Canadian Youth Criminality and Identity Formation: A South Asian (Sikh) Perspective

This thesis explores the experiences of second generation Sikh males in Canada, focusing on involvement in criminal activities during adolescence. Using a deeply qualitative autoethnographic approach (Anderson, 2006), I conducted unstructured active interviews (Holstein & Gubrium, 1995) with seven males ranging from 20 to 26 years of age. The interviews consist of a dialogue on how these youths\u27 emerging identities as Sikh and as Canadians contributed to their adolescent experiences with crime. Findings highlight the importance of engaging youth at the level of personal experience and at the level of institutional and community influences. Specifically, an interplay of parental, cultural, institutional, and societal processes impacted participants\u27 identities and subsequent actions, including desistance from crime as the youth emerged from adolescence. The major conclusion of the thesis is that while ethnic cultural influences and ethnic pride contributed to youths\u27 involvement in various criminal activities, ethnic and especially family influences and pride also contributed to transitions to desistance. This speaks to the need for an inclusive environment that encourages integration of immigrant populations in ways that allow them to actively participate as full citizens within their families, communities and as Canadians

ASCORBIC ACID AS A GROWTH ADJUVANT IN ENCAPSULATED PROTOCORM-LIKE-BODIES OF RHYNCHOSTYLIS RETUSA BL. (ORCHIDACEAE)

In the present study, effect of ascorbic acid, a known growth adjuvant on encapsulated protocorm-like-bodies (PLBs) of Rhynchostylis retusa Bl. was investigated. PLBs were encapsulated in calcium alginate (3.5% sodium alginate and 100mM calcium chloride) prepared in Mitra et al. (1976) basal medium and supplemented with different concentration of ascorbic acid (5, 10, 15, 20mM). The encapsulated PLBs were stored at 25°C. Their germination response and germination potential was evaluated after every 4 weeks on basal media. Control set of encapsulated PLBs, failed to germinate after 32 weeks. However, PLBs with 15mM ascorbic acid in the encapsulated matrix showed the best response; nearly 90% germinated even after 32 weeks of storage. The survival and germination frequency was directly proportional to the level of ascorbic acid in the alginate mix upto 15mM level but declined on further increase. Differentiation of PLBs into plantlet was better in synthetic seeds containing lower concentration of ascorbic acid (5mM) as compared to higher levels (15, 20mM) whereas multiplication of secondary PLBs was more pronounced at higher levels. Chlorophyll content was inversely proportional to the level of ascorbic acid in the nutrient mix; lush green PLBs were observed at low concentration of ascorbic acid (5mM). This study highlights the potential of ascorbic acid as an aid to growth and survival of encapsulated PLBs upon storage

An okadaic acid-sensitive pathway involved in the phenobarbital-mediated induction of CYP2B gene expression in primary rat hepatocyte cultures

ABSTRACT We have previously demonstrated that specific activation of a cAMP-dependent protein kinase A (PKA) pathway resulted in complete repression of phenobarbital (PB)-inducible CYP gene expression in primary rat hepatocyte cultures. In the current investigation, we examined the role of protein phosphatase pathways as potential co-regulators of this repressive response. Primary rat hepatocytes were treated with increasing concentrations (0.1-25 nM) of okadaic acid, a potent inhibitor of serine/threonine-specific protein phosphatases PP1 and PP2A. PB induction responses were assessed by use of specific hybridization probes to CYP2B1 and CYP2B2 mRNAs. Okadaic acid completely inhibited the PB induction process in a concentration-dependent manner (IC 50 , ϳ1.5-2 nM). Similar repression was obtained with low concentrations of other highly specific phosphatase inhibitors, tautomycin and calyculin A. In contrast, exposure of hepatocytes to 1-nor-okadaone or okadaol, negative analogs of okadaic acid largely devoid of phosphatase inhibitory activity, was without effect on the PB induction process. At similar concentrations, okadaic acid produced only comparatively weak modulation of the ␤-naphthoflavone-inducible CYP1A1 gene expression pathway. In additional experiments, hepatocytes were treated with suboptimal concentrations of PKA activators together with phosphatase inhibitors. Okadaic acid markedly potentiated the repressive effects of dibutyryl-cAMP on the PB induction process. Together, these results indicate that both PKA and protein phosphatase (PP1 and/or PP2A) pathways exert potent and complementary control of the intracellular processes modulating the signaling of PB in cultured primary rat hepatocytes

Cadmium Induced p53-Dependent Activation of Stress Signaling, Accumulation of Ubiquitinated Proteins, and Apoptosis in Mouse Embryonic Fibroblast Cells

The tumor suppressor oncoprotein, p53, is a critical regulator of stress-induced growth arrest and apoptosis. p53 activity is regulated through the ubiquitin proteasome system (UPS) with stress-induced disruption leading to increased accumulation of p53, resulting in growth arrest. In the present study, we investigate the role of p53 to determine sensitivity to cadmium (Cd) and whether induction of stress signaling responses and perturbation of the UPS are involved in Cd-induced cytotoxicity and apoptosis. We treated synchronously cultured p53 transgenic mouse embryonic fibroblasts, both wild-type p53+/+ and knockout p53−/− cells, with cadmium chloride (Cd, 0.5–20μM) for 24 h. Cd-induced cytotoxicity was assessed by cellular morphology disruption and neutral red dye uptake assay. Proteins in the stress signaling pathway, including p38 mitogen-activated protein kinase (MAPK) and stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK); ubiquitination, such as high-molecular weight of polyubiquitinated proteins (HMW-polyUb); and apoptotic pathways, were all measured. We found that Cd induced p53-dependent cytotoxicity in the p53+/+ cells, which exhibited a twofold greater sensitivity. We observed a dose-dependent stimulation of p38 MAPK and SAPK/JNK phosphorylation that corresponded to accumulation of HMW-polyUb conjugates and lead to the induction of apoptosis, as evidenced by the elevation of cleaved caspase-3. Our study suggests that Cd-mediated cytotoxicity and induction of stress signaling responses, elevated accumulation of HMW-polyUb conjugates, and resulting apoptosis are all dependent on p53 status