Abstract. The aim of our review was to identify the current information with regard to the pathogenesis and malignant transformation of adenomyosis. The current literature was reviewed by searching MEDLINE/PubMed, using the following keywords: adenomyosis, myometrium, stromal cells, malignant transformation, pathogenesis, etiology, genome-wide and microarray. Early signs of the development of adenomyosis are considered to be the penetration of stromal cells into the inner layer of the myometrium. Adenomyosis smooth muscle cells are developed, possibly, through a remodeling pathway via reactivation of coelomic epithelial cells as a result of estrogeninduced epithelial mesenchymal transition. Smooth muscle cell hyperplasia and hypertrophy are a reflection of a reaction of the surrounding tissue. The development of adenocarcinoma arising from adenomyosis is a relatively rare occurrence. In our literature review, to date, 44 cases of malignant tumors arising from adenomyosis have been documented. Studies reporting results of genetic abnormalities, epigenetic changes, monoclonal expansion, mutational analysis and the inactivation of specific tumor suppressor genes are very few in this field. In conclusion, adenomyosis can be a precursor of some carcinomas. The exact molecular mechanisms that lead to the malignant transformation are poorly understood.

Uterine sarcoma is a rare neoplasm, accounting for only 5% of uterine malignancies. The pathogenesis of uterine sarcoma remains largely unknown, although recent basic science and pre-clinical animal models have provided a better understanding of tumor biology. The aim of this study was to review the clinical features, imaging characteristics, genetic aberrations and therapeutic approaches in uterine sarcoma. This study reviewed the English-language literature on clinical and basic studies on uterine sarcoma. The common variants of uterine sarcoma are carcinosarcoma, leiomyosarcoma and endometrial stromal sarcoma (ESS). Genetic profiling efforts have identified amplification, overexpression and mutation, while the molecular mechanisms of tumorigenesis driven by these genomic and genetic aberrations have yet to be fully elucidated yet. Recent genome-wide studies have also identified complex chromosomal rearrangements as oncogenic mechanisms. The cell cycle regulators, p16 and p53, are frequently over-expressed and appear to be involved in key modifications of sarcomagenesis. Molecular-targeted therapy has now been evaluated in clinical trials for certain subtypes. In conclusion, aberrations of cell cycle control would be a critical step in the development of uterine sarcoma. This review has provided new areas of study targeting molecular and genetic pathways.

Nutrient starvation or inactivation of target of rapamycin complex 1 (TORC1) in budding yeast induces nucleophagy, a selective autophagy process that preferentially degrades nucleolar components. DNA, including ribosomal DNA (rDNA), is not degraded by nucleophagy, even though rDNA is embedded in the nucleolus. Here, we show that TORC1 inactivation promotes relocalization of nucleolar proteins and rDNA to different sites. Nucleolar proteins move to sites proximal to the nuclear-vacuolar junction (NVJ), where micronucleophagy (or piecemeal microautophagy of the nucleus) occurs, whereas rDNA dissociates from nucleolar proteins and moves to sites distal to NVJs. CLIP and cohibin, which tether rDNA to the inner nuclear membrane, were required for repositioning of nucleolar proteins and rDNA, as well as effective nucleophagic degradation of the nucleolar proteins. Furthermore, micronucleophagy itself was necessary for the repositioning of rDNA and nucleolar proteins. However, rDNA escaped from nucleophagic degradation in CLIP- or cohibin-deficient cells. This study reveals that rDNA-nucleolar protein separation is important for the nucleophagic degradation of nucleolar proteins.

No abstract

Target of rapamycin complex 1 (TORC1) phosphorylates autophagy-related Atg13 and represses autophagy under nutrient-rich conditions. However, when TORC1 becomes inactive upon nutrient depletion or treatment with the TORC1 inhibitor rapamycin, Atg13 dephosphorylation occurs rapidly, and autophagy is induced. At present, the phosphatases involved in Atg13 dephosphorylation remain unknown. Here, we show that two protein phosphatase 2A (PP2A) phosphatases, PP2A-Cdc55 and PP2A-Rts1, which are activated by inactivation of TORC1, are required for sufficient Atg13 dephosphorylation and autophagy induction after TORC1 inactivation in budding yeast. After rapamycin treatment, dephosphorylation of Atg13, activation of Atg1 kinase, pre-autophagosomal structure (PAS) formation and autophagy induction are all impaired in PP2A-deleted cells. Conversely, overexpression of non-phosphorylatable Atg13 suppressed defects in autophagy in PP2A mutant. This study revealed that the orchestrated action of PP2A antagonizes Atg13 phosphorylation and promotes autophagy after the inactivation of TORC1.

Abstract. The relationship between the percent phagocytosis of platelets by differentiated THP-1 cells was examined using flowcytometry and the peripheral platelet counts as well as platelet-associated IgG (PAIgG) in 36 patients with secondary dengue virus (DV) infections. The percent phagocytosis and the levels of PAIgG were significantly increased in these patients during the acute phase compared with the healthy volunteers. The increased percent phagocytosis and PAIgG found during the acute phase significantly decreased during the convalescent phase. An inverse correlation between platelet count and the percent phagocytosis ( P = 0.011) and the levels of PAIgG ( P = 0.041) was found among these patients during the acute phase. No correlation was found, however, between the percent phagocytosis and the levels of PAIgG. Our present data suggest that accelerated platelet phagocytosis occurs during the acute phase of secondary DV infections, and it is one of the mechanisms of thrombocytopenia in this disease.

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Mononuclear cordinatively unsaturated iron(II) complexes having a triazacyclononane ligand were developed as highly efficient and environmentally friendly catalysts for the atom-transfer radical polymerization (ATRP). These iron catalysts showed high performance in the well-controlled ATRP of styrene, methacrylates, and acrylates. The high reactivity of these catalysts led to well-controlled polymerization and block copolymerization even with lower catalyst concentrations.Keywords: atom transfer radical polymerization; environmentally friendly catalyst; iron; ligand design; polymerization Transition metal-catalyzed atom-transfer radical polymerization (ATRP) is a representative example of controlled radical polymerization (CRP), which is an important methodology to construct well-defined polymers on both laboratory and industrial scales. [1,2] In ideal cases, good catalysts for ATRP realize: 1) access to polymers with the desired molecular weight and narrow molecular weight distribution, 2) high reaction rate and durability to achieve complete monomer conversion in the construction of block co-polymers, 3) versatile applicability to several monomers, and 4) minimum residual heavy metal catalysts in the product. While the first three points are general requirements for CRP, the fourth point is a special problem for transition metal-catalyzed reactions. It is known that residual metals make the properties of the formed polymers worse and can be potentially harmful. Facile removal of the catalyst from the polymer has thus been investigated using biphasic systems, solid-supported catalysts, and solubility control of catalysts. [3][4][5][6][7][8] Recent results by Matyjaszewski and coworkers showed that reduction of the catalyst concentration to be a solution for this problem as well. [9]