The PHA-induced and serum levels of IFN-alpha and -gamma, TNF-alpha, IL-4, IL-6, IL-8, IL-RA, as well as CD3, CD4, CD8, CD20, CD56 lymphocytic subpopulations and serum IgG, IgM, and IgA were studied in 53 patients with multiple trauma to detect the most informative parameters of laboratory monitoring of the immunodeficiency developing during treatment. The stages of the study corresponded to the phases of development of an immune response: (1) an induction phase (days 1-4); (2) an immunoregulatory phase (days 5-10); (3) an effector phase (days 11-24). The findings suggest that at the early stage of the study, the drastic reduction was revealed in CD3, CD4 T-lymphocytic subpopulations, accompanied by inadequate humoral immunological parameters. By Stage 3 of the study, the majority of these parameters became normal; the serum levels of IgG and IgM remained lower only in patients with a fatal outcome. Throughout all the 3 stages of the study, the serum concentration of IFN-alpha remained in the almost normal ranges; there was no significant elevation in both the serum and induced levels of IL-4 either. The serum content of TNF-alpha in the examinees was significantly higher than the normal levels, by remaining virtually at the same level up to the end of treatment. The elevated serum levels of TNF-alpha were attended by its increased induction in vitro, without reducing up to Stage 3. From Stage 3, only some patients with a fatal outcome were observed to have the reduced induced and spontaneous levels of TNF-alpha. According to the findings, at Stage 1 of the study, the production of IFN-gamma in all patients was much increased, by significantly dropping by the end of treatment (by more than twice), without achieving, however, the normal levels, except the examinees with a fatal outcome, in whom the concentration of IFN-alpha increased or underwent no changes. A relationship was also found between the serum levels of IL-6 and IL-8 and the outcome of the disease: throughout the observation, their concentrations remained invariably high in patients with a fatal outcome whereas in those with a good outcome, there was a uniform decrease in the content of both cytokines by the end of the observation. Thus, the simultaneous increase in the levels of IFN-gamma, IL-6, IL-8, and TNF-alpha and accompanying reductions in CD3, CD4 and serum IgG, IgM are poor prognostic factors and may be used both as additional immunodiagnostic criteria and for immunotherapy monitoring in patients with polytrauma.
Download full-text PDF |
Source |
---|
Background: Lecanemab is a humanized IgG1 monoclonal antibody that binds with high affinity to Aβ soluble protofibrils. In two clinical studies (phase 2, NCT01767311 and phase 3 ClarityAD, NCT03887455) in early Alzheimer's disease, lecanemab substantially reduced amyloid PET and significantly slowed clinical decline on multiple measures of cognition and function, including CDR-SB at 18 months. Models describing the change in amyloid PET and CDR-SB in response to lecanemab treatment were used to explore the impact of changing from the initial dosage regimen (10 mg/kg every 2 weeks [Q2W]) to a less intensive maintenance dosing regimen (10 mg/kg every 4 weeks [Q4W]) on clinical efficacy, and to explore the optimal duration of the initial dosing regimen.
View Article and Find Full Text PDFBackground: Senile dementia (SD) is a deteriorative organic brain disorder and it comprises Alzheimer's disease (AD) as a major variant. SD is shown impairment of mental capacities whereas AD is degeneration of neurons. According to World Health Organization (WHO) report; more than 55 million peoples have dementia and it is raising 10 million new cases every year.
View Article and Find Full Text PDFBackground: Previously, we demonstrated therapeutic benefits following intraperitoneal delivery of the TGR5 agonist HY209 in 5xFAD, a transgenic mouse model of Alzheimer's Disease (AD). Given the desirability of a more acceptable administration route for prolonged AD treatment, we assessed the efficacy of HY209 via oral delivery. This study aims to elucidate the therapeutic potential of NuCerin, an oral formulation of HY209, in the aforementioned AD model, while simultaneously identifying potential blood biomarkers indicative of NuCerin's therapeutic action.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
L & J Bio, Co., Ltd, Seoul, Songpa-Gu, Korea, Republic of (South).
Background: Neurofibrillary tangles (NFTs), along with amyloid beta plaque, are neuropathological aggregates of Alzheimer's Disease (AD). Hyperphosphorylated tau is responsible for the NFTs formation and further neurodegeneration in AD. The hippocampal region and the entorhinal cortex (EC) have been a major focus of AD research because the deposits of hyperphosphorylated tau protein and NFT in these regions are correlated with memory deficits.
View Article and Find Full Text PDFBackground: VY-TAU01 is a recombinant humanized IgG4 monoclonal antibody (mAb) directed against pathological tau for the treatment of patients with mild dementia or mild cognitive impairment due to Alzheimer's disease (AD). Both VY-TAU01 and its parental mouse IgG1 mAb Ab-01 target an epitope in the C-terminus of tau, bind pathological tau with high affinity and selectivity over wild-type tau, block paired helical filament seed-induced tau aggregates in vitro, and selectively stain tau tangles in AD and P301S mouse (C57/B6J-Tg[Thy1-MAPT*P301S]2541Godt) brain. Ab-01 robustly inhibits seeding and propagation of pathological tau in a P301S mouse seeding model.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!