Structured, functional histology practical modules: An answer to medical students' histology nightmare and the way forward for relevant histology instruction in the Indian undergraduate medical curriculum?

Background: . It is often a challenge to make histology instruction relevant and interesting. We assessed whether structured, worksheet-based histology practical modules with emphasis on functional histology and clinical application, would improve the learning experience and help students focus on relevant functional and clinical correlates. Methods: . In eight practical sessions, 100 students worked as two groups, one group undergoing new intervention practical modules and another group undergoing the routine laboratory practical exercises as a control group. For every pair of laboratory practical exercises, the groups alternated. Spot tests administered in the following week assessed identification ability as well as application of knowledge. Feedback was collected in the form of written questionnaires from faculty and students, student focus group discussion and in-depth interviews. Analysis of test scores as well as feedback was done. Results: . Test scores were better following the intervention method when comparing the overall score as well as its subcomponents of identification and analysis-type questions (p<0.001). The weaker performers in the class as well as high achievers showed better test scores with the intervention method (p<0.001). Feedback from faculty and students reflected better student experience with the intervention method. Suggestions were made to improve the approach further. Conclusion: . Studying histology through structured modules, which emphasize functional and clinical correlates, appears to improve the identification and application ability of the student as well as the student experience.

Clinical anatomy of the inferior epigastric artery with special relevance to invasive procedures of the anterior abdominal wall.

INTRODUCTION: Injury to the inferior epigastric artery (IEA) has been reported following lower abdominal wall surgical incisions, abdominal peritoneocentesis and trocar placements at laparoscopic port sites, resulting in the formation of abdominal wall haematomas that may expand considerably due to lack of tissue resistance. The aim of this study was to localise its course in relation to standard anatomic landmarks and suggest safe areas for performance of invasive procedures. MATERIALS AND METHODS: Sixty IEAs of 30 adult cadavers (male = 19; female = 11) were dissected and the course of the IEA noted in relation to the mid-inguinal point, anterior superior iliac spine (ASIS) and umbilicus. RESULTS: The mean distance of the IEA from the midline was 4.45 ± 1.42 cm at the level of the mid-inguinal point, 4.10 ± 1.15 cm at the level of ASIS and 4.49 ± 1.15 cm at the level of umbilicus. There was an average of 3.3 branches per IEA with more branches arising from its lateral aspect. The IEA was situated within one-third (32%) of the distance between the midline and the sagittal plane through ASIS at all levels. CONCLUSION: To avoid injury to IEA, trocars can be safely inserted 5.5 cm [mean + 1 standard deviation (SD)] away from the midline (or) slightly more than one-third of the distance between the midline and a sagittal plane running through ASIS. These findings may be useful not only for laparoscopic procedures but also for image-guided biopsy, abdominal paracentesis, and placement of abdominal drains.

Topography of inferior epigastric artery relevant to laparoscopy: a CT angiographic study.

PURPOSE: The incidence of inferior epigastric artery (IEA) injury is 0.2-2 %. The aim of this study was to trace the position and course of the inferior epigastric artery in the anterior abdominal wall above the inguinal ligament at three important landmarks, i.e., at the mid-inguinal point, Anterior Superior Iliac Spine (ASIS) and umbilicus in abdominal CT Angiograms. The study also correlates the relationship of body build and the position of the inferior epigastric artery. METHODS: In 50 CT Abdominal angiograms, the course of the inferior epigastric artery was traced and distance between the artery and midline was measured at the above landmarks using measurement tool on the picture archival and communication system. The measurements were analyzed using SPSS version 16 and expressed as mean and standard deviation. Mann-Whitney test was used to compare the mean values and ratios in males and females. Linear regression was done to derive formulas by which the position of the inferior epigastric artery could be found. RESULTS: The mean distance of the inferior epigastric artery from the midline was 5.17 ± 0.93 cm at the level of mid-inguinal point, 4.57 ± 1.05 cm at the level of ASIS and 5.27 ± 1.17 cm at the level of umbilicus. There was a definitive predictive pattern in the course of the artery as seen in correlation and regression analysis. CONCLUSION: The security distance for safe trocar placement was 6 cm at the level of ASIS and 9 cm at the level of umbilicus. Preoperative IEA assessment is helpful in reducing injuries to IEA.

Mitochondrial dysfunction and electron transport chain complex defect in a rat model of tenofovir disoproxil fumarate nephrotoxicity.

The long-term use of tenofovir, a commonly used anti-HIV drug, can result in renal damage. The mechanism of tenofovir disoproxil fumarate (TDF) nephrotoxicity is not clear, although it has been shown to target proximal tubular mitochondria. In the present study, the effects of chronic TDF treatment on the proximal tubular function, renal mitochondrial function, and the activities of the electron transport chain (ETC) complexes were studied in rats. Damage to proximal tubular mitochondria and proximal tubular dysfunction was observed. The impaired mitochondrial function such as the respiratory control ratio, 2-(4,5-dimethyl-2-thiazolyl)-3,5-diphenyl-2H-tetrazolium bromide (MTT) reduction, and mitochondrial swelling was observed. The activities of the electron chain complexes I, II, IV, and V were decreased by 46%, 20%, 26%, and 21%, respectively, in the TDF-treated rat kidneys. It is suggested that TDF induced proximal tubular mitochondrial dysfunction and ETC defects may impair ATP production, resulting in proximal tubular damage and dysfunction.

Depletion of the cellular antioxidant system contributes to tenofovir disoproxil fumarate - induced mitochondrial damage and increased oxido-nitrosative stress in the kidney.

BACKGROUND: Nephrotoxicity is a dose limiting side effect of tenofovir, a reverse transcriptase inhibitor that is used for the treatment of HIV infection. The mechanism of tenofovir nephrotoxicity is not clear. Tenofovir is specifically toxic to the proximal convoluted tubules and proximal tubular mitochondria are the targets of tenofovir cytotoxicity. Damaged mitochondria are major sources of reactive oxygen species and cellular damage is reported to occur after the antioxidants are depleted. The purpose of the study is to investigate the alterations in cellular antioxidant system in tenofovir induced renal damage using a rat model. RESULTS: Chronic tenofovir administration to adult Wistar rats resulted in proximal tubular damage (as evidenced by light microscopy), proximal tubular dysfunction (as shown by Fanconi syndrome and tubular proteinuria), and extensive proximal tubular mitochondrial injury (as revealed by electron microscopy). A 50% increase in protein carbonyl content was observed in the kidneys of TDF treated rats as compared with the control. Reduced glutathione was decreased by 50%. The activity of superoxide dismutase was decreased by 57%, glutathione peroxidase by 45%, and glutathione reductase by 150% as compared with control. Carbonic Anhydrase activity was decreased by 45% in the TDF treated rat kidneys as compared with control. Succinate dehydrogenase activity, an indicator of mitochondrial activity was decreased by 29% in the TDF treated rat kidneys as compared with controls, suggesting mitochondrial dysfunction. CONCLUSION: Tenofovir- induced mitochondrial damage and increased oxidative stress in the rat kidneys may be due to depletion of the antioxidant system particularly, the glutathione dependent system and MnSOD.

Preclinical efficacy of melatonin to reduce methotrexate-induced oxidative stress and small intestinal damage in rats.

BACKGROUND: Methotrexate is widely used as a chemotherapeutic agent for leukemia and other malignancies. The efficacy of this drug is often limited by mucositis and intestinal injury, which are the major causes of morbidity in children and adults. AIM: The present study investigates whether melatonin, a powerful antioxidant, could have a protective effect. METHOD: Rats were pretreated with melatonin (20 and 40 mg/kg body weight) daily 1 h before methotrexate (7 mg/kg body weight) administration for three consecutive days. After the final dose of methotrexate, the rats were sacrificed and the small intestine was used for light microscopy and biochemical assays. Intestinal homogenates were used for assay of oxidative stress parameters malondialdehyde and protein carbonyl content, and myeloperoxidase activity, a marker of neutrophil infiltration as well as for the activities of the antioxidant enzymes. RESULT: Pretreatment with melatonin had a dose-dependent protective effect on methotrexate (MTX)-induced alterations in small intestinal morphology. Morphology was saved to some extent with 20 mg melatonin pretreatment and near normal morphology was achieved with 40 mg melatonin pretreatment. Biochemically, pretreatment with melatonin significantly attenuated MTX-induced oxidative stress (P < 0.01 for MDA, P < 0.001 for protein carbonyl content) and restored the activities of the antioxidant enzymes (glutathione reductase P < 0.05, superoxide dismutase P < 0.01). CONCLUSION: The results of the present study demonstrate that supplementation by exogenous melatonin significantly reduces MTX-induced small intestinal damage, indicating that it may be beneficial in ameliorating MTX-induced enteritis in humans.

Melatonin protects against tenofovir-induced nephrotoxicity in rats by targeting multiple cellular pathways.

Nephrotoxicity is a dose-limiting side effect of long-term use of tenofovir, a reverse transcriptase inhibitor that is used for the treatment of HIV infection and chronic hepatitis B infection. Identifying an agent that prevents tenofovir disoproxil fumarate (TDF)-induced renal injury can lead to its better tolerance, and a more effective treatment can be achieved. The present study is aimed at investigating whether melatonin, a potent antioxidant and anti-inflammatory agent, protects against TDF nephrotoxicity in rats and to determine its cellular targets. Rats were divided into groups and treated as follows. Group I (control): Rats in this group (n = 6) received sterile water only by gavage for 35 days. Group II: Rats (n = 6) in this group received 600 mg/kg body weight TDF in sterile water by gavage for 35 days. Group III: Rats (n = 6) in this group received once daily 20 mg/kg bodyweight melatonin i.p. 2 h before the administration of 600 mg/kg body weight TDF in sterile water by gavage for 35 days. Group IV: Rats were pretreated daily with 20 mg/kg body weight melatonin i.p. 2 h before the administration of sterile water by gavage. All the rats were sacrificed on the 36th day, after overnight fast. Melatonin pretreatment protected the rats against TDF nephrotoxicity both histologically and biochemically. Biochemically, melatonin pretreatment attenuated TDF-induced, oxidative stress, nitrosative stress, mitochondrial pathway of apoptosis, PARP overactivation and preserved proximal tubular function (p < 0.01). This suggests that melatonin may be useful in ameliorating TDF nephrotoxicity.

Neutrophil infiltration and oxidative stress may play a critical role in methotrexate-induced renal damage.

BACKGROUND: Nephrotoxicity is one of the adverse side effects of methotrexate (MTX) chemotherapy. The mechanism of renotoxicity of MTX is not fully understood. It is essential to understand the mechanism of nephrotoxicity of MTX in order to diminish the side effects and hence maximize the benefits of chemotherapy. OBJECTIVES: The aim of the study was to verify whether oxidative stress and neutrophil infiltration play a role in MTX-induced renal damage using a rat model. METHODS: Adult male rats were administered MTX at the dose of 7 mg/kg body weight intraperitoneally for 3 consecutive days and sacrificed 12 or 24 h after the last dose. Vehicle-treated rats served as controls. The kidneys were removed and used for light microscopic and biochemical studies. Myeloperoxidase activity, a marker of neutrophil infiltration was measured in kidney homogenates along with the markers of oxidative damage including protein carbonyl content, protein thiol and malondialdehyde. The activities of the antioxidant enzymes, namely glutathione peroxidase, glutathione S-transferase, superoxide dismutase and catalase, were also assayed. RESULTS: MTX treatment induced damage to the glomeruli and tubules. Plasma creatinine levels in the MTX-treated rats were significantly elevated compared with controls. A significant increase in myeloperoxidase activity (p<0.05) was observed in the kidneys of MTX-treated rats. Protein carbonyl content and malondialdehyde, sensitive and reliable markers of oxidative damage to proteins and lipids, respectively, were significantly elevated (p<0.01) in the kidneys of MTX-treated rats compared with controls. The activities of the antioxidant enzymes, namely, superoxide dismutase and glutathione peroxidase, were significantly elevated (p<0.01 and p<0.05, respectively) in kidneys of rats following MTX treatment. CONCLUSION: The results of the present study provide evidence for the role of neutrophil infiltration and oxidative stress in MTX-induced renal damage. Administration of inhibitors of myeloperoxidase or scavenging hypochlorous acid, the product of myeloperoxidase, by supplementation with antioxidants as an adjuvant therapy may be promising in alleviating the renal side effect of MTX.

NF-κB-iNOS-COX2-TNF α inflammatory signaling pathway plays an important role in methotrexate induced small intestinal injury in rats.

Although methotrexate is widely used in clinics as an anticancer agent, it's utility is limited by its gastrointestinal toxicity, the mechanism of which is unclear. The role of NFκB inflammatory pathway in MTX induced mucositis was investigated in the present study. GI injury was induced in adult Wistar rats by the administration of 3 consecutive i.p . injections of MTX. On the fourth day, the rats were sacrificed and the small intestine was removed; A piece was used for light microscopy, immunohistochemistry, immunofluorescence studies . The mucosa was collected and used for the analysis of protein and mRNA expressions of NFκB and its target genes by the western blot, RT-PCR respectively. MTX treatment resulted in NFκB activation and nuclear translocation as evidenced by immunofluorescence, immunohistochemistry , and western blot. NFκB mRNA was also increased. There was increased protein and mRNA expressions of NFκB target genes, TNF-α, iNOS, COX-2, PLA2, HO-1, HSP70, MMPs 2 and 9 . Aminoguanidine pretreatment (30mg/ 50mg /kg body wt.) attenuated MTX induced activation of NFκB and its proinflammatory target genes and improved MTX induced morphological changes. Aminoguanidine has protective effects against MTX induced gastrointestinal mucositis in rats.

Role for NF-κB inflammatory signalling pathway in tenofovir disoproxil fumarate (TDF) induced renal damage in rats.

Nephrotoxicity due to tenofovir treatment of HIV patients has been reported. However, the mechanism of tenofovir nephrotoxicity is not clear. NFκB is an important proinflammatory transcription factor that plays a pivotal role in oxidative stress-induced inflammation. We hypothesized that NFκB proinflammatory signalling pathway may play a role in tenofovir induced renal damage. Renal damage was induced in adult male Wistar rats by the oral administration of 600 mg/kg body wt. daily for 5 consecutive weeks. Kidneys were removed and used for histological and biochemical analysis. The protein and mRNA expressions of NFκB and its target genes namely iNOS, COX-2 and TNFα, and its inhibitor IκB-alpha were analysed by immunohistochemical methods, western blot and quantitative RT PCR. NFκBp65 activity was determined by ELISA. The protein and mRNA expressions of NFκB p65, iNOS, COX-2 and TNFα were increased in the kidneys of TDF treated rats. The activity of NFκBp65 was increased by 28 fold in the nuclear fractions of the TDF treated rat kidneys. Pretreatment with melatonin, a NFκB inhibitor attenuated TDF induced renal damage. It is concluded that the activation of NFκB and its downstream proinflammatory target genes iNOS, COX-2, and TNF-α may contribute to the pathophysiology of TDF induced renal damage.

Protective effect of ebselen, a selenoorganic drug, against gentamicin-induced renal damage in rats.

Gentamicin is an antibiotic that is widely used against serious and life-threatening gram-negative infections. However, its clinical use is limited by its nephrotoxicity. Oxidative stress and nitrosative stress are reported to play important role in gentamicin nephrotoxicity. In the present study we investigated whether ebselen, an inhibitor of oxidative stress and nitrosative stress prevents or reduces gentamicin-induced renal damage in the rat. For this purpose male Wistar rats were divided into five groups and treated as follows. Group 1 (control group): dimethyl sulphoxide, intraperitoneally, Group 2: Gentamicin 100 mg/kg b.wt. subcutaneously, Group 3: 5 mg/g b.wt. ebselen intraperitoneally, Group 4: 2.5 mg/kg b.wt. ebselen followed by 100 mg/kg b.wt. gentamicin subcutaneously one hour later, and Group 5: 5 mg/kg b.wt. of ebselen followed by 100 mg/kg b.wt. gentamicin one hour later for four consecutive days. Nephrotoxicity was evaluated histopathologically by light microscopy, and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as reduced glutathione, malondialdehyde, and activities of superoxide dismutase and glutathione peroxidase were measured in the kidney. Serum nitrite and nitrate were measured as indicators of nitrosative stress. Treatment of rats with gentamicin resulted in statistically significant reduction in reduced glutathione levels (51%) and the activities of antioxidant enzymes superoxide dismutase (56%) and glutathione peroxidase (39%) as compared with the controls in the kidneys. Renal malondialdehyde level was increased significantly (43%) as compared with the controls. Plasma creatinine levels, urea levels and nitrite levels were significantly increased (4, 4.5 and 160% times respectively) as compared with the controls. Histologically, damage to the renal cortex and medulla was observed moderate to severe tubular necrosis and glomerular congestion. Pretreatment with 2.5 mg/kg b.wt. ebselen prevented gentamicin induced damage to medulla; however, renal cortex showed mild damage and biochemically indicators of oxidative stress and nitrosative stress were significantly reduced. Pretreatment with 5 mg/kg b.wt. ebselen prevented gentamicin-induced oxidative damage and nitrosative damage and renal damage almost completely in 78% of the rats, in the other 22% of the rats, ebselen pretreatment reduced gentamicin-induced renal damage. The results of the present study suggest that ebselen may be useful as a nephroprotective agent.

Preclinical efficacy of melatonin in the amelioration of tenofovir nephrotoxicity by the attenuation of oxidative stress, nitrosative stress, and inflammation in rats.

Abstract Background: Nephrotoxicity is a dose-limiting side effect of long-term use of tenofovir, a reverse transcriptase inhibitor that is used for the treatment of human immunodeficiency virus (HIV) infection. Identifying an agent that prevents tenofovir disoproxil fumarate (TDF)-induced renal injury can lead to better tolerance to TDF, and a more effective treatment can be achieved in HIV infected patients. Recent studies show that oxidative stress, nitrosative stress, and inflammation play a role in TDF nephrotoxicity. The present study is aimed at investigating whether melatonin, a potent antioxidant and anti-inflammatory agent, protects against TDF nephrotoxicity in rats. Methods: Adult male rats were used for the study. Some rats received 600 mg/kg body weight TDF by gavage for 35 days, while others received once daily 20 mg/kg body weight melatonin i.p. 2 h before TDF administration. All the rats were sacrificed on the 36th day, after overnight fast. Results: Melatonin pretreatment protected the rats against TDF nephrotoxicity both histologically and biochemically. Biochemically, melatonin pretreatment attenuated TDF-induced renal oxidative stress, nitrosative stress, and inflammation and preserved proximal tubular function. Histologically, melatonin pretreatment prevented TDF-induced proximal tubular injury and mitochondrial injury such as swelling, disruption of cristae, and deposition of amorphous material in the matrix. It restored the lysosomal and mitochondrial numbers in the proximal tubules also. Conclusions: Melatonin pretreatment protects rats from tenofovir-induced damage to proximal tubular mitochondria by attenuating oxidative stress, nitrosative stress, and inflammation. This suggests that it may be useful in ameliorating TDF nephrotoxicity in humans.

A preclinical study on the protective effect of melatonin against methotrexate-induced small intestinal damage: effect mediated by attenuation of nitrosative stress, protein tyrosine nitration, and PARP activation.

PURPOSE: One of the major toxic side effects of methotrexate (MTX) is enterocolitis. To date, there is no efficient standard treatment for this side effect. Nitrosative stress is reported to play a critical role in MTX-induced mucositis. The purpose of this study is to investigate whether pretreatment with melatonin, an inhibitor of nitro-oxidative stress, prevents MTX-induced mucositis in rats. METHODS: Rats were pretreated with melatonin (20 and 40 mg/kg body weight) i.p. daily 1 h before MTX (7 mg/kg body weight) administration for three consecutive days. After the final dose of MTX, the rats were killed and the small intestines were used for analysis. RESULTS: The small intestines of MTX-treated rats showed moderate to severe injury. The villi were distorted, blunted, and atrophied and focally absent in various segments of the small intestines. Crypt abscesses were also found, suggesting an inflammatory response. Pretreatment with melatonin had a dose-dependent protective effect on MTX-induced mucositis. Morphology was saved to a moderate extent with 20 mg melatonin pretreatment, and near-normal morphology was achieved with 40 mg melatonin pretreatment. Damage to the villi and crypt abscess was reduced. The villi/crypt ratio was almost restored. Melatonin pretreatment protected the small intestines from MTX-induced damage by attenuating nitrosative stress, protein tyrosine nitration and PARP expression. CONCLUSION: Because of its versatility in protecting against nitro-oxidative stress and reducing inflammation, we suggest that melatonin could be beneficial in ameliorating MTX-induced enteritis in humans.

The effects of oral glutamine on cyclophosphamide-induced nephrotoxicity in rats.

Nephrotoxicity is one of the adverse side effects of cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim of the study was to verify whether glutamine, the precursor for glutathione synthesis, prevents CP-induced oxidative stress and renal damage using a rat model. Adult male rats were administered a single dose of 150 mg/ kg body weight of CP intraperitoneally. The glutamine-pretreated rats were administered 1 gm/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutamine-treated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The kidneys were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, reduced glutathione and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in kidney homogenates. CP treatment-induced damage to kidney involved the glomeruli and the tubules. Pretreatment with glutamine reduced CP-induced glutathione depletion and increased myeloperoxidase activity. However, it did not prevent CP-induced lipid peroxidation, protein carbonylation and renal damage. The results of the present study suggest that glutamine pretreatment does not prevent CP-induced lipid peroxidation and renal damage, although it prevents CP-induced glutathione depletion and neutrophil infiltration significantly. It is suggested that mechanisms other than oxidative stress may also be involved and/or oxidative stress may be consequence and not the cause of CP induced renal damage.

Ultrastructural changes in the rat kidney after single dose of cyclophosphamide--possible roles for peroxisome proliferation and lysosomal dysfunction in cyclophosphamide-induced renal damage.

Electron microscopy was used to examine changes in the subcellular organelles of the rat kidney at different time intervals after a single exposure to cyclophosphamide (CP). The morphological changes were studied at different time points (6 hrs, 16 hrs and 24 hrs) after a single-dose administration of CP. Six rats were killed at each time intervals after the administration of CP. Saline-treated rats served as controls. CP administration resulted in alterations in various subcellular organelles including peroxisomes, lysosomes, mitochondria, and the endoplasmic reticulum (ER) of the renal tubular epithelium as well as damage to the glomerulus. The basement membrane of the glomerulus was thickened. Many podocytes were destroyed. The nucleoplasm of the endothelial cell showed fewer granularities. The tubules were distorted and the brush border was destroyed. Two striking features in the renal tubular cells are increase in number and size of the peroxisomes (peroxisome proliferation) and decrease in the number of lysosomes. The mitochondria were elongated and the number was increased in the tubules of CP-treated rats. The ER was dilated. Cell necrosis was also seen. This study is an evidence of changes in morphology of rat kidney after induction of renal damage by a single dose of CP. Since transmission electron microscopy is the highest magnification tool at present, it can be useful in estimating the degree of injury and outcome of alternative treatment strategies in the management of CP-induced renal damage after establishing a scoring system.

Oral glutamine attenuates cyclophosphamide-induced oxidative stress in the bladder but does not prevent hemorrhagic cystitis in rats.

Cyclophosphamide (CP) is widely used in the treatment of cancer and non-malignant disease states such as rheumatoid arthritis. Hemorrhagic cystitis is a major dose-limiting side effect of CP. The incidence of this side effect is related to the dosage and can be as high as 75%. Elimination of the side effects of CP can lead to better tolerance of the drug, and a more efficient therapy can be achieved for patients in need of CP treatment. Several studies have demonstrated that oxidative stress and neutrophil infiltration play important roles in CP-induced bladder damage. Glutamine is utilized under clinical conditions for preventing chemotherapeutic drug-induced side effects, based on its ability to attenuate oxidative stress. The aim of the study is to verify whether glutamine prevents CP-induced oxidative stress and bladder damage using a rat model. Adult male rats were administered 150 mg/kg body weight of CP intraperitoneally. Glutamine pretreated rats were administered 1 g/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutamine-treated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The urinary bladders were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in bladder homogenates. CP treatment induced hemorrhagic cystitis in the rats. Pretreatment with glutamine significantly reduced CP-induced lipid peroxidation (p < 0.01), protein oxidation (p < 0.01), and increase in myeloperoxidase activity (p < 0.05). However, it did not prevent CP-induced bladder damage. The results of the present study show that glutamine pretreatment does not attenuate CP-induced hemorrhagic cystitis, although it prevents CP-induced oxidative stress and neutrophil infiltration significantly. It is therefore necessary to clarify the utility of glutamine as a chemoprotective agent before it is recommended in the market as a nutrient supplement.

Anatomy education in a changing medical curriculum in India: medical student feedback on duration and emphasis of gross anatomy teaching.

Authors report here a survey of medical student feedback on the effectiveness of two different anatomy curricula at Christian Medical College, Vellore, India. Undergraduate medical students seeking the Bachelor in Medicine and Bachelor in Surgery (M.B.B.S.) degrees were divided into two groups by the duration of their respective anatomy curriculum. Group 1 students had completed a longer, 18-month curriculum whereas Group 2 counterparts followed a shorter, 12-month curriculum. Students' responses to a questionnaire were studied. Analysis of feedback from Groups 1 and 2 contrasted the effectiveness of the two anatomy curricula. The coverage of gross anatomy was rated adequate or more than adequate by 98% of Group 1 and 91% of Group 2. A desire for greater emphasis on gross anatomy teaching was expressed by 24% of Group 1 and 50% of Group 2 (P = 0.000). Two-thirds of all students felt that the one-year program was not adequate, and 90% of Group 1 and 74% of Group 2 felt that clinically oriented anatomy teaching required more emphasis. Dissection was helpful or very helpful for 94% of Group 1 and 88% of Group 2. This study suggests that a better understanding of gross anatomy was gained from a course of longer duration (18 months with 915 contact hr vs. 12 months with 671 contact hr). Students who completed the longer anatomy course had greater appreciation of the need for clinically oriented anatomy teaching and dissection.