Search

Biodegradable films based on sodium alginate and aloe vera were prepared by casting technique. The resulting films were characterized by swelling behavior, scanning electron microscopy, biodegradation, as well as mechanical and barrier properties. The aloe vera gel exerted a positive influence on mechanical and physico-chemical properties. Aloe vera gel improved the tensile strength of the films giving maximum value of 21.20 N/[mm.sup.2] at 20% gel. Water vapor permeability of the composite films was reduced which made the film more effective as a moisture barrier, giving the most efficient result of 1.16 * [10.sup.-10] g [m.sup.-1] [s.sup.-1] [Pa.sup.-]1 at 50% aloe vera gel. The present study demonstrates the viability of the composite alginate aloe vera films as a biodegradable alternative to synthetic plastic films for the packaging of food materials. KEYWORDS aloe vera gel, biodegradable film, glycerol, sodium alginate, 1 | INTRODUCTION The purpose of food packaging films is to retain the quality and safety of food products during transportation and storage until consumption. [1,2] The films protect food [...]

Background: A diverse spectrum of long COVID symptoms (LCS) have the scope of physical rehabilitation. Due to limited resources, very little is known about the physiotherapy and rehabilitation interventions for LCS and their clinical application. This study aims to explore the role of physiotherapy and rehabilitation interventions in the management of musculoskeletal, neurological, cognitive, cardiorespiratory, mental health, and functional impairments of LCS. Methods: The study was a systematic scoping review of the literature published between April 2020 and July 2022. Results: 87 articles were extracted followed by a standard process of The Preferred Reporting Items for Systematic reviews and meta-analysis (PRISMA) extension for Scoping reviews (PRISMA-ScR). The included studies had a 3223 LCS population. All types of primary and secondary articles were retrieved except for qualitative studies. The evidence was evaluated by an appraisal scoring tool followed by the guidelines of the “Enhancing the Quality and Transparency of Health Research ( EQUATOR) network”. The included papers had a mean appraisal score of 0.7807 on a 0 to 1 scale (SD 0.08), the minimum score was for study protocols (0.5870), and the maximum score was for Cohort studies (.8977). Sixty seven (67) evidence-based interventions were documented from 17 clinical categories. The most weighted interventions were treating underlying symptoms of long COVID (Adjusted score 1/1), management of fatigue (Adjusted score 0.963/1), aerobic exercise and balance training (Adjusted score 0.951/1), multidisciplinary rehabilitation (Adjusted score 0.926/1), and low resistance training and aerobic exercise (Adjusted score 0.889/1). Conclusion: We recommend Long COVID rehabilitation in a multidisciplinary approach by treating the individual symptoms, especially fatigue. Physiotherapy interventions play a significant role as most of the recommended interventions were exercise, modalities, patient education, respiratory rehabilitation, and telerehabilitation Scoping reviews do not require protocol registration from PROSPERO.

Background: A diverse spectrum of long COVID symptoms (LCS) have the scope of physical rehabilitation. Due to limited resources, very little is known about the physiotherapy and rehabilitation interventions for LCS and their clinical application. This study aims to explore the role of physiotherapy and rehabilitation interventions in the management of musculoskeletal, neurological, cognitive, cardiorespiratory, mental health, and functional impairments of LCS. Methods: The study was a systematic scoping review of the literature published between April 2020 and July 2022. Results: 87 articles were extracted followed by a standard process of The Preferred Reporting Items for Systematic reviews and meta-analysis (PRISMA) extension for Scoping reviews (PRISMA-ScR). The included studies had a 3223 LCS population. All types of primary and secondary articles were retrieved except for qualitative studies. The evidence was evaluated by an appraisal scoring tool followed by the guidelines of the “Enhancing the Quality and Transparency of health Research ( EQUATOR) network”. The included papers had a mean appraisal score of 0.7807 on a 0 to 1 scale (SD 0.08), the minimum score was for study protocols (0.5870), and the maximum score was for Cohort studies (.8977). Sixty seven (67) evidence-based interventions were documented from 17 clinical categories. Conclusion: LCS can be treated by physiotherapy, exercise, and physical rehabilitation for musculoskeletal, neurological, cognitive, cardio-respiratory, mental health, and functional impairments at home or in clinical setups such as primary care settings by in-person care or telerehabilitation.

BackgroundMyriad challenges to the proper folding and structural maturation of secretory pathway client proteins in the endoplasmic reticulum (ER) - a condition referred to as "ER stress" - activate intracellular signaling pathways termed the unfolded protein response (UPR).Scope of reviewThrough executing transcriptional and translational programs the UPR restores homeostasis in those cells experiencing manageable levels of ER stress. But the UPR also actively triggers cell degeneration and apoptosis in those cells that are encountering ER stress levels that exceed irremediable thresholds. Thus, UPR outputs are "double-edged". In pancreatic islet β-cells, numerous genetic mutations affecting the balance between these opposing UPR functions cause diabetes mellitus in both rodents and humans, amply demonstrating the principle that the UPR is critical for the proper functioning and survival of the cell.Major conclusionsSpecifically, we have found that the UPR master regulator IRE1α kinase/endoribonuclease (RNase) triggers apoptosis, β-cell degeneration, and diabetes, when ER stress reaches critical levels. Based on these mechanistic findings, we find that novel small molecule compounds that inhibit IRE1α during such "terminal" UPR signaling can spare ER stressed β-cells from death, perhaps affording future opportunities to test new drug candidates for disease modification in patients suffering from diabetes.

Multitarget pharmacology of small-molecule cancer drugs significantly contributes to their mechanism of action, side effects, and emergence of drug resistance and opens ways to repurpose, combine, or customize drug therapy. In most cases, the set of targets affected at therapeutic concentrations is not fully characterized and/or the interaction efficacy values are not accurately quantified. We collected information about multiple targets for each cancer drug along with their experimental effective concentrations or binding activities from multiple sources. All multitarget activity values for each drug then were used to build two proximity network pharmacology maps of anticancer drugs and targets of those drugs, respectively. Together with the network map, we showed that the majority of the cancer drugs had substantial multitarget pharmacology based on our current knowledge. In addition, most of the cancer drugs simultaneously affect macromolecular targets from different classes and types. The target subset can further be accentuated and personalized by patient sample-specific expression data. The network maps of cancer drugs and targets as well as all quantified activity data were integrated into a freely available database, CancerDrugMap (http://ruben.ucsd.edu/dnet/maps/drugnet.html). The identified multitarget pharmacology of cancer drugs is essential for improving the efficacy of individually prescribed drugs and drug combinations and minimization of adverse effects.

Diverse perturbations to endoplasmic reticulum (ER) functions compromise the proper folding and structural maturation of secretory proteins. To study secretory pathway physiology during such "ER stress," we employed an ER-targeted, redox-responsive, green fluorescent protein-eroGFP-that reports on ambient changes in oxidizing potential. Here we find that diverse ER stress regimes cause properly folded, ER-resident eroGFP (and other ER luminal proteins) to "reflux" back to the reducing environment of the cytosol as intact, folded proteins. By utilizing eroGFP in a comprehensive genetic screen in Saccharomyces cerevisiae, we show that ER protein reflux during ER stress requires specific chaperones and cochaperones residing in both the ER and the cytosol. Chaperone-mediated ER protein reflux does not require E3 ligase activity, and proceeds even more vigorously when these ER-associated degradation (ERAD) factors are crippled, suggesting that reflux may work in parallel with ERAD. In summary, chaperone-mediated ER protein reflux may be a conserved protein quality control process that evolved to maintain secretory pathway homeostasis during ER protein-folding stress.

Endoplasmic reticulum stress (ER stress) has been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF), a disease of progressive fibrosis and respiratory failure. ER stress activates a signaling pathway called the unfolded protein response (UPR) that either restores homeostasis or promotes apoptosis. The bifunctional kinase/RNase IRE1α is a UPR sensor/effector that promotes apoptosis if ER stress remains high and irremediable (i.e., a "terminal" UPR). Using multiple small molecule inhibitors against IRE1α, we show that ER stress-induced apoptosis of murine alveolar epithelial cells can be mitigated in vitro. In vivo, we show that bleomycin exposure to murine lungs causes early ER stress to activate IRE1α and the terminal UPR prior to development of pulmonary fibrosis. Small-molecule IRE1α kinase-inhibiting RNase attenuators (KIRAs) that we developed were used to evaluate the contribution of IRE1α activation to bleomycin-induced pulmonary fibrosis. One such KIRA-KIRA7-provided systemically to mice at the time of bleomycin exposure decreases terminal UPR signaling and prevents lung fibrosis. Administration of KIRA7 14 days after bleomycin exposure even promoted the reversal of established fibrosis. Finally, we show that KIRA8, a nanomolar-potent, monoselective KIRA compound derived from a completely different scaffold than KIRA7, likewise promoted reversal of established fibrosis. These results demonstrate that IRE1α may be a promising target in pulmonary fibrosis and that kinase inhibitors of IRE1α may eventually be developed into efficacious anti-fibrotic drugs.