PSYCHOSOCIAL FACTORS AS RISK FACTOR IN SUICIDAL POISONING: A CROSS-SECTIONAL STUDY

  Objective: Suicide is known to be a phenomenon in low-, middle-, and high-income countries and occurs in all sociodemographic groups. It ranges from acute to fatal lethal attempts which occur in the context of a social crisis. Deliberate self-poisoning for suicide is a growing public health concern with frequent emergency department admissions. An epidemiological surveillance is essential for every region to understand the pattern, underlying psychological factors, and the scope of preventive measures.Methods: The 2-year retrospective study describes the epidemiology and influencing factors of suicides by self-poisoning in patients admitted to a Government Hospital and a Teaching Hospital in Pune, Maharashtra, from January 1, 2014 to December 31, 2015.Result: Out of 1010 poisoning cases reported, 539 were suicidal self-poisoning. Significantly males more than females were brought to the hospitals due to deliberate self-poisoning (1:0.86, χ2=38.05; p<0.001). The age group most recorded was 20-35 years (67.7%). Psychosocial factors were associated with increased risk of suicidal self-poisoning attempts (risk ratio 4.76, 95% confidence interval 4.07-5.57; p<0.001). Psychosocial factors were interpersonal conflict (52.4%), stress (30.4), dissatisfaction in life (6%), and alcoholism or mental disorders (11.1%). Household and agricultural products (71.8%) were the popular choices of the toxic agent in self-poisoning with phenols (20%) being the most common. 19 cases (3.5%) were severe, out of which 15 cases lead to death (2.8% mortality).Conclusion: There is an urgent need to develop and implement preventative and treatment strategies for high-risk groups attempting suicide by self-poisoning

Differing functions of ATR kinase in human epidermal keratinocytes exposed to Ultraviolet B Radiation

Ataxia-telangiectasia and Rad-3 related (ATR) is a DNA damage response protein kinase that is upregulated in various cancer cell types and has key roles in cell cycle progression, DNA repair and apoptosis. Small molecule ATR kinase inhibitors are of importance as antineoplastic agents because they sensitize cancer cells to DNA damaging chemotherapy drugs. However, only a few studies have looked at the effects of ATR kinase inhibitors on non-replicating cells, which constitute the majority of cells in the human body and have suggested an opposite, pro-apoptotic role for ATR kinase signaling in non-replicating cells in comparison to a pro-survival function in replicating cells. Therefore, experimentations were conducted to explore this new role by using chemical inhibitors of ATR kinase in quiescent human keratinocytes in vitro and skin explants ex vivo irradiated with UVB. ATR kinase was activated in quiescent keratinocytes in DNA translocase and repair factor XPB-dependent manner whereas ATR inhibition reduced apoptotic signaling and apoptotic sunburn cells in Human skin epidermis. ATR kinase acutely protected the cells from DNA damage-induced cytotoxicity and cell death and upon cell cycle re-entry, conserves cell proliferation and limits mutagenesis at the hypoxanthine phosphoribosyltransferase locus. Loss of ATR kinase activated TLS polymerase dependent mutagenic Translesion DNA synthesis for gap filling followed by Nucleotide excision repair in quiescent keratinocytes exposed to DNA damaging UVB. In conclusion, these results indicate that the ATR kinase has a pro-proliferative role in quiescent keratinocytes whereas it has a pro-apoptotic role in human skin epidermis. It has important roles in promoting cell viability and proliferation and in preventing mutagenesis following UVB exposure even in cells that are not actively synthesizing DNA. Also, the mutagenic consequences of ATR inhibition in these cells have implications for the use of small molecule ATR kinase inhibitors in chemotherapy

Differing functions of ATR kinase in human epidermal keratinocytes exposed to Ultraviolet B Radiation

Ataxia-telangiectasia and Rad-3 related (ATR) is a DNA damage response protein kinase that is upregulated in various cancer cell types and has key roles in cell cycle progression, DNA repair and apoptosis. Small molecule ATR kinase inhibitors are of importance as antineoplastic agents because they sensitize cancer cells to DNA damaging chemotherapy drugs. However, only a few studies have looked at the effects of ATR kinase inhibitors on non-replicating cells, which constitute the majority of cells in the human body and have suggested an opposite, pro-apoptotic role for ATR kinase signaling in non-replicating cells in comparison to a pro-survival function in replicating cells. Therefore, experimentations were conducted to explore this new role by using chemical inhibitors of ATR kinase in quiescent human keratinocytes in vitro and skin explants ex vivo irradiated with UVB. ATR kinase was activated in quiescent keratinocytes in DNA translocase and repair factor XPB-dependent manner whereas ATR inhibition reduced apoptotic signaling and apoptotic sunburn cells in Human skin epidermis. ATR kinase acutely protected the cells from DNA damage-induced cytotoxicity and cell death and upon cell cycle re-entry, conserves cell proliferation and limits mutagenesis at the hypoxanthine phosphoribosyltransferase locus. Loss of ATR kinase activated TLS polymerase dependent mutagenic Translesion DNA synthesis for gap filling followed by Nucleotide excision repair in quiescent keratinocytes exposed to DNA damaging UVB. In conclusion, these results indicate that the ATR kinase has a pro-proliferative role in quiescent keratinocytes whereas it has a pro-apoptotic role in human skin epidermis. It has important roles in promoting cell viability and proliferation and in preventing mutagenesis following UVB exposure even in cells that are not actively synthesizing DNA. Also, the mutagenic consequences of ATR inhibition in these cells have implications for the use of small molecule ATR kinase inhibitors in chemotherapy