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This folio of test items, contributed by a number of colleges and universities from their course, placement, entrance, or other institutional examinations, was compiled to aid teachers in constructing tests. Only those science courses offered in the first two years of college are represented by the scope of the items. The test items may also serve as models for those who are relatively inexperienced in item writing. A major consideration in using these items is that of relating them to the testing of various objectives. These questions and problems are arranged under some thirty subject matter headings in each of the two major subdivisions: Biological Science and Physical Science. The items are classified according to Bloom's taxonomy under the following major headings: Knowledge; Comprehension; Application; Analysis; Synthesis; and Evaluation. (AG)

Limbah pewarna tekstil yang mempunyai komponen utamanya zat pewarna sintesis berbahaya bagi lingkungan sekitar. Pengolahan limbah pewarna tekstil secara fisika dan biologi kurang efektif. Elektrolisis plasma dengan menggunakan metode Contact Glow Discharge Electrolysis (CGDE) merupakan bagian dari pengolahan secara kimiawi, yang efektif dalam mengolah limbah pewarna batik. Parameter kedalaman anoda sangat mempengaruhi dalam proses elektrolisis plasma metode CGDE. Tujuan penelitian ini adalah untuk mengetahui pengaruh kedalaman anoda terhadap produksi •OH, energi yang digunakan proses degradasi, persen dekolorisasi Remazol Red RB 133, serta mengetahui penurunan konsentrasi COD limbah pewarna batik Remazol Red RB 133. Kedalaman anoda dalam penelitian ini adalah 1,5 cm dimana produksi •OH sebesar 11,63 mmol dan energi proses selama 30 menit adalah 806,4 KJ. Persen dekolorisasi Remazol Red RB 133 pada konsentrasi 250 ppm, terbesar selama 30 menit mencapai 99,66 %, pada kedalaman 4,5 cm dengan energi 1075,212 KJ. Nilai COD limbah pewarna batik Remazol Red RB 133 menurun dari 169 mg/L menjadi 3,6 mg/L setelah proses CGDE selama 180 menit (sesuai dengan baku mutu limbah). Textile dye waste having the main component of synthetic dye is hazardous to the surrounding environment. Textile dye waste treatment is physically and biologically less effective. Electrolysis plasma that used Contact Glow Discharge Electrolysis (CGDE) method is part of chemical treatment. The anode depth parameters greatly affect the electrolysis CGDE method. The purpose of this study was to determine the effect of anode depth on • OH production, the energy used in the degradation process, percent decolorization of Remazol Red RB 133, as well as knowing the decrease in COD concentration of Remazol Red batik dye RB 133. The anode depth in this study is 1.5 cm where the production of OH • 11.63 mmol and the processing energy for 30 minutes is 806.4 KJ. The largest Percentage degradation of Remazol Red RB 133 at concentration 250 ppm is 99,66%, that’s reach at depth 4.5 cm for 30 minutes with energy 1075,212 KJ. COD value has decreased from 169 mg/L to 3,6 mg/L after 180 minutes CGDE process (conform to waste quality standards).

Organisms across all domains of life have developed elegant strategies to produce specialized metabolites, also referred to as natural products, for defense, structure, and communication. Natural products provide novel inspiration for pharmaceutical development given their potent biological activities and structural diversity. Recent advancements in DNA sequencing technology and the development of predictive bioinformatics tools have unveiled a vast collection of biosynthetic machinery responsible for generating this structural diversity that may be harnessed by synthetic chemists. Many of the enzymes encoded by biosynthetic genes catalyze chemical reactions that are difficult to replicate with the same selectivity by traditional synthetic methods. An example of this discrepancy is illustrated by the current enzymatic and chemical methods known to generate a highly reactive ortho-quinone methide (o-QM) intermediate. The utility of o-QMs in total synthesis has been hampered by complications that surround the preparation of their precursors, the harsh generation methods, and poor chemo-, regio-, and stereoselective control. In contrast, multiple enzymes have been reported to catalyze o-QM formation under mild conditions with remarkable selectivity. Chapter 1 of this dissertation examines several different enzymatic strategies developed to generate o-QMs. Chapter 2 describes progress towards the biomimetic total synthesis of (–)-chlorizidine A that aims to synthetically replicate the final biosynthetic intramolecular cyclization via an o-QM intermediate. Chapter 3 reports the discovery of tetrachlorizine, a novel tetrachlorinated marine natural product, and the identification of its associated biosynthetic gene cluster. Biochemical characterization of a pivotal flavin-dependent oxidase revealed a dehydrogenation reaction that proceeds via an unprecedented o-QM mechanism. This oxidase was then repurposed to generate an isolable o-QM, an extremely rare chemical motif. Chapter 4 investigates the structure-function relationships of two homologous flavin-dependent oxidases with divergent reaction selectivities and highlights their favorable biocatalytic properties. This chapter also discloses the first reported bacterial enzymes capable of performing oxidative cyclization reactions to produce cannabinoids.

Modulation of proteasome function by pharmacological interventions and molecular biology tools is an active area of research in cancer biology and neurodegenerative diseases. Curcumin (diferuloylmethane) is a naturally occurring polyphenol that affects multiple signaling pathways and known to modulate PKC activities. The therapeutic significance of curcumin is often considered to reside in its anti-inflammatory, antioxidant, anti-angiogenic, or anti-apoptotic properties. However, recent research suggests that the therapeutic efficacy of curcumin may be due to its activity as a potent inhibitor of the proteasome. In this study, we show that both curcumin and its synthetic polyphenolic derivative (didemethylcurcumin), CUIII modulated proteasome activity in a biphasic manner. Curcumin and CUIII increased proteasome activity at nanomolar concentrations but inhibited proteasome activity at micromolar concentrations. Curcumin was more effective than CUIII in relative proteasome activity increase at nanomolar concentrations. Also, curcumin was more effective than CUIII in relative proteasome activity inhibition at micromolar concentration. The docking study was conducted on the 20S proteasome catalytic subunit. Estimated Kd values for curcumin and didemethylcurcumin are 0.0054μM and 1.3167μM, respectively. These values correlate well with the results of the effectiveness of modulation by curcumin compare to CUIII. The small size of CUIII makes its dock to the narrow cavity of the active site, but the binding interaction is not strong compare to curcumin. This study suggests that curcumin and its didemethyl derivative can be used to modulate proteasome activity. This communication implicates the reason why curcumin and its didemethyl derivative can be used to two different disease mechanisms, neurodegeneration, and cancer.

Data availability: The datasets analyzed for the current study reflect collaborative efforts of two research consortia: ALLFTD and GENFI. Each consortium provides clinical data access based on established policies for data use: processes for request are available for review at allftd.org/data for ALLFTD data and by emailing genfi@ucl.ac.uk. Certain data elements from both consortia (for example raw MRI images) may be restricted due to the potential for identifiability in the context of the sensitive nature of the genetic data. The deidentified combined dataset will be available for request through the FTD Prevention Initiative in 2023 (https://www.thefpi.org/). Code availability: Custom R code is available at https://doi.org/10.5281/zenodo.6687486. Copyright © The Author(s). Unlike familial Alzheimer’s disease, we have been unable to accurately predict symptom onset in presymptomatic familial frontotemporal dementia (f-FTD) mutation carriers, which is a major hurdle to designing disease prevention trials. We developed multimodal models for f-FTD disease progression and estimated clinical trial sample sizes in C9orf72, GRN and MAPT mutation carriers. Models included longitudinal clinical and neuropsychological scores, regional brain volumes and plasma neurofilament light chain (NfL) in 796 carriers and 412 noncarrier controls. We found that the temporal ordering of clinical and biomarker progression differed by genotype. In prevention-trial simulations using model-based patient selection, atrophy and NfL were the best endpoints, whereas clinical measures were potential endpoints in early symptomatic trials. f-FTD prevention trials are feasible but will likely require global recruitment efforts. These disease progression models will facilitate the planning of f-FTD clinical trials, including the selection of optimal endpoints and enrollment criteria to maximize power to detect treatment effects. Data collection and dissemination of the data presented in this paper were supported by the ALLFTD Consortium (U19: AG063911, funded by the National Institute on Aging and the National Institute of Neurological Diseases and Stroke) and the former ARTFL and LEFFTDS Consortia (ARTFL: U54 NS092089, funded by the National Institute of Neurological Diseases and Stroke and National Center for Advancing Translational Sciences; LEFFTDS: U01 AG045390, funded by the National Institute on Aging and the National Institute of Neurological Diseases and Stroke). The manuscript was reviewed by the ALLFTD Executive Committee for scientific content. The authors acknowledge the invaluable contributions of the study participants and families as well as the assistance of the support staffs at each of the participating sites. This work is also supported by the Association for Frontotemporal Degeneration (including the FTD Biomarkers Initiative), the Bluefield Project to Cure FTD, Larry L. Hillblom Foundation (2018-A-025-FEL (A.M.S.)), the National Institutes of Health (AG038791 (A.L.B.), AG032306 (H.J.R.), AG016976 (W.K.), AG062677 (Ron C. Peterson), AG019724 (B.L.M.), AG058233 (Suzee E. Lee), AG072122 (Walter Kukull), P30 AG062422 (B.L.M.), K12 HD001459 (N.G.), K23AG061253 (A.M.S.), AG062422 (RCP), K24AG045333 (H.J.R.)) and the Rainwater Charitable Foundation. Samples from the National Centralized Repository for Alzheimer Disease and Related Dementias (NCRAD), which receives government support under a cooperative agreement grant (U24 AG021886 (T.F.)) awarded by the National Institute on Aging (NIA), were used in this study. This work was also supported by Medical Research Council UK GENFI grant MR/M023664/1 (J.D.R.), the Bluefield Project, the National Institute for Health Research including awards to Cambridge and UCL Biomedical Research Centres and a JPND GENFI-PROX grant (2019–02248). Several authors of this publication are members of the European Reference Network for Rare Neurologic Diseases, project 739510. J.D.R. and L.L.R. are also supported by the National Institute for Health and Care Research (NIHR) UCL/H Biomedical Research Centre, the Leonard Wolfson Experimental Neurology Centre Clinical Research Facility and the UK Dementia Research Institute, which receives its funding from UK DRI Ltd, funded by the UK Medical Research Council, Alzheimer’s Society and Alzheimer’s Research UK. J.D.R. is also supported by the Miriam Marks Brain Research UK Senior Fellowship and has received funding from an MRC Clinician Scientist Fellowship (MR/M008525/1) and the NIHR Rare Disease Translational Research Collaboration (BRC149/NS/MH). M.B. is supported by a Fellowship award from the Alzheimer’s Society, UK (AS-JF-19a-004-517). RC and C.G. are supported by a Frontotemporal Dementia Research Studentships in Memory of David Blechner funded through The National Brain Appeal (RCN 290173). J.B.R. is supported by NIHR Cambridge Biomedical Research Centre (BRC-1215-20014; the views expressed are those of the authors and not necessarily those of the NIHR or the Department of Health and Social Care), the Wellcome Trust (220258), the Cambridge Centre for Parkinson-plus and the Medical Research Council (SUAG/092 G116768); I.L.B. is supported by ANR-PRTS PREV-DemAls, PHRC PREDICT-PGRN, and several authors of this publication are members of the European Reference Network for Rare Neurological Diseases (project 739510). J.L. is funded by the Deutsche Forschungsgemeinschaft (German Research Foundation) under Germany’s Excellence Strategy within the framework of the Munich Cluster for Systems Neurology (EXC 2145 SyNergy – ID 390857198). R.S.-V. was funded at the Hospital Clinic de Barcelona by Instituto de Salud Carlos III, Spain (grant code PI20/00448 to RSV) and Fundació Marató TV3, Spain (grant code 20143810 to R.S.-V.). M.M. was, in part, funded by the UK Medical Research Council, the Italian Ministry of Health and the Canadian Institutes of Health Research as part of a Centres of Excellence in Neurodegeneration grant, by Canadian Institutes of Health Research operating grants (MOP- 371851 and PJT-175242) and by funding from the Weston Brain Institute. R.L. is supported by the Canadian Institutes of Health Research and the Chaire de Recherche sur les Aphasies Primaires Progressives Fondation Famille Lemaire. C.G. is supported by the Swedish Frontotemporal Dementia Initiative Schörling Foundation, Swedish Research Council, JPND Prefrontals, 2015–02926,2018–02754, Swedish Alzheimer Foundation, Swedish Brain Foundation, Karolinska Institutet Doctoral Funding, KI Strat-Neuro, Swedish Dementia Foundation, and Stockholm County Council ALF/Region Stockholm. J.L. is supported by Germany’s Excellence Strategy within the framework of the Munich Cluster for Systems Neurology (German Research Foundation, EXC 2145 Synergy 390857198). The Dementia Research Centre is supported by Alzheimer’s Research UK, Alzheimer’s Society, Brain Research UK, and The Wolfson Foundation. This work was supported by the National Institute for Health Research UCL/H Biomedical Research Centre, the Leonard Wolfson Experimental Neurology Centre Clinical Research Facility and the UK Dementia Research Institute, which receives its funding from UK DRI Ltd, funded by the UK Medical Research Council, Alzheimer’s Society, and Alzheimer’s Research UK.

Biodegradable stents have tremendous theoretical potential as an alternative to bare metal stents and drug-eluting stents for the treatment of obstructive coronary artery disease. Any bioresorbable or biodegradable scaffold material needs to possess optimal mechanical properties and uniform degradation behavior that avoids local and systemic toxicity. Recently, molybdenum (Mo) has been investigated as a potential novel biodegradable material for this purpose. With its proven moderate degradation rate and excellent mechanical properties, Mo may represent an ideal source material for clinical cardiac and vascular applications. The present study was performed to evaluate the mechanical performance of metallic Mo in vitro and the biodegradation properties in vivo. The results demonstrated favorable mechanical behavior and a uniform degradation profile as desired for a new generation ultra-thin degradable endovascular stent material. Moreover, Mo implants in mouse arteries avoided the typical cellular response that contributes to restenosis. There was minimal neointimal hyperplasia over 6 months, an absence of excessive smooth muscle cell (SMC) proliferation or inflammation near the implant, and avoidance of significant harm to regenerating endothelial cells (EC). Qualitative inspection of kidney sections showed a potentially pathological remodeling of kidney Bowman's capsule and glomeruli, indicative of impaired filtering function and development of kidney disease, although quantifications of these morphological changes were not statistically significant. Together, the results suggest that the products of Mo corrosion may exert beneficial or inert effects on the activities of inflammatory and arterial cells, while exerting potentially toxic effects in the kidneys that warrant further investigation.

Background: Experimental and epidemiological studies indicate an association between exposure to particulate matter (PM) air pollution and increased risk of type 2 diabetes. In view of the high and increasing prevalence of diabetes, we aimed to quantify the burden of type 2 diabetes attributable to PM2·5 originating from ambient and household air pollution.Methods: We systematically compiled all relevant cohort and case-control studies assessing the effect of exposure to household and ambient fine particulate matter (PM2·5) air pollution on type 2 diabetes incidence and mortality. We derived an exposure–response curve from the extracted relative risk estimates using the MR-BRT (meta-regression—Bayesian, regularised, trimmed) tool. The estimated curve was linked to ambient and household PM2·5 exposures from the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, and estimates of the attributable burden (population attributable fractions and rates per 100 000 population of deaths and disability-adjusted life-years) for 204 countries from 1990 to 2019 were calculated. We also assessed the role of changes in exposure, population size, age, and type 2 diabetes incidence in the observed trend in PM2·5-attributable type 2 diabetes burden. All estimates are presented with 95% uncertainty intervals.Findings: In 2019, approximately a fifth of the global burden of type 2 diabetes was attributable to PM2·5 exposure, with an estimated 3·78 (95% uncertainty interval 2·68–4·83) deaths per 100 000 population and 167 (117–223) disability-adjusted life-years (DALYs) per 100 000 population. Approximately 13·4% (9·49–17·5) of deaths and 13·6% (9·73–17·9) of DALYs due to type 2 diabetes were contributed by ambient PM2·5, and 6·50% (4·22–9·53) of deaths and 5·92% (3·81–8·64) of DALYs by household air pollution. High burdens, in terms of numbers as well as rates, were estimated in Asia, sub-Saharan Africa, and South America. Since 1990, the attributable burden has increased by 50%, driven largely by population growth and ageing. Globally, the impact of reductions in household air pollution was largely offset by increased ambient PM2·5.Interpretation: Air pollution is a major risk factor for diabetes. We estimated that about a fifth of the global burden of type 2 diabetes is attributable PM2·5 pollution. Air pollution mitigation therefore might have an essential role in reducing the global disease burden resulting from type 2 diabetes.Funding: Bill & Melinda Gates Foundation.

Acid hydrolysis and hydrogenation reactions were capable to convert xylose obtained from biomass materials using heterogeneous catalysts based on Ni and Ru. Xylose was extracted from sugar cane bagasse using dilute acid sulfuric solutions, and then xylitol was obtained through xylose catalytic hydrogenation. A bimetallic catalyst (Ni 10.0 wt.% and Ru 1.0 wt.%) was prepared by the wet impregnation method, supporting the metallic phase in activated carbon. Sugarcane bagasse was delignified in a three-step pretreatment (acid, basic and organic extractions, respectively), allowing effective hydrolysis of the resulting holocellulose. The acid hydrolysis process for xylose extraction was more effective at the highest concentration of sulfuric acid in the study (2.5% v/v), obtaining a xylose-rich hydrolysate with concentration over 10 g L−1. For the xylose hydrogenation process, conversion of xylose and selectivity to xylitol was near 90 % after 1 h of reaction. Kinetic evolutions were evaluated through a mathematical model in terms of operating time and temperature, providing hydrogenation activation energy values of the order of 40.76 kJ mol−1.

Objective: Glomerular injury is a recognized complication of diabetic ketoacidosis (DKA), yet the tubular lesions are poorly understood. The aim of this prospective study was to evaluate the presence and reversibility of tubular injury during DKA in children with type 1 diabetes (T1D). Research Design and Methods: Blood and urine samples were collected from 40 children with DKA (52% boys, mean age 11 ± 4 years, venous pH7.2 ± 0.1, glucose 451 ± 163 mg/dL) at three timepoints: 0–8 and 12–24 h after starting insulin, and 3 months after discharge. Mixed-effects models evaluated the changes in tubular injury markers over time (neutrophil gelatinase-associated lipocalin [NGAL], kidney injury molecule 1 [KIM-1], and interleukin 18 [IL-18]). We also evaluated the relationships among the tubular injury biomarkers, copeptin, a vasopressin surrogate, and serum uric acid (SUA). Results: Serum NGAL, KIM-1, and IL-18 were highest at 0–8h (306.5 ± 45.9ng/mL, 128.9 ± 10.1pg/mL, and 564.3 ± 39.2pg/mL, respectively) and significantly decreased over 3 months (p=0.03, p=0.01, and p < 0.001, respectively). There were strong relationships among increases in copeptin and SUA and rises in tubular injury biomarkers. At 0–8h, participants with acute kidney injury (AKI) [17%] showed significantly higher concentrations of tubular injury markers, copeptin, and SUA. Conclusions: DKA was characterized by tubular injury, and the degree of injury associated with elevated copeptin and SUA. Tubular injury biomarkers, copeptin and SUA may be able to predict AKI in DKA.

The process of fermentation renders the superior quality of mulberry wine based on the microorganisms utilized. The present study aimed at investigating the changes and correlation between phenols and product quality of mulberry wine fermented with Lactiplantibacillus plantarum and Saccharomyces cerevisiae combinatorially. Total anthocyanins concentration (TAC), polyphenols concentration (TPC), flavonoids concentration (TFC), and antioxidant capacity decreased significantly with high correlation in the fermentation process. TAC gradually reduced with a loss rate of 47.98% from 0 to third day of fermentation. Fermented mulberry wine obtained indicated a dynamic balance due to the presence of p‐hydroxybenzoic acids as compared to the primary phenolic constituent. Chlorogenic acid usually presents in mulberry juice. The relative intensity of sourness was the most prominent and reached the maximum (10.93) on day 2 of fermentation. A total of 21 volatile esters were quantified (6621.59 μg/L), which contributed significantly to the aroma of mulberry wine. The enhanced quality of fermented mulberry wine showed contraindications with decreased constituents and escalated wine quality. Rather than usual single inoculum, fermentation combination of LAB and yeast holistically influenced the color, taste, fragrance, phenolic profiles, and antioxidant properties in mulberry wine, ensuring palatability and fit for commercialization prospects., Active substances and the antioxidant capacity of mulberry wine decreased in the fermentation process. Esters and alcohols were the main volatile substances in the aroma of mulberry wine. The taste turned to sour at the end of fermentation. Combination of LAB and yeast fermentation holistically influenced the color, taste, fragrance, phenolic profiles, and antioxidant properties in mulberry wine, ensuring palatability and fit for commercialization prospects.

Background: Adenosine is a natural nucleoside present in a variety of organs and tissues, where it acts as a modulator of diverse physiological and pathophysiological processes. These actions are mediated by at least four G protein-coupled receptors, which are widely and differentially expressed in tissues. Interestingly, high concentrations of adenosine have been reported in a variety of tumors. In this context, the final output of adenosine in tumorigenesis will likely depend on the constellation of adenosine receptors expressed by tumor and stromal cells. Notably, activation of the A3 receptor can reduce the proliferative capacity of various cancer cells. Objective: This study aimed to describe the anti-proliferative effects of two previously synthesized adenosine derivatives with A3 agonist action (compounds 2b and 2f) through in vitro assays. Methods: We used gastric and breast cancer cell lines expressing the A3 receptor as in vitro models and theoretical experiments for molecular dynamics and determination of ADME properties. Results: The antiproliferative effects of adenosine derivatives (after determining IC50 values) were comparable or even higher than those described for IB-MECA, a commercially available A3 agonist. Among possible mechanisms involved, apoptosis was found to be induced in MCF-7 cells but not in AGS or MDA-MB-231 cells. Surprisingly, we were unable to observe cellular senescence induction upon treatment with compounds 2b and 2f in any of the cell lines studied, although we cannot rule out other forms of cell cycles exit at this point. Conclusion: Both adenosine derivatives showed antiproliferative effects on gastric and breast cancer cell lines, and were able to induce apoptosis, at least in the MCF-7 cell line. Further studies will be necessary to unveil receptor specificity and mechanisms accounting for the antiproliferative properties of these novel semi-synthetic compounds.

Durante 1986-89 se llevó a cabo un estudio de campo en la Subestación de Lajas para evaluar los herbicidas registrados ametryn, diuron, asulam, hexazinone (Velpar) y metribuzin y los no registrados terbutryn, pendimethalin e imazapyr para controlar la yerba peluda (Roftboellia exaltata) en caña de azúcar en cultivos sucesivos de plantilla y primer retoño. Imazapyr, pendimethalin, terbutryn y ametryn a las dosis recomendadas de 0.28, 1.78, 2.69 y 4.49 kg/ha. controlaron la yerba peluda con efectividad comparable al desyerbo a mano en caña de plantilla. En el retoño todos los herbicidas usados demostraron una efectividad mayor debido, posiblemente, a una menor población del yerbajo. El herbicida imazapyr causó fitotoxicidad a las plántulas de caña, la cual fue más severa en el retoño. Las parcelas tratadas con los herbicidas mencionados produjeron rendimientos de azúcar por hectárea para la plantilla entre 14.92 y 17.02 toneladas comparables estadísticamente con el tratamiento de desyerbo a mano (17.5 tons/ha.), pero superiores significativamente a los de tratamientos de diuron, asulam y el testigo sin desyerbo. La producción de azúcar por ha. para el retoño siguió más o menos el mismo patrón que en la plantilla, excepto que las parcelas tratadas con asulam y diuron produjeron más y las tratadas con imazapyr y ametryn produjeron menos. La producción combinada de azúcar de la plantilla y el retoño en el tratamiento con pendimethalin fue estadísticamente igual que para el desyerbo a mano, pero solo significativamente superior a hexaxinone, imazapyr y el tratamiento sin desyerbar.

In this study, we investigated the action of varespladib (VPL) alone or in combination with a coral snake antivenom (CAV) on the local and systemic effects induced by Micrurus corallinus venom in rats. Adult male Wistar rats were exposed to venom (1.5 mg/kg – i.m.) and immediately treated with CAV (antivenom:venom ratio 1:1.5 ‘v/w’ – i.p.), VPL (0.5 mg/kg – i.p.), or both of these treatments. The animals were monitored for 120 min and then anesthetized to collect blood samples used for haematological and serum biochemical analysis; after euthanasia, skeletal muscle, renal and hepatic tissue samples were collected for histopathological analysis. M. corallinus venom caused local oedema without subcutaneous haemorrhage or apparent necrosis formation, although there was accentuated muscle morphological damage; none of the treatments prevented oedema formation but the combination of CAV and VPL reduced venom-induced myonecrosis. Venom caused neuromuscular paralysis and respiratory impairment in approximately 60 min following envenomation; CAV alone did not prevent the neurotoxic action, whereas VPL alone prevented neurotoxic symptoms developing as did the combination of CAV and VPL. Venom induced significant increase of serum CK and AST release, mostly due to local and systemic myotoxicity, which was partially prevented by the combination of CAV and VPL. The release of hepatotoxic serum biomarkers (LDH and ALP) induced by M. corallinus venom was not prevented by CAV and VPL when individually administered; their combination effectively prevented ALP release. The venom-induced nephrotoxicity (increase in serum creatinine concentration) was prevented by all the treatments. VPL alone or in combination with CAV significantly prevented the venom-induced lymphocytosis. In conclusion, VPL shows to be effective at preventing the neurotoxic, nephrotoxic, and inflammatory activities of M. corallinus venom. In addition, VPL acts synergistically with antivenom to prevent a number of systemic effects caused by M. corallinus venom. Fundação de Amparo à Pesquisa do Estado de São Paulo/[No.2020/04287-6]/FAPESP/Brasil Fundação de Amparo à Pesquisa do Estado de São Paulo/[No.2020/14191-6]/FAPESP/Brasil Conselho Nacional de Desenvolvimento Científico e Tecnológico/[No.309320/2016-0]/CNPq/Brasil University of the West of São Paulo/[No.2020/04287-6]/UNOESTE/Brasil UCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias de la Salud::Instituto Clodomiro Picado (ICP) UCR::Vicerrectoría de Docencia::Salud::Facultad de Microbiología

In the present work, nanostructured porous silicon (nPSi) thin films were used as a substrate for the deposition of green synthesized silver nanoparticles (AgNPs). Different kinds of AgNPs were green synthesized by using Peumo extract and changing AgNO3 concentration. UV-vis spectroscopy confirmed the success of the synthesis, and TEM characterization showed AgNPs with a like-spherical shape and an average diameter, which ranges from 4 to 25 nm, depending on the AgNO3 concentration used. Then, AgNPs were introduced into the nPSi layer with a mean pore diameter of 46 nm and 75% of porosity by capillary suction. Hybrid layers nPSi/AgNPs were characterized by SEM, XRD, and RBS, confirming that AgNPs were introduced into nPSi layers. The catalytic activity of the hybrid layer in the reduction of organic dyes in water was studied using methylene blue (MB) as a model dye. Experimental results showed a high catalytic activity in comparison with other hybrid systems. The kinetic reduction could be fitted to the first-order equation obtaining the best degradation rate of 8.6 min−1 with AgNPs synthetized with 2 mM of AgNO3. In addition, the reusability of these layers was demonstrated after five cycles, showing promising results for their use in wastewater management.

Background There are multiple tools available to visualize the retinal and choroidal vasculature of the posterior globe. However, there are currently no reliable in vivo imaging techniques that can visualize the entire retrobulbar course of the retinal and ciliary vessels. Purpose To identify and characterize the central retinal artery (CRA) using cone-beam CT (CBCT) images obtained as part of diagnostic cerebral angiography. Materials and Methods In this retrospective study, patients with catheter DSA performed between October 2019 and October 2020 were included if CBCT angiography included the orbit in the field of view. The CBCT angiography data sets were postprocessed with a small field-of-view volume centered in the posterior globe to a maximum resolution of 0.2 mm. The following were evaluated: CRA origin, CRA course, CRA point of penetration into the optic nerve sheath, bifurcation of the CRA at the papilla, visualization of anatomic variants, and visualization of the central retinal vein. Descriptive statistical analysis was performed. Results Twenty-one patients with 24 visualized orbits were included in the analysis (mean age, 55 years ± 15; 14 women). Indications for angiography were as follows: diagnostic angiography (n = 8), aneurysm treatment (n = 6), or other (n = 7). The CRA was identified in all orbits; the origin, course, point of penetration of the CRA into the optic nerve sheath, and termination in the papilla were visualized in all orbits. The average length of the intraneural segment was 10.6 mm (range, 7-18 mm). The central retinal vein was identified in six of 24 orbits. Conclusion Cone-beam CT, performed during diagnostic angiography, consistently demonstrated the in vivo central retinal artery, demonstrating excellent potential for multiple diagnostic and therapeutic applications. © RSNA, 2021 Online supplemental material is available for this article.