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This seminal work examines the concurrence of childhood rebellion and conformity in Bengali literary texts (including adult texts), a pertinent yet unexplored area, making it a first of its kind. It is a study of the voice of child protagonists across children's and adult literature in Bengali vis-à-vis the institutions of family, the education system, and the nationalist movement in the ninenteenth and twentieth centuries.

Repeated daily dosing of rats with the occupational chemical 4-vinylcyclohexene diepoxide (VCD) depletes the ovary of primordial and primary follicles through an increase in the natural process of atresia. Additionally, in vitro exposure of Postnatal Day 4 (PND 4) rat ovaries to VCD causes similar follicular depletion. This study was designed to investigate survival signaling pathways that may be associated with VCD-induced ovotoxicity in small preantral follicles. Female Fischer 344 rats (PND 28) were dosed daily (80 mg/kg/day VCD i.p.; 12 days in vivo), and PND 4 ovaries were cultured (VCD 20 or 30 μM; 8 days in vitro). Microarray analysis identified a subset of 14 genes whose expression was increased or decreased by VCD in both experiments (i.e., via both exposure routes). Particularly, the analysis showed that relative to controls, VCD did not affect mRNA expression of growth and differentiation factor 9 (Gdf9), whereas there were decreases in mRNA encoding bone morphogenic protein receptor 1a (Bmpr1a) and Kit. To confirm findings from microarray, the genes Gdf9, Bmpr1a, and Kit were further examined. When growth factors associated with these pathways were added to ovarian cultures during VCD exposure, GDF9 and BMP4 had no effect on VCD-induced ovotoxicity; however, KITL attenuated this follicle loss. Additionally, there was a decrease in Kit and an increase in Kitl expression (mRNA and protein) following VCD exposure, relative to control. These results support that VCD compromises KIT/KITL signaling, which is critical for follicular survival in primordial and primary follicles.

Dibutyl phthalate (DBP) is present in consumer products and the coating of some oralmedications. Acetyl tributyl citrate (ATBC) has been proposed as an alternative to DBP because DBP causes endocrine disruption in animal models. Following ingestion, DBP is converted to its main metabolite mono-butyl phthalate (MBP) which has been detected in >90% of human follicular fluid samples. Previous studies show that DBP reduces the number of antral follicles present in the ovaries of mice. Thus, this study was designed to evaluate the effects of DBP, MBP, and ATBC on in vitro growth and viability of mouse ovarian antral follicles. Antral follicles were isolated from CD-1 females (PND32-37) and treated with vehicle, DBP, MBP, or ATBC (starting at 0.001 and up to 1000µg/ml for DBP; 24–72 h). Follicle diameter, ATP production, qPCR, and TUNEL were used to measure follicle growth, viability, cell cycle and apoptosis gene expression, and cell death-associated DNA fragmentation, respectively. While MBP did not cause toxicity, DBP exposure at ≥10µg/ml resulted in growth inhibition followed by cytoxicity at ≥500 µg/ml. ATBC increased the number of nongrowing follicles at 0.01 µg/ml and did not affect ATP production, but increased TUNEL positive area in treated follicles. Gene expression results suggest that cytotoxicity in DBP-treated follicles occurs via activation of cell cycle arrest prior to follicular death. These findings suggest that concentrations of DBP ≥10 µg/ml are detrimental to antral follicles and that ATBC should be examined further as it may disrupt antral follicle function at low concentrations. Summary Sentence DBP and ATBC exposures resulted in dose-specific follicle growth inhibition with high concentrations of DBP causing cytoxicity via activation of cyclin-dependent kinase inhibitors and subsequent apoptosis.

This seminal work examines the concurrence of childhood rebellion and conformity in Bengali literary texts (including adult texts), a pertinent yet unexplored area, making it a first of its kind. It is a study of the voice of child protagonists across children's and adult literature in Bengali vis-à-vis the institutions of family, the education system, and the nationalist movement in the ninenteenth and twentieth centuries.

Repeated daily dosing of rats with the occupational chemical 4-vinylcyclohexene diepoxide (VCD) depletes the ovary of primordial and primary follicles through an increase in the natural process of atresia. Additionally, in vitro exposure of Postnatal Day 4 (PND 4) rat ovaries to VCD causes similar follicular depletion. This study was designed to investigate survival signaling pathways that may be associated with VCD-induced ovotoxicity in small preantral follicles. Female Fischer 344 rats (PND 28) were dosed daily (80 mg/kg/day VCD i.p.; 12 days in vivo), and PND 4 ovaries were cultured (VCD 20 or 30 μM; 8 days in vitro). Microarray analysis identified a subset of 14 genes whose expression was increased or decreased by VCD in both experiments (i.e., via both exposure routes). Particularly, the analysis showed that relative to controls, VCD did not affect mRNA expression of growth and differentiation factor 9 (Gdf9), whereas there were decreases in mRNA encoding bone morphogenic protein receptor 1a (Bmpr1a) and Kit. To confirm findings from microarray, the genes Gdf9, Bmpr1a, and Kit were further examined. When growth factors associated with these pathways were added to ovarian cultures during VCD exposure, GDF9 and BMP4 had no effect on VCD-induced ovotoxicity; however, KITL attenuated this follicle loss. Additionally, there was a decrease in Kit and an increase in Kitl expression (mRNA and protein) following VCD exposure, relative to control. These results support that VCD compromises KIT/KITL signaling, which is critical for follicular survival in primordial and primary follicles.

4-Vinylcyclohexene diepoxide (VCD) is an occupational chemical that selectively destroys small pre-antral follicles in ovaries of rats and mice. VCD can be detoxified in the ovary to an inactive tetrol metabolite, 4-[1,2-dihydroxy] ethyl-1,2-dihydroxycyclohexane by microsomal epoxide hydrolase (EPHX1) or by conjugation with glutathione by glutathione-S-transferase (GST). This selective destruction is via acceleration of the natural process of atresia (apoptosis) and requires repeated daily dosing (in vivo) or continuous exposure (in vitro). In mice, a previous study determined that increased expression of ovarian Ephx1, Gstp and Gstm mRNA and protein caused by VCD preceded onset of VCD-induced ovotoxicity. Therefore, the present study was designed to investigate whether this effect would also be seen in rats. A post-natal day 4 (PND4) rat whole ovary culture system (enriched in targeted small pre-antral follicles) was employed to examine a timeline for VCD-induced ovotoxicity. Previously it was determined in cultured neonatal rat ovaries that VCD (30μM) exposure for 8 days results in loss (P<0.05) of small pre-antral ovarian follicles. PND4 Fischer 344 (F344) rat ovaries were incubated in control medium or medium containing VCD (30μM) for 2, 4, 6, or 8d (n=3; 10 ovaries per pool). Expression of mRNA encoding the detoxification enzymes EPHX1, GSTP and GSTM were examined using Real-Time PCR at each timepoint. Additionally, western blotting was employed to evaluate changes in EPHX1, GSTP and GSTM protein levels after 4 and 8 days of VCD exposure. There was no difference in Ephx1, Gstp or Gstm mRNA levels between control and VCD-exposed ovaries on day 2. Relative to control, VCD exposure resulted in an increase (P<0.05) in Ephx1 mRNA by 0.61-fold on day 4 and in Gstp mRNA by 0.9-, 1.2- and 1-fold on days 4, 6 and 8, respectively. In contrast, VCD exposure did not have an effect (P>0.05) on Gstm mRNA expression at any timepoint. No changes in protein levels of the three enzymes occurred after 4 days of VCD exposure. However, on day 8, relative to controls, protein for EPHX1, GSTP and GSTM increased (P<0.05) by 17%, 27% and 10%, respectively, in response to VCD. These findings demonstrate that, as with mice, increased expression of ovarian detoxification enzymes in response to VCD precedes VCD-induced ovotoxicity in rats. This suggests a model in which up-regulation of these pathways by xenobiotic (VCD) exposure affords initial protection by detoxification of VCD but eventually the ovary becomes overwhelmed by repeated exposure, resulting in ovotoxicity. (ES09246 and Center grant 06694).

By the ruins of terror's triumph children build their castles.

Schools seem to me one of the most anti-democratic, most authoritarian, most dangerous and most destructive institutions of modern society.