Hormonal, follicular and endometrial dynamics in letrozole-treated versus natural cycles in patients undergoing controlled ovarian stimulation

Background

To investigate the effect of pelvic floor Neuromuscular Electrical Stimulation (NMES) Therapy in improving endometrial thickness in women with thin endometrium.

Methods

41 patients undergoing assisted reproduction with a thin endometrium (less than or equal to7 mm) were recruited and advised to go for a pelvic floor NMES in frozen-thawed embryo transfer cycle. PHENIX Neuromuscular Electrical Stimulation Therapy System was used according to the manufacturer's recommended protocol for 20 to 30 minutes of intermittent vaginal electrical stimulation on the treatment days.

Results

A total of 20 and 21 were included in the NMES and non-NMES groups respectively. 12 out of 20 (60%) patients developed endometrial thickness equal to or more than 8 mm after the NMES therapy, which was the primary outcome. The mean thickness of endometrium before and after was respectively 5.60 mm (0.82 mm) and 7.93 mm (1.42 mm) in the therapy group versus 5.50 mm (1.00) and 6.78 mm (0.47) in the control group; the difference was statistically significant (P = 0.002). There was higher pregnancy rate in the NMES group (42% versus 35%) but the difference was not statistically significant.

Conclusion

Neuromuscular Electrical stimulation therapy may be effective for the patients with a thin endometrium. Further studies are needed to investigate its effectiveness.     

Morphological plasticity promotes resistance to phagocyte killing of uropathogenic Escherichia coli

Uropathogenic Escherichia coli proceed through a complex intracellular developmental pathway that includes multiple morphological changes. During intracellular growth within Toll-like receptor 4-activated superficial bladder epithelial cells, a subpopulation of uropathogenic E. coli initiates SulA-mediated filamentation. In this study, we directly investigated the role of bacterial morphology in the survival of uropathogenic E. coli from killing by phagocytes. We initially determined that both polymorphonuclear neutrophils and macrophages are recruited to murine bladder epithelium at times coincident with extracellular bacillary and filamentous uropathogenic E. coli. We further determined that bacillary uropathogenic E. coli were preferentially destroyed when mixed uropathogenic E. coli populations were challenged with cultured murine macrophages in vitro. Consistent with studies using elliptical-shaped polymers, the initial point of contact between the phagocyte and filamentous uropathogenic E. coli influenced the efficacy of internalization. These findings demonstrate that filamentous morphology provides a selective advantage for uropathogenic E. coli evasion of killing by phagocytes and defines a mechanism for the essential role for SulA during bacterial cystitis. Thus, morphological plasticity can be viewed as a distinct class of mechanism used by bacterial pathogens to subvert host immunity.     

Mapping of genes associated with leptine content of tetraploid potato

High content of leptine glycoalkaloids present in Solanum chacoense has been associated with genetic resistance to Colorado potato beetle (Leptinotarsa decemlineata [Say]). From an unrecorded accession of S. chacoense, the North Dakota State University breeding program has developed a tetraploid genotype, ND4382-19, that contains foliar leptines. In this study, using a segregating population, ND5873 (ND4382-19 × Chipeta), and GC-MS to analyze foliar content of alkaloids, two loci, involved in the synthesis of leptines were identified. They segregated as two complementary epistatic genes that allowed the synthesis of leptinidine (Lep) and acetyl-leptinidine (AL), respectively. Partial AFLP maps for both parents were developed using 97 individuals from population ND5873. The total lengths mapped for ND4382-19 and Chipeta were 1,883 and 1,021 cM, respectively. The marker for Lep was located at the distal end of simplex-coupling linkage group R37. Expansion of the initial mapping population and analysis of Lep-containing individuals allowed us to identify the linkage group (R35) that enabled synthesis of AL. By the use of simple sequence repeat markers, linkage group R37 (Lep) and linkage group R35 (AL) have been identified as homologs of chromosomes II and VIII, respectively.H. Casper (deceased)     

Carbon isotope fractionation during acetoclastic methanogenesis by Methanosaeta concilii in culture and a lake sediment

The isotope enrichment factors (epsilon) in Methanosaeta concilii and in a lake sediment, where acetate was consumed only by Methanosaeta spp., were clearly less negative than the epsilon usually observed for Methanosarcina spp. The fraction of methane produced from acetate in the sediment, as determined by using stable isotope signatures, was 10 to 15% lower when the appropriate epsilon of Methanosaeta spp. was used.     

Heat-shock protein 27 is a major methylglyoxal-modified protein in endothelial cells

In endothelial cells cultured under high glucose conditions, methylglyoxal is the major intracellular precursor in the formation of advanced glycation endproducts. We found that endothelial cells incubated with 30 mM d-glucose produced approximately 2-fold higher levels of methylglyoxal but not 3-deoxyglucosone and glyoxal, as compared to 5 mM d-glucose. Under hyperglycaemic conditions, the methylglyoxal-arginine adduct argpyrimidine as detected with a specific antibody, but not N(e)-(carboxymethyl)lysine and N(e)-(carboxyethyl)lysine, was significantly elevated. The glyoxylase I inhibitor HCCG and the PPARgamma ligand troglitazone also increased argpyrimidine levels. Increased levels of argpyrimidine by glucose, HCCG and troglitazone are accompanied by a decrease in proliferation of endothelial cells. A 27 kDa protein was detected as a major argpyrimidine-modified protein. With in-gel digestion and mass spectrometric analysis, we identified this major protein as heat-shock protein 27 (Hsp27). This argpyrimidine modification of Hsp27 may contribute to changes in endothelial cell function associated to diabetes.     

Sites of genetic instability in mitosis and cancer

Certain chromosomal regions called common fragile sites are prone to difficulty during replication. Many tumors have been shown to contain alterations at fragile sites. Several models have been proposed to explain why these sites are unstable. Here we describe work to investigate models of fragile site instability using a yeast artificial chromosome carrying human DNA from a common fragile site region. In addition, we describe a yeast system to investigate whether repair of breaks at a naturally occurring fragile site in yeast, FS2, involves mitotic recombination between homologous chromosomes, leading to loss of heterozygosity (LOH). Our initial evidence is that repair of yeast fragile site breaks does lead to LOH, suggesting that human fragile site breaks may similarly contribute to LOH in cancer. This work is focused on gaining understanding that may enable us to predict and prevent the situations and environments that promote genetic changes that contribute to tumor progression.