Successful endoscopic treatment of a fistula between the common bile duct and neobladder.
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Biliary Fistula↗
Biomedical subjects
S Narayan
Publications and source records attributed to S Narayan.
Skewing of cytokine profiles towards T helper cell type 2 response in visceral leishmaniasis patients unresponsive to sodium antimony gluconate.
Thirty-two parasitologically confirmed visceral leishmanisis (VL) patients and 23 healthy, age- and gender-matched controls were recruited between April 2001 and March 2002 and studied for intracellular cytokine production after stimulation in vitro using a Fluorescence Activated Cell Sorter-based intracellular cytokine assay. The VL patients were given i.m. sodium antimony gluconate at a dose of 20 mg/kg bodyweight daily for 28 d and were grouped as responders (n = 11) or non-responders (no response after 28 d of treatment; n = 21). Clinically, the non-responders had longer duration of illness (P < 0.05), larger spleen size (P < 0.05), and higher parasite load (P < 0.05) than responders. The percentage of T helper (Th) cells producing interferon-gamma (IFN-gamma) was significantly higher (P < 0.001) in responders than non-responders. Non-responders had higher IFN-gamma production than control subjects (P < 0.001). The percentage of Th cells producing interleukin-4 (IL-4) was significantly higher in non-responders than responders (P = 0.003) as well as in healthy subjects (P < 0.001). The frequency of IL-4 producing cells in responders and control subjects was similar (P= 0.65). The cytokine polarization index, as calculated by the formula loge IFN-gamma producing cells/loge IL-4 producing cells, was significantly lower in non-responders compared with both responders and control subjects (P = 0.003 and P < 0.001, respectively). The overall cytokine bias in non-responders was skewed towards a IL-4 dominance or Th2-like response and this was primarily due to induction of IL-4.
Adolescent↗
Caspase-dependent apoptosis induced by telomere cleavage and TRF2 loss.
Chromosomal abnormalities involving telomeric associations (TAs) often precede replicative senescence and abnormal chromosome configurations. We report here that telomere cleavage following exposure to proapoptotic agents is an early event in apoptosis. Exposure of human and murine cancer cells to a variety of pro-apoptotic stimuli (staurosporine, thapsigargin, anti-Fas antibody, and cancer chemotherapeutic agents) resulted in telomere cleavage and aggregation, and finally their extrusion from the nuclei. Telomere loss was associated with arrest of cells in G2/M phase and preceded DNA fragmentation. Telomere erosion and subsequent large-scale chromatin cleavage were inhibited by overexpression of the anti-apoptotic protein, bcl-2, and two peptide caspase inhibitors (BACMK and zVADfmk), indicating that both events are regulated by caspase activation. The results demonstrate that telomere cleavage is an early chromatin alteration detected in various cancer cell lines leading to drug-induced apoptosis, and suggest that this event contributes to mitotic catastrophe and induction of cell death. Results also suggest that the decrease of telomeric-repeat binding factor 2 (TRF2) may be the earliest event in the ara-C-induced telomere shortening, induction of endoreduplication and chromosomal fragmentation leading to cell death.
Animals↗
Rothmund-Thomson syndrome with myelodysplasia.
Rothmund-Thomson syndrome (RTS) is a rare autosomal recessive disorder that is caused by a DNA repair defect. It is characterized mainly by skin, eye, and skeletal abnormalities. Cutaneous changes appear at between 3 and 6 months of age and include poikiloderma, photosensitivity, scaling, hyperkeratosis, and disturbance of hair growth. Other abnormalities include cataracts, congenital bone defects, soft tissue contractures, and osteogenesis imperfecta. Various malignancies have been reported in association with RTS, including osteosarcoma, fibrosarcoma, and nonmelanoma skin cancers. The myelodysplastic syndromes are a group of hematologic disorders defined by morphologic abnormalities of the three cell lines. The pathogenesis of myelodysplasia is a multistep process that begins with a somatic mutation in the pluripotential stem cell, which is irreversibly altered and acquires a survival advantage. Myelodysplasia in the young and RTS are both rare conditions. We report a patient with RTS and myelodysplasia. This is the second reported case of an association between these two conditions, which are both likely to be due to a common etiologic cause of nonrepair of stem cell DNA damage. Clinicians should be aware of the potential of this complication arising in patients with RTS.
Adult↗
A correlation of APC and c-myc mRNA levels in lung cancer cell lines.
One of the functions of adenomatous polyposis coli (APC) in colorectal cancers is regulation of c-myc gene expression. However, the role of APC in lung cancers has not been elucidated. In the present study, the levels of APC and c-myc mRNA were determined in one strain of normal human bronchial epithelial (NHBE) cells, an SV-40-immortalized non-tumorigenic human bronchial epithelial cell line (BEAS-2B), 13 non-small cell lung cancer cell lines, and 4 small cell lung cancer cell lines. To establish a relationship between c-Myc and APC, we determined the ratio of c-myc and APC mRNA levels in different lung cancer cell lines. Out of 19 lung cancer cell lines, we found that 13 exhibited c-myc/APC mRNA ratio of more than two. Among the cell lines CaLu-3, NCI-H82, A427 and SW900 showed a very low level of APC mRNA and a high level of c-myc mRNA. The ratio of c-myc/APC mRNA in these cell lines was 48, 127, 325 and 708, respectively. The results of these analyses revealed an inverse relationship between APC and c-myc mRNA levels, suggesting that APC may regulate c-myc expression in lung cancer cells in a manner analogous to its role in colon cancer.
Adenomatous Polyposis Coli Protein↗
Developing clinical practice environments supporting the knowledge work of nurses.
Registered nurses represent the largest group of healthcare knowledge workers. They accomplish their knowledge work by engaging in the roles of data gatherer, information user, knowledge user, and knowledge builder. To successfully implement these roles, nurses rely on healthcare settings to provide supportive clinical practice environments that recognize their information and knowledge management needs. The authors describe the various knowledge-worker roles, delineate computerized mechanisms that can support these roles, and examine the ability of current healthcare settings to provide an environment conducive to successful knowledge-worker role performance. The article concludes with specific recommendations for development of clinical practice environments supportive of nurses' knowledge work.
Decision Making, Computer-Assisted↗