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Biomedical subjects

B Bose

Publications and source records attributed to B Bose.

At least 19 recordsLinked to original sources
PubMed1998

Anterior cervical fusion using Caspar plating: analysis of results and review of the literature.

BACKGROUND: Ninety-seven patients underwent anterior cervical fusions after discectomy and/or corpectomy. Fibular allograft was used in 13 cases and iliac crest was used in the remaining 84 patients. METHODS: Lateral cervical spine X-rays were reviewed for evaluation of fusion and instrumentation failures. RESULTS: Solid fusion was achieved in all but two patients (97.91%). Nineteen patients developed instrumentation related failures. Seven patients developed fracture of one screw each (one superior and six inferior). Ten patients developed screw back out (inferior screw) and in one patient the superior screws were found to be 2 mm posterior to the posterior cortex but did not cause any neurological deficits. Seven of these patients underwent revision surgery. No complications related to the instrumentation were encountered in the last 34 cases. There were no infections in this series. Five patients developed temporary dysphagia. Two developed temporary deltoid weakness and three patients developed transient recurrent laryngeal nerve palsy. One developed acute airway obstruction but the patient had a pre-existing epiglottic anomaly and sleep apnea disorder. CONCLUSIONS: In selected cases, the Caspar plating system affords an effective means of improving the fusion rate (97.91%) with acceptable instrumentation-related morbidity that improves with experience, (10.7% in the first 38 cases and 1.69% in the last 59 with an overall rate of 7.2%). Temporary neurological deficits seen in this series were probably not related to the Caspar plating procedure itself. Intraoperative fluoroscopic films can be misleading. Therefore regular lateral cervical spine X-rays postplating in the operating room prior to closure are recommended. Lower screws backed out in all failures and this was circumvented by using the bigger (rescue) screws at the inferior end of long constructs.

Bone Plates↗
PubMed1995

Correlation between UVA-induced changes in microviscosity, permeability and malondialdehyde formation in liposomal membrane.

The lipid peroxidation, 14C-glucose leakage and microviscosity of liposomal membrane increased linearly with increasing UVA fluence. A positive and highly significant correlation was found between these properties of the UVA-exposed liposomal membrane. The possible involvement of singlet oxygen in the UVA-induced damage of liposomal membrane is discussed.

Cell Membrane↗
PubMed1995

On the induction of protective responses in Salmonella typhimurium strain TA1535/pSK1002 by UVA (365 nm).

Exposure to UVA (365 nm) led to growth delay, loss of viability and inhibition of 3H-thymidine incorporation into the cells of Salmonella typhimurium strain TA1535 containing multiple copies of a plasmid pSK1002 carrying a umuC'-'lacZ fusion gene. Ultraviolet-A induced umu gene expression, as monitored by the estimation of beta-galactosidase, in a linear fluence-dependent manner. The induction of umu gene expression increased with the increase of postirradiation incubation period of the cells in the LB-ampicillin (LBA) medium at 37 degrees C and leveled off from 2 h onward. The induction of gene expression depended on concomitant protein synthesis and represented the induction of the SOS response in the particular S. typhimurium cells used. The exposure to low fluences (sublethal) of UVA also led to the induction of an adaptive response in the same bacterial cells, which made them resistant to subsequent challenge by a much higher fluence of the same radiation. The adaptive response, as monitored by the assays of viability and beta-galactosidase units, increased with the period of exposure to sublethal fluences of UVA, attained a maximum at the UVA exposure of 4.5 kJ/m2 (15 min) and thereafter gradually decreased with further increase of UVA exposure period. Modulation studies involving D2O, LBA growth medium, different scavengers of free radicals and quenchers of activated oxygen species indicated the involvement of both hydroxyl free radicals and singlet oxygen in the UVA-induced umu gene expression.

Bacterial Proteins↗
PubMed1994

UVA-induced peroxidation of lipid in the dried film state.

Exposure of a dried lipid thin film to UVA produced a dose-dependent linear increase in the three peroxidation products, conjugated diene, lipid hydroperoxide and malondialdehyde (MDA). All three lipid peroxidation products exhibited an inverse dose rate effect. Identical amounts of malondialdehyde were produced when the lipid film was exposed to UVA either directly or through the thickness of the Corning glass on which the film was cast. Antioxidants, alpha-tocopherol, butylated hydroxytoluene (BHT) and the singlet oxygen quencher beta-carotene significantly inhibited the UVA-induced peroxidation of the lipid film. The biological implications of the UVA-induced peroxidation of the dried lipid film are discussed.

Antioxidants↗
PubMed1993

Effect of UV-A on the linolenic acid micelles.

UV-A produced a dose-dependent linear increase of peroxidation in linolenic acid micelles as detected by the assay of (i) conjugated dienes, (ii) hydroperoxides, (iii) malondialdehyde (MDA), and (iv) the fluorescent adduct formed by the reaction of MDA with the amino acid, glycine. While sodium formate, dimethyl sulfoxide, superoxide dismutase, and ethylenediamine-tetraacetic acid produced no significant inhibition, some generally used singlet oxygen quenchers, beta-carotene, dimethylfuran, L-histidine, and sodium azide, caused significant inhibition of the UV-A-induced peroxidation of the linolenic acid micelles. alpha-Tocopherol and butylated hydroxytoluene produced more than 90% inhibition of the UV-A-induced peroxidation. ESR spectrometry revealed the formation of 2,2,6,6-tetramethylpiperidine oxide in the UV-A-irradiated aqueous solution of 2,2,6,6-tetramethylpiperidine. The involvement of singlet oxygen (1O2) in the UV-A-induced peroxidation of linolenic acid micelles is discussed.

Dose-Response Relationship, Radiation↗
PubMed1992

An audit of preschool vision screening.

An audit was carried out to clarify the dispute surrounding the vision screening test at 3.5 years. The uptake was 53.5%, sensitivity 77%, specificity 96%, and positive predictive value 50%. In particular the uptake was poor and the test needed a clear policy for the future.

Child, Preschool↗
PubMed1990

An approach towards understanding the genesis of sunlight-induced skin cancer.

The molecular basis of the sunlight-induced skin carcinogenesis has been elucidated. Of the two ultraviolet components of sunlight that reach the earth's surface the UV-B is known to be carcinogenic but the mode of action of UV-A, the predominant component of sunlight, is ill understood. Using the liposomes as a model system, it has been shown here that UV-A causes dose-dependent lipid peroxidation as estimated by measurements of conjugated dienes, lipid hydroperoxides, malondialdehydes and the fluorescent adducts (Schiff bases) produced by the reaction of MDA with glycine. Direct exposure to sunlight has also been shown to cause dose-dependent lipid peroxidation. The UV-A induced lipid peroxidation has also been shown to be dependent on dose rate. While the sodium formate, dimethyl sulphoxide, superoxide dismutase and EDTA do not have any significant effect, sodium azide, histidine, beta-carotene and dimethylfuran were shown to inhibit significantly the UV-A induced lipid peroxidation, thereby providing significant evidence of the involvement of singlet oxygen (1O2) as the initiating agent. The use of D2O in place of H2O as the liposome dispersing medium enhanced to great extent the UV-A induced lipid peroxidation, thereby lending additional support to the finding that singlet oxygen was the initiating agent. The possible mode of formation of 1O2 on exposure to UV-A was discussed. This study also highlighted the role of environmental factors on the sunlight-induced cutaneous damage. Finally, the relation between lipid peroxidation, DNA damage and carcinogenesis has been discussed in a way to suggest the possible link between sunlight exposure and causation of skin cancer.

Humans↗
PubMed1990

Membrane lipid peroxidation by UV-A: mechanism and implications.

UV-A produced a dose-dependent linear increase of lipid peroxidation in liposomal membrane, as detected by the assay of (i) conjugated dienes, (ii) lipid hydroperoxides, (iii) malondialdehydes (MDA), and (iv) the fluorescent adducts formed by the reaction of MDA with glycine and also a linear dose-dependent increase of [14C]glucose efflux from the liposomes. UV-A-induced MDA production could not be inhibited by any significant degree by sodium formate, dimethyl sulfoxide, EDTA, or superoxide dismutase but was very significantly inhibited by butylated hydroxytoluene, alpha-tocopherol, sodium azide, L-histidine, dimethylfuran, and beta-carotene. MDA formation increased with an increase in the D2O content in water, leading to a maximal amount of nearly 50% enhancement of lipid peroxidation in 100% D2O vis-à-vis water used as dispersion medium. The experimental findings indicate the involvement of singlet oxygen as the initiator of the UV-A-induced lipid peroxidation.

Antioxidants↗
PubMed1989

UV-A induced lipid peroxidation in liposomal membrane.

UV-A (365 nm) produced a dose-dependent linear increase of lipid peroxidation, as detected by the assay of malondialdehyde (MDA). MDA formation was inversely related to the UV-A dose rate. Sodium formate and ethylenediaminetetra acetic acid (EDTA) could not inhibit by any significant degree the UV-A induced MDA formation. While butylated hydroxy toluene (BHT) caused about 85% inhibition, sodium azide and L-histidine produced 45-50% inhibition of MDA formation. The involvement of singlet oxygen (1O2) in the UV-A induced lipid peroxidation is discussed.

Free Radicals↗
PubMed1989

CO2 reactivity and heterogeneity of cerebral blood flow in ischemic, border zone, and normal cortex.

Regional arterial CO2 tension (PaCO2) reactivity of cerebral blood flow (CBF) and the effect of PaCO2 on the spatial and temporal heterogeneity of CBF were investigated by using autoradiographically determined CBF in the rat middle cerebral artery occlusion model after a 2-h period under pentobarbital anesthesia to clarify the relation between PaCO2 reactivity, CBF heterogeneity, and the temporal cycling of CBF. PaCO2 was adjusted to one of four levels. CBF was determined in four cortical areas and white matter using the tissue fractionation of [14C]iodoantipyrine [( 14C]IAP) in combination with vessel mapping using in vivo 4% thioflavine S. Specific PaCO2 reactivity and CBF were normal in the nonischemic cortex, normal, although slightly depressed, in the border zone far from the ischemic core area, and depressed in the border zone adjacent to the ischemic core area (P less than 0.001) and the ischemic core (P less than 0.001). In normocapnic and hypocapnic animals, CBF heterogeneity in the form of regularly spaced CBF columns perpendicular to the cortical surface was observed in the nonischemic hemisphere but was absent in the ischemic core area. In hypercapnic rats, flow columns were present in the ischemic core areas and border zones but were absent on the nonischemic side. There was a highly significant interaction (P less than 0.0001) in observer-determined heterogeneity grades between PaCO2 level and each of three areas, normal, border zone, and ischemic core. In normal cortex, comparison of the thioflavine S-stained vessels with the flow columns provided evidence supporting the concept of capillary recruitment and cycling as a mode of normal cerebral blood flow control. The presence of flow columns in severely ischemic areas in hypercapnic animals indicates that a short period of high PaCO2 transiently augments microregional flow and could enhance the delivery of a therapeutic agent to these microregions of the ischemic core. The regional analysis of PaCO2 reactivity suggests an index of future tissue viability.

Animals↗
PubMed1988

Evolving focal cerebral ischemia in cats: spatial correlation of nuclear magnetic resonance imaging, cerebral blood flow, tetrazolium staining, and histopathology.

The spatial correlation of nuclear magnetic resonance imaging (NMRI) and cerebral blood flow (CBF) may improve our ability to identify ischemic brain lesions and may provide further insight into the pathophysiology of early cerebral ischemia. Eleven pentobarbital-anesthetized adult cats underwent exposure of the common carotid arteries bilaterally and the right middle cerebral artery through a transorbital approach. Baseline NMRI images were obtained with a single spin-echo, multislice technique using a 0.6-T field, 0.4-cm slice thickness, and a surface coil. Focal ischemia was produced with right middle cerebral artery occlusion and potentiated with bilateral common carotid artery ligation. Sequential NMRI studies were then performed at 1, 2, 4, 6, and 12 hours or until CBF was determined in the same cats using [14C]iodoantipyrine at either 2 (n = 2), 4 (n = 2), 6 (n = 2), or 12 (n = 1) hours after the time of occlusion. This protocol allowed temporal and spatial correlation of NMRI and CBF. Alternate 5-mm brain slices were incubated with 1% 2,3,5-triphenyltetrazolium chloride (TTC) for 45 minutes at 37-41 degrees C and frozen in liquid Freon for later autoradiographic CBF determination. Four cats were studied only with NMRI and TTC (not CBF). The correlation between areas of increased NMRI signal intensity observed in T2-weighted images (repetition time 2,000 msec, echo time 120 msec), vital staining with TTC, low CBF, and routine histology was evaluated. During the early phase (less than 6 hours), T2-weighted NMRI changes were localized to the central ischemic gray matter areas, as defined in the later CBF images, with no involvement of the white matter. By the twelfth hour the NMRI changes involved the entire ischemic area including gray and white matter. The initial visible changes seen on T2-weighted NMRI are suggestive of cellular edema, and the later changes are characteristic of vasogenic edema. The spread of NMRI changes compared with the ischemic area determined from autoradiographic CBF is consistent with the previously described biphasic evolution of ischemic injury. These data suggest that T2-weighted NMRI could be used clinically to delineate areas of acute ischemic stroke.

Animals↗