²⁷ (i.e., in-hospital death, intensive care unit [ICU] admission, hospital length of stay and unplanned 30-d readmission) for patients with and without a disability, overall and stratified by age. We hypothesized that patients with a disability would have worse outcomes because of a greater prevalence of comorbidities,¹⁰ physiologic characteristics that increase morbidity risk^11–13 and barriers to high-quality hospital care.^14–17     

Expressed gene clusters associated with cellular sensitivity and resistance towards anti-viral and anti-proliferative actions of interferon

Interferons (IFN) are multi-functional proteins that induce a large number of genes which mediate many biological processes including host defense, cell growth control, signaling, and metabolism. Bioinformatics analysis of the 3'-untranslated regions of IFN-stimulated genes (ISGs) showed that the AU-rich elements (ARE) exist in approximately 10% of the mRNA induced by IFN. The human epithelial cell lines, WISH and 293, and the human B cell lines, Daudi and RPMI 1788, were assessed for their response to type-I IFN. Due to their differential response to the anti-viral and anti-proliferative action of IFN-alpha, they were used as cellular models for genome wide ARE-gene expression. The anti-viral and anti-proliferative actions of IFN-alpha were substantially more potent against WISH and Daudi cells than 293 and RPMI 1788 cells, respectively. These results correlated with the Stat1-driven gene expression as assessed by monitoring the expression of Stat1-mediated IFN-inducible 6-16 mRNA. Interferons were able to induce a significant proportion of common and distinct ARE-genes, but the patterns of expression were different and dependent on the type of the cell, type of IFN, and status of the cellular sensitivity to IFN. Clustering algorithms generated two informative expressed gene clusters that were selectively associated with cellular sensitivity and resistance to the anti-viral and anti-proliferative action of IFN. Use of rationally designed microarray experiments in IFN biology yielded informative clusters that may provide candidate genes for diagnostic or for evaluation of therapeutic possibilities.     

Prothrombin Time and Activated Partial Thromboplastin Time Testing: A Comparative Effectiveness Study in a Million-Patient Sample

Background

A substantial fraction of all American healthcare expenditures are potentially wasted, and practices that are not evidence-based could contribute to such waste. We sought to characterize whether Prothrombin Time (PT) and activated Partial Thromboplastin Time (aPTT) tests of preoperative patients are used in a way unsupported by evidence and potentially wasteful.

Methods and Findings

We evaluated prospectively-collected patient data from 19 major teaching hospitals and 8 hospital-affiliated surgical centers in 7 states (Delaware, Florida, Maryland, Massachusetts, New Jersey, New York, Pennsylvania) and the District of Columbia. A total of 1,053,472 consecutive patients represented every patient admitted for elective surgery from 2009 to 2012 at all 27 settings. A subset of 682,049 patients (64.7%) had one or both tests done and history and physical (H&P) records available for analysis. Unnecessary tests for bleeding risk were defined as: PT tests done on patients with no history of abnormal bleeding, warfarin therapy, vitamin K-dependent clotting factor deficiency, or liver disease; or aPTT tests done on patients with no history of heparin treatment, hemophilia, lupus anticoagulant antibodies, or von Willebrand disease. We assessed the proportion of patients who received PT or aPTT tests who lacked evidence-based reasons for testing.

Conclusions

This study sought to bring the availability of big data together with applied comparative effectiveness research. Among preoperative patients, 26.2% received PT tests, and 94.3% of tests were unnecessary, given the absence of findings on H&P. Similarly, 23.3% of preoperative patients received aPTT tests, of which 99.9% were unnecessary. Among patients with no H&P findings suggestive of bleeding risk, 6.6% of PT tests and 7.1% of aPTT tests were either a false positive or a true positive (i.e. indicative of a previously-undiagnosed potential bleeding risk). Both PT and aPTT, designed as diagnostic tests, are apparently used as screening tests. Use of unnecessary screening tests raises concerns for the costs of such testing and the consequences of false positive results.     

De Novo Assembly and Genome Analyses of the Marine-Derived Scopulariopsis brevicaulis Strain LF580 Unravels Life-Style Traits and Anticancerous Scopularide Biosynthetic Gene Cluster

The marine-derived Scopulariopsis brevicaulis strain LF580 produces scopularides A and B, which have anticancerous properties. We carried out genome sequencing using three next-generation DNA sequencing methods. De novo hybrid assembly yielded 621 scaffolds with a total size of 32.2 Mb and 16298 putative gene models. We identified a large non-ribosomal peptide synthetase gene (nrps1) and supporting pks2 gene in the same biosynthetic gene cluster. This cluster and the genes within the cluster are functionally active as confirmed by RNA-Seq. Characterization of carbohydrate-active enzymes and major facilitator superfamily (MFS)-type transporters lead to postulate S. brevicaulis originated from a soil fungus, which came into contact with the marine sponge Tethya aurantium. This marine sponge seems to provide shelter to this fungus and micro-environment suitable for its survival in the ocean. This study also builds the platform for further investigations of the role of life-style and secondary metabolites from S. brevicaulis.