MicroRNA-181 Functions as an Antioncogene and Mediates NF-κB Pathway by Targeting RTKN2 in Ovarian Cancers.

MicroRNA (miR)-181 has been reported to participate in carcinogenesis and tumor progression in several malignant cancers, but its expression and biological functions in ovarian cancer have remained largely unclarified. Here, we first measured miR-181 expression in clinical ovarian cancers and found the expression levels of miR-181 were significantly lower in ovarian cancer tissues than that in adjacent tissues. Next, we screened and identified a direct miR-181 target, Rhotekin2 (RTKN2). A correlation between miR-181 and RTKN2 expression was also confirmed in clinical samples of ovarian cancers. Upregulation of miR-181 would specifically and markedly suppress RTKN2 expression. The miR-181-overexpressing subclones showed significant cell growth inhibition by cell apoptosis induction and significant impairment of cell invasiveness in SKOV3 and HO8910 ovarian cancer cells. To identify the mechanisms, we investigated the NF-κB pathway and found that nuclear factor-kappa B (NF-κB), B-cell lymphoma-2 (Bcl-2), and vascular endothelial growth factor (VEGF) were suppressed, whereas IκBα was promoted in miR-181-overexpressing cells. These findings indicate that miR-181 functions as a tumor suppressor and plays a substantial role in inhibiting the tumorigenesis and reversing the metastasis of ovarian cancer through RTKN2-NF-κB signaling pathway in vitro. Taken together, we believe that miR-181 may be a promising therapeutic target for treating malignant ovarian cancers.

Cannabidiol administration reduces sublesional cancellous bone loss in rats with severe spinal cord injury.

Patients with spinal cord injury (SCI) undergo severe loss of bone mineral below the level of lesion, and data on available treatment options after SCI is scarce. The aim of this work was to investigate the therapeutic effect of cannabidiol (CBD), a non-psychoactive cannabis, on sublesional bone loss in a rat model of SCI. The adult male rats were exposed to surgical transection of the cord and treated with CBD for consecutive 14 days. It was found that CBD treatment elevated the serum levels of osteocalcin, reduced the serum levels of collagen type I cross-linked C-telopeptide, and enhanced bone mineral density of tibiae and femurs. Treatment of SCI rats with CBD enhanced bone volume, trabecular thickness, and trabecular number, and reduced trabecular separation in proximal tibiae, and increased ultimate compressive load, stiffness, and energy to max force of femoral diaphysis. Treatment of SCI rats with CBD upregulated mRNA expression of alkaline phosphatase and osteoprotegerin and downregulated mRNA expression of receptor activator of NF-κB ligand and tartrate-resistant acid phosphatase in femurs. Furthermore, treatment of SCI rats with CBD enhanced mRNA expression of wnt3a, Lrp5 and ctnnb1 in femurs. In conclusion, CBD administration attenuated SCI-induced sublesional cancellous bone loss.

Bisphenol A in combination with TNF-alpha selectively induces Th2 cell-promoting dendritic cells in vitro with an estrogen-like activity.

Bisphenol A (BPA) is a monomer used in manufacturing a wide range of chemical products, including epoxy resins and polycarbonate. BPA, an important endocrine disrupting chemical that exerts estrogen-like activities, is detectable at nanomolar levels in human serum worldwide. The pregnancy associated doses of 17beta-estradiol (E2) plus tumor-necrosis factor-alpha (TNF-alpha) induce distorted maturation of human dendritic cells (DCs) that result in an increased capacity to induce T helper (Th) 2 responses. The current study demonstrated that the presence of BPA during DC maturation influences the function of human DCs, thereby polarizing the subsequent Th response. In the presence of TNF-alpha, BPA treatment enhanced the expression of CC chemokine ligand 1 (CCL1) in DCs. In addition, DCs exposed to BPA/TNF-alpha produced higher levels of IL-10 relative to those of IL-12p70 on CD40 ligation, and preferentially induced Th2 deviation. BPA exerts the same effect with E2 at the same dose (0.01-0.1 microM) with regard to DC-mediated Th2 polarization. These findings imply that DCs exposed to BPA will provide one of the initial signals driving the development and perpetuation of Th2-dominated immune response in allergic reactions.

[Comparison of platelet activators used in slide platelet aggregation test].

The study was purposed to explore the suitable platelet activators to be used in slide platelet aggregation test. Experiments were as follows: (1) to detect the intensity and time in 15 healthy donors' platelet aggregation tests induced by cationic propyl gallate (c-PG) and the usual platelet activators: ADP, collagen, epinephrine, arachidonic acid and ristocentin, respectively; (2) to detect the time in platelet aggregation tests of 15 healthy donors induced by c-PG and the above usual platelet activators respectively after addition of PGI2, cAMP or EDTA; (3) to detect the time in 15 healthy donors' platelet aggregation tests induced by c-PG after addition of heparin; (4) to detect the intensity and time of platelet aggregation induced by c-PG at the platelet count of (240-15) x 10(9)/L, (5) to detect the time of platelet aggregation induced by c-PG in eight patients each of whom had taken 100 mg aspirin per day for five days. The results showed that (1) c-PG reduced the strongest intensity of platelet aggregation and the time taken was appropriate, (2) c-PG was the most effective activator to reveal the inhibitive effect on platelet by PGI2, cAMP or EDTA, (3) 0.5 - 3 U/ml heparin did not significantly change the platelet aggregation induced by c-PG, (4) 15 healthy donors' platelet aggregation induced by c-PG displayed clearly on the slide until the platelet count below 30 x 10(9)/L, (5) The platelet aggregation time induced by c-PG was significantly prolonged in eight patients who had taken aspirin. In conclusion, compared to the usual platelet activators, c-PG has remarkable potential advantages when used in slide platelet aggregation test.

[Effects of leukocyte elimination before storage on quality of red blood cell concentration].

The objective of this study was to explore the possible effects of leukocyte elimination by filteration before storage on the quality of red blood cell concentrations (RCC) that prepared through two procedures. Eight units of red blood cell concentrations derived from whole blood after plasma separated (RCC1) and eight units of red blood cell concentrations derived from whole blood after platelet-rich plasma separated (RCC2) were divided randomly into filtered group and control group respectively. The RCC of filtered group were filtered by leukocyte deplete filter before storage. The control group didn't have any other treatments. These two groups were stored for five weeks at 4 degrees C according to AABB standard. Mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC) and plasma concentration of K(+) and lactate dehydrogenase (LDH), free hemoglobin (FHb), adenosine triphosphate (ATP) of red blood cell of all RCC were evaluated weekly, and bacteria contamination of all RCC was also detected after five weeks of storage. The results showed that there was no difference of MCV, MCH and MCHC and ATP level of red blood cell in all RCC of two groups, the ATP of red blood cell was lower than the control group on week 4 and 5. The average concentration of K(+) of the filtered group was less than the control group. The differences are significant except that of RCC1 stored till the third week. The plasma LDH concentration of filtered group was less than the control group, and the differences were exacerbate during the storing time prolonged. FHb release in the filtered group of RCC2 was significant less than that of control, but no significant difference was found between the two groups of RCC1. It was concluded that leukocyte elimination by filter before storage could be benefit to RCC preservation.