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Background: Smoking is one of the leading causes of millions of deaths worldwide. During cigarette smoking, most affected and highly exposed cells are the alveolar epithelium and generated oxidative stress in these cells leads to death and damage. Several studies suggested that oxidative stress causes membrane remodeling via Phospholipase A2s but in the case of cigarette smokers, mechanistically study is not yet fully defined. In view of present perspective, we evaluated the involvement of cytosolic phospholipase A2 (cPLA2) IVA as therapeutic target in cigarette smoke induced pathologies in transformed type I and type II alveolar epithelial cells. Methods: Transformed type I (WI26) and type II (A549) alveolar epithelial cells were used for the present study. Cigarette smoke condensate (CSC) was prepared from most commonly used cigarette (Gold Flake with filter) by the Indian population. CSC-induced molecular changes were evaluated through cell viability using MTT assay, reactive oxygen species (ROS) measurement using 2,7 dichlorodihydrofluorescin diacetate (DCFH-DA), cell membrane integrity using fluorescein diacetate (FDA) and ethidium bromide (EtBr) staining, super oxide dismutase (SOD) levels, cPLA2 activity and molecular involvement of specific cPLA2s at selected 24 h time period. Results: CSC-induced response on both type of epithelial cells shown significantly reduction in cell viability, declined membrane integrity, with differential escalation of ROS levels in the range of 1.5-15 folds and pointedly increased cPLA2 activity (p < 0.05). Likewise, we observed distinction antioxidant potential in these two types of lineages as type I cells had considerably higher SOD levels when compared to type II cells (p < 0.05). Further molecular expression of all cPLA2s increased significantly in a dose dependent manner, specifically cytosolic phospholipase A2 IVA with maximum manifestation of 3.8 folds. Interestingly, CSC-induced ROS levels and cPLA2s expression were relatively higher in A549 cells as compared to WI26 cells. Conclusions: The present study indicates that among all cPLA2s, specific cPLA2 IVA are the main enzymes involved in cigarette smoke induced anomalies in type I and type II lung epithelial cells and targeting them holds tremendous possibilities in cigarette smoke induced lung pathologies. [ABSTRACT FROM AUTHOR]

Background and Aims 14 C-urea breath test (14 C- UBT) is considered as 'gold standard' for detection of active gastric H. pylori infection. However, till date no comparative study using encapsulated and non-encapsulated 14 C- UBT protocols has been conducted in same subjects in identical conditions. We monitored gastric fate of capsule containing 14 C-urea with real time display and compared sensitivities of these protocols at different time points of breath collection. Methods Non-encapsulated 14 C- UBT was performed using 74 k Bq of 14 C-urea in 100 dyspeptic patients by collecting breath samples at 10, 15 and 20 minutes. Thereafter, within 2 days a gelatin capsule containing 14 C-urea along with 6.0 MBq of 99m Tc-diethylene triamine penta-acetic acid was administered to each patient for real time display of capsule movement and its fate in gastrointestinal tract by gamma camera. Simultaneously, breath samples were collected for 14 CO2 measurement during image acquisition. Results Employing non-encapsulated 14 C- UBT, 74 out of 100 dyspeptic patients were found to be H. pylori positive. Discordant 14 C- UBT results were obtained in 4/74 (5.4%) cases using these two protocols. By employing encapsulated and nonencapsulated 14 C- UBT protocols, sensitivities of 14 C- UBT were found to be 90.5 versus 98.6% at 10 and 91.8 versus 97.2% at 15 minutes respectively; while these were 94.6 versus 100, 90.7 versus 98.6 and 83.7 versus 93.2% considering any one, two or all three positive values respectively. Conclusions Incomplete/non-resolution of 14 C-urea capsule in stomach during the phase of breath collections appears to decrease sensitivity of encapsulated 14 C- UBT as compared to nonencapsulated protocol for detection of H. pylori infection. [ABSTRACT FROM AUTHOR]

Background and Aim: Previous studies have shown that while performing the 14C-urea breath test (14C-UBT) for the detection of Helicobacter pylori (H. pylori), there is possibility of false-positive results due to the other urease producing bacteria present in oropharynx, if breath samples are obtained within 30 min after administration of non-capsulated 14C-urea. Therefore, we have exclusively evaluated the kinetics of 14carbon dioxide (14CO2) excretion by oral commensal flora to theoretically propose optimum breath collection timings for 14C-UBT. Methods: Multiple breath samples up to 15 min were collected in 0.25 mmol benzethonium hydroxide from 25 healthy volunteers after they withheld 37 kBq (1 μCi) of 14C-urea in their mouths for 15 s and then expectorated the tracer. The test was repeated on the same subjects without and with mouth cleansing protocols. Breath 14CO2 content was measured by the Liquid Scintillation Counter (1409; Wallac, Turku, Finland) and results were expressed as 14CO2 excretion per mmol breath CO2 (% administered dose). Results: Peak breath radioactivity at 1 min in the former protocol was 3.53 times higher than the latter which declined subsequently with a half time of 1 min and 2.5 min, and reached baseline levels by 15 and 10 min, respectively. The peak radioactivity (100%) at 1 min declined by 94% and 97.8% in the former and later protocols, respectively, at 15 min. Although magnitude of the peak varied in different subjects, the shape of curve remained almost similar in all cases. Conclusions: Without mouth cleansing, oral micro flora excreted more 14CO2 up to 15 min after administration of non-capsulated 14C-urea. Therefore, it is proposed that two breath samples may be obtained either at 15 and 20 min without or at 10 and 15 min with mouth cleansing protocols for reliable analysis of 14C-UBT data for H. pylori detection. [ABSTRACT FROM AUTHOR]

14C-urea breath test (UBT) is considered to be an accurate diagnostic test for the detection of active Helicobacter pylori infection. Various test meals are used in 14C-UBT to slow down gastric emptying, and to enhance the gastric distribution, in order to increase the time and area of contact between microorganisms and the tracer substrate. The aim of the present paper was to evaluate the effect of gastric environment on the performance of 14C-UBT using an alkaline and an acidic liquid test meal having gastric emptying retardant effect. The comparison of 14C-UBT was done with liquid test meals (200 mL water) comprising (i) plain drinking water (PDW); (ii) 1.3 g or 3.0 g citric acid (CA); and (iii) 3.0 g trisodium citrate (TSC). Eighteen patients (37 ± 12 years, range 18–57 years) with complaints of dyspepsia participated in the study. The status of H. pylori was confirmed by histology and rapid urease test. A total of 93 kBq of 14C-urea (0.5 mL) in a gelatin capsule was orally administered along with liquid test meals to the overnight fasting subjects. Breath samples were collected and radioactivity measured. Results were expressed as 14CO2/mmol exhaled CO2 as percentage of administered radioactive urea. Higher acidic gastric environment (pH approx. 2.0) with CA was found to increase the exhaled 14CO2 level in a dose-dependent manner as compared to PDW and TSC meal ( P < 0.05) at all time points. With TSC test meal, the expired 14CO2 level decreased in the lower acidic gastric environment (pH approx. 5.3). The peaks of exhaled 14CO2 with TSC test meal were observed at the same time points as that with PDW and CA test meals. The 14C-UBT with TSC was found to be positive in 77% of patients (10/13). Better interaction between the microbial urease and 14C-urea, caused by a test meal that retards gastric emptying and that changes gastric pH, plays an important role in hydrolysis of the administered 14C-urea by H. pylori urease. © 2005 Blackwell Publishing Asia Pty Ltd [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Increased Superoxide Formation Induced by Irradiation Preconditioning Triggers Kidney Resistance to Ischemia-Reperfusion Injury in Mice," by Jinu Kim et al. in a 2009 issue.

Background: 14C-urea breath test (14C-UBT) is employed as a 'gold standard' technique for the detection of active gastric Helicobacter pylori infection and is recommended as the best option for "test-and-treat" strategy in primary health care centers., Aim: To compare the performance of capsulated and non-capsulated 14C-UBT protocols for the detection of H. pylori infection in patients., Methods: Fifty eight H. pylori infected patients underwent routine upper GI endoscopy and biopsies were processed for rapid urease test (RUT) and histopathology examination. Capsulated 14C-UBT was done in a novel way by using 74 kBq of 14C-urea along with 6.0 MBq of 99mTc-diethylene triamine penta-acetic acid (99mTc-DTPA) to simultaneously monitor the movement and the fate of ingested capsule after delineating the stomach contour by using 20.0 MBq of 99mTechnetium pertechnetate (99mTcO4-) under dual head gamma camera. Non-capsulated 14C-UBT was performed within 2 days of the previous test and the results of these protocols were compared., Results: In 3 out of 58 H. pylori positive cases (5.17%), 14C-UBT results were found to be negative by using the capsulated method. Interestingly, on monitoring the real time images of the capsule in these cases it was found that misdiagnosis of H. pylori infection occurred mainly due to either rapid transit of the 14C-urea containing capsule from the upper gastric tract or its incomplete resolution in the stomach during the phase of breath collection., Conclusion: Use of non-capsulated '4C-UBT protocol appears to be a superior option than the conventional capsule based technique for the detection of H. pylori infection.