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Background The purpose of this research was to investigate the relationship between Menopause Specific Quality of Life (MENQOL), Perceived Social Support (PSS) and factors associated with MENQOL among a group of Iranian Postmenopausal women in 2018. Methods In this cross-sectional study 410 of Postmenopausal Iranian women in Neyshabur are examined. QOL was assessed using MENQOL questionnaire, and social support was assessed through administration of a modified Sarason’s Social Support Questionnaire. The data were analyzed through conduction of a Pearson correlation coefficient and Linear regression analysis using SPSS software package 20. Results It was found that the average age of PMW was 53.92 ± 3.86 years. The total scores of the QOL ranged from 10 to 30, with a mean of 37.83 (SD = 12.9). Mean scores of Sexual, psychological, physical, and Vasomotor domain of QOL were 12.55 ± 6.96, 14.66 ± 2.20, 18.11 ± 1.85, 12.02 ± 4.93. Perceived social support was positively correlated with the overall QOL (r = 0.68; P ≤ 0.001). Moreover, perceived social support was associated with Vasomotor (r = .55, p ≤ .001), Psychosocial (r = .65, p ≤.001), Physical (r = .59, p ≤ .001), Sexual (r = .48, p ≤ .001) subscales of QOL. Conclusions The results of the current study showed a significant relationship between perceived social support and QOL in PMW. Further research is suggested to investigate other variables among PMW in Iran.Mapping the normal eye proteome in healthy persons is essential to unravel the molecular basis of diseases impacting visual health. The vitreous occupies a large portion of the human eye between the lens and the retina and plays a significant role in vitreoretinal diseases as well as maintaining clarity in the visual field, providing nutrition to the lens, and protecting the eye from mechanical shocks. It comprises four distinct anatomical regions, namely the vitreous core, vitreous cortex, vitreous base, and anterior hyaloid. Among these, the vitreous is attached to other substructures in the eye by the vitreous base, which is its strongest point of attachment. Alterations in vitreous substructures have been reported in several vitreoretinal disorders, including vitreomacular traction, vitreoretinopathies, and age-related macular degeneration. There has been limited knowledge on proteomics variations at a resolution of vitreous substructures, including the functionally and pathophysiologically significant vitreous base. We report here new findings on the proteome map of the vitreous base in normal healthy tissue. We employed a global, unbiased proteomic profiling approach resulting in the identification of 6511 proteins. Of these, 302 proteins were involved in metabolic processes essential for energy utilization. Moreover, we identified several structural and nutrient transport proteins. Notably, the identified proteome repertoire indicates that the vitreous base might possess additional physiological functions and may not be a passive structure. This study constitutes the most extensive catalog of vitreous base proteins to our knowledge and offers novel insights as a baseline for future studies on the pathobiology of various eye diseases. These data also invite us to consider a potentially more active functional role for the vitreous base in eye physiology and visual health.Solid tumors have complex biology and structure comprising cancer cells, stromal cells, and the extracellular matrix. While most therapeutics target the cancer cells, recent data suggest that cancer cell behavior and response to treatment are markedly influenced by the tumor microenvironment (TME). In particular, the cancer-associated fibroblasts (CAFs) are the most abundant stromal cells, and play a significant contextual role in shaping tumor initiation, progression, and metastasis. MSDC-0160 nmr CAFs have therefore emerged as part of the next-generation cancer drug design and discovery innovation strategy. We report here new findings on differential expression and prognostic significance of CAF markers in several cancers. We utilized two publicly available resources The Cancer Genomic Atlas and Gene Expression Profiling Interactive Analysis. We examined the expression of CAF markers, ACTA2, S100A4, platelet-derived growth factor receptor-beta [PDGFR-β], CD10, and fibroblast activation protein-alpha (FAP-α), in tumor tissues versus the adjacent normal tissues. We found that CAF markers were differentially expressed in various different tumors such as colon, breast, and esophageal cancers and melanoma. No CAF marker is expressed in the same pattern in all cancers, however. Importantly, we report that patients with colon adenocarcinoma and esophageal carcinoma expressing high FAP-α and CD10, respectively, had significantly shorter overall survival, compared with those with low levels of these CAF markers (p less then 0.05). We call for continued research on TME biology and clinical evaluation of the CAF markers ACTA2, S100A4, PDGFR-β, CD10, and FAP-α in relation to prognosis of solid cancers in large population samples. An effective cancer drug design and discovery roadmap in the 21st century ought to be broadly framed, and include molecular targets informed by both cancer cell and TME variations.The tumor stroma, a key component of the tumor microenvironment (TME), is a key determinant of response and resistance to cancer treatment. The stromal cells, extracellular matrix (ECM), and blood vessels influence cancer cell response to therapy and play key roles in tumor relapse and therapeutic outcomes. Of the stromal cells present in the TME, much attention has been given to cancer-associated fibroblasts (CAFs) as they are the most abundant and important in cancer initiation, progression, and therapy resistance. Besides releasing several factors, CAFs also synthesize the ECM, a key component of the tumor stroma. In this expert review, we examine the role of CAFs in the regulation of tumor cell behavior and reveal how CAF-derived factors and signaling influence tumor cell heterogeneity and development of novel strategies to combat cancer. Importantly, CAFs display both phenotypic and functional heterogeneity, with significant ramifications on CAF-directed therapies. Principal anti-cancer therapies targeting CAFs take the form of (1) CAFs’ ablation through use of immunotherapies, (2) re-education of CAFs to normalize the cells, (3) cellular therapies involving CAFs delivering drugs such as oncolytic adenoviruses, and (4) stromal depletion via targeting the ECM and its related signaling.