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Biomedical subjects

Mohamed Salem

Publications and source records attributed to Mohamed Salem.

13 recordsLinked to original sources
PubMed2006

Can two planar sources with the same sets of Stokes parameters generate beams with different degrees of polarization?

It is shown that two stochastic electromagnetic beams that propagate from the source plane z = 0 into the half-space z > 0 may have different degrees of polarization throughout the half-space, even though they have the same sets of Stokes parameters in the source plane. This fact is due to a possible difference in the coherence properties of the field in that plane, but other reasons are also possible. The result is illustrated by an example.

Journal Article↗
PubMed2006

Microarray gene expression analysis in atrophying rainbow trout muscle: a unique nonmammalian muscle degradation model.

Muscle atrophy is a physiological response to diverse physiological and pathological conditions that trigger muscle deterioration through specific cellular mechanisms. Despite different signals, the biochemical changes in atrophying muscle share many common cascades. Muscle deterioration as a physiological response to the energetic demands of fish vitellogenesis represents a unique model for studying the mechanisms of muscle degradation in non-mammalian animals. A salmonid microarray, containing 16,006 cDNAs, was used to study the transcriptome response to atrophy of fast-switch muscles from gravid rainbow trout compared with sterile fish. Eighty-two unique transcripts were upregulated and 120 transcripts were downregulated in atrophying muscles. Transcripts having gene ontology identifiers were grouped according to their functions. Muscle deterioration was associated with elevated expression of genes involved in the catheptic and collagenase proteolytic pathways; the aerobic production, buffering, and utilization of ATP; and growth arrest; whereas atrophying muscle showed downregulation of genes encoding a serine proteinase inhibitor, enzymes of anaerobic respiration, muscle proteins as well as genes required for RNA and protein biosynthesis/processing. Therefore, gene transcription of the trout muscle atrophy changed in a manner similar to mammalian muscle atrophy. These changes result in an arrest of normal cell growth, protein degradation, and decreased glycolytic cellular respiration that is characteristic of the fast-switch muscle. For the first time, other changes/mechanisms unique to fish were discussed including genes associated with muscle atrophy.

Animals↗
PubMed2006

Anabolic effects of feeding beta2-adrenergic agonists on rainbow trout muscle proteases and proteins.

beta2-Adrenergic agonists (BAAs) act as repartitioning agents in domestic animals by redistributing nutrients away from adipose tissue and towards muscle accretion. The mechanism involves altering the rates of protein degradation and synthesis. The aim of this study was to test the effects of chronic feeding of the BAAs clenbuterol (CLEN) and ractopamine (RACT) on rainbow trout (RBT) muscle. Specifically, we examined the activities and mRNA levels of genes in the major proteolytic pathways including calpains, the multi-catalytic proteasome and cathepsins, and the mRNA levels of genes encoding the myofibrillar proteins, fast-twitch and slow-twitch myosin heavy chains (f-MHC and s-MHC, respectively), and the cytoskeletal protein, beta-actin. RACT feeding significantly increased mRNA transcripts of the calpain catalytic subunit (Capn1), the regulatory subunit (cpns), and the calpastatin large isoform (CAST-L), without affecting the calpain enzyme activity. CLEN feeding significantly increased mRNA levels of the proteasome alpha subunit without a corresponding change in 20S enzyme activity. RACT significantly decreased cathepsin D activity without affecting mRNA levels suggesting that the action of RACT may be at the post-transcriptional level. In addition, both CLEN and RACT significantly increased mRNA transcripts of f-MHC and beta-actin genes suggesting an anabolic role of BAAs on myofibrillar and cytoskeletal proteins. Neither CLEN nor RACT altered mRNA expression of the s-MHC gene indicating no transformation of muscle fiber-types. This study supports a role for BAAs in inducing RBT muscle accretion by altering both protein synthesis and degradation.

Activating Transcription Factor 1↗
PubMed2006

Long-term results following percutaneous myocardial laser therapy.

OBJECTIVES: The usefulness and safety of percutaneous myocardial laser therapy in selected patients have been identified in previous 1-year randomized trial reports, including that from a double-blind, sham-controlled trial we independently conducted. We aimed to determine whether the 1-year effects are maintained through a long-term, longitudinal follow-up. METHODS: Patients (n=77) with chronic, stable, medically refractory angina (class III or IV) not amenable to conventional revascularization and with evidence of reversible ischemia, ejection fraction > or =25%, and myocardial wall thickness > or =8 mm were treated with percutaneous myocardial laser. After the 1-year follow-up and disclosure of all randomized assignments as prespecified in the respective study protocol, patients were followed up longitudinally for a mean of 3 years for angina class, left ventricular ejection fraction, medication usage, and adverse events. RESULTS: No procedural mortality, myocardial infarction, or cerebral embolism occurred. Pericardiocentesis was required in two patients (2.6%). Cardiac event-free survival was 88% at 1 year and 66% at late follow-up. Mean Canadian Cardiovascular Society angina class was significantly improved from baseline (3.2+/-0.4) at 1 year (2.2+/-1.1, P<0.001) and at a mean of 3 years (1.9+/-1.2, P<0.001). Nitrate usage was significantly reduced at late follow-up; however, ejection fraction did not change over time. In a multivariate analysis, angina improvement at 1 year was found to be a significant independent predictor of both survival and angina improvement at late follow-up. CONCLUSION: We conclude that percutaneous myocardial laser therapy in selected patients with severe, medically refractory angina not treatable with conventional revascularization induces significant and sustained symptomatic benefit.

Aged↗
PubMed2005

Identification and molecular characterization of the rainbow trout calpains (Capn1 and Capn2): their expression in muscle wasting during starvation.

Calpains are calcium regulated proteases involved in cellular functions that include muscle proteolysis both ante- and postmortem. Here, we describe the molecular characterization of the rainbow trout catalytic subunits of the mu- and m-calpains, respectively. The cDNA sequence for Capn1 encodes a protein of 704 amino acids with a calculated molecular mass of 79.9 kDa. The amino acid sequence shows 66% and 86% identity with the mouse and zebrafish Capn1, respectively. The Capn2 cDNA codes for a protein consisting of 701 amino acid residues with a calculated molecular mass of 78.2 kDa. The protein shows 65% amino acid sequence identity with the mouse and chicken Capn2. The two isozymes of rainbow trout have the characteristic domains: I (propeptide), II (cysteine catalytic site), III (electrostatic switch), and IV (contains five EF-hands). Because starvation induces muscle wasting, the hypothesis of this study was that starvation could affect regulation of the calpain system in muscle. Starvation of rainbow trout fingerlings (15-20 g) for 35 days stimulated the expression of Capn1 (2.2-fold increase, P < 0.01), Capn2 (6.0-fold increase, P < 0.01), and calpastatins (1.6-fold increase, P < 0.05) as measured by quantitative real-time RT-PCR. The mRNA changes led to a 1.23-fold increase in the calpain catalytic activity. The results suggest a potential role of calpains in protein mobilization as a source of energy under fasting condition.

Amino Acid Sequence↗
PubMed2005

Characterization of calpastatin gene in fish: its potential role in muscle growth and fillet quality.

Calpastatin (CAST), the specific inhibitor of the calpain proteases, plays a role in muscle growth and meat quality. In rainbow trout (RBT), we identified cDNAs coding for two CAST isoforms, a long (CAST-L) and a short isoform (CAST-S), apparently derived from two different genes. Zebrafish and pufferfish CAST cDNA and genomic sequences were retrieved from GenBank and their exon/intron structures were characterized. Fish CASTs are novel in that they have fewer repetitive inhibitory domains as compared to their mammalian counterparts (one or two vs. four). The expressions of CAST mRNAs were measured in three RBT strains with different growth rates and fillet firmness that were fed either high energy or control diets. CAST-L and S expressions were significantly lower (p<0.01) in the strain that has the slowest growth rate and yielded the softest fillet. Strain or diet did not affect level of calpain mRNAs. However, the decrease in the CAST/calpain ratio at the mRNA level did not lead to a corresponding change in the calpain catalytic activity. Further investigation should reveal a potential use of the CAST gene as a tool to monitor fish muscle growth and fillet firmness.

Amino Acid Sequence↗
PubMed2004

EpCAM is overexpressed in breast cancer and is a potential target for breast cancer gene therapy.

EpCAM (epithelial cell adhesion molecule) is a cell surface molecule that is known to be highly expressed in colon and other epithelial carcinomas. EpCAM is involved in cell-to-cell adhesion and has been the target of antibody therapy in several clinical trials. To assess the value of EpCAM as a novel target for breast cancer gene therapy, we performed real-time reverse transcription-PCR to quantify the level of EpCAM mRNA expression in normal breast tissue and primary and metastatic breast cancers. We found that EpCAM is overexpressed 100- to 1000-fold in primary and metastatic breast cancer. Silencing EpCAM gene expression with EpCAM short interfering RNA (siRNA) resulted in a 35-80% decrease in the rate of cell proliferation in four different breast cancer cell lines. EpCAM siRNA treatment decreased cell migration by 91.8% and cell invasion by 96.4% in the breast cancer cell line MDA-MB-231 in vitro. EpCAM siRNA treatment was also associated with an increase in the detergent-insoluble protein fraction of E-cadherin, alpha-catenin, and beta-catenin, consistent with the known biology of EpCAM as a regulator of cell adhesion. Our hypothesis is that modulation of EpCAM expression can affect cell migration, invasion, and proliferation by enhancing E-cadherin-mediated cell-to-cell adhesion. These data provide compelling evidence that EpCAM is a potential novel target for breast cancer gene therapy and offer insights into the mechanisms associated with EpCAM gene silencing.

Antigens, Neoplasm↗
PubMed2004

Beam conditions for radiation generated by an electromagnetic Gaussian Schell-model source.

It was shown recently that the basic properties of a fluctuating electromagnetic beam can be derived from knowledge of a 2 x 2 cross-spectral density matrix of the electric field in the source plane. However, not every such matrix represents a source that will generate a beamlike field. We derive conditions that the matrix must satisfy for the source to generate an electromagnetic Gaussian Schell-model beam.

Journal Article↗
PubMed2004

Only transient increase of vascular growth factors and microvascular density after percutaneous myocardial laser.

OBJECTIVE: We tested the hypothesis that percutaneous myocardial laser may stimulate microvascular growth in areas surrounding the laser channels. METHODS: We conducted a study of 24 domestic pigs, which underwent percutaneous myocardial laser to left ventricular myocardium using holmium:YAG laser. The pigs were sacrificed in groups of four after one day, 3-4 days, one week, three weeks and six weeks. Frozen sections from both normal and treated myocardium were prepared for immunofluorescence microscopy and stained with antibodies against von Willebrand factor, vascular endothelial growth factor (VEGF) and Extra Domain-A cellular fibronectin (ED-AcFN). Microvascular density (MVD) and vascular area (VA) were determined in sections stained with antibodies against von Willebrand factor VIII using a digitised image analysis system. When determined in laser treated areas, channel core remnants were excluded from analysis. RESULTS: Within the laser channel remnants and in the tissue closely surrounding these, expression of VEGF and ED-AcFN increased significantly after treatment at one, 3-4, and seven days and decreased to normal at three and six weeks. Expression of ED-AcFN was detected adjacent to endothelial cells of microvessels. The original laser channels were rapidly invaded by granulation tissue. There was no sign of recanalization at any stage during the six weeks. Morphometric analysis showed no increase in MVD and VA in the myocardium surrounding the laser channels. CONCLUSION: An increase of VEGF and ED-AcFN after myocardial laser is transient and is not associated with increase of MVD or VA in myocardium not involving laser channel remnants.

Animals↗
PubMed2004

[Place of endoscopic variceal ligation for the prophylaxis of rebleeding from oesophageal varices. Prospective study about 102 cases].

The aim of this study was to assess the efficacy and morbidity of endoscopic variceal ligation for the prophylaxis of rebleeding from oesophageal varices. This work is a prospective study including 102 patients having had at least one episode of variceal bleeding. The mean age is 52.5 years. Oesophageal varices were eradicated in 83.3% of cases after an average of 3.5 sessions. Recurrence of oesophageal varices after eradication was observed in 22% after an average follow-up of 7 months. 10 patients died before eradication of oesophageal varices from causes unrelated to the technique. The endoscopic variceal ligation is effective for eradication of oesophageal varices, with a low morbidity. This technique appears to be a method of choice in the prophylaxis of rebleeding from oesophageal varices.

Adolescent↗
PubMed2004

[Bone mineral density in patients with Crohn's disease. Contribution of bone densitometry in 53 cases].

Fifty-three patients with Crohn disease were included in a prospective study. Bone mineral density was measured at the femoral neck and lumbar spine by dual-energy X-ray absorptiometry. Ten variables were analyzed in search of an association with bone demineralization; Age, sex, nutritional state, smoking, duration of the disease, hormonal status, inflammatory syndrome, site of disease: ileal, colic or ileocolic, accumulated doses of corticoids and intestinal resection. A bone demineralization was observed in 58.5% of cases. The ileum location and the corticothérapie were predictives of bone demineralization. Crohn disease is a disease at high risk of bone demineralization. Predictors of the bone loss were smoking, long duration of the disease, ileal site and systematic corticotherapy.

Absorptiometry, Photon↗
PubMed2003

Effects of simvastatin and L-arginine on vasodilation, nitric oxide metabolites and endogenous NOS inhibitors in hypercholesterolemic subjects.

Hypercholesterolemia is linked to endothelial dysfunction and enhancement of the endogenous inhibitor of NO synthase. The statins have lipid-lowering and pleiotropic properties, which could exert protective effects on the endothelium in hypercholesterolemia. The association of L-arginine with simvastatin could promote a further improvement on endothelial function in this condition. Thus, we investigated whether simvastatin, with or without supplementation with L-arginine, could improve endothelium-dependent vasodilation. In this study, 25 hypercholesterolemic subjects were treated according to the following protocol: washout period of 1 month; simvastatin (20 mg/day) for 2 months; simvastatin (20 mg/day) + L-arginine (7 g/day) for 2 months. From these patients, 10 were chosen at random for evaluation of vascular function by high resolution ultrasonography of the brachial artery. In subjects treated with simvastatin plus L-arginine, an increase of L-arginine levels (68%) and L-arginine/asymmetric dimethylarginine (ADMA) ratio (67%) were observed. Simvastatin reduced the plasma concentrations of NO metabolites nitrite + nitrate (NOx: 34%), S-nitrosothiols (RSNO: 42%), total cholesterol (25%), low density lipoprotein (LDL)-cholesterol (36%) and the LDL-cholesterol/high density lipoprotein (HDL-cholesterol ratio (34%). Simvastatin, associated or not to L-arginine, did not affect ADMA levels and endothelium-dependent vasodilation. Our data showed that simvastatin reduced the plasma concentrations of NOx and RSNO without affecting either the levels of ADMA or endothelium-dependent vasodilation in hypercholesterolemia.

Anticholesteremic Agents↗