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Biomedical subjects

V Kapoor

Publications and source records attributed to V Kapoor.

At least 37 records · Page 2Linked to original sources
PubMed2001

Vertebral mass resulting from a chronic-contained rupture of an abdominal aortic aneurysm repair graft.

We describe a case of a 63-year-old man with chronic-contained rupture of an abdominal aortic aneurysm at the site of prior graft repair of the aneurysm. Initially misinterpreted as osteomyelitis on the basis of CT findings, this chronic-contained rupture of the abdominal aorta eroding the vertebrae was preoperatively diagnosed at MR imaging and confirmed at surgery. A conventional angiogram failed to show the pseudoaneurysm. Owing to a major difference in the management of a contained aortic aneurysm rupture versus that for osteomyelitis, MR imaging with CT or MR angiography is recommended before any operative or invasive procedure.

Aortic Aneurysm, Abdominal↗
PubMed2001

Wireless telemetry and Internet technologies for medical management: a Martian analogy.

BACKGROUND: The NASA Haughton-Mars Project Base Camp on Devon Island, Canada (approximately 75 degrees north) was the site for transmission of vital signs from two "terranauts" (individuals who acted as Earthbound astronauts) back to the United States in (artificially delayed) real-time. METHODS: The subjects became "physiologic ciphers" for status monitoring using readily available technologies that affordably captured and distributed vital signs to a variety of platforms. This study of nominal monitoring and simulated medical emergency used wireless technologies and the Internet. RESULTS: Basic vital signs and images can be sent using wireless topologies and completely automated functions. Due to the lightweight transport requirements, existing low data rate connections can easily handle the volume of traffic. CONCLUSIONS: Monitoring, the health of space travelers will be an important component for both low-Earth orbiting spacecraft and long-term missions to distant planets. However, terrestrial applications represent the primary application of such technologies because the home can be a remote and hazardous environment as well.

Aerospace Medicine↗
PubMed2000

Termination of psychotherapy: a training perspective.

Given the constraints of the prevailing mental health system in the United States, it has become very challenging for psychiatrists to offer psychotherapy services to patients in need of this modality of treatment. In spite of this situation, the profession has made a consistent effort not only to retain this type of psychiatric care but also to train psychiatric residents in this psychiatric intervention technique and its appropriate indications. In this article, the authors highlight a very important aspect of psychotherapy treatment-the termination phase. They review relevant literature on this subject, discuss some of the most common problems faced by psychiatrists, especially psychiatric residents, when addressing the termination phase of psychotherapy, and then present two cases to illustrate these issues.

Journal Article↗
PubMed2000

Induction of indolamine 2,3-dioxygenase in primary human macrophages by human immunodeficiency virus type 1 is strain dependent.

Increased kynurenine pathway metabolism has been implicated in the etiology of AIDS dementia complex (ADC). The rate-limiting enzyme for this pathway is indolamine 2,3-dioxygenase (IDO). We tested the efficacy of different strains of human immunodeficiency virus type 1 (HIV1-BaL, HIV1-JRFL, and HIV1-631) to induce IDO in cultured human monocyte-derived macrophages (MDM). A significant increase in both IDO protein and kynurenine synthesis was observed after 48 h in MDM infected with the brain-derived HIV-1 isolates, laboratory-adapted (LA) HIV1-JRFL, and primary isolate HIV1-631. In contrast, almost no kynurenine production or IDO protein was evident in MDM infected with the highly replicating macrophage-tropic LA strain HIV1-BaL. The induction of IDO and kynurenine synthesis by HIV1-JRFL and HIV1-631 declined to baseline levels by day 8 postinfection. Abundant HIV-1 replication did not reduce the ability of exogenous gamma interferon (IFN-gamma) to induce IDO and kynurenine synthesis in HIV-infected MDM. The addition of anti-IFN-gamma antibody to MDM infected with HIV1-JRFL resulted in an absence of detectable IDO protein after 48 h and a decrease of 64% +/- 1% in supernatant kynurenine concentration. Together, these results indicate that only selected strains of HIV-1 are capable of inducing IDO synthesis and subsequent kynurenine metabolism in MDM. The induction of IDO, while apparently independent of replication capacity, appears to be mediated by a transient production of IFN-gamma in MDM responding to the initial infection with selected strains of HIV-1.

Cells, Cultured↗
PubMed2000

IDO induction in IFN-gamma activated astroglia: a role in improving cell viability during oxidative stress.

In the central nervous system (CNS), astrocytes play an integral role in the maintenance of neuronal viability and function. Inflammation within the CNS increases the concentration of oxidative metabolites and, therefore, the potential for NAD depletion through increased poly-(ADP-ribose) polymerase (PARP) activity. However, the activity of indoleamine 2,3-dioxygenase (IDO), the rate limiting enzyme for de novo NAD synthesis, is also markedly increased in astrocytes during inflammation. This study investigated the role of IDO induction in the maintenance of intracellular NAD and its relationship to improved cell viability under conditions of increased oxidative stress in the human astroglioma cell line, HTB-138. Treatment with the pro-inflammatory cytokine IFN-gamma increased IDO activity in these cells. Intracellular NAD levels also increased significantly after treatment with IFN-gamma in the presence of a PARP inhibitor. Pretreatment of astroglial cells with IFN-gamma significantly moderated both the drop in intracellular NAD concentration and cell death following exposure to hydrogen peroxide. These results suggest that induction of IDO and subsequent de novo NAD synthesis may contribute to the maintenance of intracellular NAD levels and cell viability under conditions of increased oxidative stress.

Astrocytes↗
PubMed2000

Induction of indoleamine 2,3-dioxygenase in primary human macrophages by HIV-1.

Increased kynurenine pathway metabolism has been implicated in the aetiology of the AIDS dementia complex (ADC). The rate limiting enzyme for this pathway is indoleamine 2,3-dioxygenase (IDO). We tested the efficacy of different strains of HIV-1 (HIV1-BaL, HIV1-JRFL and HIV1-631) to induce IDO in cultured human monocyte-derived macrophages (MDM). A significant increase in both IDO protein and kynurenine synthesis was observed after 48 h in MDM infected with the brain derived HIV-1 isolates, laboratory adapted (LA) HIV1-JRFL, and primary isolate HIV1-631. In contrast, almost no kynurenine production or IDO protein was evident in MDM infected with the high replicating macrophage tropic LA strain, HIV1-BaL. The induction of IDO and kynurenine synthesis by HIV1-JRFL and HIV1-631 declined to baseline levels by day-8 post-infection. Together, these results indicate that only selected strains of HIV-1 are capable of inducing IDO synthesis and subsequent oxidative tryptophan catabolism in MDM.

Brain↗
PubMed2000

Characterisation of kynurenine pathway metabolism in human astrocytes and implications in neuropathogenesis.

The role of astrocytes in the production of the neurotoxin quinolinic acid (QUIN) and other products of the kynurenine pathway (KP) is controversial. Using cytokine-stimulated human astrocytes, we assayed key enzymes and products of the KP. We found that astrocytes lack kynurenine-hydroxylase so that large amounts of kynurenine (KYN) and kynurenic acid (KYNA) were produced, while minor amounts of QUIN were synthesised that were completely degraded. We then showed that kynurenine added to macrophages led to significant production of QUIN. These results suggest that astrocytes alone are neuroprotective by minimising QUIN production and maximising synthesis of KYNA. However, it is likely that, in the presence of macrophages and/or microglia, astrocytes are neurotoxic by producing large concentrations of KYN that can be metabolised by neighbouring monocytic cells to QUIN.

Astrocytes↗
PubMed2000

Screening marine natural products for selective inhibitors of key kynurenine pathway enzymes.

Kynurenine, a metabolite of tryptophan along the 'kynurenine pathway', is at a branch point of the pathway which can lead to the synthesis of both quinolinic acid (QUIN) and kynurenic acid (KYNA). KYNA is an antagonist of glutamate receptors; however, QUIN is a selective agonist of NMDA receptors, and has been shown to act as an excitotoxic agent. A high QUIN/KYNA ratio has been implicated in a variety of neurological diseases in which excitotoxic neuronal cell death is found, e.g. AIDS-related dementia, stroke, etc. Inhibiting the key enzymes of this pathway (i.e. kynureninase and kynurenine 3-hydroxylase) would lower the QUIN/KYNA ratio, which may potentially have neuroprotective effects. We have developed high through-put assays for kynurenine pathway enzymes which allow us to screen extracts from marine organisms for selective enzyme inhibitors. Active metabolites are purified, isolated and identified by HPLC, high-field NMR and mass spectral techniques. Extracts from a sponge of the Aka species were found to contain a selective inhibitor of kynureninase. We have recently purified and identified the active principal as being serotonin sulfate. Related indoleamines, serotonin and 5-hydroxyindoleacetic acids are inactive. This finding may be suggestive of a novel interaction between the serotoninergic and excitatory amino acid pathways.

Animals↗
PubMed1999

Evidence for increased de novo synthesis of NAD in immune-activated RAW264.7 macrophages: a self-protective mechanism?

The parent pyridine nucleotide NAD is the end product of oxidative tryptophan catabolism via the kynurenine pathway. Indoleamine 2, 3-dioxygenase, the rate-limiting enzyme for this pathway, is induced by the proinflammatory cytokine interferon-gamma. The aim of this study was to investigate the effect of interferon-gamma treatment on intracellular NAD concentration in the murine macrophage cell line, RAW 264.7. A significant increase in intracellular NAD concentration was observed following 24 h exposure to interferon-gamma. This cytokine-mediated increase in NAD concentration was markedly enhanced by the inhibition of poly(ADP-ribose) polymerase or nitric oxide synthase or following treatment with the synthetic glucocorticoid dexamethasone. NAD production was dependent on both the presence of tryptophan in the culture medium and on functional indoleamine 2,3-dioxygenase activity. In agreement with previous studies a marked increase in nitric oxide production was observed in these cells following activation with interferon-gamma. These results provide evidence for the first time that de novo synthesis of NAD from tryptophan is increased concomitantly with free radical production in RAW 264.7 macrophages stimulated with interferon-gamma. This increase in NAD biosynthesis may provide an improved supply of substrate to the nuclear repair enzyme poly(ADP-ribose) polymerase assisting in DNA repair and hence cell viability.

Animals↗
PubMed1999

Solitary cellular schwannoma (neurilemmoma) showing malignant changes: evaluation through magnetic resonance imaging (M.R.I.), surgical intervention, and histopathology.

Schwannoma (neurilemmoma) are common benign tumors arising from the peripheral nerve sheath. Malignant transformation is uncommon. A unique case showing such a transformation is reported highlighting the roles of magnetic resonance imaging, surgical intervention, and histopathology. The case was thoroughly investigated by learning the details of the sequence of events leading to the current status. The evaluation was made through magnetic resonance imaging. In addition, computed tomography and conventional radiography were used to locate any foci of calcification. Subsequently, the tumor's gross and microscopic morphology was defined by surgical intervention and histopathology. Malignant schwannoma of the left leg occupying the entire calf is extremely uncommon. Only ten cases have been reported thus far, including the current one from the Indian subcontinent. Malignant transformation in a schwannoma differs significantly from malignant nerve sheath tumors (erroneously called malignant schwannomas). An endeavour has been made to differentiate malignant transformation in schwannoma from other malignant peripheral nerve sheath tumors. An innovation in this direction is magnetic resonance imaging. This investigate procedure is imperative in such situations, along with surgery and histopathology, which may also help in classifying the condition.

Humans↗
PubMed1998

ErbB2 expression increases the spectrum and potency of ligand-mediated signal transduction through ErbB4.

Interleukin 3-dependent murine 32D cells do not detectably express members of the ErbB receptor family and do not proliferate in response to known ligands for these receptors. 32D transfectants were generated expressing human ErbB4 alone (32D.E4) or with ErbB2 (32D.E2/E4). Epidermal growth factor (EGF), neuregulin 1-beta (NRG1-beta), betacellulin (BTC), transforming growth factor-alpha (TGF-alpha), heparin binding-EGF (HB-EGF), and amphiregulin were analyzed for their ability to mediate mitogenesis in these transfectants. 32D.E4 responded mitogenically to NRG1-beta and BTC. Surprisingly, EGF also induced significant DNA synthesis and TGF-alpha was negligibly mitogenic on 32D.E4 cells, whereas HB-EGF and amphiregulin were inactive. Although coexpression of ErbB2 with ErbB4 in 32D.E2/E4 cells did not significantly alter DNA synthesis in response to NRG1-beta or BTC, it greatly enhanced mitogenesis elicited by EGF and TGF-alpha and unmasked the ability of HB-EGF to induce proliferation. EGF-related ligands that exhibited potent mitogenic activity on 32D.E2/E4 cells at low concentrations induced adherence, morphological alterations, and up-regulation of the Mac-1 integrin and FcgammaRII/III at higher concentrations. While 125I-EGF could be specifically crosslinked to both 32D.E4 and 32D.E2/E4 cells, its crosslinking capacity was greatly enhanced in the cotransfected cells. The ability of the various ligands to mediate proliferation and/or adhesion in the two transfectants correlated with their capacity to induce substrate tyrosine phosphorylation and to initiate and sustain activation of mitogen-activated protein kinase. We conclude that the ability of ErbB4 to mediate signal transduction through EGF-like ligands is broader than previously assumed and can be profoundly altered by the concomitant expression of ErbB2.

Amphiregulin↗
PubMed1998

Reduced kynurenine aminotransferase-I activity in SHR rats may be due to lack of KAT-Ib activity.

Kynurenine aminotransferase I (KAT-I), which also shows glutamine transaminase K (GTK) activity, catalyses the conversion of kynurenine to kynurenic acid, an endogenous glutamate antagonist. Both the GTK and KAT enzyme activities were found to be significantly reduced in kidney, brain and medulla oblongata homogenates of spontaneously hypertensive (SHR) compared to Wistar-Kyoto (WKY) rats. Enzyme activity stains on native gel separations of partially purified kidney homogenates was associated with two major bands of GTK (KAT-I)-activity in WKY and Wistar rats, KAT-Ia and KAT-Ib. SHR rats however showed only KAT-Ia activity. These findings suggest that the absence of KAT-Ib activity may result in a reduced ability to synthesise kynurenic acid in SHR rats, this may help to explain the enhanced sensitivity to glutamate seen in this strain.

Animals↗
PubMed1998

Murine glial cells regenerate NAD, after peroxide-induced depletion, using either nicotinic acid, nicotinamide, or quinolinic acid as substrates.

The potential for regeneration of intracellular pyridine nucleotide levels from different precursors, after peroxide-induced NAD depletion, in cultured glial cells was investigated. Cultured murine glial cells showed a decrease in intracellular NAD levels of >40% after treatment with H2O2 (100 microM). Removal of the H2O2 followed by a 2-h incubation did not result in NAD recovery in the absence of precursors. However, NAD levels increased significantly in these cells after the following substrate additions, at minimum effective concentrations of 1 mM for quinolinic acid (QUIN), 500 microM for nicotinamide, and 2 microM for nicotinic acid. The regeneration of significant amounts of NAD from nicotinic acid at doses 250 and 500 times lower than either nicotinamide or QUIN indicates a preferred route for NAD biosynthesis in glial cells in vitro, probably via nicotinic acid phosphoribosylation.

Animals↗
PubMed1998

Quality control of white cell-reduced red cells: white cell preservation and simplified counting.

BACKGROUND: White cell (WBC) degradation restricts the interval between the filtration process and the assay for residual WBCs. Maintaining WBC integrity would permit extended sample storage for batching and/or shipment to centralized laboratories. The usual quality control assay for WBC-reduced red cell units requires determining the number of WBCs in the entire counting area of a Nageotte hemocytometer, which consists of 40 rows. Reducing the counting area would simplify the quality control procedure. STUDY DESIGN AND METHODS: Adsol red cell units were prepared either on the day of collection (Day 0) or on Day 1 and WBC reduced by filtration on the same day. By using prefiltration and postfiltration red cells, samples containing WBC concentrations of 15, 10, and 3 WBCs per microL were prepared by serial dilution. Identical samples were treated with glutaraldehyde and stored at either 20 to 24 degrees C or 1 to 6 degrees C. All samples were assayed on the day of component preparation and on Days 7 and 14. The numbers of WBCs corresponding to 10- and 40-row areas of the Nageotte hemocytometer were determined. RESULTS: For the conditions and WBC concentration range studied, no significant changes in WBC concentrations were observed through Day 14 for glutaraldehyde-treated samples stored at either temperature, although there were substantial decreases in untreated samples. A 10-row measurement was determined to be sufficient for identifying WBC-reduced red cell units passing the present limit of 5 x 10(6) residual WBCs. CONCLUSION: Glutaraldehyde treatment can preserve WBCs in red cell samples at least up to Day 14, which provides increased efficiency in quality control for laboratories. Current red cell WBC-reduction filters produce components that, when assayed, contain fewer than 10 WBCs per full counting area. The simplified procedure would allow reduction of the counting area by 75 percent.

Blood Preservation↗
PubMed1998

Protein kinase C-delta is an important signaling molecule in insulin-like growth factor I receptor-mediated cell transformation.

To investigate the potential role of protein kinase C-delta (PKC-delta) in insulin-like growth factor I receptor (IGF-IR)-mediated cell transformation, an oncogenic gag-IGF-IR beta-fusion receptor lacking the entire extracellular domain, which was designated NM1, and a full-length IGF-IR were coexpressed with either wild-type PKC-delta (PKC-deltaWT) or an ATP-binding mutant of PKC-delta (PKC-deltaK376R) in NIH 3T3 fibroblasts. While overexpression of PKC-deltaWT did not affect NM1- and IGF-IR-induced focus and colony formation of NIH 3T3 cells, expression of PKC-deltaK376R severely impaired these events. In contrast, NM1-mediated cell growth in monolayer was not affected by coexpressing PKC-deltaK376R. PKC-deltaWT and PKC-deltaK376R were constitutively phosphorylated on a tyrosine residue(s) in the NM1- and IGF-IR-expressing cells and were associated with them in an IGF-I-independent manner. Activated IGF-IR was able to phosphorylate purified PKC-delta in vitro and stimulated its kinase activity. Furthermore, the level of endogenous PKC-delta protein was up-regulated through transcriptional activation in response to long-term IGF-IR activation. Taken together, our results demonstrate that PKC-delta plays an important role in IGF-IR-mediated cell transformation, probably via association of the receptor with PKC-delta and its activation through protein up-regulation and tyrosine phosphorylation. Competition with endogenous PKC-delta for NM1 and IGF-IR association by PKC-deltaK376R is probably an important mechanism underlying the PKC-deltaK376R-mediated inhibition of cell transformation by NM1 and IGF-IR.

3T3 Cells↗
PubMed1997

Immuno-localization of kynurenine aminotransferase (KAT) in the rat medulla and spinal cord.

In the mammalian brain, kynurenine aminotransferase (KAT) is pivotal to the synthesis of kynurenic acid, a preferential antagonist at the strychnine-insensitive NMDA-glycine site. As NMDA receptors are involved in autonomic function, we have examined the immunohistochemical localization of KAT in the medulla and spinal cord of the rat. KAT immunoreactivity (KAT-li) was found throughout these areas, in both glia and neurons. Unlike the mainly astrocytic localization in forebrain structures, KAT-li was predominantly neuronal, notably in areas important for blood pressure and heart rate regulation: ventral medulla, nucleus ambiguus, nucleus of the solitary tract and intramediolateral cell column of the spinal cord. The presence of KAT in these nuclei supports a neuromodulatory role for kynurenic acid in NMDA-mediated autonomic function.

Animals↗