Aktivitas Antioksidan Berbagai Fraksi Dan Ekstrak Metanolik Daun Beluntas (Pluchea Indica Less)

This study has been done to investigate the antioxidant activity of various fractions and methanolic extract of beluntasleaves by using several test system, such as DPPH, superoxide and hydroxyl radical-scavenging activities, hydrogenperoxide scavenging activity, ferric reducing power, iron and haemoglobin chelating capacities and b-carotene–linoleicbleaching assay. The results showed that methanolic extract of beluntas leaves (EMB) and its fractions (ethyl acetatefraction (FEA), water fraction (FA) and n-butanol fraction (FNB)) had scavenging activity of DPPH radical. EMBwhich had highest phenolic content and the strongest ferric reducing power, exhibited b-carotene–linoleic bleachinginhibition and the highest superoxide scavenging activity, while FEA showed antioxidant activity based on superoxideradical-scavenging activity, iron and haemoglobin chelating capacities and ferric reducing power

PF-23 Canine Pancytopenia with Normocytic-Normochromic Anemia: Case Reports in Three Dogs [2016-2017]

Canine pancytopenia is a disease that occurs in dogs caused by a decrease in the number of erythrocytes, leukocytes and thrombocytes/platelets in the blood. Canine pancytopenia often attacks dogs that live in the tropic climates. The diseases can be caused by an agent infection, excessive cell proliferation and through an immune intermediary. A decreasing in the number of erythrocytes followed by a decreasing of hemoglobin and hematocrit causes anemic condition. Non-regenerative anemia that often occurs when pancytopenia is normocytic-normochromic anemia [1]

Central Nervous System Targets and Routes for SARS-CoV-2: Current Views and New Hypotheses

As the coronavirus disease 2019 (COVID-19) pandemic unfolds, neurological signs and symptoms reflect the involvement of targets beyond the primary lung effects. The etiological agent of COVID-19, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibits neurotropism for central and peripheral nervous systems. Various infective mechanisms and paths can be exploited by the virus to reach the central nervous system, some of which bypass the blood-brain barrier; others alter its integrity. Numerous studies have established beyond doubt that the membrane-bound metalloprotease angiotensin-converting enzyme 2 (ACE2) performs the role of SARS-CoV-2 host-cell receptor. Histochemical studies and more recently transcriptomics of mRNA have dissected the cellular localization of the ACE2 enzyme in various tissues, including the central nervous system. Epithelial cells lining the nasal mucosae, the upper respiratory tract, and the oral cavity, bronchoalveolar cells type II in the pulmonary parenchyma, and intestinal enterocytes display ACE2 binding sites at their cell surfaces, making these epithelial mucosae the most likely viral entry points. Neuronal and glial cells and endothelial cells in the central nervous system also express ACE2. This short review analyzes the known entry points and routes followed by the SARS-CoV-2 to reach the central nervous system and postulates new hypothetical pathways stemming from the enterocytes lining the intestinal lumen.Fil: Barrantes, Francisco Jose. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentin

SARS-CoV-2 infection produces chronic pulmonary epithelial and immune cell dysfunction with fibrosis in mice

A subset of individuals who recover from coronavirus disease 2019 (COVID-19) develop post-acute sequelae of SARS-CoV-2 (PASC), but the mechanistic basis of PASC-associated lung abnormalities suffers from a lack of longitudinal tissue samples. The mouse-adapted severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strain MA10 produces an acute respiratory distress syndrome (ARDS) in mice similar to humans. To investigate PASC pathogenesis, studies of MA10-infected mice were extended from acute to clinical recovery phases. At 15 to 120 days post-virus clearance, pulmonary histologic findings included subpleural lesions composed of collagen, proliferative fibroblasts, and chronic inflammation, including tertiary lymphoid structures. Longitudinal spatial transcriptional profiling identified global reparative and fibrotic pathways dysregulated in diseased regions, similar to human COVID-19. Populations of alveolar intermediate cells, coupled with focal up-regulation of pro-fibrotic markers, were identified in persistently diseased regions. Early intervention with antiviral EIDD-2801 reduced chronic disease, and early anti-fibrotic agent (nintedanib) intervention modified early disease severity. This murine model provides opportunities to identify pathways associated with persistent SARS-CoV-2 pulmonary disease and test countermeasures to ameliorate PASC., After recovery from acute SARS-CoV-2 infection, mice exhibit chronic lung disease similar to some humans, allowing for testing of therapeutics

Correlations between serum levels of beta amyloid, cerebrospinal levels of tau and phospho tau, and delayed response tasks in young and aged cynomolgus monkeys (Macaca fascicularis)

Background In an attempt to explore cynomolgus monkeys as an animal model for Alzheimer's disease, the present study focused on the Alzheimer's biomarkers beta amyloid 142 (A42) in serum, and total tau (t-tau) and phosphorylated tau (p-tau) levels in cerebrospinal fluid. Methods We measured biomarker levels in Young and Aged cynomolgus monkeys and correlated these with performance on three delayed response tasks. Results The A42 concentration of the Aged monkeys was significantly lower than in the Young subjects, while the t-tau and p-tau did not significantly differ between the groups. The Young subjects performed significantly better than the Aged individuals on the memory tests. Only A42 levels were significantly correlated with performance in the three delayed response tasks. Conclusions Circulating A42 levels were lower in Aged monkeys and were correlated with inferior performance on delayed response tasks in Aged animals; therefore, both measures may be useful in establishing cynomolgus monkeys as models for studies of AD.</p

Whole genome sequencing association and gene-by-air-pollution interaction analyses identified kitlg as a novel baseline lung function gene candidate among African American children with asthma

RATIONALE: Baseline lung function, quantified as the forced expiratory volume in the first second of exhalation (FEV1), is a standard diagnostic criterion used by clinicians to identify and classify lung diseases. FEV1 is a complex phenotype that is heavily influenced by both environmental and genetic factors, with estimated heritability as high as 55%. Epidemiological studies have shown that early-life exposure to air pollution is a significant predictor of baseline lung function, while several genetic loci have been associated with FEV1 and genetic ancestry contributes to its variation. Despite numerous studies linking genetic and environmental factors to variation in FEV1, the majority of its heritability remains unexplained. We hypothesized that a portion of this missing heritability is due to gene-by-environment (GxE) interactions. METHODS: Using whole genome sequencing data on 876 African American children with asthma from the Trans-Omics for Precision Medicine (TOPMed) program, we performed a genome-wide association study of FEV1 using the ENCORE tool. Potential gene targets of associated variants were identified using long range chromatin interaction data available in the HUGIN browser. RNA-Seq data of nasal epithelial cells from minority children with asthma was used to identify eQTLs of potential gene targets. FEV1-associated variants were overlapped with candidate cisregulatory elements (ccRE) from ENCODE to identify variants with potential regulatory function. Gene-by-air pollution analyses using early-life and past-year exposure to air pollution were performed. All models were adjusted for age, sex, height, the first five genetic principal components, use of controller medications and sequencing batches. RESULTS AND CONCLUSION: We identified a novel genome-wide significant locus on chromosome 12 (rs73429450) that was associated with FEV1 (p = 1.26 x 10-8, β =0.302). Publicly available Hi-C and in-house eQTL data supported a regulatory role of the novel locus on the KITLG gene. Additional gene-by-air-pollution interaction analyses found that candidate variants interacted with SO2 in the first year of life (rs73440122, p = 0.049, β = 0.009) and past-year exposure (rs58475486, p = 0.003, β = 0.539) to modify association with FEV1. Thus, we identified KITLG as a novel gene candidate with variants that have protective genetic association and gene-by-SO2 interactions with baseline lung function (FEV1) among African American children with asthma