Macleanhede8159

Radiotherapy has been widely used in the treatment of hepatocellular carcinoma (HCC). However, whether the patients should receive radiotherapy before or after surgical treatment has not been studied. The objective of the study was to compare the efficacy of the treatment in HCC patients who received pre-surgery and post-surgery radiotherapy.

Data from the Surveillance, Epidemiology, and End Results (SEER) database were analyzed. Patients with surgery combined with radiotherapy were included into the study. The outcome measures were overall survival (OS) and cancer-specific survival (CSS). Propensity score matching (PSM) was used to reduce selection bias.

Before PSM, the median OS (mOS 82 months) and median CSS (mCSS NA) in the pre-surgery group were longer than in the post-surgery group (mOS 21 months; mCSS 20 months; P<0.001 for both). After PSM, the mOS and mCSS in the pre-surgery group were longer than in the post-surgery group (mOS 45 vs. 26 months, P=0.011; mCSS 60 vs. 26 months, P=0.003). The subgroup analysis documented that patients with single tumor, liver resection, and American Joint Committee on Cancer (AJCC) stage I and II had longer mOS and mCSS if they received pre-surgery rather than post-surgery radiotherapy (all P<0.05). Multivariate regression analysis showed patients with post-surgery radiotherapy had a higher risk of mortality than patients with post-surgery radiotherapy.

HCC patients with single tumor, AJCC stage I and II, or with liver resection who received pre-surgery radiotherapy have better survival benefits than patients receiving post-surgery radiotherapy, particularly if internal radiotherapy was used.

HCC patients with single tumor, AJCC stage I and II, or with liver resection who received pre-surgery radiotherapy have better survival benefits than patients receiving post-surgery radiotherapy, particularly if internal radiotherapy was used.Psoriasis is widely accepted as a metabolic syndrome with significantly abnormal lipid metabolism and high level of blood lipids that induce a persistent low level of inflammatory condition in patients. T cell mediated immune response plays a critical role in the occurrence and persistence of psoriasis lesions. Hyperlipidemia and associated inflammatory reaction are believed to be the major risk factors for the onset and recurrence of psoriasis. Peroxisome proliferator activated receptor-gamma (PPAR-γ) is known to effectively regulate the blood lipid level and inhibit inflammatory reaction. In this study, we examined the efficacy of ozonated autohemotherapy (OAHT) treatment on psoriatic patients by evaluating the Psoriasis Area and Severity Index (PASI) score and blood lipid level. In addition, PPAR-γ expression level and the correlation of PASI scores or blood lipid level with the PPAR-γ expression were also assessed to determine the psoriasis-associate targets of OAHT. We found that OAHT significantly decreased patients' PASI scores and increased blood HDL-C level. Furthermore, we found that PPAR-γ expression in CD4+ T cells from psoriasis patients was significantly lower than healthy controls, and OAHT treatment increased the expression of PPAR-γ. In conclusion, OAHT attenuates the psoriatic severity in patients and increased blood HDL-C level, which may be associated with increased PPAR-γ expression. Our data suggests that OAHT is an effective treatment in psoriasis and deserves further evaluations in clinical applications.Age-related macular degeneration (AMD) is one of the leading causes of blindness among the elderly. However, the correlation between vascular change and cognitive impairment in AMD disease is still unknown. In our study, we investigate the blood flow change among different layers of the retina in the AMD eye and normal fellow eye of AMD patients and its influence with patients' cognition. Our study applies optical coherence tomography angiography (OCTA) to assess the blood flow of the retina in AMD patients and the healthy controls (HCs). Magnetic resonance imaging (MRI) and Montreal Cognitive Assessment (MoCA) were performed to evaluate the cognitive change of the individuals. VEGFR inhibitor The results showed that deep capillary plexus density, superficial capillary plexus density, retina thickness and retinal nerve fiber layer thickness deduction existed in both eyes of the AMD patient compared with the HCs. The reduced vessel density in the choroidal layer only existed in the AMD eye of the patients while the fellow eye of patients and HCs did not change much. Furthermore, the AMD patient got a lower MoCA score compared to the HCs. Our results illustrate that the fellow eye of the AMD patient underwent vessel density change, which may lead to the early stage of AMD. The lower score of the MoCA test in AMD patients refers to the cognitive impairment. These findings show the significance of taking actions to prevent the progress of AMD in the fellow eye, as well as paying more attention to the development of cognitive impairment of these patients.

PARK2, a Parkinson's disease-associated gene, functions as an E3 ubiquitin ligase regulating the degradation of proteins via ubiquitination. Our study was designed to explore its role in allergic asthma and the underlying mechanisms.

Airway epithelial cell line BEAS-2B was treated with house dust mite (HDM) to mimic allergic asthma in vitro. Lentivirus oePARK2 and siPARK2 were constructed to overexpress and knock down PARK2 expression, respectively. RT-qPCR, western blot, co-immunoprecipitation, and ubiquitination assay were performed to investigate the interaction between PARK2 and NLRP3. NLRP3 inflammasome activity, IL-1β and IL-18 secretion, pyroptosis, and epithelial barrier integrity were detected to explore the role of PARK2 in allergic asthma.

PARK2 expression was remarkably down-regulated in HDM-treated BEAS-2B cells. In BEAS-2B cells, NLRP3 protein was reduced by PARK2 overexpression and increased by PARK2 knockdown. Interestingly, PARK2 overexpression and knockdown didn't affect NLRP3 mRNA. Cose of inflammatory cytokines, pyroptosis, and barrier impairment in airway epithelial cells by ubiquitinating NLRP3.