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S Sebastian

Publications and source records attributed to S Sebastian.

At least 19 recordsLinked to original sources
PubMed2005

Molecular and cytogenetic characterization of a novel rearrangement involving chromosomes 9, 12, and 17 resulting in ETV6 (TEL) and ABL fusion.

We performed chromosome analysis on the bone marrow of a patient with BCR/ABL negative chronic myelogenous leukemia (CML). By interphase fluorescence in situ hybridization (FISH), an extra ABL signal was present in interphase nuclei and appeared to be located at 17p in the metaphase cells. Chromosome analysis showed a subtle abnormality at 17p13 and 12p13 but no visible rearrangement at 9q34 (ABL). Additional FISH experiments disclosed a rearrangement between the short arms of chromosomes 12 and 17 at approximately bands 12p13 and 17p13, respectively. In addition, subtelomeric FISH analysis confirmed the presence of terminal 12p at 17p13 and showed terminal 9q34 to be intact on each chromosome 9. Taken together, these results indicated a rearrangement involving chromosomes 9, 12, and 17 that suggested the possibility of juxtaposition of part of the ETV6 (also known as TEL) locus (12p13) with a portion of ABL (9q34) together at 17p13. The ETV6/ABL fusion was confirmed by RT-PCR, which showed that the first 5 exons of ETV6 were fused in frame with ABL at exon 2. Wild-type ETV6 and ABL were also expressed, in accordance with the FISH results that showed no loss of the second ETV6 or ABL allele.

Aged↗
PubMed2004

Endoscopic argon plasma coagulation for the treatment of gastric antral vascular ectasia (watermelon stomach): long-term results.

INTRODUCTION: Gastric antral vascular ectasia is a rare but well-recognised cause of occult gastrointestinal bleeding. Various endoscopic treatments have been tried in this condition. We report our experience with argon plasma coagulation in the treatment of gastric antral vascular ectasia. PATIENTS AND METHODS: Twelve patients with endoscopically proved gastric antral vascular ectasia were included. All patients received argon plasma coagulation with power of 40 W at a median interval of 4 weeks. The pre-treatment haemoglobin and transfusion requirements were compared with the post-treatment values. RESULTS: There was a sustained increase in mean haemoglobin levels post-treatment. The mean haemoglobin levels pre- and post-treatment were 8.13 +/- 0.70 and 12.2 +/- 0.32 g/dl, respectively (P = 0.008). All patients were anaemic and 58.3% of the patients were transfusion dependent. The mean number of units of blood transfusion in the period 6 months prior to treatment was 11.3 +/- 5.68. Following argon plasma coagulation, the number of transfusions decreased significantly to 1.1 +/- 0.57 units (P = 0.018). No significant procedure-related complications were identified. CONCLUSION: Argon plasma coagulation is a safe and effective alternative to the currently available endoscopic modalities of treatment for gastric antral vascular ectasia.

Aged↗
PubMed2004

Painful ascites.

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Aged↗
PubMed2003

Review article: current therapeutic options for gastric antral vascular ectasia.

Gastric antral vascular ectasia, or 'watermelon stomach', is a rare but important cause of gastrointestinal blood loss and anaemia, which has characteristic endoscopic and histological features. The pathogenesis of this condition remains unclear; however, many associated disorders have been documented. Various medical, surgical and endoscopic therapeutic modalities have been attempted with variable success. Leading contenders for the therapeutic modality of choice include hormonal therapy, endoscopic Nd:YAG laser and argon plasma coagulation. Randomized controlled trials to identify the ideal treatment method are lacking at present.

Adrenal Cortex Hormones↗
PubMed2003

Induction of cyclooxygenase-2 in human endometrial stromal cells by malignant endometrial epithelial cells: evidence for the involvement of extracellularly regulated kinases and CCAAT/enhancer binding proteins.

We previously reported that human malignant endometrial epithelial cell conditioned medium (MECM) up-regulated cyclooxygenase (COX)-2 mRNA and protein levels in human normal endometrial stromal cells (ESC). Here we showed that pretreatment with a selective inhibitor of the extracellularly regulated kinase (ERK)1/2 signaling pathway blocked the MECM-induced COX-2 expression in ESC. Transient transfection assays indicated critical roles of a cAMP response element (CRE,-59/-53 bp) and a nuclear factor for interleukin (IL)-6 expression (NF-IL6) site (-132/-124 bp) in the regulation of basal and MECM-induced activity of COX-2 gene promoter in ESC. Employing electrophoretic mobility shift assays, we demonstrated that increased functional binding of CCAAT/enhancer binding protein (C/EBP)alpha, C/EBPbeta and upstream stimulatory factor-2 to the CRE and C/EBPalpha and C/EBPbeta to the NF-IL6 site were, at least in part, responsible for MECM-induced COX-2 expression in ESC. Moreover, overexpression of C/EBPalpha and C/EBPbeta significantly induced COX-2 promoter activity in ESC. Collectively, these results suggest that the basal and MECM-induced transcription of the COX-2 gene in ESC is regulated through a combination of the CRE and the NF-IL6 site by functional interactions of C/EBPalpha and C/EBPbeta.

Base Sequence↗
PubMed2002

Microwave conductivity and penetration depth in the heavy fermion superconductor CeCoIn5.

The electrodynamic properties of the quasi-two-dimensional heavy fermion superconductor CeCoIn5 have been investigated by microwave surface impedance measurements over a wide range of microwave frequencies and temperatures. We derive a value penetration depth lambda(0) approximately 190 nm, with a strong linear term in the temperature dependence of lambda(T) below T(c)/3, consistent with a superconducting gap with line nodes. The real part of the conductivity displays a broad peak at low temperatures consistent with a decreased scattering rate of almost 2 orders of magnitude below T(c). CeCoIn5 has remarkably similar properties to those of the high-T(c) cuprates.

Journal Article↗
PubMed2001

The human gene for the type III isozyme of hexokinase: structure, basal promoter, and evolution.

The structure of the gene for the Type III isozyme of human hexokinase is nearly identical to that of previously characterized genes for other isozymes of hexokinase. The most striking difference is that the 5'-untranslated sequence and the initial coding sequence are contained in two exons in the Type III hexokinase gene but in a single exon in genes for the other isozymes. Sequence at the transcriptional start site for rat Type III hexokinase (S. Sebastian, J. A. White, and J. E. Wilson, 1999, J. Biol. Chem. 274, 31700-31706) is conserved in the human gene, as is an Oct-1 site, in reverse orientation, approximately 30 bp upstream from the start site. This site has been shown to regulate transcription of both human and rat genes for Type III hexokinase. Comparison of the genes for the various mammalian isozymes of hexokinase indicates that a major feature in the evolution of this isozyme family has been acquisition of alternative first exons.

Base Sequence↗
PubMed2001

Malignant breast epithelial cells stimulate aromatase expression via promoter II in human adipose fibroblasts: an epithelial-stromal interaction in breast tumors mediated by CCAAT/enhancer binding protein beta.

Expression of aromatase P450 (P450arom), which catalyzes the formation of estrogens, is aberrantly increased in adipose fibroblasts surrounding breast carcinomas, giving rise to proliferation of malignant cells. Aromatase in human adipose tissue is primarily expressed in undifferentiated fibroblasts under the control of several distinct and alternatively used P450arom promoters. In tumor-free breast adipose tissue, P450arom is usually expressed at low levels via a distal promoter (I.4), whereas in the breast adipose tissue bearing a tumor, P450arom is increased through the activation of two proximal promoters, II and I.3. Because the in vivo activation of P450arom promoter II is a key event responsible for aberrantly high P450arom expression in breast tumors, we studied the molecular basis for the enhancement of P450arom promoter II using human adipose fibroblasts (HAFs) in primary culture treated with T47D breast cancer cell-conditioned medium (TCM) as a model system. Upon treatment with TCM, HAFs displayed a striking induction of P450arom mRNA levels via promoter II usage. This effect appeared to be specific for malignant breast epithelial cells, because conditioned media from breast cancer cell lines T47D and MCF-7 induced promoter II activity, whereas normal breast epithelial cells or liver or prostate cancer cell lines did not produce such an effect. Although treatment with a cyclic AMP analogue also caused a switch in the promoter use from I.4 to II in cultured HAFs, TCM-induced promoter II use was found to be mediated via a cyclic AMP-independent pathway. Use of serial deletion mutants of the promoter II 5'-flanking sequence revealed the presence of critical cis-acting elements in the -517/-278 bp region, which regulate the baseline activity. TCM caused a 5.7-fold induction of the -517-bp promoter II construct, whereas site-directed mutagenesis of a CCAAT/enhancer binding protein (C/EBP) binding site (-317/-304 bp) abolished both baseline and TCM-induced activities. Ectopic expressions of C/EBPalpha and C/EBPbeta, but not C/EBPdelta, significantly induced promoter II activity. Moreover, we demonstrated the presence of both C/EBPbeta and C/EBPdelta but not C/EBPalpha in a DNA-protein complex formed by the nuclear extract from TCM-treated HAFs and a probe containing this critical C/EBP binding element (-317/-304 bp). Finally, treatment of HAFs with TCM strikingly induced C/EBPbeta expression, whereas this did not affect the levels of C/EBPalpha or C/EBPdelta transcripts. In conclusion, malignant breast epithelial cells secrete factors, which induce aromatase expression in adipose fibroblasts via promoter II. This is, at least in part, mediated by a TCM-induced up-regulation and enhanced binding of C/EBPbeta to a promoter II regulatory element.

Adipose Tissue↗
PubMed2001

Treatment-refractory schizophrenia.

Treatment-refractory schizophrenia is common. Refinements in pharmacologic and psychosocial treatments of schizophrenia offer the expectation of superior outcomes for this disadvantaged patient group. This article critically reviews those articles that were published during the year 2000 that address this treatment-refractory population.

Antipsychotic Agents↗
PubMed2001

Role of aromatase in endometrial disease.

Aromatase is the key enzyme for estrogen biosynthesis. It is normally expressed in the human ovary, skin, adipose tissue and brain. Aromatase activity is not detectable in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis and is stimulated by PGE2. This results in local production of estrogen, which induces PGE2 formation and establishes a positive feedback cycle. Another abnormality in endometriosis, i.e. deficient 17beta-hydroxysteroid dehydrogenase (17beta-HSD) type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE2 in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of post-menopausal endometriosis using an aromatase inhibitor.

Aromatase↗
PubMed2000

Anabolic function of the type II isozyme of hexokinase in hepatic lipid synthesis.

The mRNA encoding the Type II isozyme of hexokinase was markedly elevated in livers of transgenic mice overexpressing the transcriptionally active nuclear form of sterol regulatory element binding protein-1a (nSREBP-1a), but not in transgenic mice overexpressing the nSREBP-1c or nSREBP-2 isoforms. Cellulose acetate electrophoresis and immunoblotting results confirmed selective increase of the Type II isozyme in livers of transgenic mice expressing nSREBP-1a. SREBP-1a has previously been shown to activate transcription of genes encoding enzymes involved in biosynthesis of fatty acids and glycerolipids and to a lesser extent the enzymes of cholesterol biosynthesis. Thus, these results are consistent with the view that the Type II isozyme serves an anabolic function, providing precursors and reducing equivalents required for increased rates of hepatic lipid synthesis.

Animals↗
PubMed2000

Developmental Gerstmann's syndrome: a distinct clinical entity of learning disabilities.

The symptom complex of finger anomia, right-left disorientation, dysgraphia, and dyscalculia constitutes Gerstmann's syndrome. It is mostly described in adults and is caused by acquired lesions of the dominant parietal lobe. It is infrequently described in children with learning disabilities and has been designated developmental Gerstmann's syndrome. Developmental Gerstmann's syndrome goes unnoticed if not specifically sought by clinicians. A detailed evaluation will reveal subtle neurologic deficits, behavioral problems, and neuropsychologic and specific speech and language abnormalities. Ten such patients are reported; six of the children demonstrated improvement with intensive speech training. Early identification and intervention is therefore crucial, and even more important in cultures in which students are required to be biliterate or triliterate, further increasing the constraints on writing. A selective writing, reading, or calculation abnormality in the presence of normal oral communication triggers several interesting possibilities for the brain mechanisms behind normal language processing. Similarly, the association of acalculia with finger anomia and agraphia with right-left disorientation may have specific implications in the neuropsychologic processing of the evolution of calculation and writing. A theoretical possibility of oral and written language processing from the observation of the language behavior of these children is also described.

Adolescent↗