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Biomedical subjects

B Agarwal

Publications and source records attributed to B Agarwal.

16 recordsLinked to original sources
PubMed2002

Regional variation in the distribution of subtypes of lymphoid neoplasms in India.

Lymphoid malignancies (LM) are a heterogeneous group of tumours. The relative frequencies of the various types of LMs vary across geographic regions. The pattern in India shows significant differences from the rest of the world. As India is a vast country, we set out to investigate whether there are regional differences in the relative frequencies of the various LMs. A total of 562 LMs from three different regions in India--Barshi (western India, 102 cases), Pondicherry (southern India, 156 cases) and Jaipur (northern India, 304 cases) were analysed according to the WHO classification. The non-Hodgkin lymphoma (NHL) to Hodgkin disease (HD) ratio was 6.28 in Barshi, 1.26 in Pondicherry and 2.27 in Jaipur. The frequency of HD's various subtypes did not significantly differ among the three regions. While T-cell NHLs constituted only 12.5% of NHLs at Barshi, they accounted for 31 and 27.5% of all NHLs at Pondicherry and Jaipur, respectively. There were also notable differences in the specific subtypes of NHL between the three different geographic regions in India.

Demography↗
PubMed2001

Endoscopic ultrasonography in the diagnosis and staging of pancreatic neoplasms.

BACKGROUND: Pancreatic cancer is the fourth leading cause of death among Americans. Twenty-eight thousand cases of pancreatic cancer are diagnosed annually and about the same number of patients die of pancreatic cancer every year. Most patients with pancreatic cancer are diagnosed when the tumor is 3 cm or more in diameter. Most pancreatic cancers are metastatic at the time of diagnosis and the median survival is only 18-20 mo. Overall, actual 5-yr survival is about 10% and has not changed much over several decades. Curative surgical resection is currently believed to offer the only chance of long-term survival in these patients. Difficulty in the early diagnosis of pancreatic cancer remains a major obstacle in improving outcomes in these patients. Screening for pancreatic cancer is currently not recommended. However, recent developments in endoscopic ultrasound (EUS) and cytological EUS-guided fine-needle aspiration (FNA) allow early diagnosis of pancreatic cancer with histological confirmation. EUS-FNA in conjunction with helical CT also provides reliable preoperative staging of pancreatic tumors. EUS with FNA therefore appears to be a promising tool in the fight against pancreatic cancer.

Biopsy, Needle↗
PubMed1999

Lovastatin augments sulindac-induced apoptosis in colon cancer cells and potentiates chemopreventive effects of sulindac.

BACKGROUND & AIMS: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (HRIs) were found incidentally to reduce new cases of colon cancer in 2 large clinical trials evaluating coronary events, although most patients in both treatment and control group were taking nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs are associated with reduced colon cancer incidence, predominantly by increasing apoptosis. We showed previously that lovastatin induces apoptosis in colon cancer cells. In the present study we evaluated the potential of combining lovastatin with sulindac for colon cancer chemoprevention. RESULTS: Lovastatin, 10-30 micromol/L, augmented sulindac-induced apoptosis up to 5-fold in 3 colon cancer cell lines. This was prevented by mevalonate (100 micromol/L) or geranylgeranylpyrophosphate (10 micromol/L) but not farnesylpyrophosphate (100 micromol/L), suggesting inhibition of geranylgeranylation of target protein(s) as the predominant mechanism. In an azoxymethane rat model of chemical-induced carcinogenesis, the total number of colonic aberrant crypt foci per animal (control, 161 +/- 11) and the number of foci with 4+ crypts (control, 40 +/- 4.5) decreased to 142 +/- 14 (NS) and 43 +/- 2.9 (NS), respectively, with 50 ppm lovastatin alone; to 137 +/- 5.4 (P = 0.053) and 36 +/- 2.1 (NS) with 80 ppm sulindac alone; and to 116 +/- 8.1 (P = 0.004) and 28 +/- 3.4 (P = 0.02) when 50 ppm lovastatin and 80 ppm sulindac were combined. CONCLUSIONS: Addition of an HRI such as lovastatin may augment chemopreventive effects of NSAIDs or/and may allow lower, less toxic doses of these drugs to be used.

Animals↗
PubMed1999

Lovastatin augments apoptosis induced by chemotherapeutic agents in colon cancer cells.

Beta-hydroxy-beta-methylglutaryl coA reductase inhibitors (HRIs) inhibit isoprenylation of several members of the Ras superfamily of proteins and therefore have important cellular effects, including the reduction of proliferation and increasing apoptosis. Significant toxicity at high doses has precluded the use of HRIs as a monotherapy for cancers. We therefore studied whether combinations of the HRI lovastatin with standard chemotherapeutic agents would augment apoptosis in colon cancer cells. In the colon cancer cell lines SW480, HCT116, LoVo, and HT29, lovastatin induced apoptosis with differing sensitivity. Pretreatment with lovastatin significantly increased apoptosis induced by 5-fluorouracil (5-FU) or cisplatin in all four cell lines. Lovastatin treatment resulted in decreased expression of the antiapoptotic protein bcl-2 and increased the expression of the proapoptotic protein bax. The addition of geranylgeranylpyrophospate (10 microM) prevented lovastatin-induced augmentation of 5-FU and cisplatin-induced apoptosis; mevalonate (100 microM) was partially effective, whereas cotreatment with farnesyl pyrophosphate (100 microM) had no effect. These data imply that lovastatin acts by inhibiting geranylgeranylation and not farnesylation of target protein(s). Our data suggest that lovastatin may potentially be combined with 5-FU or cisplatin as chemotherapy for colon cancers.

Antineoplastic Agents↗
PubMed1996

Increased intestinal Bak expression results in apoptosis.

Cells in the human intestinal epithelium have a life-span of around 5 days before being lost by apoptosis at the luminal surface. We examined changes in expression of the Bcl-2 gene family which may be responsible for epithelial cell loss. In the normal and neoplastic colon, mucosal expression of immunoreactive Bak co-localized with sites of epithelial cell apoptosis. Inducing apoptosis in the human colon cancer cell line HT29 and the rat normal small intestinal cell line IEC 18 in culture was accompanied by increased Bak expression without consistent changes in expression of other Bcl-2 homologous proteins. Bak appears to be the endogenous Bcl-2 family member best correlated with intestinal cell apoptosis.

Animals↗
PubMed1996

Induction of gastric epithelial apoptosis by Helicobacter pylori.

BACKGROUND: Helicobacter pylori may promote gastric carcinogenesis through increasing gastric epithelial cell proliferation. How H pylori does so is unknown. Programmed, non-necrotic, cell death (apoptosis) occurs throughout the gut and is linked to proliferation. It was hypothesised that H pylori may induce hyper-proliferation through increasing apoptosis. AIM: To measure the effect of H pylori infection on gastric epithelial apoptosis in situ. PATIENTS: Patients with duodenal ulcers treated to eradicate H pylori and patients with H pylori negative non-ulcer dyspepsia. METHODS: Retrospective quantification of apoptotic epithelial cells in situ from formalin fixed biopsy specimens, counted after staining by terminal uridine deoxynucleotidyl nick end-labelling. RESULTS: In the uninfected stomach, apoptotic cells were rare and situated in the most superficial portion of gastric glands (mean 2.9% of epithelial cells). In H pylori infection, they were more numerous and were located throughout the depth of gastric glands, comprising 16.8% of epithelial cells, falling to 3.1% after H pylori eradication, p = 0.017. Apoptotic cell number did not correlate with the degree of histological gastritis. CONCLUSIONS: These results suggest that H pylori induces epithelial apoptosis in vivo. Increased apoptosis may be the stimulus for a compensatory hyperproliferative and potentially preneoplastic response in chronic H pylori infection.

Adult↗
PubMed1994

Gender, resistance and land: interlinked struggles over resources and meanings in South Asia.

This article examines the nature of women's resistance to gender inequities in resource distribution and ideological representation. It argues that to understand how women perceive these inequities it is necessary to take into account not only their overt protests but also the many covert forms their resistance might take. At the same time, to significantly alter gendered structures of property and power it appears necessary to move beyond 'individual-covert' to 'group-overt' (organized collective) resistance. These issues are examined here especially in the context of women's struggles for land rights and gender equality in South Asia. Although historically South Asian women have been important participants in peasant movements, these movements have not been typified by women demanding independent land rights or contesting iniquitous gender relations within the movements and within their families. Some recent challenges in this direction indicate that attaining gender equality in the distribution of productive resources will require a simultaneous struggle against constraining ideological constructions of gender, including (in many regions) associated social practices such as purdah. And in both types of struggle (namely concerning resources and gender ideologies), group-overt resistance is likely to be of critical importance.

Agriculture↗
PubMed1991

Penile cancer--the sentinel lymph node controversy.

The management of lymph nodes in penile cancer has always been a problem. Sentinel lymph node biopsy was supposed to solve this problem but has not been universally accepted due to conflicting results. We herein present a case of penile cancer with bilateral pathologically positive inguinal lymph nodes associated with concurrent negative sentinel lymph node biopsies. We discuss the possible reasons for this situation and suggest guidelines to study this issue.

Biopsy↗
PubMed1978

Pharmacology of intraperitoneal cefazolin in patients undergoing peritoneal dialysis.

Cefazolin was added to dialysis fluid in nine patients with renal failure undergoing peritoneal dialysis with 2 liters/h per exchange. With 50 mg/liter (three patients), the first measurable mean serum concentration was 3.7 mug/ml (range, 2.4 to 4.9 mug/ml) after three exchanges and was 30.3 mug/ml (range, 13.3 to 44.3 mug/ml) after 24 exchanges. After 18 to 24 more exchanges without cefazolin, the mean serum concentration was 12.3 mug/ml (range, 3.8 to 24.6 mug/ml). The mean concentration in the dialysis outflow was 26.9 mug/ml (range, 2.5 to 58.5 mug/ml). With 150 mg/liter (six patients), the mean serum concentration was 5.2 mug/ml (range, 3.6 to 7.8 mug/ml) after the first exchange and 8.4 (range, 6.1 to 14.0 mug/ml), 15.0 (range, 8.2 to 23.5 mug/ml), and 71.9 (range, 26.2 to 142.1 mug/ml) mug/ml after the second, third, and twenty-fourth exchanges, respectively. After 17 to 24 more exchanges without cefazolin, the mean serum concentration was 38.2 mug/ml (range, 15.4 to 65.7 mug/ml). The mean concentration in the dialysis outflow was 71.4 mug/ml (range, 21.9 to 150.8 mug/ml). After 1 g of cefazolin was given intraperitoneally with no more dialysis, serum concentrations rose by a mean of 62.5 mug/ml (range, 18.9 to 107.8 mug/ml). The maximum rise occurred within 2 h with two-thirds of the rise occurring within 30 min. During the subsequent 22 h levels dropped to 65.4% of the peak.

Acute Kidney Injury↗
PubMed1975

Resolution of an iatrogenic coronary artery thromboembolus.

A patient with an iatrogenic coronary thromboemboulus, sustained during selective left coronary catheterization is presented. The embolus was identified by angiography and its complete resolution was documented in the same manner three months later. Despite chest pain and elevation of the cardiac enzymes, the electrocardiogram showed only nonspecific changes and the absence of macroscopically identifiable infarction was demonstrated at thoracotomy. Thromboembolization may be a more common cause of complication with the Judkins technique than generally realized but may be compatible with complete recovery and be avoided by special catheterization practices.

Cardiac Catheterization↗
PubMedDate not supplied

Autoimmune hemolytic anemia.

Immune hemolytic anemia can be either isoimmune or autoimmune. Autoimmune hemolytic anemias (AIHA) consist of group of disorders whose common characteristics are the presence of an antibody which in turn causes short red blood cell (RBC) life. The rate and site of hemolysis and hence the clinical manifestations depends on the type of antibody attached and its propensity to fix complement. Antibodies of the IgG class are most commonly responsible for AIHA in children. Rh erythrocyte antigen is involved in more than 70% of cases. Since the antibody has its maximal activity at 37 degrees C, the resultant hemolysis is called warm antibody induced hemolytic anemia. This is a severe life threatening condition, the clinical features are: sudden onset of pallor, jaundice and dark urine. The cornerstone of diagnosis is a positive Coomb's antiglobulin test in the presence of hemolysis. Coomb's test has false negative and false positive rates in about 2-4% and 8% of all cases respectively. The modalities for treatment of warm AIHA include blood transfusion, steroid therapy, intravenous gammaglobulin, plasma-pheresis and splenectomy. The choice depends on the severity of the disease and child's response to therapy.

Anemia, Hemolytic, Autoimmune↗