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Biomedical subjects

S K Agrawal

Publications and source records attributed to S K Agrawal.

At least 19 recordsLinked to original sources
PubMed2004

A new heterobifunctional reagent for immobilization of biomolecules on glass surface.

Synthesis of a new heterobifunctional reagent, [N-(2-trifluoroethanesulfonatoethyl)-N-(methyl)-triethoxysilylpropyl-3-amine] (NTMTA) is described for the immobilization of a variety of biomolecules on glass surface. Its triethoxysilyl group reacts with glass surface and trifluoroethanesulfonate ester structure reacts selectively with aminoalkyl/mercaptoalkyl function in biomolecules. The immobilization can be achieved by two ways involving two steps. The first route involves the reaction of NTMTA with glass beads followed by attachment of aminoalkyl- or mercaptoalkylated biomolecules. The second one involves the reaction of biomolecules, viz., oligonucleotides, proteins, etc., with NTMTA via their aminoalkyl or mercaptoalkyl functions to form a biomolecule conjugate, which is then reacted with glass beads (unmodified) to complete immobilization process. This has been demonstrated by successful immobilization of 5'-mercaptoalkyl- or aminoalkylated oligonucleotides and some commonly used enzymes on glass beads using NTMTA reagent.

Glass↗
PubMed2002

Role of RyRs and IP3 receptors after traumatic injury to spinal cord white matter.

Calcium influx and elevation of intracellular free calcium (Ca2+i), with subsequent activation of degenerative enzymes is hypothesized to cause cell injury and death after trauma. We examined the effects of traumatic compressive injury on (Ca2+)i dynamics in spinal cord white matter. We conducted electrophysiological studies with ryanodine and inositol (1,4,5)-triphosphate (IP3) receptor agonists and antagonists in an in vitro model of spinal cord injury (SCI). A 25-30-mm length of dorsal column was isolated from the spinal cord of adult rats, pinned in an in vitro recording chamber (37 degrees C) and injured with a modified clip (2-g closing force) for 15 sec. The functional integrity of the dorsal column was monitored electrophysiologically by quantitatively measuring the compound action potential (CAP) with glass microelectrodes. The CAP decreased to 55.2+/-6.8% of control (p < 0.05) after spinal cord injury (SCI). Chelation of Ca2+i with BAPTA-AM (a high-affinity calcium chelator) promoted significantly greater recovery of CAP amplitude (83.2+/-4.2% of control; p < 0.05) after injury. Infusion of caffeine (1 and 10 mM) exacerbated CAP amplitude decline (45.1+/-5.9% of control; p < 0.05; 44.6+/-3.1% of control; p < 0.05) postinjury. Blockade of Ca2+i release through ryanodine-sensitive receptors (RyRs) with dantrolene (10 microM) and ryanodine (50 microM), conferred significant (p < 0.05) improvement in CAP amplitude after injury. On the other hand, blockade of Ca2+i with inositol (1,4,5)-triphosphate receptor (IP3Rs) blocker 2APB (10 microM) also conferred significant improvement in CAP amplitude after injury (82.9+/-7.9%; p < 0.05). In conclusion, the injurious effects of Ca2+i in traumatic central nervous system (CNS) white matter injury appear to be mediated both by RyRs and through IP3Rs calcium-induced calcium release receptors (CICRs).

Action Potentials↗
PubMed2002

A pilot study on observations on CD4 & CD8 counts in healthy HIV seronegative individuals.

BACKGROUND & OBJECTIVES: CD4 T lymphocyte count is used to measure the progression of HIV infection and is recommended as part of the standard care of HIV infected person. Information on reference CD4 counts and CD4:CD8 ratio in healthy individuals is lacking in India. Therefore the present study was undertaken to obtain base-line data on CD4 counts and CD4:CD8 ratio of healthy population from north India and to assess the feasibility of using the values as reference in an extended larger study. METHODS: In this pilot study 84 HIV negative healthy volunteers (56 males, 28 females) in the age group of 20-59 yr and who were willing to participate in the study were enrolled after proper counseling. Blood specimens were collected from each subject and processed for anti-HIV antibodies for exclusion of HIV. CD4 and CD8 counts of the samples were performed by fluorescence activated cell sorting (FACS). RESULTS: The mean +/- SD of the absolute numbers of CD4 and CD8 lymphocytes/microliter was 763.6 +/- 226 and 547.5 +/- 190 in males and 797.9 +/- 263 and 567.7 +/- 250 in females. The range of the CD4 and CD8 counts was 365-1328 and 264-991 in males and 415-1257 and 224-1126 in females respectively. The mean +/- SD of the CD4:CD8 ratio was 1.47 +/- 0.42 in males and 1.52 +/- 0.45 in females. INTERPRETATION & CONCLUSION: The results of this study showed that there is wide variability in CD4 count in our population, as is seen in studies reported from other parts of India. A large multicentric study could define the normal range for CD4 and CD8 counts and CD4:CD8 ratio in the Indian population.

Adult↗
PubMed2001

Human experience with canal plugging.

Canal occlusion/plugging is a very effective technique with a low risk to hearing. The series of posterior semicircular canal occlusions described in this review now becomes the largest in the literature to date. It continues to support this procedure as the treatment of choice for intractable benign paroxysmal positional vertigo (BPPV). All 44 operated ears were relieved of BPPV, with one patient having an atypical late recurrence. Of the 40 ears with normal preoperative hearing, one had a delayed (3-month) sudden and permanent profound loss, while one other had a mild (20 dB) loss. Six patients had protracted courses of imbalance and motion sensitivity. Canal plugging has led to several new and innovative developments including the partial labyrinthectomy for difficult-to-access skull base lesions and superior semicircular canal plugging for dehiscence. These new procedures and their development are reviewed in this paper.

Humans↗
PubMed2000

Role of L- and N-type calcium channels in the pathophysiology of traumatic spinal cord white matter injury.

Recent work has suggested a potential role for voltage-gated Ca(2+) channels in the pathophysiology of anoxic central nervous system white matter injury. To examine the relevance of these findings to neurotrauma, we conducted electrophysiological studies with inorganic Ca(2+) channels blockers and L- and N-subtype-specific calcium channel antagonists in an in vitro model of spinal cord injury. Confocal immunohistochemistry was used to examine for localization of L- and N-type calcium channels in spinal cord white matter tracts. A 30-mm length of dorsal column was isolated from the spinal cord of adult rats, pinned in an in vitro recording chamber and injured with a modified clip (2g closing force) for 15s. The functional integrity of the dorsal column was monitored electrophysiologically by quantitatively measuring the compound action potential at two points with glass microelectrodes. The compound action potential decreased to 71.4+/-2.0% of control (P<0. 05) after spinal cord injury. Removal of extracellular Ca(2+) promoted significantly greater recovery of compound action potential amplitude (86.3+/-7.6% of control; P< 0.05) after injury. Partial blockade of voltage-gated Ca(2+) channels with cobalt (20 microM) or cadmium (200 microM) conferred improvement in compound action potential amplitude. Application of the L-type Ca(2+) channel blockers diltiazem (50 microM) or verapamil (90 microM), and the N-type antagonist omega-conotoxin GVIA (1 microM), significantly enhanced the recovery of compound action potential amplitude postinjury. Co-application of the L-type antagonist diltiazem with the N-type blocker omega-conotoxin GVIA showed significantly greater (P<0.05) improvement in compound action potential amplitude than application of either drug alone. Confocal immunohistochemistry with double labelling for glial fibrillary acidic protein, GalC and NF200 demonstrated L- and N-type Ca(2+) channels on astrocytes and oligodendrocytes, but not axons, in spinal cord white matter. In conclusion, the injurious effects of Ca(2+) in traumatic central nervous system white matter injury appear to be partially mediated by voltage-gated Ca(2+) channels. The presence of L- and N-type Ca(2+) channels on periaxonal astrocytes and oligodendrocytes suggests a role for these cells in post-traumatic axonal conduction failure.

Animals↗
PubMed2000

Effects of methylprednisolone and MK-801 on functional recovery after experimental chronic spinal cord injury.

STUDY DESIGN: An experimental study was conducted to evaluate the effects of methylprednisolone and MK-801 after the compressive injury of spinal cord in rats. OBJECTIVES: To investigate the effect of methylprednisolone and non-competitive NMDA antagonist MK-801 in long-term functional outcome after spinal cord injury (SCI). METHODS: A randomized group A of Sprague-Dawley rats were treated with MK-801 (1.0 mg/kg, n=10; Group A) after a compression injury. A group of methylprednisolone (MP)-treated (30 mg/kg, n=10; Group B) and non-treated animals (n=9; Group C) were included for comparison. The functional motor outcome such as inclined plane (IP), toe spreading reflex (TSR), and modified Tarlov scale (TS) were measured in each animal at regular time points up to 8 weeks post-treatment. Histologically the injury site was scored in four groups and immunohistochemically Wallerian Degeneration (WD), astrocytosis and expression of beta-amyloid protein was identified. RESULTS: In examining the IP data, no significant difference was recognized between the group means (P-value>0.5). For the TSR, there were no differences in the group responses. For the TS, the differences were not statistically significant. Only group B showed significance in cavitation scores compared to group A (P>0.0094), WD was significantly different than group C (P>0.03), astrocytosis was significantly higher than group A (P>0.001) and modest presence of beta-amyloid protein. CONCLUSION: Our data indicate that one time bolus administration of MK-801 lacks any significant effect on axonal function in chronically injured rats. Daily bolus administration of MP at 30 mg/kg also did not ensure a better functional outcome. Immunohistochemically we have been able to show significant differences in WD, astrocytosis and small insignificant changes in beta-amyloid protein.

Amyloid beta-Peptides↗
PubMed2000

Tremor suppression through impedance control.

This paper presents a method for designing tremor suppression systems that achieve a specified reduction in pathological tremor power through controlling the impedance of the human-machine interface. Position, rate, and acceleration feedback are examined and two techniques for the selection of feedback coefficients are discussed. Both techniques seek a desired closed-loop human-machine frequency response and require the development of open-loop human-machine models through system identification. The design techniques were used to develop a tremor suppression system that was subsequently evaluated using human subjects. It is concluded that nonadaptive tremor suppression systems that utilize impedance control to achieve a specified reduction in tremor power can be successfully designed when accurate open-loop human-machine models are available.

Acceleration↗
PubMed1998

Role of group I metabotropic glutamate receptors in traumatic spinal cord white matter injury.

Metabotropic glutamate receptors (mGluRs) participate in glutamate neural transmission, but their role in the pathophysiology of spinal cord injury (SCI) has not been explored. Accordingly, we examined the role of group I mGluRs, which are linked to phospholipase C, in mediating SCI using an in vitro model. A dorsal column segment was isolated from the spinal cord of adult rats, maintained in vitro, and injured by compression for 15 sec with a clip having a 2 g closing force. Under control conditions after SCI, the compound action potential (CAP) amplitude was reduced to 69.1 +/- 5.4% of baseline. Blockade of group I mGluR receptors with MCPG, 4CPG, or AIDA resulted in improved recovery of CAP amplitude (82.2 +/- 2.0%, 86.2 +/- 3.9%, and 86.0 +/- 2.5% of baseline, respectively). The group I/II agonist trans-ACPD and selective group I agonist DHPG exacerbated the posttraumatic reduction of CAP amplitude. The phospholipase C inhibitor U-73122 improved recovery of CAP amplitude after traumatic spinal cord axonal injury. Western blotting and immunocytochemistry demonstrated the presence of mGluR1alpha-immunopositive astrocytes and the absence of mGluR5 in spinal cord white matter. These studies are consistent with the hypothesis that activation of group I mGluR receptors after SCI exacerbates posttraumatic axonal injury through a phospholipase C dependent mechanism. The presence of mGluR1alpha labeling on astrocytes suggests a role for these cells in the pathophysiology of SCI. Additional studies in vivo, are required to further clarify the role of mGluRs in acute traumatic SCI.

Age Factors↗
PubMed1997

Role of NMDA and non-NMDA ionotropic glutamate receptors in traumatic spinal cord axonal injury.

We examined the role of glutamatergic mechanisms in acute injury to rat spinal cord white matter. Compound action potentials (CAPs) were recorded from isolated dorsal column segments in vitro. Under control conditions (Ringer's solution), the CAPs decreased to 71.4 +/- 2.0% of preinjury values after compression injury with a clip exerting a closing force of 2 g. The combination of the NMDA receptor blocker APV (50 microM) and the AMPA/kainate (KA) receptor blocker CNQX (10 microM) resulted in significantly improved recovery of CAP amplitude postinjury; however, the NMDA receptor antagonist APV alone did not enhance postinjury recovery, and infusion of NMDA (10 microM) did not affect recovery of the CAPs. In contrast, the AMPA/KA receptor blockers NBQX (10 microM) or CNQX (10 microM) significantly enhanced the recovery of CAP amplitude postinjury. The agonists AMPA (100 microM) or KA (100 microM) resulted in significant attenuation of CAP amplitude postinjury. Coapplication of AMPA/KA plus NBQX and CNQX was also associated with improved functional recovery. After incubation with AMPA and KA, Co(2+)-positive glia were visualized in spinal cord white matter. Similar results were seen after compressive injury but not in control cords. Immunohistochemistry and Western blot analysis demonstrated AMPA (GluR4)- and KA (GluR6/7 and KA2)-positive astrocytes in spinal cord white matter. In summary, non-NMDA ionotropic glutamate receptors seem to be involved in the pathophysiology of traumatic spinal cord injury. The presence of AMPA (GluR4) and KA (GluR6/7 and KA2) receptors on periaxonal astrocytes suggests a role for these cells in glutamatergic white matter injury.

Animals↗
PubMed1997

Sinus venosus atrial septal defects: surgical follow-up.

OBJECTIVE: To assess early and later results after surgery for sinus venous atrial septal defects (ASDs). METHODS: Forty-four patients of sinus venosus ASDs with anomalous drainage of the right superior pulmonary vein into the superior vena cava, were operated upon between January 1985 and June 1995. Defects were approached by an incision starting from the tip of the right atrial appendage then extending upward along the atrial crest to the medial wall of the superior vena cava. Atrial defects were closed by an autologous pericardial patch. Another pericardial patch was used to enlarge the superior vena cava-right atrial junction to avoid the narrowing of the superior vena cava. RESULTS: There was no operative mortality. The total duration of follow-up was 4 +/- 0.7 years. Follow-up of the echocardiographic study at 6 months and 2 years after surgery revealed a normal study. Two patients developed sinus node dysfunction of short duration in the immediate postoperative period. Follow-up of the electrocardiographic study at 6 months and 2 years revealed sinus node dysfunction in one and two patients, respectively.

Adolescent↗
PubMed1997

The effect of the sodium channel blocker QX-314 on recovery after acute spinal cord injury.

There is evidence that elevated intracellular sodium ([Na+]i) activity potentiates spinal cord injury (SCI) and the hypoxic/ischemic cell death. In this study, we examined the effect of QX-314, a potent Na+ channel blocker, on recovery after SCI in vivo. QX-314 (2.0 and 10 nmol) or vehicle was microinjected (2 microL) into the injury site 15 min after SCI. Injury was performed by compression of the spinal cord at C7-T1 for 1 min with a modified aneurysm clip exerting a closing force of 35 g. Neurological function was assessed 1 day after injury and weekly thereafter until 6 weeks by the inclined plane method and by the modified Tarlov technique. After 6 weeks of injury, the origin of descending axons at the injury site was determined by retrograde labeling with fluorogold (FG), and a computer-assisted morphometric assessment of the injury site was performed. There was a significant improvement in counts of retrogradely labeled neurons in the red nucleus and rostral ventrolateral medulla (RVLM) in rats treated with either 2 nM (1338 +/- 366 and 28.8 +/- 16) or 10 nM (1390 +/- 511 and 46.3 +/- 31) QX-314 as compared to vehicle (902 +/- 403 and 13.8 +/- 8). There was a trend to increased neuronal counts in the sensorimotor cortex (170.8 +/- 226.8) and vestibular nuclei (1096.2 +/- 970.2) with QX-314 (10 nM) as compared to the vehicle-treated group. There was no significant difference in the extent of neurological recovery between the control and treated groups. Our results suggest that the Na+ channel blocker QX-314 partially preserves the integrity of descending motor axons after SCI. However, in this study, the effects were insufficient to result in sustained improvements in behavioral neurological function.

Anesthetics, Local↗
PubMed1996

Mechanisms of secondary injury to spinal cord axons in vitro: role of Na+, Na(+)-K(+)-ATPase, the Na(+)-H+ exchanger, and the Na(+)-Ca2+ exchanger.

There is evidence that intracellular Na+ entry potentiates hypoxic-ischemic cell death by causing cytotoxic cell edema, intracellular acidosis, and gating of Ca2+ entry by reverse activation of the Na(+)-Ca2+ exchanger. In this study, we examined the role of Na+ in mediating traumatic injury to spinal cord axons. Dorsal column segments from adult rats (n = 87) were isolated and maintained in an in vitro recording chamber while being superfused with oxygenated Ringer's solution (95% O2/5% CO2, 25 degrees C). Selected experiments (n = 10) also were done at 33 degrees C. Compound action potentials (CAP) were recorded from microelectrodes. Injury was performed by compression of the dorsal column segment for 15 sec with a modified aneurysm clip exerting a closing force of 2 gm. With injury, the CAP decreased to 72.1 +/- 9.6% of baseline values. Removal of extracellular Na+ and replacement with the impermeant cation N-methyl-D-glucamine enhanced recovery of the CAP to 98.3 +/- 18.3% (p < 0.05) of baseline. The Na+ channel blockers tetrodotoxin and procaine also improved recovery of the CAP to 96.3 +/- 23.7% (p < 0.05) and 82.8 +/- 4.6% (p < 0.05) of baseline values, respectively. In contrast, increasing Na+ permeability with veratridine resulted in greater attenuation of CAP amplitude after 1 hr of trauma (60.1 +/- 8.4%, p < 0.05). Similarly, prevention of extrusion of Na+ from the intracellular compartment by inhibiting the Na(+)-K(+)-ATPase pump with ouabain resulted in greater attenuation of CAP amplitude at 1 hr after trauma (56.7 +/- 3.6%, p < 0.05). The Na(+)-H+ exchange blockers amiloride (100 microM) and harmaline (100 microM) significantly improved recovery after injury to 89.6 +/- 17.0% (p < 0.05) and 85.7 +/- 7.2% (p < 0.05) of baseline, respectively. However, administration of the Na(+)-Ca2+ exchange blockers benzamil (100 or 500 microM) and bepridil (50 microM) was ineffective. In summary, reduction of extracellular Na+ confers neuroprotection after spinal cord injury in vitro. Intracellular sodium rises appear to be mediated by voltage-gated Na+ channels. Blockade of the Na(+)-H+ exchanger also is neuroprotective, possibly by reducing intracellular acidosis. Furthermore, prevention of extrusion of intracellular Na+ by the Na(+)-K(+)-ATPase pump exacerbates the effects of compression trauma. However, reverse operation of the Na(+)-Ca2+ exchanger does not explain the injurious effects of Na+ in traumatically injured CNS white matter.

Animals↗
PubMed1994

Balloon angioplasty for treatment of in-stent restenosis: feasibility, safety, and efficacy.

Sixty patients with 1 or 2 stainless steel intracoronary stents (Cook, Inc.) underwent balloon angioplasty for in-stent restenosis 1.5-13.5 months after stenting. Seventy-five in-stent redilatation procedures were performed. Seventy-three restenotic lesions (97%) were successfully recrossed and dilated, reducing the mean pre-angioplasty intrastent diameter stenosis from 77 +/- 12% to 20 +/- 11% residual. Although one angioplasty (1.3%) was complicated by non-Q-wave infarction, no angioplasty-related death, acute closure, need for additional stenting, emergent coronary bypass surgery, side branch occlusion, or vascular sequelae occurred. Post-procedure heparin was not used in 83% of successful cases. Most patients were discharged the day following redilatation (mean in-hospital stay 1.7 +/- 1.3 days). At 5.4 +/- 3.4 months following in-stent angioplasty, 84% of patients were in Canadian Cardiovascular Society class 0 or I. In conclusion, balloon dilatation in this stent for restenosis appears simple and efficacious in the short term, and may entail less risk than dilatation of unprotected coronary vessels.

Adult↗
PubMed1993

Clinically guided closure of femoral arterial pseudoaneurysms complicating cardiac catheterization and coronary angioplasty.

Femoral artery pseudoaneurysm formation is a significant problem in patients undergoing cardiac catheterization and interventional cardiac procedures. It is especially more common with the use of anticoagulant and antiplatelet therapy and the use of intracoronary stents. We describe our initial experience with clinically guided bedside compression of femoral pseudoaneurysms in such patients. Eleven patients, 10 undergoing coronary angioplasty (including 3 with intracoronary stents) and 1 undergoing diagnostic cardiac catheterization, developed a femoral pseudoaneurysm. All patients had a femoral bruit and 9 had an expansile groin hematoma. The diagnosis was confirmed in each case by Doppler ultrasound. Seven patients were receiving heparin while 4 were on oral anticoagulants at the time of detection of the pseudoaneurysm. These patients underwent clinically guided graded external compression to close the pseudoaneurysm neck while maintaining femoral arterial flow. External compression for 104.1 +/- 63 min resulted in successful clinical resolution of pseudoaneurysm in all patients without complications. The results were confirmed by Doppler ultrasound at least 12 hr later. Bedside compression of femoral pseudoaneurysms guided by clinical clues is simple and appears to be an effective and safe technique to manage this iatrogenic problem.

Aged↗
PubMed1993

Early removal of catheter following transurethral resection of the prostate.

This study was conducted on 83 patients who underwent an uncomplicated transurethral resection of the prostate for carcinoma or benign hyperplasia. In all cases the urethral catheter was removed within 24 h of surgery. Only 2 patients failed to void because of clot retention. The total hospital stay was 3 days in 67 patients. There were no significant complications due to early removal of the catheter.

Adult↗
PubMed1992

Nonsurgical closure of femoral pseudoaneurysms complicating cardiac catheterization and percutaneous transluminal coronary angioplasty.

OBJECTIVES: This study was performed to describe the initial experience and follow-up of ultrasound-guided compression of pseudoaneurysms in patients receiving systemic anticoagulant or antiplatelet therapy, or both, after recent cardiac catheterization or percutaneous transluminal coronary angioplasty. BACKGROUND: Femoral artery pseudoaneurysm formation after an interventional procedure is becoming more common as larger caliber catheters and prolonged anticoagulant and antiplatelet therapy are being used. Traditional treatment of this complication has been surgical repair. This study describes a new method of closing femoral pseudoaneurysms by using external compression guided by Doppler color flow imaging. METHODS: Fifteen patients, 3 undergoing cardiac catheterization and 12 undergoing coronary angioplasty, developed an expansile groin mass at the vascular access site diagnosed as a femoral artery pseudoaneurysm by Doppler ultrasound. Seven of the patients had undergone coronary stenting and were receiving postprocedural anticoagulant therapy. These patients underwent progressive graded mechanical (C-clamp) external compression guided by ultrasound. The mechanical compression was titrated to obliterate the vascular tracts to these aneurysms and maintain adequate flow in the femoral artery. RESULTS: After an average compression time of 30 min (range 10 to 120), these tracts remained closed. Follow-up ultrasound examination at 24 h or later confirmed continued closure in all. CONCLUSIONS: This study suggests that nonsurgical closure of femoral pseudoaneurysms is feasible. This technique may be valuable in managing vascular access-related complications after diagnostic and interventional procedures, even in patients requiring prolonged anticoagulant therapy.

Adult↗