<abstract> <p>Vitamin C stands as an essential water-soluble vitamin, antioxidant and has been shown to enhance immunity. SARS-CoV-2 has been spreading rapidly across the worldwide, several cellular processes of innate and adaptive immunity are aided by vitamin C, which strengthens the immune system overall. Multiple lines of evidence in the literature associate vitamin C with antioxidant, anti-inflammatory, anticoagulant and immunomodulatory actions. Pneumonia and sepsis patients had poor ascorbic acid status and high oxidative stress, according to many studies. Pneumonia patients who get vitamin C may have less severe symptoms and a longer course of the illness if they do. To standardize plasma levels in sepsis patients, gram measurements of the vitamin must be administered intravenously (IV). This intervention has been shown in a few trials to reduce mortality. COVID-19 management in China and the United States has exhibited remarkable results when using a high percentage of intravenous vitamins C. It's acceptable to include vitamin C in the COVID-19 treatment protocol as a secondary measure based on the current active clinical studies looking at the impact of vitamin C on the management of COVID-19. Patients with hypovitaminosis C or severe respiratory illnesses, such as COVID-19, may benefit from taking vitamin C, due to its good safety profile, simplicity of use, and potential for rapid production scaling. The study's goal was to see whether high dosage intravenous vitamin C had any impact on individuals with severe COVID-19 (HDIVC). Finally we discuss recent research that has been published on the efficacy of vitamin C administration in the treatment of viral infection and life-threatening conditions. The purpose of this manuscript is to summarise existing research on the efficacy of vitamin C as a treatment for COVID-19 and to discuss possible explanations for why it may work in some individuals but not in others.</p> </abstract>

Mediator complex subunit 1 (MED1) is a component of the mediator complex and functions as a coactivator involved in the regulated transcription of nearly all RNA polymerase II-dependent genes. Previously, we showed that MED1 in macrophages has a protective effect on atherosclerosis; however, the effect of MED1 on intimal hyperplasia and mechanisms regulating proinflammatory cytokine production after macrophage MED1 deletion are still unknown. In this study, we report that MED1 macrophage-specific knockout (MED1ΔMac) mice showed aggravated neointimal hyperplasia, vascular smooth muscle cells (VSMCs), and macrophage accumulation in injured arteries. Moreover, MED1ΔMac mice showed increased proinflammatory cytokine production after an injury to the artery. After lipopolysaccharide (LPS) treatment, MED1ΔMac macrophages showed increased generation of reactive oxygen species (ROS) and reduced expression of peroxisome proliferative activated receptor gamma coactivator-1α (PGC1α) and antioxidant enzymes, including catalase and glutathione reductase. The overexpression of PGC1α attenuated the effects of MED1 deficiency in macrophages. In vitro, conditioned media from MED1ΔMac macrophages induced more proliferation and migration of VSMCs. To explore the potential mechanisms by which MED1 affects inflammation, macrophages were treated with BAY11-7082 before LPS treatment, and the results showed that MED1ΔMac macrophages exhibited increased expression of phosphorylated-p65 and phosphorylated signal transducer and activator of transcription 1 (p-STAT1) compared with the control macrophages, suggesting the enhanced activation of NF-κB and STAT1. In summary, these data showed that MED1 deficiency enhanced inflammation and the proliferation and migration of VSMCs in injured vascular tissue, which may result from the activation of NF-κB and STAT1 due to the accumulation of ROS.

Aim of study This study investigated whether pre-activated bone marrow cells with sodium nitro prusside have effectiveness in the inhibition of diabetic wound healing in diabetic rabbits. In diabetic skin disorders and conditions involved redox state disturbances. The aim was to determine the effect of two minimum dosages of sodium nitro prusside, and its’ potential with bone marrow cells for chronic wound healing in-vivo. Methods Full-thickness skin dorsal wounds were created on diabetic rabbits. The effects of two minimum concentrations of sodium nitro prusside solution with bone marrow cells on wound healing were studied. The useful combination of sodium nitro prusside with bone marrow cells on wound repair may be attributed to its functional influences on inflammation, angiogenesis, cell proliferation, matrix deposition, and remodeling. Results The in-vivo experiments confirmed that pre-activated bone marrow cells contributed to wound healing by alleviating oxidative stress, increasing proliferation and migration, decreasing apoptosis. In histological results, improved collagen deposition, enhanced re-epithelization, angiogenesis, and decreased inflammatory infiltration were also detected in wound biopsies. Conclusions For the treatment of chronic wounds, cell-based therapy was an attractive approach. Bone marrow cells have a low ability to differentiate various types of cells or late healing without pretreatment. So it was needed to increase their potency of differentiation. The transplantation of pretreated bone marrow cells with a prime quantity of sodium nitro prusside solution improved chronic wound healing with a greater level of growth factors and a minimum level of oxidative stress.

Summary The low efficiency of somatic cell nuclear transfer (SCNT) greatly limits its application. Compared with the fertilized embryo, cloned embryos display abnormal epigenetic modification and other inferior developmental properties. In this study, small RNAs were isolated, and miR-34c and miR-125b were quantified by real-time PCR; results showed that these micro-RNAs were highly expressed in sperm. The test sample was divided into three groups: one was the fertilized group, one was the SCNT control group (NT-C group), and the third group consisted of SCNT embryos injected with sperm-borne small RNA (NT-T group). The level of tri-methylation of lysine 9 on histone H3 (H3K9me3) at the 8-cell stage was determined by immunofluorescence staining, and the cleavage ratio, blastocyst ratio, apoptotic cell index of the blastocyst and total cell number of blastocysts in each group were analyzed. Results showed that the H3K9me3 level was significantly higher in the NT-C group than in the fertilized group and the NT-T group. The apoptosis index of blastocysts in the NT-C group was significantly higher than that in the fertilized group and the NT-T group. The total cell number of SCNT embryos was significantly lower than that of fertilized embryos, and injecting sperm-borne small RNAs could significantly increase the total cell number of SCNT blastocysts. Our study not only demonstrates that sperm-borne small RNAs have an important role in embryo development, but also provides a new strategy for improving the efficiency of SCNT in rabbit.

Background Rabbits are well-domesticated animals. As a crucial economic animal, rabbit has been successfully bred into wool-use, meat-use and fur-use breeds. Hair length is one of the most economically important traits affecting profitability in wool rabbits. In this study, to identify selection signatures with the long-hair trait, whole-genomic resequencing of long-haired rabbits (Angora rabbits) and short-haired rabbits (Rex and New Zealand rabbits) was performed. Results By genome-wide selective sweeping analysis based on population comparison, we identified a total of 5.85 Mb regions (containing 174 candidate genes) with strong selection signals. Six of these genes (Dusp1, Ihh, Fam134a, Map3k1, Spata16, and Fgf5) were enriched in the MAPK signalling and Hedgehog signalling pathways, both of which are closely associated with hair growth regulation. Among these genes, Fgf5 encodes the FGF5 protein, which is a well-established regulator of hair growth. There was a nonsynonymous nucleotide substitution (T19234C) in the Fgf5 gene. At this locus, the C allele was present in all of the tested Angora rabbits, while the T allele was dominant in New Zealand and Rex rabbits. We further confirmed that the C allele was conserved in Angora rabbits by screening an additional 135 rabbits. Moreover, the results of functional predictions and co-immunoprecipitation revealed that the T19234C mutation impaired the binding capacity of FGF5 to its receptor FGFR1. Conclusions We discovered that the homozygous missense mutation T19234C within Fgf5 might contribute to the long-hair trait of Angora rabbits by reducing its receptor binding capacity. This finding will provide new insights into the genetic basis underlying the genetic improvement of Angora rabbits and benefit the improvement of rabbit breeding in the future.