Ectoplasmic specialization: a friend or a foe of spermatogenesis?

The ectoplasmic specialization (ES) is a testis-specific, actin-based hybrid anchoring and tight junction. It is confined to the interface between Sertoli cells at the blood-testis barrier, known as the basal ES, as well as between Sertoli cells and developing spermatids designated the apical ES. The ES shares features of adherens junctions, tight junctions and focal contacts. By adopting the best features of each junction type, this hybrid nature of ES facilitates the extensive junction-restructuring events in the seminiferous epithelium during spermatogenesis. For instance, the alpha6beta1-integrin-laminin 333 complex, which is usually limited to the cell-matrix interface in other epithelia to facilitate cell movement, is a putative apical ES constituent. Furthermore, JAM-C and CAR, two tight junction integral membrane proteins, are also components of apical ES involving in spermatid orientation. We discuss herein the mechanisms that maintain the cross-talk between ES and blood-testis barrier to facilitate cell movement and orientation in the seminiferous epithelium.     

Clear cell carcinoma of the ovary diagnosed in ascitic fluid. A case report

BACKGROUND: Clear cell carcinoma of the ovary (CCC) is a rare variety of ovarian cancer. CASE: A case of CCC in a 49-year-old woman was diagnosed in asciticfluid on thin-layer preparations. Peritoneal fluid cytology revealed papillary clusters of cells with clear cytoplasm and extracellular hyaline material generally without neoplastic cells. The tumor was excised, and the histologic sections confirmed the cytologic diagnosis. CONCLUSION: CCC has a distinctive cytomorphologic appearance, and the entity may be diagnosed on ascitic fluid cytology.     

A hypocaloric diet enriched in legumes specifically mitigates lipid peroxidation in obese subjects

Legume intake could specifically protect against lipid peroxidation in addition to the effects associated to weight loss when included in hypocaloric diets. Thus, 30 obese subjects (age: 36 +/- 8 years and BMI: 32.0 +/- 5.3 kg/m(2)) were nutritionally treated by a 8-week energy restriction ( - 30% energy expenditure) with a legume enriched diet (4 days/week servings, [image omitted] ) or without legumes (control diet (CD), [image omitted] ). Body weight, circulating cholesterol, oxidized LDL (ox-LDL), malondialdehyde (MDA) and urinary 8-isoprostane F(2alpha) (8-iso-PGF(2alpha)) were measured at baseline and at endpoint. After the nutritional intervention, all obese subjects lost weight, specially those individuals who followed the legumes-enriched diet as compared to the CD ( - 7.7 +/- 3 vs. - 5.3 +/- 2.7%; p = 0.023), which was accompanied by marked decreases in total cholesterol levels (p < 0.001) and statistically significant diet-related reductions on plasma ox-LDL, plasma MDA and urinary 8-iso-PGF(2alpha) output. Therefore, a balanced diet with moderate caloric restriction including 4 day/week legume servings empowered the oxidative stress improvement related to weight loss through a reduction in lipid peroxidation as compared to a control hypocaloric diet.     

ZO-1 is required for protein kinase C gamma-driven disassembly of connexin 43

We have previously reported that protein kinase C gamma (PKC-gamma) is activated by phorbol-12-myristate-13-acetate (TPA) and that this causes PKC-gamma translocation to membranes and phosphorylation of the gap junction protein, connexin 43 (Cx43). This phosphorylation, on S368 of Cx43, causes disassembly of Cx43 out of cell junctional plaques resulting in the inhibition of dye transfer. The purpose of this study is to identify the specific role of zonula occludens protein-1 (ZO-1), a tight junction protein with recently established effects on gap junctions, in this PKC-gamma-driven Cx43 disassembly. For this purpose, ZO-1 levels in lens epithelial cells in culture were decreased by up to 70% using specific siRNA. The down-regulation of ZO-1 caused a stable interaction of PKC-gamma with Cx43 even without normal enzyme activation by TPA. However, after TPA activation of the PKC-gamma, the Cx43 did not disassemble out of plaques even though the PKC-gamma enzyme was activated and the Cx43 was phosphorylated on S368. Confocal microscopy demonstrated that the siRNA treatment caused a loss of ZO-1 from borders of large junctional Cx43 cell-to-cell plaques and resulted in the accumulation of Cx43 aggregates inside of cells. Loss of the specific "plaquetosome" arrangement of large Cx43 plaques surrounded by ZO-1 was accompanied by a complete loss of functional dye transfer. These results suggest that ZO-1 is required for Cx43 control, both for dye transfer, and, for the PKC-gamma-driven disassembly response.     

Regulation of the Glycine Transporter GLYT1 by microRNAs

Neurochemical Research - The glycine transporter GLYT1 participates in inhibitory and excitatory neurotransmission by controlling the reuptake of this neuroactive substance from synapses. Over the...