RESUMEN
BACKGROUND: A gastric stromal tumor (GST) is a mesenchymal tumor that occurs in the gastrointestinal tract; its biological characteristics are highly complex. Clinically, the severity of a GST is often evaluated by factors such as risk classification, tumor size, and mitotic figures. However, these indicators are not very accurate. Even patients classified as low risk are also at risk of metastasis and recurrence. Therefore, more accurate and objective clinical biological behavior evaluations are urgently needed. AIM: To determine the relationship between Ki-67 and CD44 expression in GSTs and microvessel formation and prognosis. METHODS: Eighty-six GST tissue specimens from our hospital were selected for this study. The immunohistochemical staining technique was used to detect Ki-67, CD44, and microvessel density (MVD) in the collected samples to analyze the different risk grades and mitotic figures. In addition, this approach was used to determine the differences in the expression of Ki-67 and CD44 in GST tissues with varying lesion diameters. RESULTS: In GSTs with positive expression of the Ki-67 protein, the proportions of patients with medium-to-high risk and more than five mitotic counts were 24.07% and 38.89%, respectively. In GSTs with positive expression of the CD44 protein, the proportions of patients with medium-to-high risk and more than five mitotic counts were 23.73% and 38.98%, respectively. In GSTs with negative expression of the Ki-67 protein, these values were relatively high (3.70% and 11.11%, respectively). The MVD in GSTs with positive and negative expression of the CD44 protein was 15.92 ± 2.94 and 13.86 ± 2.98/Hp, respectively; the difference between the two groups was significant (P < 0.05). CONCLUSION: Ki-67 and CD44 expression in GSTs is correlated with the grade of tumor risk and mitotic figures. CD44 expression is correlated with microvessel formation in tumor tissues.
RESUMEN
Ovarian hormone deprivation is associated with mood disorders, such as depression, and estradiol therapy is significantly more effective than placebos in treating major depression associated with menopause onset. However, the effect of estradiol on neuronal plasticity and its mechanisms remain to be further elucidated. In this study, behavioral assessments were used to examine the antidepressant effect of estradiol in ovariectomized (OVX) B6.Cg-TgN (Thy-YFP-H)-2Jrs transgenic mice on chronic restraint stress (CRS)-induced dendrite and dendritic spine loss; Yellow fluorescent protein (YFP) is characteristically expressed in excitatory neurons in transgenic mice, and its three-dimensional images were used to evaluate the effect of estradiol on the density of different types of dendritic spines. Quantification and distribution of cofilin1 and p-cofilin1 were determined by qPCR, Western blots, and immunohistochemistry, respectively. The results revealed that treatment with estradiol or clomipramine significantly improved depression-like behaviors. Estradiol treatment also significantly upregulated the dendritic density in all areas examined and increased the density of filopodia-type, thin-type and mushroom-type spines in the hippocampal CA1 and elevated the thin-type and mushroom-type spine density in the PFC. Consistent with these changes, estradiol treatment significantly increased the density of p-cofilin1 immunopositive dendritic spines. Thus, these data reveal a possible estradiol antidepressant mechanism, in that estradiol promoted the phosphorylation of cofilin1 and reduced the loss of dendrites and dendritic spines, which of these dendritic spines include not only immature spines such as filopodia-type, but also mature spines such as mushroom-type, and attenuated the depression-like behavior.
