Incidental finding of a Sertoli-Leydig cell tumor in a postmenopausal woman with complex endometrial hyperplasia

Sertoli-Leydig cell tumors (SLCTs) arise from the non-germ cell component of the ovary and typically present in young women with evidence of hyperandrogenism such as precocious puberty, amenorrhea, hirsutism and virilization. It is very rare accounting for less than 0.2% of all ovarian tumors, and because of the rarity, no standardized treatment approach has reached a consensus. The prognosis is generally good with complete reversion of symptoms after surgery, although some cases have been reported to be malignant. Recently the need for DICER1 mutations testing in paediatric patients has been emphasized for the surveillance of possible synchronous tumors and affected family members. Authors present here a case of Sertoli-Leydig cell tumor incidentally found while performing a hysterectomy with bilateral salpingo-oophorectomy in a postmenopausal woman with endometrial hyperplasia that caused intractable vaginal bleeding

Autonomous control of terminal erythropoiesis via physical interactions among erythroid cells

AbstractIn vitro erythropoiesis has been studied extensively for its application in the manufacture of transfusable erythrocytes. Unfortunately, culture conditions have not been as effective as in vivo growth conditions, where bone marrow macrophages are known to be a key regulator of erythropoiesis. This study focused on the fact that some erythroblasts are detached from macrophages and only contact other erythroblasts. We hypothesized that additional factors regulate erythroblasts, likely through either physical contact or secreted factors. To further elucidate these critical factors, human erythroblasts derived from cord blood were cultured at high density to mimic marrow conditions. This growth condition resulted in a significantly increased erythroid enucleation rate and viability. We found several novel contact-related signals in erythroblasts: intercellular adhesion molecule-4 (ICAM-4) and deleted in liver cancer-1 (DLC-1). DLC-1, a Rho-GTPase-activating protein, has not previously been reported in erythroid cells, but its interaction with ICAM-4 was demonstrated here. We further confirmed the presence of a secreted form of human ICAM-4 for the first time. When soluble ICAM-4 was added to media, cell viability and enucleation increased with decreased nuclear dysplasia, suggesting that ICAM-4 is a key factor in contact between cells. These results highlight potential new mechanisms for autonomous control of erythropoiesis. The application of these procedures to erythrocyte manufacturing could enhance in vitro erythrocyte production for clinical use

RBFOX3 regulates Claudin-1 expression in human lung tissue via attenuation of proteasomal degradation

RBFOX3, a nuclear RNA-binding protein, is well known as a regulator of alternative pre-mRNA splicing during neuronal development. However, other functions of RBFOX3 are poorly understood. Here, we investigated the function of RBFOX3 in the cytoplasm with respect to regulation of Claudin-1 expression. In human lung tissue, Claudin-1 is higher in RBFOX3-positive cells than in RBFOX3-negative cells. Immunostaining and mRNA quantification revealed that protein levels, but not mRNA levels, of Claudin-1 are increased by RBFOX3. In addition, cycloheximide treatment of human lung cancer cells revealed that RB-FOX3 increases the stability of Claudin-1 through attenuation of its ubiquitination. Our study provides insights into the molecular mechanisms by which RBFOX3 regulates Claudin-1 expression in human lung tissue

The effect of a culturally tailored web-based physical activity promotion program on Asian American midlife women’s depressive symptoms

The benefits of physical activities on depressive symptoms have increasingly been reported in the literature, but the effect through which a Web-based physical activity promotion program alleviates depressive symptoms is not clearly known, especially among ethnic minority midlife women. The purpose of this pilot randomized control study is to examine the preliminary efficacy of the Web-based physical activity promotion program in enhancing the depressive symptoms of Asian American midlife women through increasing physical activity. This study adopted a randomized repeated measures pretest/posttest control group design. This study consisted of two groups of research participants: 18 in an intervention group and 15 in a control group. By using multiple instruments, the participants’ background and health status, depressive symptom experience, and physical activity experience were measured at three time points (pre-, post 1-month, and post 3-months). The data were analyzed using a modified intent-to-treat linear mixed-model growth curve analysis. After controlling for covariates, random intercept, and random slope, only discrimination stress showed statistical significances in the group effect (0.18, p = .08 for control) and time effect (-0.04, p = .04), but not in the group × time effect (p = .51). The active living habits scores showed statistical significances in the group effect (0.82, p \u3c 0.01 for control), time effect (0.29, p \u3c 0.01), and group × time effect (-0.31, p = 0.03 for control). Findings support the significant effect of the Web-based physical activity promotion program on the women’s discrimination stress and active living habits

Control of mammalian G protein signaling by N-terminal acetylation and the N-end rule pathway

Rgs2, a regulator of G proteins, lowers blood pressure by decreasing signaling through Gαq. Human patients expressing Met-Leu-Rgs2 (ML-Rgs2) or Met-Arg-Rgs2 (MR-Rgs2) are hypertensive relative to people expressing wild-type Met-Gln-Rgs2 (MQ-Rgs2). We found that wild-type MQ-Rgs2 and its mutant, MR-Rgs2, were destroyed by the Ac/N-end rule pathway, which recognizes Nα-terminally acetylated (Nt-acetylated) proteins. The shortest-lived mutant, ML-Rgs2, was targeted by both the Ac/N-end rule and Arg/N-end rule pathways. The latter pathway recognizes unacetylated N-terminal residues. Thus, the Nt-acetylated Ac-MX-Rgs2 (X = Arg, Gln, Leu) proteins are specific substrates of the mammalian Ac/N-end rule pathway. Furthermore, the Ac/N-degron of Ac-MQ-Rgs2 was conditional, and Teb4, an endoplasmic reticulum (ER) membrane-embedded ubiquitin ligase, was able to regulate G protein signaling by targeting Ac-MX-Rgs2 proteins for degradation through their N^α-terminal acetyl group