Suchergebnisse

Menopause is the lack of menstrual cycle for at least six months. Due to hormonal changes, the alternation of lipid profile as a risk factor related to heart disease increases during menopause . One hundred twenty Iraqi women, aged between 40-65 years, were selected for this study. They were divided into two groups: 60 premenopausal and 60 postmenopausal women, and then each group was further divided into two subgroups: 20 women with hyperthyroidism and 20 with hypothyroidism, as well as 20 healthy women as control group. Blood samples were collected to estimate hormonal parameter by enzyme linked immunosorbent assay (ELISA) and lipid profile using enzymatic technique. The results showed that alterations in lipid profile included decrease in the cholesterol levels, triglyceride, LDL and VLDL. Whereas HDL increased in hyperthyroidism as compared to hypothyroidism and control groups in premenopausal women. In women with postmenopause, alterations of lipid profiles included a decrease in the cholesterol level, triglyceride, high density lipoprotein (HDL), very low density lipoprotein (VLDL) except an increase in low density lipoprotein (LDL) in hyperthyroidism as compared to hypothyroidism and control groups. Also, the level of lipid profiles increased in hypothyroidism rather than hyperthyroidism both in pre and postmenopause. According to this study, the conclusion was reached that there was an increase in the lipid profile level in postmenopausal women than premenopausal women with hypothyroidism when compared to hyperthyroidism.

Postmenopausal women with hypertension may be linked with cardiovascular risk factors like visceral obesity. Changes in antioxidant levels and lipid profile are considered risk factors concerning heart disease that arises during postmenopausal. Ninety Iraqi women aged between 53-70 years, sixty women with postmenopausal hypertension, and thirty healthy postmenopausal women were selected as control for this study. Blood samples were taken to measure some antioxidants through enzyme-linked immune sorbent assay (ELISA) and lipid profile by enzymatic technique. Results showed that the mean of catalase levels was significantly lower in patients (257.62±6.99) compared towith the control group (499.30±13.08). Glutathione results were significantly lower in patients (10.99±0.26) compared with the healthy control (39.32±2.03). Cholesterol levels were significantly higher in patients (236.09±1.91), while lower levels were observed in the control group (172.67±4.92). Triglyceride levels were significantly higher both in patients (182.10±2.68) and the healthy group (145.92±5.85). HDL levels were significantly lower in patients (29.91±0.37) compared with the control group (43.02±1.38). VLDL levels were significantly higher in patients (36.49±0.54) compared with the control (29.16±1.17). LDL levels were significantly higher in patients (169.74±2.20) than in the control group (1 00.48±5.41). It can be concluded from the results that antioxidant levels decreased in postmenopausal women than in the control group. Elevation in lipid profile of postmenopausal women was observed compared with the control group.

Abstract
Pancreatic ductal adenocarcinoma (PDAC) is associated with a vast stromal reaction that arises mainly from cancer-associated fibroblasts (CAFs) and promotes both immune escape and tumor growth. Here, we used a mouse model with deletion of the activin A receptor ALK4 in the context of the KrasG12D mutation, which strongly drives collagen deposition that leads to tissue stiffness. By ligand–receptor analysis of single-cell RNA-sequencing data, we identified that, in stiff conditions, neoplastic ductal cells instructed CAFs through sustained platelet-derived growth factor (PDGF) signaling. Tumor-associated tissue rigidity resulted in the emergence of stiffness-induced CAFs (siCAFs) in vitro and in vivo. Similar results were confirmed in human data. siCAFs were able to strongly inhibit CD8+ T-cell responses in vitro and in vivo, promoting local immunosuppression. More importantly, targeting PDGF signaling led to diminished siCAF and reduced tumor growth. Our data show for the first time that early paracrine signaling leads to profound changes in tissue mechanics, impacting immune responses and tumor progression. Our study highlights that PDGF ligand neutralization can normalize the tissue architecture independent of the genetic background, indicating that finely tuned stromal therapy may open new therapeutic avenues in pancreatic cancer.