PubMed Health⌕ Search

Biomedical subjects

S K Banerjee

Publications and source records attributed to S K Banerjee.

At least 55 records · Page 3Linked to original sources
PubMed1999

Prospective long-term endoscopic and histologic follow-up of gastric lymphoproliferative disease of early stage IE low-grade B-cell mucosa-associated lymphoid tissue type following Helicobacter pylori eradication treatment.

Long-term endoscopic and histologic follow-up of Stage IE gastric lymphoproliferative disease of the low-grade B-cell mucosa-associated lymphoid tissue (MALT) type following cure of H. pylori was undertaken. Clinical and endoscopic features (age, race, endoscopic appearance, cure of H. pylori and duration of follow-up) were also evaluated as potential prognostic indicators for complete or near-complete regression of low-grade MALT lymphoma. Sixty-eight MALT lymphoma patients prospectively underwent H. pylori eradication. follow-up at periodic intervals with endoscopy and extensive mucosal biopsy protocol on 65 patients ranging from 12 weeks up to 73 months (mean +/- SD of 22.5+/-15.8 months) has been completed. H. pylori was eradicated in 89.2% of MALT lymphoma patients with complete histologic regression noted in 58.5%, near-complete regression in 18.5%, partial in 4.6%, and no change in 18.5%. Univariate analysis revealed two factors predictive of complete and/or near complete MALT lymphoma regression, H. pylori cure (p=0. 001) and duration of follow-up (p=0.001). Stepwise logistic regression also demonstrated that both H. pylori cure (p<0.0001) and duration of follow-up (p<0.02) were independently associated with complete and near complete MALT lymphoma regression. Age, race, and endoscopic appearance were not predictive of regression. We conclude that this lymphoproliferative disease predictably undergoes complete to near-complete histologic regression at variable rates following cure of H. pylori in a majority of patients.

Adult↗
PubMed1999

Cold stress-induced modulation of cell immunity during acute Toxoplasma gondii infection in mice.

Infection with Toxoplasma gondii in the acute phase results in nonspecific suppression of immunologic function in mice and humans. The present study examined the effects of a physical stressor, i.e., cold stress (CS), on macrophage function (nitrite production, parasite survival) and splenic blastogenesis in the acute phase of murine T. gondii infection. In our stress paradigm, female BALB/c mice were placed in cold water (1 +/- 0.5 C), 5 min each day for 8 days. Nitrite production and parasite survival were measured in cultured peritoneal macrophages obtained from mice subjected to CS after in vivo activation with interferon-gamma/lipopolysaccharide (CS + ACT), and in vitro infection with T. gondii tachyzoites. Peritoneal macrophages from CS + ACT mice showed decreased nitrite production compared to control but activated cells (ACT). Spleen cell proliferation to in vitro stimulation with the mitogens concanavalin A (Con A) and anti-CD3, and Toxoplasma lysate antigen (TLA) was measured in splenocytes obtained from BALB/c mice during the acute phase of infection with T. gondii. Mice subjected to CS and infection (CS + INF) had maximum splenocyte proliferation on days 8 and 15 followed by a subsequent decline on day 28 postinoculation (PI). In contrast, infected mice not subjected to stress (INF) showed decreased splenocyte proliferation on days 8 and 15 followed by an increase on day 28 PI. The rate of mortality was decreased in the CS + INF compared to the INF group during acute infection. These results suggest that CS may alter the pathogenesis of T. gondii infection by modulating acute-phase responses, provoking a state of transient disequilibrium between the host and parasite.

Acute Disease↗
PubMed1999

Cold stress-induced modulation of inflammatory responses and intracerebral cytokine mRNA expression in acute murine toxoplasmosis.

The effects of a physical stressor, cold water stress (CWS), within the central nervous system were investigated in the acute phase of infection with Toxoplasma gondii. Female BALB/c mice were subjected to CWS for 5 min each day for 8 days prior to oral infection with 20 cysts of the low virulent ME 49 strain. Animals were killed at 10-day intervals to detect inflammation, gliosis, and expression of intracerebral cytokine mRNAs. Zones of inflammation were detected by Nissl staining and gliosis by immunoreactivity to glial fibrillary acidic protein. Larger zones of inflammation and reactive astrogliosis were consistently observed in mice subjected to CWS and infected (CWS +INF) compared to control infected (INF) mice. Expression of interleukin (IL)-1beta, IL-2, IL-12, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and inducible nitric oxide synthase (iNOS) were decreased in CWS+INF mice at 10 days postinoculation (PI), followed by a gradual increase after day 20 PI. This was in contrast to increased expression of these cytokines at 10 days PI in INF mice with a gradual decline thereafter. Inflammation and astrogliosis in CWS+INF mice were associated with an increased expression of IL-1beta, IL-6, IL-12, and TNF-alpha between 20 and 30 days PI. These findings correlated with the continuous gene expression of tachyzoite surface antigen (SAG)-1 mRNA in CWS+INF mice compared to its sharp decline in INF mice after 20 days PI. These results suggest that CWS delays regulation and control of intracerebral Toxoplasma gondii during acute infection in BALB/c mice by decreasing the early expression of IFN-gamma, IL-2, TNF-alpha, iNOS, IL-1beta, and IL-12, while increasing the expression of IL-6, a counterregulatory cytokine.

Acute Disease↗
PubMed1998

Identification of an ABC transporter gene that exhibits mRNA level overexpression in fluoroquinolone-resistant Mycobacterium smegmatis.

We describe here the PCR amplification of a DNA fragment (mtp1) from Mycobacterium smegmatis using primers derived from consensus sequences of the ABC family of transporters. The fragment encodes amino acid sequences that exhibited significant homology with different ABC transporters. Amino acid sequence alignment of the full length gene with other transporters identified the ABC protein as the B-subunit of the phosphate specific transporter. Strikingly, a M. smegmatis colony which exhibited a high level of ciprofloxacin resistance showed mRNA level overexpression of mtp1. Thus this is the first report in any prokaryote indicating differential expression of an ABC transporter in a fluoroquinolone resistant colony.

ATP-Binding Cassette Transporters↗
PubMed1998

Specificity of polymerase chain reaction monoclonality for diagnosis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma: direct comparison to Southern blot gene rearrangement.

The specificity of polymerase chain reaction monoclonality in the diagnosis of gastric lymphoma was prospectively evaluated. Gastric mucosal tissue from normal gastric mucosa (N = 13), benign gastric ulcers (N = 3), chronic Helicobacter pylori gastritis (N = 3), gastric mucosa-associated lymphoid tissue (N = 16), and gastric lymphoma (N = 15) was obtained. Polymerase chain reaction amplification of the heavy-chain framework 2A gene was performed. The sensitivity and specificity of heavy-chain clonality, in the detection of gastric lymphoma, were 73.3% and 45.7%, respectively. Determination of monoclonality by polymerase chain reaction methodology is not an acceptable technique for confirming the diagnosis of gastric lymphoma as it is too sensitive, detecting minute populations of clonal lymphocytes that occur in benign diseases as well as larger populations of clonal lymphocytes associated with malignant gastric lymphoproliferative diseases. Southern blot gene rearrangement testing should be utilized to determine clonality in the evaluation of gastric lymphocytic infiltrates.

Autoradiography↗
PubMed1998

Quick-FISH: a rapid fluorescence in situ hybridization technique for molecular cytogenetic analysis.

A rapid and simplified fluorescence in situ hybridization (FISH) technique for the detection of human chromosome-specific centromeric probes is described. Using chromosomes 1-, 4-, 11- and Y-specific fluorescence-labeled probes, the modified, or quick-FISH technique, was compared to two conventional FISH methods. The modified FISH technique detected human chromosomes without sacrificing sensitivity or signal quality in both fresh-frozen and paraffin-embedded tissue sections. Further studies demonstrated that this technique can be used with simultaneous application of dual-color probes. This novel technique offers the advantages of being simpler to perform and faster than conventional techniques. The quick-FISH technique can be substituted for any sensitive conventional FISH method for molecular cytogenetic analysis in fresh, fresh-frozen or paraffin-embedded tissues.

Aneuploidy↗
PubMed1997

Non-random loss of chromosome 3 during transition of Helicobacter pylori-associated gastric MALT to B-cell MALT lymphoma revealed by fluorescence in situ hybridization.

Acquired gastric mucosa-associated lymphoid tissue (MALT) accumulates as a result of long-standing Helicobacter pylori (H. pylori) infection and from this acquired MALT, low-grade B-cell MALT lymphoma may develop. Carcinogenesis is a multistep, multifactorial process involving the progressive accumulation of genetic changes. To determine whether numerical chromosomal alterations are involved in the transition of H. pylori-associated human gastric MALT to low-grade B-cell MALT lymphoma, frozen biopsy specimens prospectively obtained from H. pylori positive gastric MALT and gastric MALT lymphoma patients, as well as normal control patients (normal gastroscopy/gastric mucosal histology/H. pylori negative), were analyzed by fluorescence in situ hybridization (FISH). Fluorescent, directly labeled alpha-satellite DNA probes, specific for the centromeres of chromosomes 1, 3, 4, 11, 17 and Y were used in this study. The non-random loss of chromosome 3 was detected in two MALT patients and in all five MALT lymphoma patients. Trisomy 17 was detected in one MALT patient and one MALT lymphoma patient. Trisomy 1 was detected in a single MALT lymphoma patient as was trisomy 3. None of the MALT patients had trisomy 3 or trisomy 1. Monosomy 17 was noted in one MALT lymphoma patient. Clonal aneusomy was not observed in any patient for chromosomes Y, 4 or 11. These results suggest that the consistent loss of chromosome 3 may be an important genetic alteration in the transformation of H. pylori-associated gastric MALT into low-grade B-cell gastric MALT lymphoma.

Adult↗
PubMed1997

Biphasic estrogen response on bovine adrenal medulla capillary endothelial cell adhesion, proliferation and tube formation.

Abnormal angiogenesis underlies many pathological conditions and is critical for the growth and maintenance of various types of tumors, including hormone-dependent cancers. Since estrogens are potent carcinogens in humans and rodents, and are involved in regulating angiogenesis, this study was designed to examine the effect of estrogen on the behavior of an established bovine capillary endothelial cell line, a simple and physiologically relevant model of the capillary wall. The results demonstrate that 17beta-estradiol (E2), at different conditions, exerts both stimulatory and inhibitory effects on endothelial cell adhesion, proliferation and tube formation in vitro. Utilizing a cellular attachment assay, chronic exposure to nanomolar concentrations of E2 (i.e. 1 and 10 nM) increased endothelial cell adhesion significantly compared to vehicle treated controls. Cellular adhesion was inhibited by micromolar concentrations of E2. Cell count, PCNA immunohistochemistry and Western blot analysis demonstrated enhanced cell proliferation at low E2 concentration in estrogen-deplete medium. Inhibition of cellular proliferation was observed in both estrogen-replete and deplete medium at higher E2 concentrations (i.e. 1 and 10 microM). Furthermore, in vitro tube formation increased up to 3.0 fold in the presence of 10 nM and higher E2 concentrations. The present observations indicate that in vitro regulation of capillary endothelial cell adhesion, proliferation and capillary tube formation by estrogen, are dose dependent.

Adrenal Medulla↗
PubMed1997

Over expression of vascular endothelial growth factor and its receptor during the development of estrogen-induced rat pituitary tumors may mediate estrogen-initiated tumor angiogenesis.

Estrogens, which have been associated with several types of human and animal cancers, can induce tumor angiogenesis in the pituitary of Fischer 344 rats. The mechanistic details of tumor angiogenesis induction, during estrogen carcinogenesis, are still unknown. To elucidate the role of estrogen in the regulation of tumor angiogenesis in the pituitary of female rats, the density of blood vessels was analysed using factor VIII related antigen (FVIIIRAg) immunohistochemistry and the expression of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) was examined by Western blot and immunohistochemical analysis. The expression of VEGF receptor (VEGFR-2/Flk-1/KDR) was also examined by immunohistochemistry. The results demonstrated that 17beta-estradiol (E2) induces neovascularization, as well as the growth and enlargement of blood vessels after 7 days of exposure. The high tumor angiogenic potential was associated with an elevated VEGF/VPF protein expression in the E2 exposed pituitary of ovariectomized (OVEX) rats. VEGF/VPF and FVIIIRAg immunohistochemistry and endothelial specific lectin (UEA1) binding studies, indicate that the elevation of VEGF protein expression initially occurred in both blood vessels and non-endothelial cells. After 15 days of E2 exposure, VEGF/VPF protein expression, in the non-endothelial cell population, sharply declined and was restricted to the blood vessels. The function of non-endothelial-derived VEGF is not clear. Furthermore, immunohistochemical studies demonstrated that VEGFR-2 (flk-1/KDR), expression was elevated significantly in the endothelial cells of microblood vessels after 7 days of E2 exposure. These findings suggest that over expression of VEGF and its receptor (VEGFR-2) may play an important role in the initial step of the regulation of estrogen induced tumor angiogenesis in the rat pituitary.

Animals↗
PubMed1997

A two-step enriched-nested PCR technique enhances sensitivity for detection of codon 12 K-ras mutations in pancreatic adenocarcinoma.

Mutations at codon 12 of the K-ras gene have been detected in pancreatic adenocarcinomas by a variety of techniques. A few of these techniques are very sensitive, identifying the mutations in 96-100% of cases. However, these sensitive techniques are labor intensive, utilizing multistep processing and radioactive material. Much simpler techniques, involving nonradioactive single-step polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) have been employed to detect K-ras mutations at codon 12 in pancreatic adenocarcinomas. However, the low sensitivity of these single-step PCR/ RFLP techniques is unacceptable. A simple and nonradio-active PCR/RFLP-based method for detection of K-ras codon 12 mutations in formalin-fixed, paraffin-embedded tissue sections of pancreatic adenocarcinoma is described and compared to the traditional PCR technique. K-ras gene mutations at codon 12 were detected by a modified two-step enrich-nested PCR (EN-PCR)/RFLP method, and their existence was confirmed by direct DNA sequencing analysis of the product. When the two-step EN-PCR/RFLP technique was compared to the single-step PCR/RFLP method, K-ras codon 12 mutations were detected in 100% of pancreatic adenocarcinomas (15/15) with the EN-PCR/RFLP method, while half as many (9/15) were detected with the single-step PCR/RFLP method. This study demonstrates that the sensitivity of the simple two-step EN-PCR/RFLP technique is comparable to that of the more complex methods for detecting K-ras mutations at codon 12 in formalin-fixed, paraffin-embedded tissue sections of pancreatic adenocarcinoma and its sensitivity is superior to that of the single-step technique.

Base Sequence↗
PubMed1996

Involvement of an efflux system in mediating high level of fluoroquinolone resistance in Mycobacterium smegmatis.

A wild type strain of Mycobacterium smegmatis mc2 155 was serially adapted to 64 fold of minimal inhibitory concentration of an antimycobacterial agent, ciprofloxacin. This clone (CIPr) exhibited cross resistance to ofloxacin and ethidium bromide. The rate of drug efflux was accelerated in CIPr compared to the wild type strain. Verapamil, a calcium channel blocker, enhanced the drug accumulation in CIPr by diminishing the efflux and thus reversed the resistant phenotype. Additionally, a missense mutation was detected in the quinolone resistance determining region of the DNA-gyrase A subunit of CIPr. Taken together, these results suggest that drug efflux plays a major role in conferring such a high level of resistance in CIPr, in addition to the mutation in the DNA-gyrase locus.

Amino Acid Sequence↗
PubMed1996

Short segment Barrett's esophagus: clinical and histological features, associated endoscopic findings, and association with gastric intestinal metaplasia.

OBJECTIVES: To prospectively determine the clinical features, associated esophageal endoscopic lesions, associated gastric intestinal metaplasia, and prevalence of dysplasia and adenocarcinoma of short segment Barrett's. METHODS: All patients undergoing upper endoscopy over a 5-month period were scrutinized for endoscopic features suggestive of short segment Barrett's, and, if present, multiple biopsies were obtained from the suspicious areas. Prevalence of gastric intestinal metaplasia was determined by obtaining biopsies from the antrum, body, and cardia. RESULTS: Two hundred thirty seven patients were examined. Short segment Barrett's was suspected in only 42 patients, and traditional Barrett's was noted in 45 patients. Short segment Barrett's was confirmed by biopsy in 48%. Clinical presentation of short segment Barrett's was that of typical or complicated gastroesophageal reflux disease in 53%. A hiatal hernia was the most common associated esophageal endoscopic finding; however, none of the endoscopic findings differed significantly from findings of patients who did not have short segment Barrett's. Diagnosis of short segment Barrett's required histological analysis. A significant difference was noted in the prevalence of intestinal metaplasia between the esophagus and stomach in patients with Barrett's. No dysplasia or adenocarcinoma was detected in patients with short segment Barrett's. CONCLUSIONS: Short segment Barrett's is a frequent finding in patients undergoing upper endoscopy. All patients with short tongues or patches of red mucosa lying less than 2 cm above the esophagogastric junction should be biopsied to exclude short segment Barrett's. Large scale endoscopic and histological surveillance studies along with long-term follow-up are required to clarify short segment Barrett's prevalence and cancer risk.

Adenocarcinoma↗
PubMed1995

Isolation, cultivation and partial characterization of a kinetoplastid flagellate from the hindgut of the water bug, Lethocerus indicus.

A new species of kinetoplastid flagellates was isolated from the hindgut of the giant water bug, Lethocerus indicus, and successfully cultured in modified glycerol beef extract medium. Light and electron microscopic studies as well as growth in various culture media are described. The flagellates were in three different shapes and sizes in the hindgut of the host as well as in the culture medium. Each form of the parasite contained a kinetoplast which was located near the basal body of the flagellate. The ultrastructural features of this species exhibit great similarity to other species of Bodo. The flagellate ingested bacteria, grew in culture, and was identical with that observed in the hindgut of the bugs. The name Bodo indica has been proposed for this kinetoplastid flagellate.

Animals↗
PubMed1994

Colocalization of prolactin and proliferating cell nuclear antigen in the anterior pituitary during estrogen-induced pituitary tumors.

Chronic estrogen treatment induces prolactin (PRL)-secreting pituitary tumors in laboratory animals. To determine earlier events of tumorigenesis, we studied cell proliferation in the pituitary following 7-30 days of estrogen administration in Fischer 344 rats. Immunohistochemical localization of proliferative cells by proliferating cell nuclear antigen (PCNA) staining and lactotropes by PRL staining revealed that estrogen treatment caused a time-dependent increase in the number of proliferative cells and lactotropes. Although the increase in lactotropic cell number paralleled the increase in PCNA-reactive cell number, only approximately 30% of lactotropes reacted simultaneously with the PCNA antibody. These results indicate that a subset population of lactotropes proliferates under the influence of estrogen during tumorigenesis.

Animals↗
PubMed1994

Induction of chromosome aberrations in Syrian hamster renal cortical cells by various estrogens.

Estrogens, both natural and synthetic, have been implicated in carcinogenesis at different organ sites in a variety of animals, including man, for more than six decades. However, the molecular mechanism(s) involved in the carcinogenic action of estrogens still remains both controversial and elusive. Cytogenetic damage in the hamster kidney has been studied after in vivo treatment with either potent or weak estrogens for varying periods. Compared to age-matched untreated control, diethylstilbestrol (DES) treatment resulted in significant increases in the number of chromatid gaps and breaks, chromosome breaks, and endoreduplicated cells in hamster renal cortical cells. These chromosomal aberrations (CA) were cumulative with continued hormone exposure from 1.0 to 5.0 months. However, chromosome exchanges as a result of the breaks were not elevated. After 5.0 months of hormone treatment, potent estrogens such as 17 beta-estradiol and Moxestrol exhibited similar frequencies of CA in the hamster kidney to that found for DES, whereas weak estrogens such as 17 alpha-estradiol and beta-dienestrol exhibited CA frequencies that were not significantly different from untreated levels. Ethinylestradiol treatment for a similar period resulted in significant increases in chromatid gaps, although these did not evolve into increases in either chromatid or chromosome breaks, and in a rise in endoreduplicated cells. These results raise the possibility that the CA generated after estrogen treatment may be involved in renal tumorigenic processes.

Analysis of Variance↗