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I Ducic

Publications and source records attributed to I Ducic.

10 recordsLinked to original sources
PubMed2006

The innervation of the medial humeral epicondyle: implications for medial epicondylar pain.

The purpose of this study was identification of the innervation of the medial humeral epicondyle which has not been described before. In 20 patients, the medial intermuscular septum was evaluated histopathologically: the nerve was identified in 15 specimens without S-100 staining, and in the remaining 5 with S-100 staining. In six fresh cadavers, bilateral dissections identified the source of this nerve as the radial nerve in the axilla, coursing adjacent to the ulnar nerve in the upper arm, then moving laterally to be superficial to, or within, the medial intermuscular septum, until the nerve terminated in the periosteum of the medial humeral epicondyle, at the origin of the flexor-pronator muscle mass. In one specimen, a branch from the ulnar nerve in the axilla contributed to this nerve to the medial humeral epicondyle.

Cadaver↗
PubMed2005

Reconstruction of the spinal accessory nerve with autograft or neurotube? Two case reports.

Injury to the spinal accessory nerve is most commonly iatrogenic, but can be related to cervical trauma or resection of tumor. Of the two most recent publications related to injury of the spinal accessory nerve, one describes transfer of the levator scapulae muscle to restore shoulder function, while the other reports on the results of six surgical repairs, three of which used a sural nerve graft to reconstruct a short neural defect. The present report describes the results obtained in two patients when an iatrogenic injury to the XIth nerve was reconstructed at 3 months after the loss of shoulder function. Denervation of the XIth nerve was confirmed by a first EMG at 6 weeks, and a second one at 12 weeks. At surgery, each XIth nerve was found to have an in-continuity neuroma, most probably related to electrocoagulation. Intraoperative electrical stimulation did not pass the region of nerve injury. In the first patient, the XIth nerve was reconstructed with an autograft from the greater auricular nerve. In the second patient, the XIth nerve was reconstructed with a bioabsorbable conduit, the Neurotube. The patient with the Neurotube reconstruction reached M5 trapezius function by 3 months after surgery, and had no nerve graft donor-site morbidity, while the patient with the autograft reached M4 function by 6 months after reconstruction, and has persistent numbness of the ear lobe. This is the first reported case of a cranial motor nerve being reconstructed with a bioabsorbable conduit.

Accessory Nerve↗
PubMed2000

The use of local muscle flaps in foot and ankle reconstruction.

Pedicled muscle flaps always should be considered as a reconstructive option when evaluating possible options to filling a defect around the foot and ankle. To gain confidence in using this option, multiple anatomic dissections with special attention to the vascular anatomy are necessary. These dissections also should give the surgeon a feel for the reach of the various flaps and their applicability in various circumstances. For optimal results, the interoperative dissections should be performed with loupes and the Doppler. This allows the surgeon to identify and protect the dominant pedicle. When insetting the flap, special attention is directed to avoid placing excessive torsion or tension on the pedicle so that the blood flow is not compromised. The flow, both arterial and venous, should be assessed after insetting the muscle with a Doppler. Pedicled muscle flaps offer a rapid and easy solution to difficult soft tissue problems around the foot and ankle. The operation can be performed with a regional block in under two hours. The postoperative stay is short, and the donor defect is minimal. Pedicled muscle flaps offer a great alternative to microsurgical free flaps, especially in the sick patient. They should be considered more often when looking at how to fill small defects with exposed bone or osteomyelitis around the foot and ankle.

Ankle↗
PubMed1998

Imaging of the liver with helical CT: a survey of scanning techniques.

OBJECTIVE: We conducted a survey of the members of the Society of Computed Body Tomography/Magnetic Resonance to assess current techniques in liver imaging using helical CT. MATERIALS AND METHODS: The survey, which was designed to update earlier surveys from 1987 and 1993, included a questionnaire distributed to 77 members of the Society of Computed Body Tomography/Magnetic Resonance. RESULTS: Forty-nine members responded, representing 28 institutions. In 1993, 19% (5/26) of institutions used helical scanners, compared with 82% (23/28) in 1996. The group of institutions with helical CT served as the focus of this survey. In 1993, 58% of institutions used 1-cm collimation: in 1996, 78% (18/23) used thinner, 7- to 8-mm collimation. In 1987, 41% used power injectors compared with 85% in 1993 and 100% in 1996. In 1996, monophasic injections were used by 96% (22/23) of institutions. In 1993, most institutions used a contrast material injection rate of 1.5-2.0 ml/sec; in 1996, most used a 2.5-3.0 ml/sec injection rate. In 1993, 96% of institutions used 125-150 ml of contrast material; in 1996, 57% (13/23) of institutions used 125-150 ml and 30% of institutions used less than 125 ml of contrast material. A delay time of 21-45 see was used by 83% of institutions in 1993, whereas in 1996, 83% (19/23) of institutions used a longer delay time of 50-80 sec. In 1996, 13% of institutions used an individual scan delay technology and all institutions performed multiphasic scanning of hypervascular lesions. CONCLUSION: The availability of helical CT has changed radiologists' approach to liver imaging. The greatest effects of which are a more widespread use of power injectors, longer delay times, thinner collimation, increased contrast material injection rates, decreased contrast material volumes, and multiphasic scanning.

Contrast Media↗
PubMed1998

Gender difference in the cycle length-dependent QT and potassium currents in rabbits.

Women are known to have a longer electrocardiographic Q-T than men, which may contribute to their being at greater risk of developing drug-induced polymorphic ventricular arrhythmias. However, little is known about the underlying mechanisms. In the present study, we evaluated potential gender differences in Q-T interval in isolated perfused rabbit hearts using the Langendorff technique and evaluated the density of outward potassium currents in single ventricular myocytes using the whole-cell patch-clamp technique. We found that female hearts demonstrated a greater Q-T lengthening (delta Q-T%) upon an increase in cycle length (CL), resulting in a significantly longer Q-T (301 +/- 4.8 ms, CL = 2.3 s) at a long CL in female hearts compared with male hearts (267 +/- 4.0 ms, P < .01). Ventricular myocytes isolated from female hearts showed a smaller IK(tail) and peak IKI outward current density. A 50% reduction in extracellular K+ and Mg++ shifted the I-V relationship of IKI and Ito and reduced their amplitude. However, neither the I-V relationship of IKr nor the gender difference in the Q-T-CL relationship was significantly altered. We conclude that 1) female rabbit ventricular myocytes have significantly lower IKr and IKl outward current densities than do male cells, which may contribute to the gender difference in Q-T, and 2) a lower base-line IKr density may contribute to the steeper Q-T-CL relationship in female hearts.

Animals↗
PubMed1997

Comparative effects of loratadine and terfenadine on cardiac K+ channels.

Nonsedating H1-receptor antagonists appear to have wide and variable effects on the QT interval, mediated through modulation of cardiac K+ channels. By using the whole-cell patch-clamp technique, we examined the effects of terfenadine, loratadine, and descarboethoxyloratadine on a large family of K+ channels in ventricular myocytes and in Xenopus oocytes expressing the HERG delayed rectifier. The channels studied included the inward rectifier (I(Kl)) of rat and guinea pig, the transient outward K+ current (I(to)) of rat, the maintained K+ current (I(ped)) of rat, and the delayed rectifier K+ channels (I(Ks) and I(Kr)) of guinea pig myocytes. Loratadine and descarboethoxyloratadine, at therapeutic concentrations (30 to 100 nM), had no measurable effect on any one of the five types of K+ channels studied. At higher concentrations, 0.3 to 1.0 microM, only terfenadine had a significant suppressive effect on I(Kl) and delayed rectifier K+ channels, I(Kr) and I(Ks). At higher concentrations (1 to 2.5 microM), there were marked differences in the ability of the three drugs to suppress the five K+ channels. Generally, terfenadine was the most and loratadine, the least effective blocker of all K+ channels examined. The most susceptible K+ channels were the delayed rectifier channels (I(Ks) and I(Kr)) in guinea pig and I(ped) in rat myocytes. Comparative effects of loratadine and terfenadine examined on the I(Kr) channel (HERG) expressed in Xenopus oocytes suggest much higher affinity of this channel to terfenadine, such that 1 microM terfenadine completely suppressed the current, whereas loratadine had little or no effect. The preferential suppressive effect of terfenadine on the expressed HERG channel was consistent with data obtained on I(Kr) in isolated guinea pig ventricular myocytes. The strong suppressive effect of terfenadine, noted particularly on the I(Kr) and to a lesser extent on I(to), I(Kl), and I(Ks), may be the cause of the reported incidence of QT prolongation and arrhythmogenesis. The absence of significant effect of loratadine and descarboethoxyloratadine, especially on I(Kr), I(to), I(ped), and I(Kl), even at 100 x highest plasma concentrations achieved, may explain the absence of significant reports of QT prolongation and arrhythmogenesis by the latter drugs.

Animals↗
PubMed1997

Suppression of mammalian K+ channel family by ebastine.

Nonsedating H1 receptor (H1-R) antagonists exert variable effects on QT interval, most likely mediated through modulation of cardiac K+ channels. We examined the effects of a novel H1-R antagonist, ebastine, on a family of K+ currents in isolated rat and guinea pig ventricular cardiomyocytes as well as on HERG-induced rapidly delayed rectifier K+ current (I(Kr)) in Xenopus laevis oocytes. The effect of ebastine was compared with that of two other H1-R antagonists, terfenadine and loratadine, with and without reported cardiotoxicity, respectively. In guinea pig ventricular myocytes, ebastine at concentrations approximating those found in plasma under certain conditions suppressed in a voltage-independent manner the I(Kr) (Kd = 0.14 microM, maximum block 74%) more effectively than the slowly delayed rectifier K+ current (I(Ks)) (Kd = 0.8 microM, maximum block 60%). Ebastine also suppressed I(Kr) in HERG-expressing X. laevis oocytes with the Kd value of 0.3 microM and a maximal block of 46% at 3 microM. The block of the rapidly activating delayed rectifier channel in rat myocytes (Iped) (Kd = 1.7 microM, maximum block 58%) had a small voltage dependence. Ebastine only minimally suppressed rat transient K+ current (Ito) (Kd = 1.1 microM, maximum block 10%). The drug was also not a very potent blocker of the inwardly rectifier K+ current (I(K1)) of rat and guinea pig (15 +/- 3% block at 3 microM). At concentrations of <100 nM, ebastine produced negligible effect on all K+ currents. We conclude that ebastine blocks various cardiac K+ channels with different potencies. The group of delayed rectifier K+ currents appeared to be most susceptible to ebastine with the order of sensitivity of I(Kr) > I(Ks) > Iped. Ebastine-induced inhibition of all K+ current types was always weaker than that observed with similar concentrations of terfenadine.

Animals↗
PubMed1996

Assessment of a technology that permits individualized scan delays on helical hepatic CT: a technique to improve efficiency in use of contrast material.

OBJECTIVE: We performed this study to assess the usefulness of a computer automated scan technology (CAST) for individualizing scan delay during helical CT to improve the efficiency of hepatic enhancement. SUBJECTS AND METHODS: We prospectively evaluated 183 patients who were randomized into five groups. Control patients received 100 or 150 ml of contrast material (320 mg I/ml) with a 60-sec delay between contrast injection at 3 ml/sec and scanning. CAST patients received 100, 125, or 150 ml. In our latter groups we used an hepatic enhancement threshold of 50 H over baseline to determine the optimum delay between contrast injection and scanning. For the intergroup comparisons, we measured the liver on baseline and enhanced helical CT scans at the upper, mid, and lower levels of the liver. RESULTS: The mean enhancement in patients who received 150 ml of contrast material was 70.7 +/- 19.4 H for the control group and 81.0 +/- 17.5 H for the CAST group (p < .05). Hepatic enhancement above 50 H was achieved in 84% of the control subjects compared with 100% of CAST subjects; more than 60 H hepatic enhancement was achieved in 73% of control subjects and in 89% of CAST subjects. The use of CAST software with 125-ml contrast doses provided enhancement equivalent to that of control subjects who received 150 ml of contrast material (mean enhancement in CAST subjects, 70.3 +/- 15.4 H). Enhancement above 50 H was reached in 98% of CAST and 84% of control patients. With 100 ml of contrast material, 24% of patients failed to initiate CAST, resulting in enhancement similar to control patients (CAST, 54.2 +/- 11.4 H; controls, 56.9 +/- 15.2 H). CONCLUSION: Using a contrast dose of 150 ml, CAST provided significantly increased hepatic enhancement than that achieved in control subjects with less variability. For equivalent hepatic enhancement, contrast doses could be decreased by 25 ml using CAST technology because it provides individualized scan delays.

Adult↗
PubMed1992

Molecular mechanisms of the partial allosteric modulatory effects of bretazenil at gamma-aminobutyric acid type A receptor.

In central nervous system gamma-aminobutyric acid (GABA) inhibits neuronal activity by acting on GABA type A (GABAA) receptors. These heterooligomeric integral membrane proteins include a GABA-gated Cl- channel and various allosteric modulatory sites where endogenous modulators and anxiolytic drugs act to regulate GABA action. In vivo, various anxiolytic drugs exhibit a wide range of variability in their modulatory efficacy and potency of GABA action. For instance, bretazenil modulatory efficacy is much lower than that of diazepam. Such low efficacy could be due either to a preferential modulation of specific GABAA receptor subtypes or to a low modulatory efficacy at every GABAA receptor subtype. To address these questions we studied drug-induced modifications of GABA-activated Cl- currents in native GABAA receptors of cortical neurons in primary cultures and in recombinant GABAA receptors transiently expressed in transformed human embryonic kidney cells (293) after transfection with cDNAs encoding different molecular forms of alpha, beta, and gamma subunits of GABAA receptors. In cortical neurons the efficacy of bretazenil was lower than that of diazepam, whereas the potency of the two drugs was similar. In cells transfected with gamma 2 subunits and various molecular forms of alpha and beta subunits bretazenil efficacy was always lower than that of diazepam. However, in cells transfected with gamma 1 or gamma 3 subunits and various forms of alpha and beta subunits the efficacy of both diazepam and bretazenil was lower and always of similar magnitude. When bretazenil and diazepam were applied together to GABAA receptors including a gamma 2 subunit, the action of diazepam was curtailed in a manner related to the dose of bretazenil.

Allosteric Regulation↗