Factors associated with suicide/self-inflicted injuries among women aged 18-65 years in the United States: A 13-year retrospective analysis of the National Inpatient Sample database.

BACKGROUND: Suicide is a significant cause of mortality in the United States, accounting for 14.5 deaths/100,000. Although there are data on gender disparity in suicide/self-inflicted injury rates in the United States, few studies have examined the factors associated with suicide/self-inflicted injury in females. OBJECTIVE: To determine factors associated with suicide/self-inflicted injuries among women aged 18-65 years in the United States. METHODS: Hospitalizations for suicide or self-inflicted injuries were identified using the National Inpatient Sample database from 2003-2015 using sample weights to generate national estimates. Independent predictors of suicide/self-inflicted injuries were identified using multivariable regression models. Interaction term analysis to identify the interaction between race/ethnicity and income were conducted. RESULTS: There were 1,031,693 adult women hospitalizations in the U.S. with a primary diagnosis of suicide/self-inflicted injury in the study period. The highest suicide/self-inflicted injury risk was among women aged 31-45years (OR = 1.23, CI = 1.19-1.27, p < 0.05). Blacks in the highest income strata had a 20% increase in the odds of suicide/self-inflicted injury compared to Whites in the lowest socioeconomic strata (OR = 1.20, CI = 1.05-1.37, p <0.05). Intimate partner violence increased suicide/self-inflicted injury risk 6-fold (OR = 5.77, CI = 5.01-6.65, p < 0.05). CONCLUSION: Suicide risk is among women aged 31-45 years, higher earning Black women, intimate partner violence victims, uninsured, and current smokers. Interventions and policies that reduce smoking, prevents intimate partner violence, addresses racial discrimination and bias, and provides universal health coverage are needed to prevent excess mortality from suicide deaths.

M3, a 1,4-Dihydropyridine Derivative and Mixed L-/T-Type Calcium Channel Blocker, Attenuates Isoproterenol-Induced Toxicity in Male Wistar Rats.

Recent evidence indicates that Ca2+ dysregulation is involved in the pathogenesis of isoproterenol (ISP)-induced biochemical toxicity and associated oxidative stress. In this study, we investigated the chemopreventive benefit of M3, a 1,4-dihydropyridine calcium channel blocker, against ISP-induced toxicity in male Wistar rats. Adult rats were divided into eight groups of six rats/group. Groups 1-5 received normal saline (control, 10 mL/kg/day, p.o.), ISP (85 mg/kg/day, s.c.), M3 lower dose (M3LD, 5 mg/kg, p.o.), M3 upper dose (M3UD, 20 mg/kg/day, p.o.), and Nifedipine (NFD, 20 mg/kg/day, p.o.), respectively. Others (groups 6-8) were pretreated with either M3LD, M3UD or NFD one hour before ISP administration. All rats were sacrificed 24 h after the last administration and changes in biochemical, hematological, and antioxidant parameters were assessed. Histologic examination of the heart, liver and kidney was also conducted. ISP elevated (p < 0.05) Ca2+, alanine aminotransferase, lactate dehydrogenase, triglycerides, and low-density lipoprotein levels when compared with control. Similarly, ISP increased levels of markers of renal function (p < 0.01), C-reactive protein (148.1%) and myocardial malondialdehyde (MDA, 88.7%) and tumor necrosis factor-alpha (109.2%). Platelet level was reduced (p < 0.05) in the ISP-intoxicated control rats. M3 exhibited antioxidant property, reduced levels of triglycerides, MDA and improved biochemical and hematological alterations associated with ISP toxicity. M3, however, was not effective in restoring histological changes that characterized ISP toxicity at the doses used. M3 offers chemopreventive benefits against ISP toxicity possibly through L-/T-type calcium channels blockade and modulatory actions on biochemical and antioxidant homeostasis.

Amlodipine, an L-type calcium channel blocker, protects against chlorpromazine-induced neurobehavioural deficits in mice.

This study investigated the modulatory and chemopreventive benefit of amlodipine (AML), a dihydropyridine calcium channel antagonist, against neurobehavioural abnormalities (NAs) associated with chlorpromazine (CPZ) toxicity in mice. Adult mice were divided into five groups of six animals/group. Group 1 (control) was administered saline (10 mL/kg i.p.). Group 2 received CPZ (2 mg/kg i.p.). Groups 3 and 4 received bromocriptine (BMC, 2.5 mg/kg s.c.) and AML (1 mg/kg s.c.), respectively, while group 5 received their combination. Groups 3-5 later received CPZ 30 min after initial treatments. Animals were subjected to neurobehavioural tests and euthanized 18 h later. CPZ-induced NAs were characterized by significant increase (P < 0.001) in cataleptic behaviour and lowered (P < 0.05) spontaneous activity reaction time in mice. There were also significant (P < 0.001) increases in malondialdehyde levels and decreased locomotion plus learning and memory parameters (P < 0.05-0.001). AML pretreatment alone did not alleviate CPZ-induced motor deficits in the mice. While pretreatment with BMC alone attenuated CPZ-associated catalepsy, its combination with AML further protected mice against NAs. Furthermore, BMC pretreatment did not affect CPZ-induced increase in malondialdehyde level, but AML or BMC+AML significantly (P < 0.05) decreased malondialdehyde in the CPZ-treated rats. Reduced glutathione levels and activities of superoxide dismutase and catalase remained elevated in all treatment groups. In conclusion, data from this study suggest possible chemopreventive benefit of AML alone or in combination with BMC against CPZ-associated neurobehavioural deficits. The ameliorative effect of AML may be related to its antioxidant and/or calcium channel blocking property.