Epilepsy, a chronic seizure disorder, can cause elevated fatigue and reduced quality of life (QOL) of the sufferers. Hence, improving QOL, seizure severity (SS) and fatigue are important areas of therapeutic interventions for people living with epilepsy (PLWE). Therefore, there is need to ascertain the levels and interrelationships among these constructs in PLWE. This study compared fatigue and QOL of PLWE with those of apparently healthy individuals (AHIs) and also determined the interrelationships between fatigue, QOL and SS in PLWE. This cross-sectional survey involved 91 PLWE and 101 AHIs consecutively recruited from purposively selected hospitals and hosting communities. The Short-form Health Survey (SF-36) questionnaire, the Fatigue Severity Scale, the Modified Fatigue Impact Scale and the Seizure Severity Questionnaire were used to evaluate QOL, fatigue severity (FS), fatigue impact (FI) and SS respectively. Data was analyzed using frequency count, proportions, mean and standard deviation, range, Chi-square test, Mann-Whitney U test and Spearman-rank order correlation. Alpha level was set at 0.05. PLWE had significantly lower QOL compared to AHIs (U = 3057.00;p < 0.01). The two groups however experienced similar fatigue severity, but PWE suffered greater fatigue impact (U = 2798.00;p < 0.01). Significant relationships existed among FI, FS, SS and QOL in PLWE (p < 0.01). Compared with AHIs, PLWE had poorer QOL, similar FS, and higher FI. QOL of PLWE was negatively associated with SS, FI and FS. Clinical interventions geared towards minimizing seizure, severity and impact of fatigue may improve the QOL of PLWE.Compared with AHIs, PLWE had poorer QOL, similar FS, and higher FI. QOL of PLWE was negatively associated with SS, FI and FS. Clinical interventions geared towards minimizing seizure, severity and impact of fatigue may improve the QOL of PLWE.Cancer immunotherapy aims to augment the response of the patient's own immune system against cancer cells. Despite effective for some patients and some cancer types, the therapeutic efficacy of this treatment is limited by the composition of the tumor microenvironment (TME), which is not well-suited for the fitness of anti-tumoral immune cells. However, the TME differs between cancer types and tissues, thus complicating the possibility of the development of therapies that would be effective in a large range of patients. A possible scenario is that each type of cancer cell, granted by its own mutations and reminiscent of the functions of the tissue of origin, has a specific metabolism that will impinge on the metabolic composition of the TME, which in turn specifically affects T cell fitness. Therefore, targeting cancer or T cell metabolism could increase the efficacy and specificity of existing immunotherapies, improving disease outcome and minimizing adverse reactions.Acute lung injury (ALI), a devastating illness induced by systemic inflammation e.g., sepsis or local lung inflammation e.g., COVID-19 mediated severe pneumonia, has an unacceptably high mortality and has no effective therapy. ALI is associated with increased pulmonary microvascular hyperpermeability and alveolar flooding. The small Rho GTPases, RhoA and Rac1 are central regulators of vascular permeability through cytoskeleton rearrangements. RhoA and Rac1 have opposing functional outcome RhoA induces an endothelial contractile phenotype and barrier disruption, while Rac1 stabilizes endothelial junctions and increases barrier integrity. In ALI, RhoA activity is increased while Rac1 activity is reduced. We have shown that the activation of RhoA in lipopolysaccharide (LPS)-mediated ALI, is dependent, at least in part, on a single nitration event at tyrosine (Y)34. Thus, the purpose of this study was to determine if the inhibition of Rac1 is also dependent on its nitration. Our data show that Rac1 inhibition by LPS is associated with its nitration that mass spectrometry identified as Y32, within the switch I region adjacent to the nucleotide-binding site. Using a molecular modeling approach, we designed a nitration shielding peptide for Rac1, designated NipR2 (nitration inhibitor peptide for the Rho GTPases 2), which attenuated the LPS-induced nitration of Rac1 at Y32, preserves Rac1 activity and attenuates the LPS-mediated disruption of the endothelial barrier in human lung microvascular endothelial cells (HLMVEC). Using a murine model of ALI induced by intratracheal installation of LPS we found that NipR2 successfully prevented Rac1 nitration and Rac1 inhibition, and more importantly attenuated pulmonary inflammation, reduced lung injury and prevented the loss of lung function. Together, our data identify a new post-translational mechanism of Rac1 inhibition through its nitration at Y32. As NipR2 also reduces sepsis induced ALI in the mouse lung, we conclude that Rac1 nitration is a therapeutic target in ALI.Avian coccidiosis leads to severe economic losses on the global poultry industry. Immune mapped protein-1 (IMP1) is a novel membrane protein, and was reported to be a candidate protective antigen. https://www.selleckchem.com/products/cloperastine-fendizoate.html However, production and utilization modes of IMP1 using Lactococcus lactis as delivery vector were not reported untill now. In the present study, Eimeria tenella IMP1 (EtIMP1) protein was expressed in L. lactis under the nisin-inducible promoter, and EtIMP1 protein was produced in cytoplasmic, cell wall-anchored and secreted forms. Each chicken was orally immunized with one of the three live EtIMP1-expressing lactococci three times at 2 weeks intervals (immunized group), or with live bacteria harboring empty vector (immunized control group). Chickens in immunized and immunized control group were challenged with E. tenella sporulated oocysts to assess the immune responses. The results showed that proliferative responses of peripheral blood T lymphocytes, mRNA expression levels of IL-2, IL-4, IL-10 and IFN-γ in spleen tissues, levels of serum IgG and secretory IgA (sIgA) in cecal lavage fluids from chickens in immunized group were all significantly elevated compared to that in immunized control group. All three the live EtIMP1-expressing lactococci significantly decreased oocyst shedding, alleviated pathological damage in cecum and improved weight gain compared with bacteria harboring empty vector. These results suggested EtIMP1 protein delivered by L. lactis might be a promising candidate in developing novel vaccines against Eimeria infection.