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Biomedical subjects

N Kanaan

Publications and source records attributed to N Kanaan.

14 recordsLinked to original sources
PubMed2006

Lamivudine for nephrotic syndrome related to hepatitis B virus (HBV) infection.

A 57-year-old man presented with nephrotic syndrome associated with active HBV infection. Liver biopsy showed severe portal and moderate lobular inflammation, patchy necrosis, moderate fibrosis and several "ground glass" cells. Immunofluorescence microscopical view of the renal biopsy showed diffuse granular IgG deposits along the glomerular basement membrane, compatible with MN. As symptomatic therapy with ACE inhibitors did not improve the nephrotic syndrome, lamivudine 100 mg o.d. was initiated. HBV-DNA became undetectable after 10 weeks and seroconversion of HBeAg and HBsAg to anti-HBe and anti-HBs occurred after 2 additional months; proteinuria normalized subsequently. This observation documents for the first time in an adult the beneficial effect of lamivudine in glomerulonephritis related to HBV infection with HBV seroconversion and complete remission of the nephrotic syndrome.

Biopsy↗
PubMed2004

Multiple bilateral fibroadenomas of the breasts requiring mastectomy in a renal transplant patient.

Fibroadenomas of the breast have been reported in female renal graft recipients and associated with the use of cyclosporin A (CsA). We report the case of a young patient given CsA who developed multiple bilateral fibroadenomas of the breasts 3 years after renal transplantation, leading to bilateral mastectomy. We discuss the association of CsA with fibroadenomas, the mechanisms by which the drug can act and review the literature. Based on these observations, an early conversion from CsA to tacrolimus should be considered; further observations are needed to assess the reversibility of the breast(s) lesions after such immunosuppressive regimen switch.

Adolescent↗
PubMed2001

Proteasome activity is required for T lymphocyte aggregation after mitogen activation.

The proteasome is a multicatalytic complex of proteases involved in T lymphocyte proliferation and activation through multiple mechanisms. In this study, we investigated its role in lymphocyte aggregation. We found that blocking proteasome activity by a proteasome-specific inhibitor lactacystin (LAC) prevented clustering of T lymphocytes after stimulation with various mitogens. Expression of adhesion molecules ICAM-1 and LFA-1 at cell surfaces of activated T cells was decreased after treatment with LAC. Mechanisms by which the proteasome intervenes in the expression of these adhesion molecules were different. LAC inhibited ICAM-1 expression at the mRNA level, whereas LFA-1 inhibition was probably at a post-translational level. Downregulation of these molecules after proteasome inhibition likely contributes to the observed repression of T cell aggregation. Our results show that the proteasome plays an important role in cell-cell interaction during T cell activation.

Acetylcysteine↗
PubMed2001

Proteasomes modulate balance among proapoptotic and antiapoptotic Bcl-2 family members and compromise functioning of the electron transport chain in leukemic cells.

The mechanism underlying apoptosis induced by proteasome inhibition in leukemic Jurkat and Namalwa cells was investigated in this study. The proteasome inhibitor lactacystin differentially regulated the protein levels of proapoptotic Bcl-2 family members and Bik was accumulated at the mitochondria. Bik overexpression sufficed to induce apoptosis in these cells. Detailed examination along the respiration chain showed that lactacystin compromised a step after complex III, and exogenous cytochrome c could overcome this compromise. Probably as a result, the succinate-stimulated generation of mitochondrial membrane potential was significantly diminished. Bcl-x(L) interacted with Bik in the cells, and Bcl-x(L) overexpression prevented cytochrome c leakage out of the mitochondria, corrected the mitochondrial membrane potential defect, and protected the cells from apoptosis. These results show that proteasomes can modulate apoptosis of lymphocytes by affecting the half-life of Bcl-2 family members, Bik being one of them.

Acetylcysteine↗
PubMed2001

Nocturnal leg cramps. Clinically mysterious and painful--but manageable.

Nocturnal leg cramps are common occurrences among older, generally healthy adults. Although there are many known causes--endocrinologic, neurologic, and vascular disorders, treatment with certain drugs, and occupational factors--a significant portion of cases are idiopathic. History, physical exam, and laboratory testing can provide clues for distinguishing between cramps with identifiable causes and idiopathic cases. For nonidiopathic cases, management consists of treating the underlying cause whenever possible. A nonpharmacologic approach (massaging and stretching) is the recommended first-line treatment for idiopathic cases. Quinine sulfate also appears to offer safe and effective symptom management of idiopathic cases, although its efficacy has not been definitively established in clinical trials.

Age Distribution↗
PubMed2001

Carpal tunnel syndrome: modern diagnostic and management techniques.

Carpal tunnel syndrome is a common disorder characterised by the classical symptoms of numbness and paraesthesiae along the distribution of the median nerve. Thenar muscle weakness is a late manifestation of advanced disease. Tinel's and Phalen's signs are helpful in suggesting the diagnosis. The symptoms and signs arise from entrapment of the median nerve. Electrophysiological tests are helpful in confirming the diagnosis and magnetic resonance imaging may be used in the diagnosis of atypical cases. Ergonomic manoeuvers and steroid injections may alleviate symptoms in mild cases. Surgery is reserved for severe cases and those who do not respond to conservative therapy. Open carpal tunnel release is the classical surgery with usually excellent results. Endoscopic carpal tunnel release surgery was introduced to decrease the morbidity of open surgery. This latter technique also has its complications and is still being refined.

Carpal Tunnel Syndrome↗
PubMed2000

The proteasome controls the expression of a proliferation-associated nuclear antigen Ki-67.

The proteasome is a protease complex responsible for rapid, selective, and irreversible removal of regulatory proteins, as well as many other cellular proteins. In this study, we have demonstrated that a proliferation-associated nuclear protein Ki-67 depended on the proteasome for its rapid degradation. A proteasome-specific inhibitor lactacystin augmented Ki-67 protein levels in pancreatic cancer BxPC-3 cells while repressed the level of steady-state Ki-67 mRNA. Inhibition of the proteasome also led to accumulation of two CDK inhibitors p27(kip1) and p21(cip1) in the BxPC-3 cells. Failed reduction of Ki-67 protein and enhanced levels of the two CDK inhibitors are likely contributing factors for the suppressed BxPC-3 proliferation after proteasome inhibition.

Acetylcysteine↗
PubMed1997

Ventricular tachycardia in healing canine myocardial infarction: evidence for multiple reentrant mechanisms.

Prior studies have demonstrated that unimorphic VT, sometimes due to epicardial reentry, can be induced in healing canine MI; however, the characterization of the types of reentry involved has differed among prior studies. The purpose of this study was to further characterize the spectrum of epicardial reentrant circuits during induced VT in experimental canine MI. Experimental MI was created by total occlusion of the LAD in dogs. Five days later, programmed stimulation was used to induce VT, which was mapped on the epicardium using a combination of vector and isochronal techniques. Pathological analysis was used to determine regions of transmural MI. Epicardial reentrant circuits were identified in eight dogs. The mean cycle length of induced VT was 212 +/- 32 ms. In 3 of 8 experiments, a region of transmural MI was present, which formed at least a portion of a central zone of block around which reentrant impulses circulated. In five experiments, reentry was functional in nature, although the characteristics of the region of functional conduction block were variable. Long lines of functional block, short lines of block with slow conduction transverse to fiber orientation, and leading circle reentry were each observed in different experiments. Although a zone of slow conduction was identified in seven of the experiments, slow conduction transverse to fiber orientation appeared crucial in maintaining reentry in only three experiments. Multiple reentrant mechanisms of VT may be present in this single canine infarction model. Although a zone of slow conduction is usually present, the characteristics of the region of block are highly variable. However, epicardial reentry accounted for only a minority of induced arrhythmia episodes.

Animals↗
PubMed1991

Monophasic action potential duration during programmed electrical stimulation.

UNLABELLED: To examine changes in monophasic action potential duration (APD) with a pacing protocol similar to that used during electrophysiological testing, action potentials were recorded in vivo from the left ventricular apical endocardium of 12 normal mongrel dogs. The atrioventricular node was ablated and the dogs paced from the anterior right ventricle at a baseline cycle length of 1000 ms between interventions. Mean steady-state APD (APDss) was 266 +/- 7 ms at a pacing cycle length (PCL) of 1000 ms. Two pacing protocols were used. The first consisted of a sudden acceleration in pacing from a cycle length of 1000 ms to one between 300 and 600 ms. The second consisted of an 8-beat train at a cycle length of 400 ms followed by a premature beat at a coupling interval of 280 ms followed by a pause. The inter-train pause varied between 1 second and 32 seconds. With a sudden acceleration in pacing rate, steady-state values for APD at the faster PCLs were significantly smaller than APDss at 1000 ms with a change to cycle lengths of 600 ms (247 +/- 29 ms), 500 ms (229 +/- 21 ms), 400 ms (220 +/- 17 ms), and 300 ms (203 +/- 31 ms; P less than 0.01 for all comparisons). The time constant of the change in APD was shorter at a PCL of 300 ms (14.9 +/- 0.8 s) than 600 ms (20.3 +/- 4.7 s; P less than 0.05). With drive train pacing and incorporating an inter-train pause, the percent drop in steady-state APD compared to APD for the first train ranged from 10.1% with a 1-second inter-train pause to 2.1% with a 32-second pause. The difference in APD between the first drive train and drive trains after at least 3 minutes of pacing when APD had stabilized was not significant for an inter-train pause exceeding 8 seconds. IN CONCLUSION: (1) with a sudden acceleration in pacing rate, endocardial APD in vivo decreases exponentially. The faster the new rate, the shorter the new steady-state APD and the shorter the time constant. (2) When pacing using an 8-beat drive train and an inter-train pause, there is a decremental shortening in APD for pause lengths shorter than 16 seconds. Thus, while performing programmed stimulation using a pause, a conditioning period of at least 2 minutes should be used prior to diastole scanning to allow APD to achieve a steady state.

Action Potentials↗
PubMed1990

An automatic microcomputer system for analysis of monophasic action potentials.

A computer system for rapid measurement and analysis of monophasic action potentials (MAPs) recorded in vivo was developed. MAPs recorded from the epicardium of mongrel dogs using a contact electrode were digitized by analog-to-digital conversion at a sampling rate of 1 kHz per channel for computer data acquisition. Activation time was detected using a sliding 10-point window at the location where the average positive dV/dT exceeds an adjustable threshold value in order to eliminate spurious detection due to baseline variability or motion artifact. Action potential duration (APD) was determined at 50% and 90% (APD50, APD90) repolarization levels at the first sample point below these detection levels. In addition, a tangent algorithm (APDtan) that detects peak negative dV/dT during repolarization was developed. APDtan was determined from the location of onset of activation to the intersection of tangent and baseline. APDtan allowed estimation of APD in the presence of subsequent premature beats when APD90 was not measurable. To validate activation time measurements, 4,600 action potentials were analyzed during fixed rate pacing. Over a range of paced coupling intervals from 200 to 1000 msec, an R2 value of 0.99968 and a slope of 0.9959 were obtained by linear regression between paced and calculated intervals. To validate APD measurements, 5035 action potentials were analyzed in five animals during fixed rate pacing (longer than 3 minutes) when action potential duration should be constant. Average coefficient of variation of 1.25%, 1.65%, and 1.14% were obtained for APD50, APD90, and APDtan, respectively. This algorithm provides a rapid and accurate method to analyze MAP activation and duration for basic physiological studies such as the determination of initiation of arrhythmias.

Action Potentials↗
PubMedDate not supplied

Pasteurella multocida in peritoneal dialysis: a rare cause of peritonitis associated with exposure to domestic cats.

Pasteurella multocida is a rare cause of peritonitis in peritoneal dialysis patients with only 10 cases reported in the literature so far. All cases were observed in patients with close contact with cats, usually with a direct puncture of the dialysis tubing. We report a case of Pasteurella multocida peritonitis in a patient maintained under continuous cycling peritoneal dialysis (CCPD), who had frequent and close contact with cats. Patients should be made aware of this potential complication and advised to keep domestic animals away from the location of their peritoneal exchanges.

Adult↗