Comment on "Early Life Food Desert Status Is Associated With Alpha and Gamma-Tocopherol Levels and Infant Lung Function".
Shridevi Kotina K, Doiphode Megha M, Mishra Rakhi R, Dhyani Archana A et al.
Reliance Life Sciences Private Limited · IFNAR2 · 重组蛋白
rhIFN-alpha 是一种重组蛋白,由Reliance Life Sciences Private Limited研发。该药已获批,用于治疗相关适应症,给药途径:Injectable (Others)、Intramuscular (IM) Injection、Intravenous (IV)、Subcutaneous Injection。
| 商品名 | ReliFeron |
| 公司 | Reliance Life Sciences Private Limited |
| 药物类别 | 重组蛋白 |
| 分子靶点 | IFNAR2 |
| 给药途径 | Injectable (Others), Intramuscular (IM) Injection, Intravenous (IV), Subcutaneous Injection |
| 状态 | Approved |
rhIFN-alpha 作用于 1 个分子靶点:
| IFNAR2 | interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC) |
rhIFN-alpha 针对 8 个适应症,涉及 2 个治疗领域。
| 治疗领域 | 疾病/病症 | 分期 |
|---|---|---|
| Neoplasms benign, malignant and unspecified (incl cysts and polyps) | Hairy cell leukaemia | ✓ Approved |
| Infections and infestations | Hepatitis B | ✓ Approved |
| Infections and infestations | Hepatitis C | ✓ Approved |
| Neoplasms benign, malignant and unspecified (incl cysts and polyps) | Kaposi's sarcoma | ✓ Approved |
| Neoplasms benign, malignant and unspecified (incl cysts and polyps) | Non-Hodgkin's lymphoma | ✓ Approved |
注册免费账户还可查看另外 3 个适应症
免费注册查看全部适应症 →Shridevi Kotina K, Doiphode Megha M, Mishra Rakhi R, Dhyani Archana A et al.
Mahida Kishankumar K, Jagtap Snehal Rajendra SR
Abalenikhina Yu V YV, Breslavets D I DI, Mylnikov P Yu PY, Builina S G SG et al.
The effect of tumor necrosis factor alpha (TNFα) on the barrier function of the nasal epithelium (RPMI 2650 cell line) was studied in in vitro experiments. It was shown that short-term exposure to the cytokine (6 h) increased transepithelial electrical resistance and decreased paracellular permeability for mannitol, which was accompanied by elevated expression of the tight junction proteins occludin and claudin-1. Prolonged exposure (48 h) caused an opposite effect, i.e., a significant decrease in the barrier function and a decrease in the content of the studied proteins. These results indicate that the proinflammatory cytokine TNFα modulates the permeability of the nasal epithelium, which should be taken into account when developing strategies for intranasal drug delivery.
Han Jieun J, Kim Seohan S, Ha Sangseok S, Sung Wonmo W
Objective.This study investigated the microdosimetric characteristics of auger electrons (AEs) and their DNA damage-related physical properties, specifically evaluating the microdosimetric quantity as a physical predictor of initial DNA damage across different radiation types.Approach.Monte Carlo simulations using OpenTOPAS were conducted to calculate the frequency-mean lineal energy (yF) and the dose-mean lineal energy (yD) in spherical water targets (radii: 10-500 nm) for monoenergetic electrons (3-15 keV). DNA damage yields were quantified using TOPAS-nBio with a linear plasmid DNA model. The correlations between microdosimetric quantities and DNA damage were analyzed not only for AEs but also for protons and alpha particles to assess the universality ofyFandyDas potential biological predictors.Main results.AEs demonstrated a pronounced site-radius dependency for bothyFandyDwithin the 10-100 nm target region. Across these biologically relevant nano-scale targets, both strand break (SB) and double-SB (DSB) yields exhibited strong power-law correlations with microdosimetric quantities (R2⩾ 0.94 foryFandR2⩾ 0.89 foryD). Low-energy electrons, protons, and alpha particles aligned along a continuous microdosimetric-damage relationship despite differences in particle identity. Specifically,yFprovided a more sensitive physical predictor thanyDfor Auger electron-induced initial DNA damage in the low-lineal-energy region below 10 keVμm-1.Significance.These findings show thatyFandyDreflect nanoscale energy-deposition patterns governing initial DNA strand-break induction. This microdosimetry-damage relationship extends to low-energy AEs as well as proton and alpha particles.
Cruz Meryl M, Martínez-Huélamo Miriam M, Yubero-Serrano Elena M EM, Cubedo-Cullere Marta M et al.
Metabolomics contributes to the understanding of mechanisms by which dietary interventions can minimize the progression of mild cognitive impairment (MCI) to dementia. In this study, changes in metabolomics profiles were analyzed to assess the effects of a 24-week intervention with a Mediterranean diet (MD), with and without probiotics, and a low-fat diet (according to the World Health Organization recommendations) in 47 older adults (aged ≥60 years, 42.6% women) with MCI. The plasma metabolome was analyzed using a quantitative LC-MS/MS targeted assay to assess metabolite changes derived from dietary intervention. Multivariate methods were employed to assess the impact of diets on the plasma metabolome, as well as the associations between the changes in metabolite profiles and cognitive evaluation scores (assessed through ADAS-Cog-11 and a complete neuropsychological test battery). Our results showed that the MD increased the levels of acetoacetic acid and various metabolites linked to the tricarboxylic acid (TCA) cycle and decreased the levels of branched-chain amino acids (BCAAs), particularly isoleucine. Increases in alpha-ketoglutarate, alpha-ketoisovalerate, and 2-oxocaproate, as well as decreases in beta-alanine, L-carnitine, and alpha-aminobutyric acid concentrations, were associated with improved cognitive scores. The MD, but not the low-fat diet, promoted ketone body production and increased the availability of TCA cycle intermediates, suggesting an increase in metabolic flexibility in older adults with MCI. Targeted dietary and/or pharmacological strategies aimed at enhancing metabolic flexibility may open new avenues for preventing the progression of MCI. This study is registered with ClinicalTrials.gov (NCT05029765).
Gopalakrishnan Raghavan R, Malan Nitesh Singh NS, Sonneborn Claire C, Hogue Olivia O et al.
Maladaptive pain avoidance plays a critical role in chronic pain development and maintenance. Pain avoidance reinforced instrumentally through action-outcome contingencies remains poorly understood, specifically in complex regional pain syndrome (CRPS), a nociplastic condition. We aim to identify mechanisms underlying maladaptive avoidance to inform interventions and improve quality of life. Twenty-eight lower extremity CRPS and twenty-seven healthy (HC) participants performed an instrumental pain avoidance task in which they chose between two options linked to different probabilities of receiving pain, enabling assessment of avoidance learning and decision-making. Pain was delivered to the affected or non-affected extremity in CRPS and to either hand in HC. A reinforcement learning model estimated threat and safety learning, choice stochasticity, and trial-wise pain expectancies based on task behaviour. Resting-state magnetoencephalography was used to quantify intrinsic alpha-band activity, a frequency linked to chronic pain experience, in relation to pain avoidance. Threat and safety learning did not differ between extremities in CRPS. CRPS exhibited significantly elevated threat and safety learning than HC, accompanied by increased choice stochasticity, despite similar pain exposure. Pain expectancies directly influenced avoidance decisions independent of perceived pain in both groups; however, this expectancy-decision relationship was significantly weaker in CRPS. Increased threat learning in CRPS was statistically accounted for by elevated anxiety, sentimental personality, and reduced resting-state alpha power in the prefrontal cortex. Collectively, compared to HC, CRPS exhibited higher learning from recent outcomes and diminished expectancy-guided control of behaviour. Prefrontal alpha partially mediated the effects of pain severity on threat learning. The study was registered in Clinicaltrials.gov [NCT04603417]. CRPS is a debilitating condition associated with disproportionate pain, sensorimotor abnormalities, and autonomic dysfunction, often arising without underlying structural or organic causes. Maladaptive pain avoidance, driven by fear of pain, severely hinders physical therapy and rehabilitation by creating a cycle of inactivity, physical deconditioning, and increased pain sensitivity. This work highlights specific behavioural and neural mechanisms underlying pain avoidance for the development of novel psychosocial and neuromodulatory interventions that can be incorporated in clinical practice to treat CRPS.
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