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Biomedical subjects

A Rafiq

Publications and source records attributed to A Rafiq.

17 recordsLinked to original sources
PubMed2006

Skill performance in open videoscopic surgery.

INTRODUCTION: Application of minimally invasive surgery represents the future of modern surgical care. Previous studies by our group provided a novel way for viewing open surgery using a rigid endoscope attached to charged coupled device (CCD) camera in proximity to the surgical field using a robotic arm (AESOP) and a stabilizing fulcrum (Alpha port). MATERIALS AND METHODS: This study is a follow-up to investigate the technical feasibility, advantages, and disadvantages of relying only on video images displayed on standard monitors in performing open surgical procedures instead of direct binocular eye vision. This study used two surgeons as participants with training in basic surgical skill and previous experience in performing an intestinal anastomosis in an ordinary fashion. The standard task consisted of anastomosing porcine intestine in two layers with digital viewing of the operative field. A total of 40 anastomoses (20 by each surgeon) were compared with 10 control performances using direct vision of the field. RESULTS: All the resulting anastomoses were accurate, well coapted, and fully patent with no leakage. Time for task performance was approximately twice as long (p < 0.05) with videoscopic vision as with direct vision. DISCUSSION: These findings suggest it is technically feasible to conduct open surgeries with visualization of the open surgical field limited to video display on standard monitors.

Anastomosis, Surgical↗
PubMed2005

Telementoring versus on-site mentoring in virtual reality-based surgical training.

BACKGROUND: Telementoring can be an adjunct to surgical training using virtual reality surgical simulation. Telementoring is hypothesized to be as effective as a local mentor for surgical skills training. METHODS: In this study, 20 Romanian medical students trained using a virtual reality surgical simulator (LapSim) with a telementor or local mentor. All the students watched an instructional module at the beginning of the exercise. The telementor, in the United States, interacted by videoconferencing. Before and after training sessions, tool path length and time for task completion were measured. RESULTS: Instructional media and training with mentoring resulted in similar levels of performance between locally mentored and telementored groups. Right- and left-hand path length and time decreased significantly within each group from the initial to the final evaluation (p < 0.05) for most tasks (grasping, cutting, suturing). No significant difference was achieved for clip-applying. CONCLUSIONS: Integration of instructional media with telementoring can be as effective for the development of surgical skills as local mentoring.

Education, Medical↗
PubMed2005

Ergonomics and human factors in endoscopic surgery: a comparison of manual vs telerobotic simulation systems.

BACKGROUND: Minimally invasive surgical techniques expose surgeons to a variety of occupational hazards that may promote musculoskeletal disorders. Telerobotic systems for minimally invasive surgery may help to reduce these stressors. The objective of this study was to compare manual and telerobotic endoscopic surgery in terms of postural and mental stress. METHODS: Thirteen participants with no experience as primary surgeons in endoscopic surgery performed a set of simulated surgical tasks using two different techniques--a telerobotic master--slave system and a manual endoscopic surgery system. The tasks consisted of passing a soft spherical object through a series of parallel rings, suturing along a line 5-cm long, running a 32-in ribbon, and cannulation. The Job Strain Index (JSI) and Rapid Upper Limb Assessment (RULA) were used to quantify upper extremity exposure to postural and force risk factors. Task duration was quantified in seconds. A questionnaire provided measures of the participants' intuitiveness and mental stress. RESULTS: The JSI and RULA scores for all four tasks were significantly lower for the telerobotic technique than for the manual one. Task duration was significantly longer for telerobotic than for manual tasks. Participants reported that the telerobotic technique was as intuitive as, and no more stressful than, the manual technique. CONCLUSIONS: Given identical tasks, the time to completion is longer using the telerobotic technique than its manual counterpart. For the given simulated tasks in the laboratory setting, the better scores for the upper extremity postural analysis indicate that telerobotic surgery provides a more comfortable environment for the surgeon without any additional mental stress.

Arm↗
PubMed2001

Long-term alteration of calcium homeostatic mechanisms in the pilocarpine model of temporal lobe epilepsy.

The pilocarpine model of temporal lobe epilepsy is an animal model that shares many of the clinical and pathophysiological characteristics of temporal lobe or limbic epilepsy in humans. This model of acquired epilepsy produces spontaneous recurrent seizure discharges following an initial brain injury produced by pilocarpine-induced status epilepticus. Understanding the molecular mechanisms mediating these long lasting changes in neuronal excitability would provide an important insight into developing new strategies for the treatment and possible prevention of this condition. Our laboratory has been studying the role of alterations in calcium and calcium-dependent systems in mediating some of the long-term neuroplasticity changes associated with epileptogenesis. In this study, [Ca(2+)](i) imaging fluorescence microscopy was performed on CA1 hippocampal neurons acutely isolated from control and chronically epileptic animals at 1 year after the induction of epileptogenesis with two different fluorescent dyes (Fura-2 and Fura-FF) having high and low affinities for [Ca(2+)](i). The high affinity Ca(2+) indicator Fura-2 was utilized to evaluate [Ca(2+)](i) levels up to 900 nM and the low affinity indicator Fura-FF was employed for evaluating [Ca(2+)](i) levels above this range. Baseline [Ca(2+)](i) levels and the ability to restore resting [Ca(2+)](i) levels after a brief exposure to several glutamate concentrations in control and epileptic neurons were evaluated. Epileptic neurons demonstrated a statistically significantly higher baseline [Ca(2+)](i) level in comparison to age-matched control animals. This alteration in basal [Ca(2+)](i) levels persisted up to 1 year after the induction of epileptogenesis. In addition, the epileptic neurons were unable to rapidly restore [Ca(2+)](i) levels to baseline following the glutamate-induced [Ca(2+)](i) loads. These changes in Ca(2+) regulation were not produced by a single seizure and were not normalized by controlling the seizures in the epileptic animals with anticonvulsant treatment. Peak [Ca(2+)](i) levels in response to different concentrations of glutamate were the same in both epileptic and control neurons. Thus, glutamate produced the same initial [Ca(2+)](i) load in both epileptic and control neurons. Characterization of the viability of acutely isolated neurons from control and epileptic animals utilizing standard techniques to identify apoptotic or necrotic neurons demonstrated that epileptic neurons had no statistically significant difference in viability compared to age-matched controls. These results provide the first direct measurement of [Ca(2+)](i) levels in an intact model of epilepsy and indicate that epileptogenesis in this model produced long-lasting alterations in [Ca(2+)](i) homeostatic mechanisms that persist for up to 1 year after induction of epileptogenesis. These observations suggest that altered [Ca(2+)](i) homeostatic mechanisms may underlie some aspects of the epileptic phenotype and contribute to the persistent neuroplasticity changes associated with epilepsy.

Animals↗
PubMed2001

Anticonvulsant activities of ethanolic extract and aqueous fraction isolated from Delphinium denudatum.

Dried roots of Delphinium denudatum Wall. are a popular folk remedy for the treatment of epilepsy in the traditional Unani system of medicine in the sub-continent. We carried out anticonvulsant screening of the ethanolic extract (EE) and aqueous fraction (AF) of this plant utilising the maximal electroshock (MEST) and subcutaneous pentylenetetrazole (scPTZ), bicuculline (scBIC), picrotoxin (scPTX) and strychnine (scSTN) tests for anticonvulsant activity. EE had weak dose-dependent anticonvulsant effects on seizures induced by PTZ and BIC. AF exhibited dose-dependent activity against hind limb tonic extension phase (HLTE) of MEST and comparatively stronger anticonvulsant activity against seizures induced by PTZ and BIC. The results suggest the presence of potent anticonvulsant compounds in AF of D. denudatum and deserve further investigation for isolation of active compounds and elucidation of the mechanism of anticonvulsant action.

Animals↗
PubMed2001

Epileptogenesis induces long-term alterations in intracellular calcium release and sequestration mechanisms in the hippocampal neuronal culture model of epilepsy.

Calcium and calcium-dependent processes have been hypothesized to be involved in the induction of epilepsy. It has been shown that epileptic neurons have altered calcium homeostatic mechanisms following epileptogenesis in the hippocampal neuronal culture (HNC) and pilocarpine models of epilepsy. To investigate the mechanisms causing these alterations in [Ca2+]i homeostatic processes following epileptogenesis, we utilized the HNC model of in vitro 'epilepsy' which produces spontaneous recurrent epileptiform discharges (SREDs). Using [Ca2+]i imaging, studies were initiated to evaluate the mechanisms mediating these changes in [Ca2+]i homeostasis. 'Epileptic' neurons required much longer to restore a glutamate induced [Ca2+]i load to baseline levels than control neurons. Inhibition of Ca2+ entry through voltage and receptor gated Ca2+ channels and stretch activated Ca2+ channels had no effect on the prolonged glutamate induced increase in [Ca2+]i in epileptic neurons. Employing thapsigargin, an inhibitor of the sarco/endoplasmic reticulum calcium ATPase (SERCA), it was shown that thapsigargin inhibited sequestration of [Ca2+]i by SERCA was significantly decreased in 'epileptic' neurons. Using Ca2+ induced Ca2+ release (CICR) cell permeable inhibitors for the ryanodine receptor (dantrolene) and the IP3 receptor (2-amino-ethoxydiphenylborate, 2APB) mediated CICR, we demonstrated that CICR was significantly augmented in the 'epileptic' neurons, and determined that the IP3 receptor mediated CICR was the major release mechanism altered in epileptogenesis. These data indicate that both inhibition of SERCA and augmentation of CICR activity contribute to the alterations accounting for the impaired calcium homeostatic processes observed in 'epileptic' neurons. The results suggest that persistent changes in [Ca2+]i levels following epileptogenesis may contribute to the long-term plasticity changes manifested in epilepsy and that understanding the basic mechanisms mediating these changes may provide an insight into the development of novel therapeutic approaches to treat epilepsy and prevent or reverse epileptogenesis.

Animals↗
PubMed2000

Transalkylation of phosphotriesters using Cob(I)alamin: toward specific determination of DNA-phosphate adducts.

The supernucleophilic cobalt compound, cob(I)alamin, has been kinetically characterized with respect to its ability to bring about transalkylation of adducts to DNA phosphates (phosphotriesters). The reactivity of cob(I)alamin toward different phosphotriesters (model compounds and methylated DNA), as well as its specificity toward DNA-phosphate adducts, has been investigated. Through nucleophilic displacement on the alkyl by cob(I)alamin, the alkyl groups (methyl and ethyl) were transferred from phosphotriesters within minutes at room temperature. In contrast, methylated nucleosides (base adducts) were stable in the presence of cob(I)alamin.

Alkylation↗
PubMed2000

Induction of spontaneous recurrent epileptiform discharges causes long-term changes in intracellular calcium homeostatic mechanisms.

Calcium and calcium-dependent systems have been long implicated in the induction of epilepsy. We have previously observed that intracellular calcium ([Ca2+]i) levels remain elevated in cells undergoing epileptogenesis in the hippocampal neuronal culture (HNC) model. In this study, we employed the hippocampal neuronal culture (HNC) model of in vitro 'epilepsy' which produces spontaneous recurrent epileptiform discharges (SREDs) for the life of the neurons in culture to investigate alterations in [Ca2+]i homeostatic mechanisms that may be associated with the 'epileptic' phenotype. [Ca2+]i imaging fluorescence microscopy was performed on control and 'epileptic' neurons with two different fluorescent dyes ranging from high to low affinities for [Ca2+]i. We measured baseline [Ca2+]i levels and the ability to restore resting [Ca2+]i levels after a brief 2-min exposure to the excitatory amino acid glutamate in control neurons and neurons with SREDs. Neurons manifesting SREDs had statistically significantly higher baseline [Ca2+]i levels that persisted for the life of the culture. In addition, the 'epileptic' phenotype was associated with an inability to rapidly restore [Ca2+]i levels to baseline following a glutamate induced [Ca2+]i load. The use of the low affinity dye Fura-FF demonstrated that the difference in restoring baseline [Ca2+]i levels was not due to saturation of the high affinity dye Indo-1, which was utilized for evaluating the [Ca2+]i kinetics at lower [Ca2+]i levels. Peak [Ca2+]i levels in response to glutamate were the same in both 'epileptic' and control neurons. While [Ca2+]i levels recovered in approximately 30 min in control cells, it took more than 90 min to reach baseline levels in cells manifesting SREDs. Alterations of [Ca2+]i homeostatic mechanisms observed with the 'epileptic' phenotype were shown to be independent of the presence of continuous SREDs and persisted for the life of the neurons in culture. Epileptogenesis was shown not to affect the degree or duration of glutamate induced neuronal depolarization in comparing control and 'epileptic' neurons. The results indicate that epileptogenesis in this in vitro model produced long-lasting alterations in [Ca2+]i regulation that may underlie the 'epileptic' phenotype and contribute to the persistent neuroplasticity changes associated with epilepsy.

Animals↗
PubMed1996

Long-lasting reduction of inhibitory function and gamma-aminobutyric acid type A receptor subunit mRNA expression in a model of temporal lobe epilepsy.

This study evaluated hippocampal inhibitory function and the level of expression of gamma-aminobutyric acid type A (GABAA) receptor mRNA in an in vivo model of epilepsy. Chronic recurrent limbic seizures were induced in rats using injections of pilocarpine. Electrophysiological studies performed on hippocampal slices prepared from control and epileptic animals 1 to 2 months after pilocarpine injections demonstrated a significant hyperexcitability in the epileptic animals. Reduced levels of mRNA expression for the alpha 2 and alpha 5 subunits of the GABAA receptors were evident in the CA1, CA2, and CA3 regions of the hippocampus of epileptic animals. No decrease in mRNA encoding alpha 1, beta 2, or gamma 2 GABAA receptor subunits was observed. In addition, no change in the mRNA levels of alpha CaM kinase II was seen. Selective decreases in mRNA expression did not correlate with neuronal cell loss. The results indicate that selective, long-lasting reduction of GABAA subunit mRNA expression and increased excitability, possibly reflecting loss of GABAergic inhibition, occur in an in vivo model of partial complex epilepsy.

Animals↗
PubMed1996

GABAA alpha 2 mRNA levels are decreased following induction of spontaneous epileptiform discharges in hippocampal-entorhinal cortical slices.

Exposure of hippocampal slices to Mg2+ free media (0 Mg) has been shown to trigger full production of stimulus-induced seizure activity after restoration of physiological conditions [1]. In the present study employing hippocampal entorhinal cortical slices (HEC), spontaneous epileptiform discharges (SEDs) were induced using 0 Mg treatment following the return of the slices to physiological conditions. To evaluate the effect of sustained epileptiform activity on gene expression in this HEC slice preparation, changes in mRNA levels of the GABAA alpha 1 and alpha 2 and beta CaM Kinase II subunits were measured using in situ hybridization. HEC slices were incubated in oxygenated artificial cerebrospinal fluid (ACSF) in the presence or absence of Mg2+ for 3 h, then placed in oxygenated ACSF containing Mg2+ for up to 3 h. Control slices were maintained in Mg2+ containing ACSF for up to 6 h. Recurrent SEDs were observed in 0 Mg pre-treated slices while no epileptiform discharges were seen in control slices. Following induction of SEDs by 0 Mg pre-treatment, a significant decrease in mRNA encoding GABAA alpha 2 was found in the CA1, CA2, CA3 and dentate gyrus (DG) regions of the hippocampus for up to 3 h after treatment. Levels of mRNA for GABAA alpha 1 and beta CaM Kinase II were not affected. The results document a decrease in GABAA alpha 2 gene expression following the induction of SEDs in the HEC slice preparation and suggest that rapid changes in neuronal gene expression may contribute to long lasting excitability changes associated with the induction of epilepsy.

Animals↗
PubMed1996

Brain injury-induced enhanced limbic epileptogenesis: anatomical and physiological parallels to an animal model of temporal lobe epilepsy.

Traumatic brain injury (TBI) is a leading cause of symptomatic epilepsy in young adults. This study examined physiological and anatomical epileptogenic consequences of a prior incident of TBI in rats. Rats were subjected to a fluid percussion brain injury one week prior to experimentation, and in vitro electrophysiological recording studies were conducted using combined hippocampal-entorhinal cortical slices (HEC slices). Results were compared to sham operated controls and rats in which a condition of chronic temporal lobe epilepsy was induced by a 2 h bout of pilocarpine-induced status epilepticus 2 months prior to recording (PILO). In field potential recording, PILO HEC slices evidenced a greater degree of disinhibition in Ca1 than did TBI or control slices. TBI slices showed greater disinhibition in the dentate gyrus than did PILO or control rats. In in vitro kindling experiments, 86% of TBI HEC slices generated self-sustaining epileptic activity within 9 stimulus trains. This type of activity was never triggered in control slices. HEC slices prepared from PILO animals generated self-sustaining epileptic activity with fewer stimulus trains than did TBI slices. In anatomical studies, both TBI and PILO hippocampi evidenced significant loss of neurons within the hilar region. TBI induces a series of changes within the limbic system of rats, which are qualitatively similar in many aspects but quantitatively less severe than changes seen in rats with chronic temporal lobe epilepsy. These physiological and anatomical TBI-associated alterations in the limbic system may contribute to the development of epilepsy following head trauma.

Adult↗
PubMed1995

Long-duration self-sustained epileptiform activity in the hippocampal-parahippocampal slice: a model of status epilepticus.

1. Combined hippocampal-parahippocampal slices were employed to study the development of complex epileptiform discharges after Schaeffer collateral stimulation in vitro. With repeated stimulation, slices generated several different types of epileptiform discharges, which were temporally linked to the preceding stimulus, and predictable in their progression. The first epileptiform discharge to be elicited by stimulation was a primary afterdischarge, which began immediately after the stimulation train and progressed with repeated stimulation until it had peaked in amplitude and duration by the third to fifth stimulus train. After development of the primary afterdischarge, a secondary afterdischarge began to appear, with a 2- to 5-min latency after the third to sixth stimulation train, and progressed in amplitude and duration with repeated stimulation, sometimes to durations > 30 min. 2. After development of the secondary afterdischarge, 65-70% of rostral slices triggered long-duration, spontaneous self-sustained activity. This activity consisted of repeated spontaneous 3- to 5-min duration ictallike discharges with a short interval (< 15 min between events), lasting for hours in many cases. These discharges were similar to activity seen in depth recordings of patients with complex partial status epilepticus. This cyclic spontaneous epileptiform activity was blocked by diazepam (100 nM to 1 microM), and potentiated by the N-methyl-D-aspartate (NMDA) antagonist 2-amino-5-phosphonovaleric acid (APV, 50 microM). Analysis of the temporal progression of epileptiform activity through multiple channel extracellular recordings demonstrated that both the interictal and ictal discharges evident during spontaneous recurrent ictal-like status epilepticus (SE) originated at a site distant from the stimulation locus, and then propagated to area CA1. 3. Intracellular recordings from CA3 neurons during spontaneous recurrent ictallike SE activity revealed the cellular correlates of this activity. Recurrent ictallike discharges were initiated at a cellular level by a large depolarization, accompanied by tonic action-potential firing. As the ictal event progressed, the neuron continued to depolarize, and a period of depolarization block ensued, which was terminated by the gradual repolarization of the neuron, with accompanying phasic burst firing. 4. A second variety of long-duration self-sustained activity was also seen in 5-10% of slices. This type of continuous sustained activity was initiated by an increase in duration of the secondary afterdischarge to 30-120 min duration with repeated stimulation. These sustained discharges were also increased in amplitude and frequency by APV (50 microM) and reduced or blocked by the benzodiazepines diazepam or clonazepam (1 microM). Sustained epileptiform discharges seen in vitro were similar to one form of seizure discharges seen in patients with SE in their frequency, duration, in their progression through a similar electrographic series of stages, and their sensitivity to benzodiazepines. 5. Intracellular recordings from CA3 neurons during continuous SE-like discharges revealed large bursts within this area during generation of generalized epileptiform activity. These bursts were coincident with extracellularly recorded population burst activity in CA1, and so were a circuit phenomenon. 6. This physiological and pharmacological correspondence between the multiple types of SE-like activity seen in vitro and in patients with SE suggests that these long-duration limbic discharges seen in slices may constitute a valuable model for study of the seizure discharges of SE. Future studies exploiting the advantages of in vitro preparations may aid in understanding physiological and pharmacological factors important in generation and control of this grave neurological condition.

Animals↗
PubMed1993

Generation and propagation of epileptiform discharges in a combined entorhinal cortex/hippocampal slice.

1. The development of epileptiform discharges in response to tetanic stimulation of the Schaeffer collaterals was studied by using extracellular field potential recordings in CA1, CA3, dentate gyrus, and entorhinal cortex and intracellular recordings in CA1 neurons in rat hippocampal-parahippocampal slices, which were cut so as to maintain reciprocal connections between entorhinal cortex and hippocampus in vitro. 2. The first type of epileptiform discharge to develop was an immediate afterdischarge, which grew in duration and amplitude with repeated stimulation trains at 10-min intervals, until it plateaued after five to nine trains at 40-s duration, on average. This afterdischarge, when fully developed, consisted of an early, high frequency tonic component, followed by a later, lower frequency clonic component. Fully developed primary afterdischarges were all-or-none, in that they had a definite threshold, and varied little in amplitude or duration when activated by threshold or suprathreshold stimulation. The primary discharge could be recorded simultaneously throughout the hippocampal-parahippocampal slice, providing evidence for the intact reciprocal connections between hippocampus and entorhinal cortex. Intracellular recordings in CA1 neurons revealed that during the tonic phase of the afterdischarge, neurons were depolarized by 15-30 mV and gradually repolarized during the clonic component. 3. After full development of the primary afterdischarge, a delayed secondary epileptiform discharge began to appear after five to nine stimulation trains. This late discharge began 2-5 min after the stimulation train and progressed in amplitude and duration with repeated stimulation, in some cases to 2-3 h long self-sustained epileptiform discharges. Like the primary afterdischarge, the secondary discharge could be recorded simultaneously throughout the hippocampal-parahippocampal slice, and individual bursts comprising the secondary discharge occurred at earliest latency in the dentate gyrus, followed by activation in CA3, CA1, and finally in the entorhinal cortex. Intracellular recordings in CA1 neurons established that the secondary discharge occurred without an accompanying depolarization. Rather, it appeared as synaptic bursts developing in an escalating frequency barrage, initiated 2-5 min after the primary afterdischarge. 4. Lesioning studies were conducted to begin determining the site of origin of the secondary epileptiform discharge. After appearance of the secondary discharge, the mossy fibers were cut. This lesion abolished the secondary discharge but did not block the primary afterdischarge. Moving the stimulating electrodes from the Schaeffer collaterals to the mossy fibers proximal to the cut reestablished a truncated secondary discharge. In a second lesioning experiment, a cut was made through the subicular region of the hippocampal-parahippocampal slice before the onset of stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Global forebrain ischemia results in decreased immunoreactivity of calcium/calmodulin-dependent protein kinase II.

Previous studies utilizing crude brain homogenates have shown that forebrain ischemia results in inhibition of calcium/calmodulin-dependent protein kinase II (CaM kinase II) activity without large-scale proteolysis of the enzyme. In this report, a monoclonal antibody (1C3-3D6) directed against the beta- (60-kDa) subunit of CaM kinase II that does not recognize ischemically altered enzyme was utilized to further investigate the ischemia-induced inhibition of CaM kinase II. Immunohistochemical investigations showed that the ischemia-induced decreased immunoreactivity of CaM kinase II occurred immediately following ischemic insult in ischemia-sensitive cells such as pyramidal cells of the hippocampus. No decrease in CaM kinase II immunoreactivity was observed in ischemia-resistant cells such as granule cells of the dentate gyrus. The decreased immunoreactivity was observed for CaM kinase II balanced for protein staining and calmodulin binding in vitro. In addition, autophosphorylation of CaM kinase II in the presence of low (7 microM) or high (500 microM) ATP did not alter immunoreactivity of the enzyme with 1C3-3D6. The data demonstrate the production of a monoclonal antibody that recognizes the beta-subunit of CaM kinase II in a highly specific manner, but does not recognize ischemic enzyme. Together with previous studies, the data support the hypothesis that rapid, ischemia-induced inhibition of CaM kinase II activity may be involved in the cascade of events that lead to selective neuronal cell loss in stroke.

Animals↗