Social disorganization and police arrest trajectories

Prior police decision-making research is limited by (1) its emphasis on individual and organizational predictors and (2) cross-sectional designs, which fail to account for the time-varying aspects of police activities and the factors explaining them. Using group-based trajectory modeling, this study tested the ability of social disorganization theory to explain arrest activity at the Census block group level in Dallas, Texas. Social disorganization variables helped predict certain arrest trajectories, but not all of them. Specifically, socio-economic status was significant in low and medium arrest trajectory groups. An interaction between racial heterogeneity and family disruption was also significant in the medium arrest trajectory group. Theoretical implications are discussed.

Neuromodulation or energy failure? Metabolic limitations silence network output in the hypoxic amphibian brainstem

Hypoxia tolerance in the vertebrate brain often involves chemical modulators that arrest neuronal activity to conserve energy. However, in intact networks, it can be difficult to determine whether hypoxia triggers modulators to stop activity in a protective manner or whether activity stops because rates of ATP synthesis are insufficient to support network function. Here, we assessed the extent to which neuromodulation or metabolic limitations arrest activity in the respiratory network of bullfrogs-a circuit that survives moderate periods of oxygen deprivation, presumably, by activating an inhibitory noradrenergic pathway. We confirmed that hypoxia and norepinephrine (NE) reduce network output, consistent with the view that hypoxia may cause the release of NE to inhibit activity. However, these responses differed qualitatively; hypoxia, but not NE, elicited a large motor burst and silenced the network. The stereotyped response to hypoxia persisted in the presence of both NE and an adrenergic receptor blocker that eliminates sensitivity to NE, indicating that noradrenergic signaling does not cause the arrest. Pharmacological inhibition of glycolysis and mitochondrial respiration recapitulated all features of hypoxia, implying that reduced ATP synthesis underlies the effects of hypoxia on network activity. Finally, activating modulatory mechanisms that dampen neuronal excitability when ATP falls, KATP channels and AMP-dependent protein kinase, did not resemble the hypoxic response. These results suggest energy failure- rather than inhibitory modulation- silences the respiratory network during hypoxia and emphasize the need to account for metabolic limitations before concluding that modulators arrest activity as an adaptation for energy conservation in the nervous system.

PHYTOCEMICALS SCREENING AND CELL CYCLE ARREST ACTIVITY OF n-HEXANE EXTRACT OF Vernonia amygdalina Delile LEAVES AGAINST PANCREATIC CANCER CELL LINE

Objective: This study aims to determined phytochemical compounds of simplex and n-hexane extract (nHE) of Vernonia amygdalina Delile Leaves and cell cycle arrest activity against PANC-1 cells. Methods: The leaves of Vernonia amygdalina Delile were dried and extracted with n-hexane, followed by evaporation and freeze-drying. Phytochemicals screening were analyzed with standard procedures. Cytotoxic activity was carried out using MTT assay method. PANC-1 cells were treated with different concentrations of nHE (500 ug/mL, 250 ug/mL, 125 ug/mL, 61.5 ug/mL and 31.25 ug/mL) for 24 hours to obtained IC50 values. The cell cycle inhibition activity of nHE was carried out used flowcytometry method and apoptosis activity used double staining method. Results: Then HE was identified contains steroids/triterpenoids. The IC50 was114.80 ± 1.21 ug/mL. The nHE inhibited cell cycle PANC-1 on M1 phase (67.39%) and it was induced apoptosis process on PANC-1 cells. Conclusions: Our results suggest that extractsn­-hexane of Vernonia amygdalina Delile Leaves had as cancer chemoprevention activities with inhibits cell cycle and spur apoptosis process on PANC-1 cells. Keywords:

The Anti-Proliferation, Cycle Arrest and Apoptotic Inducing Activity of Peperomin E on Prostate Cancer PC-3 Cell Line

Peperomin E is a natural secolignan existing distributed in the plants of the genus Peperomia. Previous investigations demonstrated that peperomin E showed potential antitumor activity in some cancer lines, but it is unclear whether peperomin E has an effect on prostate cancer cell lines. The aim of the present study is to investigate its effects on proliferation inhibition, apoptosis-inducing and cell-cycle arrest activity using a prostate cancer PC-3 cell line. The proliferation inhibition was evaluated by MTT assay, apoptosis was detected by Annexin V/propidium iodide (PI) staining and Hoechst 33258 staining, cell cycle distributions were measured by flow cytometry, and western blot analysis was used to determine specific cellular apoptotic protein expressions of Bcl-2, Bax, caspase-3 and cleaved-caspase-3. According to the results of this study, peperomin E exhibited significant anti-proliferation activity on PC-3 cell lines in vitro in a dose-dependent manner. Peperomin E treatments lead to marked morphological changes. Apoptotic cell count and cell-cycle distribution at G2/M phase significantly increased with increasing concentrations of peperomin E. The down-regulated expression level of Bcl-2 and up-regulated expression level of Bax and cleaved-caspase-3 compared with the controls were also observed after peperomin E treatment. These data suggest that peperomin E exhibited proliferation inhabitation, apoptosis-inducing and cell-cycle arrest activity on PC-3 cell lines. The anti-proliferation effect of peperomin E on PC-3 cells should result partly from its cell-cycle arrest and apoptosis-inducing activity, whereas the increasing of the Bax/Bcl-2 ratio and activation of caspases-3 play an important role in the development of apoptosis.

Revalidation of the Federal PTRA: Testing the PTRA for Predictive Biases

The pretrial risk assessment instrument (PTRA) was developed for use in the U.S. federal pretrial system. Specifically, this instrument was constructed to help officers assess the likelihood that defendants will commit pretrial violations including being rearrested for new crimes, missing court appearances, or being revoked while on pretrial release. This research evaluates the PTRA’s capacity to predict pretrial violations on 85,369 defendants with officer-completed PTRA assessments. Bivariate and multivariate models were estimated by race, ethnicity, and sex. Results show that the PTRA performs well at predicting pretrial violations as the area under the receiver operating characteristic curve ranged from 0.65 to 0.73 depending upon the subsamples and outcomes being predicted. Moreover, the PTRA predicted new criminal arrest activity equally well for non-Hispanic Whites and Blacks, while for Hispanics and females, findings show the instrument validly predicting rearrest activity, with some evidence of overprediction depending upon the outcome being examined.

CELL CYCLE ARREST ACTIVITY OF LITSEA CUBEBA LOUR: HEARTWOOD AND FRUIT EXTRACTS AGAINST T47D BREAST CANCER CELLS

Objective: This study was carried out to investigate cell cycle arrest activity toward T47D cells of Litsea cubeba heartwoods and fruits extract.Methods: Dry extracts were prepared from dry-grounded heartwoods and fruits by cold maceration using n-hexane, ethylacetate, and ethanol solvent. Cytotoxic activity were measured by [3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide] methods and interpreted with inhibitory concentration 50% (IC50) value. Cell cycle arrest was investigated by flowcytometry method.Results: IC50 values for each n-hexane, ethylacetate, and ethanol of L. cubeba heartwoods and fruits were 76.34±2.61; 67.52±2.45; 71.23±2.37; 75.59±3.24; 162.58±15.08; 63.70±2.67 μg/mL, respectively. Cell cycle arrest for ethylacetate extract of heartwoods and fruits were accumulated in G0/G1 phase (56.70% and 65.56%).Conclusion: These results suggest that L. cubeba heartwoods and fruits has cell cycle arrest activity.

SLX4-SLX1 Protein-independent Down-regulation of MUS81-EME1 Protein by HIV-1 Viral Protein R (Vpr)

Evolutionarily conserved structure-selective endonuclease MUS81 forms a complex with EME1 and further associates with another endonuclease SLX4-SLX1 to form a four-subunit complex of MUS81-EME1-SLX4-SLX1, coordinating distinctive biochemical activities of both endonucleases in DNA repair. Viral protein R (Vpr), a highly conserved accessory protein in primate lentiviruses, was previously reported to bind SLX4 to mediate down-regulation of MUS81. However, the detailed mechanism underlying MUS81 down-regulation is unclear. Here, we report that HIV-1 Vpr down-regulates both MUS81 and its cofactor EME1 by hijacking the host CRL4-DCAF1 E3 ubiquitin ligase. Multiple Vpr variants, from HIV-1 and SIV, down-regulate both MUS81 and EME1. Furthermore, a C-terminally truncated Vpr mutant and point mutants R80A and Q65R, all of which lack G2 arrest activity, are able to down-regulate MUS81-EME1, suggesting that Vpr-induced G2 arrest is not correlated with MUS81-EME1 down-regulation. We also show that neither the interaction of MUS81-EME1 with Vpr nor their down-regulation is dependent on SLX4-SLX1. Together, these data provide new insight on a conserved function of Vpr in a host endonuclease down-regulation.