The CYCLIN-A CYCA1;2/TAM Is Required for the Meiosis I to Meiosis II Transition and Cooperates with OSD1 for the Prophase to First Meiotic Division Transition

Meiosis halves the chromosome number because its two divisions follow a single round of DNA replication. This process involves two cell transitions, the transition from prophase to the first meiotic division (meiosis I) and the unique meiosis I to meiosis II transition. We show here that the A-type cyclin CYCA1;2/TAM plays a major role in both transitions in Arabidopsis. A series of tam mutants failed to enter meiosis II and thus produced diploid spores and functional diploid gametes. These diploid gametes had a recombined genotype produced through the single meiosis I division. In addition, by combining the tam-2 mutation with AtSpo11-1 and Atrec8, we obtained plants producing diploid gametes through a mitotic-like division that were genetically identical to their parents. Thus tam alleles displayed phenotypes very similar to that of the previously described osd1 mutant. Combining tam and osd1 mutations leads to a failure in the prophase to meiosis I transition during male meiosis and to the production of tetraploid spores and gametes. This suggests that TAM and OSD1 are involved in the control of both meiotic transitions

The Effect of Transcutaneous Electrical Acupoint Stimulation on Postoperative Catheter-Related Bladder Discomfort in Patients Undergoing Transurethral Resection of the Prostate

Background. Catheter-related bladder discomfort (CRBD), an extremely distressing complication secondary to an indwelling urinary catheterization, is frequently reported in patients with transurethral resection of the prostate (TURP), postoperatively. A prospective, randomized, controlled, double-blind study was designed to assess the efficacy of transcutaneous electrical acupoint stimulation (TEAS) as a treatment for CRBD in patients undergoing TURP. Methods. Seventy benign prostatic hyperplasia male patients undergoing TURP under general anesthesia requiring intraoperative urinary catheterization were enrolled for the trial. An experienced acupuncturist performed TEAS for 30 minutes before general anesthesia with acupoints RN7, RN6, RN5, RN4, and RN3 and bilateral BL32, BL33, and BL34. Mean arterial pressure (MAP), heart rate (HR), oxygen saturation (SPO2), body temperature (T), and blood samples were collected during the surgery. A series of assessments included the incidence and severity of CRBD, postoperative pain, nausea and vomiting, and physical and mental state measurements. Results. The incidence of CRBD was significantly lower in TEAS group than in control group at the time T5 [9(26%) vs. 28(80%), P<0.001], T9 [20(57%) vs. 28(80%), P=0.039], T11 [7(20%) vs. 31(89%), P<0.001], and T12 [4(11%) vs. 7(20%), P=0.003]. The severity of CRBD was significantly lower in TEAS group than in control group at the time T5 [0 vs. 10 (29%), P<0.001], T9 [2(6%) vs. 10(29%), P=0.011], and T11 [0 vs .9(26%), P=0.002]. The QoR-40 total score was higher in TEAS group at time T11 [191.7(4.4) vs. 189.1(4.3), P=0.007] and T12 [195.3(1.9) vs. 193.3(3.0), P<0.001]. The postoperative analgesia requirement was higher in control group [5.0(2.9) vs. 3.8(1.9), P=0.045]. Conclusions. TEAS could significantly prevent the incidence and severity of CRBD, reduce the postoperative analgesic requirement in the early postoperative period, and promote the quality of early recovery in patients undergoing TURP

A comparative transcriptomic analysis of uveal melanoma and normal uveal melanocyte.

BACKGROUND: Uveal melanoma is the most common primary intraocular tumor in adults in western countries. It is associated with very severe visual morbidity and may lead to distant metastases even after successful treatment of the primary tumor. In order to gain better insight into molecular mechanisms related to tumorigenesis and metastasis of uveal melanoma, we used next-generation sequencing technology (SOLiD, Life Technologies) to acquire global transcriptome alteration between posterior uveal melanoma cells and normal uveal melanocyte. RESULTS: From mRNAs of the cultured uveal melanoma cells and normal uveal melanocytes, we annotated more than 3.7 × 10(7) and 2.7 × 10(7) sequencing tags based on human Ensembl databases, respectively. For detailed analysis, we chose 5155 well-annotated genes mainly involved in the MAPK signaling pathway, cell cycle, cell adhesion junction, apoptosis, and P53 signaling pathways as well as melanogenesis. In an effort to confirm the authenticity of our sequencing results, we validated twenty-one identically differentially expressed genes by using quantitative real time PCR from cultured cell lines of other posterior uveal melanoma cells and normal uveal melanocytes. CONCLUSION: We have identified a large number of potentially interesting genes for biological investigation of uveal melanoma. The expression profiling also provides useful resources for other functional genomic and transcriptome studies. These 21 potential genes could discriminate between uveal melanoma cells and normal uveal melanocyte, which may be indicative of tumorigenesis process. Our results further suggest that high-throughput sequencing technology provides a powerful tool to study mechanisms of tumogenesis in the molecular level

Securin and not CDK1/cyclin B1 regulates sister chromatid disjunction during meiosis II in mouse eggs

Mammalian eggs remain arrested at metaphase of the second meiotic division (metII) for an indeterminate time before fertilization. During this period, which can last several hours, the continued attachment of sister chromatids is thought to be achieved by inhibition of the protease separase. Separase is known to be inhibited by binding either securin or Maturation (M-Phase)-Promoting Factor, a heterodimer of CDK1/cyclin B1. However, the relative contribution of securin and CDK/cyclin B1 to sister chromatid attachment during metII arrest has not been assessed. Although there are conditions in which either CDK1/cyclinB1 activity or securin can prevent sister chromatid disjunction, principally by overexpression of non-degradable cyclin B1 or securin, we find here that separase activity is primarily regulated by securin and not CDK1/cyclin B1. Thus the CDK1 inhibitor roscovitine and an antibody we designed to block the interaction of CDK1/cyclin B1 with separase, both failed to induce sister disjunction. In contrast, securin morpholino knockdown specifically induced loss of sister attachment, that could be restored by securin cRNA rescue. During metII arrest separase appears primarily regulated by securin binding, not CDK1/cyclin B1