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Biomedical subjects

S Mukherji

Publications and source records attributed to S Mukherji.

At least 19 recordsLinked to original sources

Mass transfer effects on microbial uptake of naphthalene from complex NAPLs.

The bioavailability of naphthalene present as a component of a complex nonaqueous phase liquid(NAPL) comprised by nine aromatic compounds was investigated. Specifically, the effects of naphthalene mass transfer from the NAPL to the aqueous phase on rates of its microbial degradation were examined. The investigations were conducted using a pure culture, ATCC 17484, and a mixed culture of naphthalene-degrading bacteria, the former having been implicated previously in the direct uptake of sorbed naphthalene. The studies were conducted in mass-transfer-limited, segregated-phase reactors(SPRs) in which both the NAPL and aqueous phases were internally well-mixed. A 30-day active biodegradation period was preceded and followed by a 5-7-day period devoid of bioactivity, during which time the rates and extents of mass transfer of components from the NAPL to the aqueous phase were quantified. The NAPL-phase naphthalene mass depletion profiles during biodegradation were compared to those predicted by assuming maximum mass depletion under mass-transfer-limited conditions using both pre- and post-biodegradation dissolution rate and equilibrium parameters. The observed mass depletion rates were high during the initial stages of biodegradation but decreased significantly in later stages. Throughout biodegradation, even in the initial rapid stage, mass depletion rates never exceeded maximum predicted rates based on pre-biodegradation mass transfer parameters. Reduced depletion rates in the later stages appear to relate to mass transfer hindrance caused by formation of biofilms at the NAPL-water interface.

Bacteria↗

Calcium/calmodulin-dependent protein kinase II inhibitor protein: localization of isoforms in rat brain.

A second isoform of Ca2+/calmodulin-dependent-kinase II inhibitor protein (CaM-KIIN) has been identified using the yeast two-hybrid screen. The 1.8kb message encodes a 78 residue CaM-KIINalpha that is 65% identical in its putative open-reading frame and 95% identical in its inhibitory domain to the previously characterized CaM-KIINbeta. CaM-KIINalpha exhibits inhibitory properties towards recombinant mouse CaM-kinase IIalpha indistinguishable from CaM-KIINbeta. The 27 amino acid inhibitory peptide (CaM-KIINtide) derived from CaM-KIIN has the ability to inhibit brain CaM-kinase II activity from multiple organisms including rat, Drosophila and goldfish. Northern analysis of various rat tissues indicates that CaM-KIINalpha is specific to brain whereas CaM-KIINbeta message is also present in testis. In situ hybridization shows a general distribution of both isoforms in rat brain with stronger localization of CaM-KIINbeta in cerebellum and hindbrain and CaM-KIINalpha in frontal cortex, hippocampus and inferior colliculus. An antibody that recognizes both isoforms shows a distribution of CaM-KIIN in rat brain that correlates with immunoreactivity of CaM-kinase II. In cultured mature hippocampal neurons, CaM-KIIN is present in cell bodies and dendrites but, unlike CaM-kinase II, does not display punctate staining at synapses. These results suggest a localized function for CaM-KIIN in inhibiting specialized pools of CaM-kinase II.

Amino Acid Sequence↗

Symbolic description of intracerebral vessels segmented from magnetic resonance angiograms and evaluation by comparison with X-ray angiograms.

We describe and evaluate methods that create detailed vessel trees by linking vessels that have been segmented from magnetic resonance angiograms (MRA). The tree-definition process can automatically exclude erroneous vessel segmentations. The parent-child connectivity information provided by our vessel trees is important to both surgical planning and to guidance of endovascular procedures. We evaluated the branch connection accuracy of our 3D vessel trees by asking two neuroradiologists to evaluate 140 parent-child connections comprising seven vascular trees against 17 digital subtraction angiography (DSA) views. Each reviewer rated each connection as (1) Correct, (2) Incorrect, (3) Partially correct (a minor error without clinical significance), or (4) Indeterminate. Analysis was summarized for each evaluator by calculating 95% confidence intervals for both the proportion completely correct and the proportion clinically acceptable (completely or partially correct). In order to protect the overall Type I error rate, alpha-splitting was done using a top down strategy. We additionally evaluated segmentation completeness by examining each slice in 11 MRA datasets in order to determine unlabeled vessels identifiable in cross-section following segmentation. Results indicate that only one vascular parent-child connection was judged incorrect by both reviewers. MRA segmentations appeared complete within MRA resolution limits. We conclude that our methods permit creation of detailed vascular trees from segmented 3D image data. We review the literature and compare other approaches to our own. We provide examples of clinically useful visualizations enabled by our methodology and taken from a visualization program now in clinical use.

Angiography, Digital Subtraction↗

Fungal diseases of the paranasal sinuses.

Fungal diseases of the paranasal sinuses can be categorized into the invasive and noninvasive varieties. The invasive form has been classified as acute fulminant fungal sinusitis, granulomatous invasive fungal sinusitis, and chronic invasive fungal sinusitis. The noninvasive form can be classified as the fungus ball and the allergic fungal sinusitis. The following review discusses the various types of fungal sinusitis with a special emphasis on the CT and MR imaging features.

Acute Disease↗

Mass transfer effects on microbial uptake of naphthalene from complex NAPLs.

The bioavailability of naphthalene present as a component of a complex nonaqueous phase liquid (NAPL) comprised by nine aromatic compounds was investigated. Specifically, the effects of naphthalene mass transfer from the NAPL to the aqueous phase on rates of its microbial degradation were examined. The investigations were conducted using a pure culture, ATCC 17484, and a mixed culture of naphthalene-degrading bacteria, the former having been implicated previously in the direct uptake of sorbed naphthalene. The studies were conducted in mass-transfer-limited, segregated-phase reactors (SPRs) in which both the NAPL and aqueous phases were internally well-mixed. A 30-day active biodegradation period was preceded and followed by a 5-7-day period devoid of bioactivity, during which time the rates and extents of mass transfer of components from the NAPL to the aqueous phase were quantified. The NAPL-phase naphthalene mass depletion profiles during biodegradation were compared to those predicted by assuming maximum mass depletion under mass-transfer-limited conditions using both pre- and post-biodegradation dissolution rate and equilibrium parameters. The observed mass depletion rates were high during the initial stages of biodegradation but decreased significantly in later stages. Throughout biodegradation, even in the initial rapid stage, mass depletion rates never exceeded maximum predicted rates based on pre-biodegradation mass transfer parameters. Reduced depletion rates in the later stages appear to relate to mass transfer hindrance caused by formation of biofilms at the NAPL-water interface.

Bacteria↗

Characterization of a calmodulin kinase II inhibitor protein in brain.

Ca2+/calmodulin-dependent protein kinase II (CaM-KII) regulates numerous physiological functions, including neuronal synaptic plasticity through the phosphorylation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors. To identify proteins that may interact with and modulate CaM-KII function, a yeast two-hybrid screen was performed by using a rat brain cDNA library. This screen identified a unique clone of 1.4 kb, which encoded a 79-aa brain-specific protein that bound the catalytic domain of CaM-KII alpha and beta and potently inhibited kinase activity with an IC50 of 50 nM. The inhibitory protein (CaM-KIIN), and a 28-residue peptide derived from it (CaM-KIINtide), was highly selective for inhibition of CaM-KII with little effect on CaM-KI, CaM-KIV, CaM-KK, protein kinase A, or protein kinase C. CaM-KIIN interacted only with activated CaM-KII (i. e., in the presence of Ca2+/CaM or after autophosphorylation) by using glutathione S-transferase/CaM-KIIN precipitations as well as coimmunoprecipitations from rat brain extracts or from HEK293 cells cotransfected with both constructs. Colocalization of CaM-KIIN with activated CaM-KII was demonstrated in COS-7 cells transfected with green fluorescent protein fused to CaM-KIIN. In COS-7 cells phosphorylation of transfected alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors by CaM-KII, but not by protein kinase C, was blocked upon cotransfection with CaM-KIIN. These results characterize a potent and specific cellular inhibitor of CaM-KII that may have an important role in the physiological regulation of this key protein kinase.

Amino Acid Sequence↗

Spinal intradural cerebellar ectopia.

An ectopic cerebellum, as in Chiari malformations and ectopic cerebellar dysplastic tissue, is a common finding; however, the presence of an organized ectopic cerebellum is exceedingly rare. We describe the MR imaging, surgical, and histologic appearance of an intraspinal ectopic cerebellum in an infant.

Cerebellum↗

Geniculate ganglion meningioma.

Primary ectopic meningiomas are rare, but may be seen in the head and neck region. The temporal bone and its neural foramen are rarely the site of a primary meningioma. This report describes the CT and MRI appearance of an ectopic meningioma arising at the anatomic location of the geniculate ganglion, and discusses the differential diagnosis as well as the possible origin of the tumor.

Adolescent↗

Effect of anthracycline antitumor antibiotics (adriamycin and nogalamycin) and cycloheximide on the biosynthesis and processing of major UsnRNAs.

In the present study, anthracycline antitumor antibiotics (e.g. adriamycin and nogalamycin), the potent RNA synthesis inhibitors and cycloheximide, the protein synthesis inhibitor, have been used to understand the events of biosynthesis and processing of major UsnRNAs (U1-U6). The anthracyclines inhibit the UsnRNAs biosynthesis (in terms of labelling) differentially in a dose dependent manner. The inhibitory effect of adriamycin and nogalamycin reached plateau at a concentration of 2.5 micrograms/ 10(6) cells/ml and 0.1 microgram/10(6) cells/ml respectively and indicates that nogalamycin is more inhibitory than adriamycin. The inhibition of the UsnRNAs synthesis (in terms of labelling) became maximum within 30 min of incubation and remained unaltered even after 2 h. Thus, it shows that the anthracyclines preferentially inhibit the initiation of the UsnRNA genes' transcription as it has been seen in cases of other large RNAs' synthesis by some other laboratories. The higher inhibitory effect of the anthracyclines on the biosynthesis of U5 and U6 compared to other UsnRNAs indicates the presence of more binding sites on the U5 and U6 snRNA genes. In presence of the anthracyclines, there was high retention of cytoplasmic major pre-UsnRNAs/ UsnRNAs which indicates that the elongation of the UsnRNA synthesis is probably impaired along with initiation; because for the proper processing of the pre-UsnRNAs, formation of the correct secondary structure of that pre-UsnRNA is necessary. Cycloheximide showed some differential effect on the pol II transcribed UsnRNAs (U1-U5) biosynthesis (in terms of labelling) however it has no effect on the pol III transcribed U6 snRNA. It implies that in the pol II transcribed UsnRNAs, some transacting labile factors, either activator or inhibitor, are involved. Whereas, the processing of the UsnRNAs (either pol II or pol III transcribed) was affected more or less in a similar fashion in presence of cycloheximide, indicating the involvement of some transacting labile factors in this event.

Animals↗

Orbital involvement by Wegener's granulomatosis: imaging findings.

OBJECTIVE: The purpose of this study was to define patterns of Wegener's granulomatosis (WG) orbital disease involvement. SUBJECTS AND METHODS: We evaluated the orbital examinations of 14 WG patients (CT for nine, MR imaging for three, and both CT and MR imaging for two) for the number of involved orbits, intraconal or extraconal location, involvement of the orbital apex, sinus involvement, bony erosion, and optic nerve compression. MR images were analyzed for signal characteristics and enhancement patterns. RESULTS: We found orbital disease to be unilateral in 12 patients (86%) and bilateral in two patients (14%) (total of 16 orbits). In 11 orbits (69%), coexistent orbital and sinus diseases with bony erosion were present. Orbital disease without sinus disease was seen in five orbits (31%). Intraorbital disease distribution was as follows: solely extraconal--seven orbits (44%) (four with involvement of muscle); intraconal with muscular involvement--one orbit (6%); combined intra- and extraconal--seven orbits (44%); and primarily orbital apex--one orbit (6%). Involvement of the apex was seen in six orbits. The WG mass was hypointense relative to orbital fat on three standard T2-weighted MR images. We saw homogeneous MR contrast enhancement in all four orbits studied on enhanced T1-weighted images. CONCLUSION: Intraorbital WG involvement is usually accompanied by paranasal sinus disease. A hypointense signal on T2-weighted MR images is helpful in suggesting the diagnosis.

Aged↗

Calcium/calmodulin-dependent kinase II and long-term potentiation enhance synaptic transmission by the same mechanism.

Ca(2+)-sensitive kinases are thought to play a role in long-term potentiation (LTP). To test the involvement of Ca2+/calmodulin-dependent kinase II (CaM-K II), truncated, constitutively active form of this kinase was directly injected into CA1 hippocampal pyramidal cells. Inclusion of CaM-K II in the recording pipette resulted in a gradual increase in the size of excitatory postsynaptic currents (EPSCs). No change in evoked responses occurred when the pipette contained heat-inactivated kinase. The effects of CaM-K II mimicked several features of LTP in that it caused a decreased incidence of synaptic failures, an increase in the size of spontaneous EPSCs, and an increase in the amplitude of responses to iontophoretically applied alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate. To determine whether the CaM-K II-induced enhancement and LTP share a common mechanism, occlusion experiments were carried out. The enhancing action of CaM-K II was greatly diminished by prior induction of LTP. In addition, following the increase in synaptic strength by CaM-K II, tetanic stimulation failed to evoke LTP. These findings indicate that CaM-K II alone is sufficient to augment synaptic strength and that this enhancement shares the same underlying mechanism as the enhancement observed with LTP.

Animals↗

Mutational analysis of Ca(2+)-independent autophosphorylation of calcium/calmodulin-dependent protein kinase II.

Previous studies with synthetic peptides indicate that residues 290-309, corresponding to the calmodulin (CaM)-binding domain of Ca2+/CaM-dependent protein kinase II interact with the catalytic core of the enzyme as a pseudosubstrate (Colbran, R. J., Smith, M. K., Schworer, C. M., Fong, Y. L., and Soderling, T. R. (1989) J. Biol. Chem. 264, 4800-4804). In the present study, we attempted to locate the pseudosubstrate motif by generation or removal of potential substrate recognition sequences (RXXS/T) at selected positions using site-directed mutagenesis. Based on previous results, Arg297, Thr305/306, and Ser314 were selected as key residues. Single mutations such as N294S, K300S, A302R, A309R, and R311A were expressed, purified, and characterized. Several of the mutants exhibited decreased binding of and activation by CaM, not surprising since the mutations were within the CaM-binding domain. None of the mutants exhibited enhanced Ca(2+)-independent kinase activity toward exogenous substrate, but the K300S and N294S mutants showed a significant enhancement in the rate and stoichiometry of 32P incorporation during Ca(2+)-independent autophosphorylation. Using two-dimensional peptide mapping and phosphoamino acid analyses, enhanced phosphorylation of the introduced Ser residue was demonstrated in the K300S mutant but not in the N294S mutant. This specific Ca(2+)-independent autophosphorylation of Ser300 is consistent with the hypothesis that Arg297 may occupy the P (-3) position in a pseudosubstrate autoinhibitory interaction with the catalytic core in the nonactivated state of the kinase.

Amino Acids↗