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Bruun Falkenberg posted an update 6 months, 3 weeks ago
t50% = 19 days for risperidone loaded Resomer® 503 H microspheres). The limited space for swelling and the rigidity of the agarose gel might mimic the tight encapsulation of the dosage form in the tissue better than the conventional liquid medium.Bromelain, a cysteine protease exhibits promising potential in amelioration of wide variety of inflammatory disorders. Its denaturation or aggregation in gastric milieu depletes its therapeutic potential along with unpredictable prophylactic hypersensitivity reactions. Hence, efficient carrier system to improve bromelain’s stability and avoid related side effects is of utmost importance. Therefore, present investigation was undertaken to prepare bromelain loaded nanostructured lipid carriers (Br-NCs) with high drug loading, stability and efficacy in rheumatoid arthritis management. Br-NCs fabricated via double emulsion solvent evaporation method were characterized for physical properties, morphology and stability. selleck chemical Optimized batch exhibited spherical shape, nanometric size (298.23 nm) and entrapment efficiency ~77% with sustained release behavior and improved gastric stability. Br-NCs exhibited 4.63-folds improvement in shelf-life compared to bromelain at room temperature. The protective potential of orally administered Br-NCs in rheumatoid arthritis was evaluated via assessing arthritis severity in wistar rats along with biochemical, hematological and immunological parameters. Br-NCs remarkably (p less then 0.05) diminished paw edema, joint stiffness, mechanical allodynia and tissue damage along with alleviation of oxidative stress and immunological markers. Radiological joint alterations were also notably preserved with Br-NCs. Thus, preclinical studies distinctly manifested that Br-NCs formulation opens new avenue for development of novel effective therapeutic modality for rheumatoid arthritis management.
To explore whether APOBEC family members are involved in the response to inappropriate expression of L1 retroelements in primary Sjögren’s syndrome (SS) and systemic lupus erythematosus (SLE), as well as in SS related lymphomagenesis.
Minor salivary glands (MSG) and kidney biopsy (KB) specimens were obtained from 41 SS patients (10 with lymphoma) and 23 patients with SLE, respectively. PBMC and sera were also collected from 73 SLE patients. Full-length L1 transcripts, members of the APOBEC and IFN family were quantitated by real time PCR. Type I IFN activity was assessed in lupus plasma by a cell assay.
APOBEC3A was increased in SS MSG, SLE KB and PBMC and correlated with L1. AID and APOBEC3G were particularly overexpressed in MSG tissues derived from SS lymphoma patients.
These data reveal a previously unappreciated role of APOBEC family proteins in the pathogenesis of systemic autoimmunity and SS related lymphomagenesis.
These data reveal a previously unappreciated role of APOBEC family proteins in the pathogenesis of systemic autoimmunity and SS related lymphomagenesis.The cut-off values used in C6 peptide-based enzyme immunoassay (EIA), a widely used test in Lyme borreliosis (LB) serology, have not been thoroughly analysed. The objective of the study was to examine the performance of the C6 EIA, and to determine optimal cut-off values for the test. The analysed data contained results of 1368 serum samples. C6 EIA index values were compared statistically with the immunoblot (IB) test results. The identified cut-off values were further tested in a well-defined LB patient cohort. Cut-off value 1.6 appeared to be optimal when C6 EIA was used as a stand-alone test. When using C6 EIA as the first-tier test, the optimal cut-off values were 0.9 and 2.4 for negative and positive results. When C6 EIA was used as a second-tier test, samples yielding C6 index values ≥3.0 could be considered positive. The identified cut-off values had also a high sensitivity to identify seropositivity among definite LB patients. The identified cut-off values refine the role of C6 EIA in LB serology. Importantly, the use of C6 EIA leads to a reduction in the number of samples that need to be analysed using an IB, thus also reducing the costs. Two alternative workflows for LB serology including the C6 EIA are suggested.Glucose-6-phospate dehydrogenase (G6PD) deficiency is estimated to affect more than 400 million people world-wide. This X-linked genetic deficiency puts stress on red blood cells (RBC), which may be further augmented under certain pathophysiological conditions and drug treatments. These conditions can cause hemolytic anemia and eventually lead to multi-organ failure and mortality. G6PD is involved in the rate-limiting step of the pentose phosphate pathway, which generates reduced nicotinamide adenine dinucleotide phosphate (NADPH). In RBCs, the NADPH/G6PD pathway is the only source for recycling reduced glutathione and provides protection from oxidative stress. Susceptibility of G6PD deficient populations to certain drug treatments and potential risks of hemolysis are important public health issues. A number of clinical trials are currently in progress investigating clinical factors associated with G6PD deficiency, validation of new diagnostic kits for G6PD deficiency, and evaluating drug safety, efficacy, and pathophysiology. More than 25 clinical studies in G6PD populations are currently in progress or have just been completed that have been examined for clinical pharmacology and potential therapeutic implications of G6PD deficiency. The information on clinical conditions, interventions, purpose, outcome, and status of these clinical trials has been studied. A critical review of ongoing clinical investigations on pharmacology and therapeutics of G6PD deficiency should be highly important for researchers, clinical pharmacologists, pharmaceutical companies, and global public health agencies. The information may be useful for developing strategies for treatment and control of hemolytic crisis and potential drug toxicities in G6PD deficient patients.The high comorbidity of psychological disorders in both functional and organic gastrointestinal diseases suggests the intimate and complex link between the brain and the gut. Termed the brain-gut axis, this bidirectional communication between the central nervous system and enteric nervous system relies on immune, endocrine, neural, and metabolic pathways. There is increasing evidence that the gut microbiome is a key part of this system, and dysregulation of the brain-gut-microbiome axis (BGMA) has been implicated in disorders of brain-gut interaction, including irritable bowel syndrome, and in neuropsychiatric disorders, including depression, Alzheimer’s disease, and autism spectrum disorder. Further, alterations in the gut microbiome have been implicated in the pathogenesis of organic gastrointestinal diseases, including inflammatory bowel disease. The BGMA is an attractive therapeutic target, as using prebiotics, probiotics, or postbiotics to modify the gut microbiome or mimic gut microbial signals could provide novel treatment options to address these debilitating diseases.
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