A Comparative Analysis of Caregivers Burden and Depression of Patients with Dementia and Malignancy

INTRODUCTION: Caregivers of individuals suffering from Dementia and Cancer illnesses are at risk of having subjected to psychiatric morbidities. There is a paucity of data comparing the caregiver burden and depression of Dementia and Cancer patients. AIM OF THE STUDY: The aim of the study is to compare the caregivers’ burden and depression of Dementia and Cancer patients and also to study the risk factors associated with caregivers’ depression. MATERIALS AND METHODS: This cross sectional study is performed on the caregivers of 40 Dementia and 40 Cancer caregivers in tertiary care hospital in Tamilnadu, from March to August 2015. The burden was assessed by ZBI scale, functional impairment by Katz ADL Index and IADL scale, and depression by MADRS scale. RESULTS: This study suggests both the groups were comparable in most sociodemographic factors, duration of caregiving, chronic illness in caregivers and functional impairment in patients. The burden and depression in Cancer caregivers were higher than Dementia caregivers such as 65% and 72.5%, and 30% and 17.5% respectively, it was statistically significant (p=0.003, p=0.0001) respectively. In both the groups whenever the burden was high, the depression was also high. CONCLUSION: Caregivers of Cancer patients have more burden and depression, than dementia patients respectively. Both the caregiver groups were vulnerable to depression, if the caregiver has more burden. So regular screening, early detection, psychiatric interventions will favor for better quality of life in both patients and caregivers

Protective Effect of Curcumin on Pulmonary and Cardiovascular Effects Induced by Repeated Exposure to Diesel Exhaust Particles in Mice

Particulate air pollution has been associated with increased risk of cardiopulmonary diseases. However, the underlying mechanisms are not fully understood. We have previously demonstrated that single dose exposure to diesel exhaust particle (DEP) causes lung inflammation and peripheral thrombotic events. Here, we exposed mice with repeated doses of DEP (15µg/animal) every 2nd day for 6 days (a total of 4 exposures), and measured several cardiopulmonary endpoints 48 h after the end of the treatments. Moreover, the potential protective effect of curcumin (the yellow pigment isolated from turmeric) on DEP-induced cardiopulmonary toxicity was assessed. DEP exposure increased macrophage and neutrophil numbers, tumor necrosis factor α (TNF α) in the bronchoalveolar lavage (BAL) fluid, and enhanced airway resistance to methacoline measured invasively using Flexivent. DEP also significantly increased plasma C-reactive protein (CRP) and TNF α concentrations, systolic blood pressure (SBP) as well as the pial arteriolar thrombosis. It also significantly enhanced the plasma D-dimer and plasminogen activator inhibitor-1 (PAI-1). Pretreatment with curcumin by oral gavage (45 mg/kg) 1h before exposure to DEP significantly prevented the influx of inflammatory cells and the increase of TNF α in BAL, and the increased airway resistance caused by DEP. Likewise, curcumin prevented the increase of SBP, CRP, TNF α, D-dimer and PAI-1. The thrombosis was partially but significantly mitigated. In conclusion, repeated exposure to DEP induced lung and systemic inflammation characterized by TNFα release, increased SBP, and accelerated coagulation. Our findings indicate that curcumin is a potent anti-inflammatory agent that prevents the release of TNFα and protects against the pulmonary and cardiovascular effects of DEP

Semaphorin 3A is a new early diagnostic biomarker of experimental and pediatric acute kidney injury.

BACKGROUND: Semaphorin 3A is a secreted protein that regulates cell motility and attachment in axon guidance, vascular growth, immune cell regulation and tumor progression. However, nothing is known about its role in kidney pathophysiology. Here, we determined whether semaphorin3A is induced after acute kidney injury (AKI) and whether urinary semaphorin 3A can predict AKI in humans undergoing cardiopulmonary bypass (CPB). METHODS AND PRINCIPAL FINDINGS: In animals, semaphorin 3A is localized in distal tubules of the kidney and excretion increased within 3 hr after reperfusion of the kidney whereas serum creatinine was significantly raised at 24 hr. In humans, using serum creatinine, AKI was detected on average only 48 hours after CPB. In contrast, urine semaphorin increased at 2 hours after CPB, peaked at 6 hours (2596±591 pg/mg creatinine), and was no longer significantly elevated 12 hours after CPB. The predictive power of semaphorin 3A as demonstrated by area under the receiver-operating characteristic curve for diagnosis of AKI at 2, 6, and 12 hours after CPB was 0.88, 0.81, and 0.74, respectively. The 2-hour urine semaphorin measurement strongly correlated with duration and severity of AKI, as well as length of hospital stay. Adjusting for CPB time and gender, the 2-hour semaphorin remained an independent predictor of AKI, with an odds ratio of 2.19. CONCLUSION: Our results suggest that semaphorin 3A is an early, predictive biomarker in experimental and pediatric AKI, and may allow for the reliable early diagnosis and prognosis of AKI after CPB, much before the rise in serum creatinine

Quantification of serum semaphorin 3A in different forms AKI and diabetes in mouse.

<p>Semaphorin 3A was quantified using ELISA kit as described in Methods. A. Circulating levels of semaphorin 3A before and different time after cisplatin administration. Cisplatin administration was significantly upregulated semaphorin 3A in the blood. *<i>p</i><0.005 vs. 0 hr. B. Circulating levels of semaphorin 3A in sham operated (0 hr) and different time after reperfusion. Ischemia reperfusion rapidly downregulated circulating semaphorin 3A. *<i>p</i><0.005 vs. 0 hr. Values are mean ± SEM. n = 4–6.</p

Quantification of urine semaphorin 3A in different forms AKI and diabetes in mouse.

<p>Semaphorin 3A was quantified using ELISA kit as described in Methods. A. Semaphorin 3A in urine from animals subjected to sham surgery (0 hr) and different time after reperfusion. Ischemia reperfusion rapidly increased urinary excretion of semaphorin 3A. *<i>p</i><0.005 vs. 0 hr. B. Serum creatinine at different time after reperfusion. *<i>p</i><0.001 vs. 0 hr. C. Semaphorin 3A excretion in urine before and different time after cisplatin administration. Cisplatin administration significantly increased the excretion of semaphorin 3A at 24, 48 and 72 hr. *<i>p</i><0.005 vs. 0 hr. D. Serum creatinine at different time after administration of cisplatin. *<i>p</i><0.05. Values are mean ± SEM. n = 6–8.</p

ROC curve analysis for urinary semaphorin at 2 hours after cardiac surgery.

<p>The values 109.8, 492.1, and 910.0 are urinary semaphorin concentrations (in picograms per milligram urine creatinine) at 2 hours after CPB, which correspond to 96% sensitivity, optimal sensitivity and specificity, and 97% specificity, respectively.</p