Kidney injury molecule-1: a urinary biomarker for contrast induced acute kidney injury.

Back ground: Urinary kidney injury molecule 1 (KIM-1) is early biomarker for renal damage. A few studies have been published analyzing the potential use of urinary kidney injury molecule-1 (KIM-1) as a biomarker for acute kidney injury. However no study has been done related to Acute Kidney Injury associated with contrast administration. Aim: To search for new markers to identify Acute Kidney Injury (ARF) associated with contrast administration earlier than serum creatinine. Material and Methods: We studied 100 consecutive patients with normal serum creatinine undergoing angiographic procedure. We assessed urine KIM-1, at 4h, 8h, and 24 hours after the angiographic procedure. Serum creatinine was measured at basal, 24h and 48 hours after the procedure. Results: There was a significant rise in urinary KIM-1 levels at 24 hours after the angiographic procedure. The presence of contrast induced nephropathy associated with acute Kidney Injury was 12%. Conclusion: The present study highlighted the importance of urinary KIM-1 in detecting Acute Kidney Injury associated with contrast administration earlier than Serum creatinine. Key words: Neutrophil-gelatinase-associated lipocalin. Contrast-induced nephropathy. Cystatin C. Glomerular Filtration Rate (GFR), Kidney injury molecule -1 (KIM-1)

Family-led rehabilitation after stroke in India (ATTEND): a randomised controlled trial

Background Most people with stroke in India have no access to organised rehabilitation services. The effectiveness of training family members to provide stroke rehabilitation is uncertain. Our primary objective was to determine whether family-led stroke rehabilitation, initiated in hospital and continued at home, would be superior to usual care in a low-resource setting. Methods The Family-led Rehabilitation after Stroke in India (ATTEND) trial was a prospectively randomised open trial with blinded endpoint done across 14 hospitals in India. Patients aged 18 years or older who had had a stroke within the past month, had residual disability and reasonable expectation of survival, and who had an informal family-nominated caregiver were randomly assigned to intervention or usual care by site coordinators using a secure web-based system with minimisation by site and stroke severity. The family members of participants in the intervention group received additional structured rehabilitation training—including information provision, joint goal setting, carer training, and task-specific training—that was started in hospital and continued at home for up to 2 months. The primary outcome was death or dependency at 6 months, defined by scores 3–6 on the modified Rankin scale (range, 0 [no symptoms] to 6 [death]) as assessed by masked observers. Analyses were by intention to treat. This trial is registered with Clinical Trials Registry-India (CTRI/2013/04/003557), Australian New Zealand Clinical Trials Registry (ACTRN12613000078752), and Universal Trial Number (U1111-1138-6707). Findings Between Jan 13, 2014, and Feb 12, 2016, 1250 patients were randomly assigned to intervention (n=623) or control (n=627) groups. 33 patients were lost to follow-up (14 intervention, 19 control) and five patients withdrew (two intervention, three control). At 6 months, 285 (47%) of 607 patients in the intervention group and 287 (47%) of 605 controls were dead or dependent (odds ratio 0·98, 95% CI 0·78–1·23, p=0·87). 72 (12%) patients in the intervention group and 86 (14%) in the control group died (p=0·27), and we observed no difference in rehospitalisation (89 [14%]patients in the intervention group vs 82 [13%] in the control group; p=0·56). We also found no difference in total non-fatal events (112 events in 82 [13%] intervention patients vs 110 events in 79 [13%] control patients; p=0·80). Interpretation Although task shifting is an attractive solution for health-care sustainability, our results do not support investment in new stroke rehabilitation services that shift tasks to family caregivers, unless new evidence emerges. A future avenue of research should be to investigate the effects of task shifting to health-care assistants or team-based community care

Effect of fish oil on mitochondrial respiration in isoproterenol induced myocardial infarction in rats

268-272<span style="font-size:14.0pt;line-height: 115%;font-family:" times="" new="" roman";mso-fareast-font-family:"times="" roman";="" color:#2a2a2a;mso-ansi-language:en-in;mso-fareast-language:en-in;mso-bidi-language:="" hi"="" lang="EN-IN">Following isoproterenol treatment mitochondrial lipid peroxidation, phosphoslipase activity, lactate and calcium increased significantly, while activities of tricarboxylic acid cycle enzymes, enzymes of respiratory chain and ATP production showed decline. Oxidative phosphorylation was also affected on isoproterenol treatment with significant reduction in all the variables. Fish oil pretreatment in isoproterenol treated rats showed improved mitochondrial energy metabolism. The results suggest cardioprotective effect of fish oil.</span

Evaluation of the diagnostic performance of new markers for acute kidney injury associated with contrast administration

Background: Contrast-induced nephropathy (CIN) is a form of acute kidney injury (AKI) that is caused by exposure to contrast media in diagnostic imaging and interventional procedures such as angiography. At present serum creatinine is the only standard test for it. A few studies have been published analyzing the potential use of neutrophil-gelatinase-associated lipocalin (NGAL) in AKI. Aim: The aim of this study is to search for new markers to identify AKI acute renal failure earlier than serum creatinine. Materials and Methods: We studied 100 consecutive patients with normal serum creatinine undergoing angiographic procedure against Urine NGAL, serum NGAL, serum Cystatin C and urinary interleukin-18 (IL-18) at basal, and 2 h, 4 h, 8 h, 24 h, and 48 h after the angiography. Results: There was a significant rise in serum NGAL levels at 2 h, 4 h, and 8 h after angiography and in urinary NGAL levels at 4 h, 8 h, and 24 h after the procedure. Cystatin C rose significantly at 8 h and 24 h after the procedure, On the other hand, there was mild rise in urinary Il-18 levels at 24 h, but not significant. The presence of CIN associated with AKI was 13%. Conclusion: The present study highlighted the importance of serum NGAL, urine NGAL and Cystatin C in detecting AKI associated with contrast administration earlier than serum creatinine

Tinospora cordifolia extract prevents cadmium-induced oxidative stress and hepatotoxicity in experimental rats

Background: Cadmium (Cd) pollution is of serious concern due to its toxic effects in both humans and animals. The study investigates the protective effect of Tinospora cordifolia stem methanolic extract (TCME) on Cd induced hepatotoxicity. Objective(s): The objective of the study was to explore the hepatoprotective effects of T. cordifolia extract. Materials and methods: Rats were administered orally with Cd (5 mg/kg) and TCME (100 mg/kg) for 28 days. At the end of the treatment period, serum and liver tissues homogenates were subjected to biochemical analysis. Results: Cd treated rats showed increased activities of the serum marker enzymes of liver damage such as AST and ALT along with increased levels of LPO and protein carbonyl content in liver tissues. Cd treatment also leads to decreased activities of endogenous antioxidants (SOD, CAT, GSH, GPx and GST), membrane ATPases (Na+K+ATPase, Ca2+ATPase and Mg2+K+ATPase) and the tissue glycoprotein levels (hexose, fucose, hexosamine and sialic acid). Histological analysis revealed vacuolar degeneration of hepatocytes with focal necrosis upon Cd administration. TCME co-treatment restored the biochemical and histological alterations caused by Cd intoxication to near normal levels. Conclusion: The results of the present investigation reveal the hepatoprotective nature of T. cordifolia against Cd induced hepatotoxicity. Keywords: Cadmium, Oxidative stress, Tinospora cordifolia, Hepatotoxicity, Antioxidan

Kidney injury molecule-1: A urinary biomarker for contrast-induced acute kidney injury

Background: Urinary kidney injury molecule 1 (KIM-1) is an early biomarker for renal damage. A few studies have been published analyzing the potential use of urinary KIM-1 as a biomarker for acute kidney injury (AKI). However, no study has been done related to AKI associated with contrast administration. Aim: To search for new markers to identify AKI associated with contrast administration earlier than serum creatinine. Materials and Methods: We studied 100 consecutive patients with normal serum creatinine undergoing angiographic procedure. We assessed urine KIM-1, at 4, 8, and 24 hours after the angiographic procedure. Serum creatinine was measured at basal, 24, and 48 hours after the procedure. Results: There was a significant rise in urinary KIM-1 levels at 24 hours after the angiographic procedure. The presence of contrast induced nephropathy associated with AKI was 12%. Conclusion: The present study highlighted the importance of urinary KIM-1 in detecting AKI associated with contrast administration earlier than Serum creatinine

Versatile Coordination Behavior of Salicylaldehydethiosemicarbazone in Ruthenium(II) Carbonyl Complexes: Synthesis, Spectral, X‑ray, Electrochemistry, DNA Binding, Cytotoxicity, and Cellular Uptake Studies

The reaction of salicylaldehydethiosemicarbazone, [H₂-(Sal-tsc)], with an equimolar amount of [RuHCl­(CO)­(PPh₃)₃] has afforded two complexes, namely [Ru­(H-Sal-tsc)­(CO)­Cl­(PPh₃)₂] (<b>1</b>) and [Ru­(Sal-tsc)­(CO)­(PPh₃)₂] (<b>2</b>), in one pot. The new complexes were separated and characterized by elemental analyses, various spectroscopic techniques (NMR, UV–vis, IR), X-ray crystallography, and cyclic voltammetry. In complex <b>1</b>, the ligand coordinated in a bidentate monobasic fashion by forming an unusual strained NS four-membered ring in 32% yield. However, in <b>2</b>, the ligand coordinated in a tridentate dibasic fashion by forming ONS five- and six-membered rings in 51% yield. Comparative biological studies such as DNA binding, cytotoxicity (MTT, LDH, and NO), and cellular uptake studies have been carried out for new ruthenium­(II) complexes (<b>1</b> and <b>2</b>). From the DNA binding studies, it is inferred that the complex <b>1</b> exhibited electrostatic binding and <b>2</b> exhibited intercalative binding modes. On comparison of the cytotoxicity of the complexes in human lung cancer cells (A549) and liver cancer cells (HepG2), complex <b>2</b> exhibited better activity than <b>1</b>; this may be due to the strong chelation and subsequent electron delocalization in <b>2</b> increasing the lipophilic character of the metal ion into cells

Tetramethylpyrazine Ameliorated Hypoxia-Induced Myocardial Cell Apoptosis via HIF-1α/JNK/p38 and IGFBP3/BNIP3 Inhibition to Upregulate PI3K/Akt Survival Signaling

Background: Hemorrhagic shock (HS) is the major cause of death from trauma. Hemorrhagic shock may lead to cellular hypoxia and organ damage. Our previous findings showed that HS induced a cardiac apoptosis pathway and synergistically caused myocardial cell damage in diabetic rats under trauma-induced HS. Tetramethylpyrazine (TMP) is a major biologically active ingredient purified from the rhizome of Ligusticum wallichii (called Chuang Xiong in Chinese). Chuan Xiong rescued cells from synergistic cardiomyoblast cell injury under high-glucose (HG) conditions plus hypoxia. TMP is one of the most important active ingredients that elevated the survival rate in ischemic brain injury and prevented inducible NO synthase expression to have anti-inflammatory effects against cell damage in different cell types. Method: Here, we further investigate whether TMP can protect against hypoxic (Results: Our results showed that hypoxia mediated through HIF-1α/JNK/p38 activation significantly elevated the levels of the hypoxia-related proteins HIF-1α, BNIP3 and IGFBP3, further enhanced the pro-apoptotic protein Bak and upregulated downstream Caspase 9 and 3, resulting in cell death. All of these phenomena were fully recovered under TMP treatment. We observed that TMP exerted this effect by activating the IGF1 receptor survival pathway, dependent primarily on PI3K/Akt. When PI3K (class I) was blocked by specific siRNA, the hypoxia-induced activated caspase 3 and cell apoptosis could not be reversed by TMP treatment. Conclusion: Our results strongly suggest that TMP could be used to restore hypoxia-induced myocardial cell apoptosis and cardiac hypoxic damage