Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.

Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability

Global wealth disparities drive adherence to COVID-safe pathways in head and neck cancer surgery

Peer reviewe

The investigations of photocatalytic degradation and defluorination of perfluorooctanoic acid using palm kernel shell activated carbon and Fe-Sn binary oxides nanocomposite under visible light irradiation

Perfluorooctanoic acid (PFOA) is a persistent pollutant in the environment that does not break down easily because its strong CF bonds strong. Current methods for degrading organic pollutants such as PFOA often have low mineralization efficiency, need a lot of energy, and cause pollution in other ways. In response to these challenges, this study presents an innovative palm kernel shell activated carbon-supported binary oxide, Fe₂O₃/SnO₂ (PKSAC-Fe₂O₃/SnO₂), as a heterojunction and multifunctional photocatalyst for the decomposition of PFOA under visible light. This research presents an innovative PKSAC-Fe₂O₃/SnO₂ nanocomposite that used the synergistic interaction among the large surface area and adsorption capacity of bio-derived activated carbon, the redox reactivity of Fe₂O₃, and the potent oxidative characteristics of SnO₂. The photocatalytic degradation performance of PKSAC-Fe₂O₃/SnO₂ nanocomposite was tested by irradiation of visible light on it. The optimum conditions were found to be pH 5, a catalyst dose of 5.0 mg, and an initial PFOA concentration of 20 ppm. After 6  of irradiation, the nanocomposite reached an impressive PFOA degradation efficiency of 92.40 % and a defluorination rate of 51.23 %, showing that the fluorinated compound had been mineralized significantly. Mechanistic investigations showed that the hydroxyl radical (•OH) and direct electron were the main species involved in the partial mineralization of PFOA with five shorter-chain intermediates identified. The catalyst's potential reusability coupled with its low-cost, biomass-derived support, present a sustainable solution for PFAS remediation. This work advanced the design of efficient, solar-driven catalysts for persisting pollutant degradation, bridging critical gaps in energy efficiency, cost-effectiveness, and environmental safety

HIV-1 drug-resistance surveillance among treatment-experienced and -naïve patients after the implementation of antiretroviral therapy in Ghana.

BACKGROUND: Limited HIV-1 drug-resistance surveillance has been carried out in Ghana since the implementation of antiretroviral therapy (ART). This study sought to provide data on the profile of HIV-1 drug resistance in ART-experienced and newly diagnosed individuals in Ghana. METHODS: Samples were collected from 101 HIV-1-infected patients (32 ART-experienced cases with virological failure and 69 newly diagnosed ART-naïve cases, including 11 children), in Koforidua, Eastern region of Ghana, from February 2009 to January 2010. The pol gene sequences were analyzed by in-house HIV-1 drug-resistance testing. RESULTS: The most prevalent HIV-1 subtype was CRF02_AG (66.3%, 67/101) followed by unique recombinant forms (25.7%, 26/101). Among 31 ART-experienced adults, 22 (71.0%) possessed at least one drug-resistance mutation, and 14 (45.2%) had two-class-resistance to nucleoside and non-nucleoside reverse-transcriptase inhibitors used in their first ART regimen. Importantly, the number of accumulated mutations clearly correlated with the duration of ART. The most prevalent mutation was lamivudine-resistance M184V (n = 12, 38.7%) followed by efavirenz/nevirapine-resistance K103N (n = 9, 29.0%), and zidovudine/stavudine-resistance T215Y/F (n = 6, 19.4%). Within the viral protease, the major nelfinavir-resistance mutation L90M was found in one case. No transmitted HIV-1 drug-resistance mutation was found in 59 ART-naïve adults, but K103N and G190S mutations were observed in one ART-naïve child. CONCLUSIONS: Despite expanding accessibility to ART in Eastern Ghana, the prevalence of transmitted HIV-1 drug resistance presently appears to be low. As ART provision with limited options is scaled up nationwide in Ghana, careful monitoring of transmitted HIV-1 drug resistance is necessary

Prevalence of 3TC-, NVP-, EFV-, AZT-, and d4T-resistance mutations by duration of ART in 31 HIV-1-infected patients ≧15 years old.

<p>(A) Bar graph and (B) details of 17 patients identified with 3TC-, NVP-, EFV-, AZT-, and d4T-resistance mutations. HIV-1 drug-resistance mutations were detected according to the latest definition of the International AIDS Society-USA panel <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0071972#pone.0071972-Johnson1" target="_blank">[10]</a>. Amino acid mutations responsible for drug resistance are shown in bold and color coded with bar graph in A. *Major NFV-resistance mutation L90M was found in the protease in the case of KF307. ART, antiretroviral therapy; AZT, zidovudine; d4T, stavudine; EFV, efavirenz; NFV, nelfinavir; NVP, nevirapine; and 3TC, lamivudine.</p

List of primers used in HIV-1 genotypic drug-resistance testing.

<p>bp, base pairs; PCR, polymerase chain reaction; and RT-PCR, reverse transcription and polymerase chain reaction.</p>a<p>Amplicon positions in the reference HIV-1 HXB2 sequence are represented.</p

HIV-1 drug-resistance mutations in patients <15 years old (<i>n</i> = 11)^a.

<p>ART, antiretroviral therapy; d4T, stavudine; EFV, efavirenz; NNRTI, non-nucleoside reverse-transcriptase inhibitor; NRTI, nucleoside reverse-transcriptase inhibitor; and 3TC, lamivudine.</p>a<p>HIV-1 drug-resistance mutations were detected according to the latest definition of the International AIDS Society-USA panel <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0071972#pone.0071972-Johnson1" target="_blank">[10]</a>. For ART-naïve patients, transmitted drug-resistance (shown in bold and underlined) was detected according to the latest definition of the WHO drug-resistance surveillance <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0071972#pone.0071972-Bennett1" target="_blank">[11]</a>.</p

Demographic and clinical characteristics of ART-experienced and -naïve HIV-1-infected patients ≧15 years old (<i>n</i> = 90).

<p>ART, antiretroviral therapy; AZT, zidovudine; CRF, circulating recombinant form; d4T, stavudine; EFV, efavirenz; IQR, interquartile range; NFV, nelfinavir; NVP, nevirapine; 3TC, lamivudine; and URF, unique recombinant form.</p>a<p>HIV serology was determined using New LAV Blot I and II (Bio-Rad Laboratories, Marnes-la-Coquette, France).</p>b<p>Good, 100% pills taken; Satisfactory, ≧95%, but <100% pills taken; Poor, <95% pills taken.</p

Molecular epidemiology of HIV-1 infections in Koforidua, Ghana.

<p>HIV-1 subtypes of 101 isolates were determined through the construction of phylogenetic trees, similarity plotting, and boot-scanning analyses. (A) Phylogenetic tree containing our 75 isolates classified into known subtypes and CRFs. (B) Phylogenetic tree containing our 26 URF isolates identified with unknown mosaic patterns of the <i>pol</i> gene. Two clusters of URF isolates are represented by #1 and #2. (C) Summary on the chimeric patterns of 26 URF isolates. The trees were constructed by the neighbor-joining method. Bootstrap values were calculated from 1,000 analyses, and values greater than 70% are shown at tree nodes. Our isolates are represented by colored circles, and subtype reference isolates are represented by their subtype and name. Scale bar represents nucleotide substitutions per site. HIV-1 group O isolate, ANT70, was used as the outgroup. CRF, circulating recombinant form; PR, protease; RT, reverse transcriptase; and URF, unique recombinant form.</p