Corporate Social Responsibility (CSR) Dalam Presfektif Hukum Islam

Issues related to Corporate Social Responsibility (CSR), it is no stranger to the world of law and the company\u27s preformance, when CSR is associated with Islamic law, if in fact Islam has been set in this regard? So that the activities undertaken by these companies is worth worship for businesses. Besides, CSR is an activity undertaken humanitarian nature. Maslahah mursalah While this is a law where there is no dail about the commands and prohibitions.CSR itself is a commitment of the Company to participate in the sustainable economic development to improve the quality of life and environment benefits the Company itself, the local community and society in general. While maslahah mursalah itself has a definition that is a benefit that is not covered by the Personality \u27and nor are the arguments sent to work or leave it, whereas if done will bring great good or benefit

Hedgehog-stimulated stem cells depend on non-canonical activity of the Notch co-activator Mastermind

Normal self-renewal of follicle stem cells (FSCs) in the Drosophila ovary requires Hedgehog (Hh) signaling. Excess Hh signaling, induced by loss of patched (ptc), causes cell-autonomous duplication of FSCs. We have used a genetic screen to identify Mastermind (Mam), the Notch pathway transcriptional co-activator, as a rare dose-dependent modifier of aberrant FSC expansion induced by excess Hh. Complete loss of Mam activity severely compromises the persistence of both normal and ptc mutant FSCs, but does not affect the maintenance of ovarian germline stem cells. Thus, Mam, like Hh, is a crucial stem cell factor that acts selectively on FSCs in the ovary. Surprisingly, other Notch pathway components, including Notch itself, are not similarly required for FSC maintenance. Furthermore, excess Notch pathway activity alone accelerates FSC loss and cannot ameliorate the more severe defects of mam mutant FSCs. This suggests an unconventional role for Mam in FSCs that is independent of Notch signaling. Loss of Mam reduces the expression of a Hh pathway reporter in FSCs but not in wing discs, suggesting that Mam might enhance Hh signaling specifically in stem cells of the Drosophila ovary

Additional file 5: Figure S1. of Sex differences in the molecular signature of the developing mouse hippocampus

Principal Component Analysis of only female samples. File contains figure of principal component analysis of 2 and 4 month old female samples to investigate variance in gene expression associated with differences in estrous stage. (PNG 96 kb

Additional file 2: of Sex differences in the molecular signature of the developing mouse hippocampus

Metadata table for RNA-seq assay. File contains information on RNA-seq samples such as sample ID, sex, timepoint, and estrous stage. (CSV 749 bytes

Transgenerational Evidence of Increases in Dopamine D2 Receptor Sensitivity in Rodents: Impact on Sensorimotor Gating, the Behavioral Response to Nicotine and BDNF

Background/Aims: Neonatal quinpirole (NQ) treatment to rats increases dopamine D2 (DAD2) receptor sensitivity in adult animals. We investigated if increased DAD2 sensitivity would be passed to the next (F1) generation, and if these animals demonstrated sensorimotor gating deficits and enhanced behavioral responses to nicotine. Methods: Male and female rats were intraperitoneal (IP) administered quinpirole (1 mg/kg) or saline (NS) from postnatal day (P)1–21. Animals were either behaviorally tested (F0) or raised to P60 and mated, creating F1 offspring. Results: Experiment 1 revealed that F1 generation animals that were the offspring of at least one NQ-treated founder increased yawning behavior, a DAD2-mediated behavioral event, in response to acute quinpirole (0.1 mg/kg). F1 generation rats also demonstrated increased striatal β arrestin-2 and decreased phospho-AKT signaling, consistent with increased G-protein independent DAD2 signaling, which was equal to F0 NQ-treated founders, although this was not observed in all groups. RNA-Seq analysis revealed significant gene expression changes in the F1 generation that were offspring of both NQ-treated founders compared to F0 NQ founders and controls, with enrichment in sensitivity to stress hormones and cell signaling pathways. In Experiment 2, all F1 generation offspring demonstrated sensorimotor gating deficits compared to controls, which were equivalent to F0 NQ-treated founders. In Experiment 3, all F1 generation animals demonstrated enhanced nicotine behavioral sensitization and nucleus accumbens (NAcc) brain-derived neurotrophic factor (BDNF) protein. Further, F1 generation rats demonstrated enhanced adolescent nicotine conditioned place preference equivalent to NQ-treated founders conditioned with nicotine. Conclusions: This represents the first demonstration of transgenerational effects of increased DAD2 sensitivity in a rodent model

Cocaine-induced nucleosome repositioning.

<p>Comparative genome hybridization of mononucleosomally-protected DNA reveals a large-scale repositioning of nucleosomes following cocaine treatment. (A) The number of loci with significant changes in nucleosome positions fluctuates with the duration of exposure. Between 5 and 20 min, there is a significant increase in the number of loci with nucleosome repositioning (from 10 at 5 min to 211 at 20 min). However, by 40 min, the majority of the nucleosomes return to their basal positions such that only 8 loci continue to show nucleosome repositioning. At 60 min, 223 loci show significant repositioning of nucleosomes. (B) Number of genes showing nucleosome repositioning that was unique to each time point and common to multiple time points is shown. The changes detected at 5 and 40 min were common across the 20 and 60 minute time points. Some changes are unique to early or late time points (104 loci specific for 10 min, 116 loci for 60 min). (C) Nucleosome repositioning upstream of the transcription start site (TSS) and throughout the 5’ end of the <i>NFKBIB</i> gene following 5, 20 and 40 min of cocaine exposure. Nucleosome positions relative to the TSS and coding sequence of the <i>NFKBIB</i> gene in the drug naïve (black) and cocaine exposed (red) states are further illustrated pictorially at the bottom of the figure. Each sphere (black or red) represents a nucleosome. Nucleosome positions do not diverge noticeably from the basal positions at 5 min following the cocaine treatment. By 20 min, there is significant repositioning, such that nucleosomes are evicted upstream of the TSS. However, the nucleosomes return to the basal position by the 40 min (60 min identical to 40 min; data not shown). The x-axis represents the genomic position showing 2 kb centered on a TSS. The y-axis is the log₂ ratio of mononucleosomally-protected DNA to genomic DNA signal at each probe on the microarray.</p

Nicotine-induced changes in nucleosome occupancy at the <i>LITAF</i>, <i>MLL3</i> and <i>DHFR</i> promoter regions.

<p>(A) Nucleosome positioning at the <i>LITAF</i> and (B) <i>MLL3</i> promoter after 10 minute nicotine exposure. Increased nucleosome occupancy in the nicotine treated cells (red line) relative to control cells (black line) is indicated by red bars. Nucleosome occupancy is enhanced, relative to control, at the regions just upstream of the TSS in both <i>LITAF</i> and <i>MLL3</i>, consistent with repressed transcription. (C) Nucleosome occupancy at <i>DHFR</i> is also enhanced at the TSS, above baseline and is enhanced upstream of the TSS, relative to the control, but not above baseline (pink bar). The 60 and 90 minute time points were similar to the 10 minute nicotine time point and therefore, were not shown. Nucleosome positions relative to the transcription start site in the drug naïve (black) and nicotine exposed (red) states are further illustrated pictorially at the bottom of the figure. Red and pink bars represent increased nicotine-induced nucleosome occupancy upstream of the TSS and are replicated on the pictoral illustrations at the bottom of the figure.</p

Nucleosome Repositioning: A Novel Mechanism for Nicotine- and Cocaine-Induced Epigenetic Changes

<div><p>Drugs of abuse modify behavior by altering gene expression in the brain. Gene expression can be regulated by changes in DNA methylation as well as by histone modifications, which alter chromatin structure, DNA compaction and DNA accessibility. In order to better understand the molecular mechanisms directing drug-induced changes in chromatin structure, we examined DNA-nucleosome interactions within promoter regions of 858 genes in human neuroblastoma cells (SH-SY5Y) exposed to nicotine or cocaine. Widespread, drug- and time-resolved repositioning of nucleosomes was identified at the transcription start site and promoter region of multiple genes. Nicotine and cocaine produced unique and shared changes in terms of the numbers and types of genes affected, as well as repositioning of nucleosomes at sites which could increase or decrease the probability of gene expression based on DNA accessibility. Half of the drug-induced nucleosome positions approximated a theoretical model of nucleosome occupancy based on physical and chemical characteristics of the DNA sequence, whereas the basal or drug naïve positions were generally DNA sequence independent. Thus we suggest that nucleosome repositioning represents an initial dynamic genome-wide alteration of the transcriptional landscape preceding more selective downstream transcriptional reprogramming, which ultimately characterizes the cell- and tissue-specific responses to drugs of abuse.</p></div

Cocaine- and nicotine-induced nucleosome repositioning comparisons.

<p>(A) Changes in nucleosome repositioning that were unique to nicotine or cocaine, and common to both the drugs. (B-E) Nucleosome repositioning in response to nicotine or cocaine exposure is shown. (B) Nucleosome repositioning upstream of TSS, at the TSS and at the beginning of the coding sequence in the <i>CDNK1C</i> gene around the TSS was induced by nicotine and not by cocaine (nicotine-specific). Nicotine exposure positioned nucleosomes upstream of the TSS, depleted the nucleosomes at the TSS, and positioned nucleosomes at the start of the coding sequence. On the other hand, cocaine exposure for 20 min, did not produce changes in nucleosome position compared to the drug naïve state. (C) Nicotine and cocaine both induced nucleosome repositioning upstream of TSS, at the TSS and at the beginning of the coding sequence in the <i>ANGPT2</i> gene. However, 60 min cocaine-specific changes were detected at the +1 nucleosome (asterisk), just downstream of the <i>ANGPT2</i> TSS. The 60 min nicotine-induced nucleosome repositioning at <i>ANGPT2</i> is similar to the 20 min time point and therefore is not shown. (D) Changes common to nicotine (10 min) and cocaine (20 min) just upstream and downstream of the TSS of <i>FNB2</i> gene. (E) Neither nicotine (10 min) nor cocaine (20 min) produced nucleosome repositioning across the promoter and 5’ region of <i>BMP3</i>. Nucleosome positions relative to the TSS and coding sequence of each gene in the drug naïve (black) and drug exposed (red) states are further illustrated pictorially at the bottom of the figure. Each sphere (black or red) represents a nucleosome.</p