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Biomedical subjects

Mohammad Ilyas

Publications and source records attributed to Mohammad Ilyas.

13 recordsLinked to original sources
PubMed2006

Evaluation by magnetic resonance imaging of aortic dilatation and coarctation in adult Turner syndrome patients.

OBJECTIVE: Turner syndrome has well-recognized cardiovascular complications that appear in up to 40% of the patients and are more common in monosomy X. Left-sided obstructive lesions are relatively more frequent and predispose to aortic root dilatation and life-threatening aortic dissection. However, bicuspid aortic valves, hypertension, coarctation and aortic stenosis are also at risk of aortic dissection. Currently there is no clear guideline regarding the best single test for detection or monitoring aortic disease progression. DESIGN: Routine thoracic aortic magnetic resonance imaging (MRI) was introduced to the dedicated Turner syndrome clinic, with repeated MRI examination every 2 years to detect or assess progression of aortic lesions. RESULTS: Seven out of a total of 17 patients developed aortic anomalies during the course of surveillance, which included coarctation as well as aortic dilatation. None of these patients had any cardiovascular symptoms and the vascular abnormalities were detected on MRI at presentation or during the course of their follow-up. In patients with previously normal aortic imaging, the time interval for the lesion to be detectable varied between 2 and 6 years. In one patient there was progression of an established lesion over the 2-year period. CONCLUSION: In the few patients presented here, regular imaging at first consultation followed by every 2 years would appear to be warranted, although the exact frequency of imaging and by what modality still need to be ascertained definitively.

Adult↗
PubMed2006

Management of childhood hypertension: a guide for primary care physicians.

Prevalence of pediatric hypertension has increased with the onset of obesity epidemic. Early detection and treatment of childhood hypertension is important due to its link with atherosclerosis in adult life. Accurate measurement of blood pressure is the key for the management and physicians should make effort to rule out the possibility of anxiety associated and white coat hypertension before the final diagnosis of hypertension. Secondary hypertension is more common in children as compared to adults but essential hypertension is also common in older children and adolescents. The younger children with severe hypertension are more likely to have secondary hypertension. Non-pharmacologic treatment should be tried before instituting the pharmacologic treatment, unless patient is symptomatic and has severe hypertension.

Adolescent↗
PubMed2005

CDC4 mutations occur in a subset of colorectal cancers but are not predicted to cause loss of function and are not associated with chromosomal instability.

CDC4/FBXW7 is part of a ubiquitin ligase complex which targets molecules such as cyclin E, c-myc, and c-jun for destruction. CDC4 mutations occur in several cancer types and are best described in colorectal tumors. Knockout of CDC4 in vitro in colorectal cancer cells causes changes suggestive of chromosomal instability (CIN). In p53(+/-) mice, radiation-induced lymphomas show deletion or mutation of one copy of CDC4 and knockdown of CDC4 leads to increased aneuploidy in mouse fibroblasts. We screened 244 colorectal tumors and 40 cell lines for CDC4 mutations and allelic loss. Six percent (18 of 284) of tumors, including near-diploid (CIN-) lesions, harbored CDC4 mutations and there was no association between mutation and CIN (polyploidy). The CDC4 mutation spectrum in colorectal tumors was heavily biased towards C:G > T:A changes, either missense mutations at critical arginine residues or nonsense changes in the 5' half of the gene. The reasons for this odd mutation spectrum were unclear but C:G > T:A changes were not found more often than expected at APC, K-ras, or p53 in the same tumors and we found no specific defects in DNA repair to account for the observations. No colorectal tumor was found to carry two CDC4 mutations predicted to abolish protein function; partial loss of CDC4 function may therefore cause tumorigenesis. The in vitro studies, therefore, did not assess the functional effects of mutant alleles which are found in vivo. CDC4 mutations may be selected primarily to drive progression through the cell cycle although CIN might be an important secondary effect in some cancers.

Adenocarcinoma↗
PubMed2005

Hyperphosphatemia in children receiving peritoneal dialysis--an educational program.

Hyperphosphatemia has been associated with the development of secondary hyperparathyroidism, renal osteodystrophy, cardiovascular calcification and increased risk of death. Using a one group, pretest-posttest study design, we sought to evaluate changes in serum phosphorus, calcium, parathyroid hormone and subject knowledge in response to a 3-month educational intervention. Mean serum phosphorus levels did not differ significantly between the three evaluation periods: pretreatment (5.69 mg/dl), treatment (5.84 mg/dl) and posttreatment (6.17 mg/dl). Mean serum calcium, calcium-phosphorus product and PTH values also did not differ significantly between the treatment periods. We observed no difference between the subject test scores between the two testing periods. Calcium-phosphorus product, serum phosphorus and PTH values on average, despite the education program, remained outside the K/DOQI target guidelines 44, 56 and 81% of the time, respectively. The results of this study suggest that an aggressive 3-month patient education program targeting dietary phosphorus knowledge, phosphate binder name and dosing, and knowledge of medical consequences associated with non-compliance had no effect on the serum phosphorus, calcium, PTH or phosphate binder need.

Adolescent↗
PubMed2005

Genetic basis of variation in adenoma multiplicity in ApcMin/+ Mom1S mice.

Apc(Min) mice have provided an example of a locus (Modifier of Min1; Mom1) modifying adenoma numbers in the intestines of inbred strains. Linkage analysis located Mom1 on chromosome 4, and further investigation identified secretory phospholipase A2 (Pla2g2a) as a candidate gene. Because of unknown variation introduced by a single founding male mouse, our Min stock, although Pla2g2a(Mom1-s), was not on a pure C57BL/6J background and exhibited several polymorphic loci, including a region on chromosome 18 distal to Apc. Through selective breeding for homozygosity for distal chromosome 18 markers, six recombinant lines that presented with limited intraline variation in adenoma numbers were established. One line (V) showed a particularly severe phenotype (mean adenoma number +/- SEM, 370 +/- 21) compared with the other lines that recorded significantly lower means (3- to 5-fold; P < 10(-3), t test). Intercrosses between lines I and V showed suppression of the severe phenotype in the N1 generation. In N2 (and subsequent) backcrosses, tumor multiplicity depended on the origins of the WT and Min Apc alleles. Mice carrying both alleles from line V had a severe phenotype; others had mild disease very similar to line I (likelihood ratio statistic > 49.0; likelihood of odds > 10; P < 10(-5)). Frequency of allele loss at Apc was increased significantly in adenomas of mice with more severe disease. We propose that a modifier gene close to Apc or structural variation on chromosome 18 modifies polyp numbers in our mice, possibly by altering the frequency of WT Apc allele loss.

Adenoma↗
PubMed2005

Wnt signalling and the mechanistic basis of tumour development.

Abnormalities in the Wnt signalling pathway are found in a wide range of cancers. The diverse origin of these malignancies implies that the contribution that disrupted Wnt signalling makes to tumourigenesis is not limited to specific tissue types and thus can be regarded as a step which is 'generic' to the process of carcinogenesis. In recent years, rapid progress has been made in the understanding of the Wnt signalling pathway, giving an insight into how inappropriate activation of this pathway may facilitate the neoplastic conversion of a normal cell. Furthermore, elucidation of the mechanisms that regulate Wnt signalling has led to the possibility of manipulating these mechanisms in order to down-regulate Wnt signalling in established tumours. In this review, the Wnt signalling pathway is described. The role of aberrant Wnt signalling in tumour development is discussed together with its clinical implications for anti-tumour therapy.

Animals↗
PubMed2005

Expression profiling of murine intestinal adenomas reveals early deregulation of multiple matrix metalloproteinase (Mmp) genes.

Initiation of intestinal tumours occurs as a consequence of aberrant Wnt signalling. This causes altered expression of a number of genes which provides the mechanistic basis of neoplastic change in normal epithelium. In order to identify these genes, expression profiles of normal intestinal mucosa and intestinal adenomas from multiple intestinal neoplasia (Min) mice were compared. A total of 116 genes were found to show significant changes in expression in adenomas compared with normal mucosa. Functional classification of these genes clearly identified the biological processes of cellular adhesion and matrix remodelling to be profoundly affected. Notably, three members of the matrix metalloproteinase (Mmp) gene family (Mmp10, Mmp13, and Mmp14) were consistently up-regulated in tumour tissue. To extend these data, expression of 17 Mmp genes was defined using quantitative reverse transcriptase-polymerase chain reaction (Q-RT-PCR). Several Mmp genes were profoundly up-regulated and every tumour showed overexpression of at least four Mmp genes. These results underscore the probable importance of interactions between the intestinal epithelium and stroma in early tumour development. Furthermore, the inferred role of Mmps at the adenomatous stage of tumourigenesis suggests that this may represent the optimal therapeutic window for the use of Mmp antagonists as anti-cancer agents.

Adenoma↗
PubMed2004

Myh deficiency enhances intestinal tumorigenesis in multiple intestinal neoplasia (ApcMin/+) mice.

Monoallelic APC and biallelic MYH (homolog of Escherichia coli mutY) germ-line mutations are independently associated with a strong predisposition to colorectal adenomas and carcinoma in humans. Whereas mice heterozygous for mutant Apc develop intestinal tumors, mice homozygous for mutant Myh do not show increased tumor susceptibility. We analyzed the phenotype of Apc(Min/+)/Myh(-/-) mice and found that they developed significantly more adenomas in the small intestine than did Apc(Min/+)/Myh(+/+) or Apc(Min/+)/Myh(+/-) mice (median 231 versus 151 versus 152). In the large bowel, Apc(Min/+)/Myh(-/-) mice showed significant increases in the number of aberrant crypt foci. In addition, Apc(Min/+)/Myh(-/-) mice developed an increased number of mammary tumors. Molecular analyses suggested that at least 19% of intestinal tumors from Apc(Min/+)/Myh(-/-) mice had acquired intragenic Apc mutations rather than allelic loss. Consistent with a defect in base excision repair, three intragenic Apc mutations in polyps without allelic loss from Apc(Min/+)/Myh(-/-) mice were shown to be G:C to T:A transversions which resulted in termination codons; no such mutations were found in polyps from Apc(Min/+)/Myh(+/+) or Apc(Min/+)/Myh(+/-) mice. Tumors from Apc(Min/+)/Myh(+/-) mice harbored neither somatic mutations nor allelic loss at Myh. Thus, homozygous, but not heterozygous, Myh deficiency enhanced intestinal tumorigenesis in Apc(Min/+) mice. The excess small-bowel adenomas in Apc(Min/+)/Myh(-/-) mice, therefore, appear to be a model of MYH-associated polyposis in humans.

Adenoma↗
PubMed2004

Hypertension and the vanishing kidney.

The diagnostic role of retrograde pyelography in children with secondary hypertension has never been discussed in the literature. We report a child with severe hypertension, who apparently has a normal renin level and a solitary kidney by renal sonography and renal scan. Retrograde pyelography was able to identify the scarred renal mass. To our knowledge this is the first report to discuss the role of retrograde pyelography in a child with a solitary kidney and severe hypertension.

Child, Preschool↗
PubMed2003

Minimal change nephrotic syndrome with Guillain-Barré syndrome.

A 17-year-old white male with a diagnosis of Guillain-Barré syndrome (GBS) developed severe proteinuria and edema 5 days later. Renal biopsy confirmed minimal change nephrotic syndrome (MCNS). To our knowledge this is the first report of such an association between ex novo MCNS and GBS in a pediatric patient. The NS responded to steroid therapy. The pertinent literature is reviewed.

Adolescent↗
PubMed2002

Cyclin D1 is not an essential target of beta-catenin signaling during intestinal tumorigenesis, but it may act as a modifier of disease severity in multiple intestinal neoplasia (Min) mice.

Deregulation of beta-catenin activity is an important step in the development of colorectal cancers. One consequence of this is transcriptional activation of cyclin D1, an oncogene known to be overexpressed in colorectal cancers. We tested the hypothesis that cyclin D1 gene activation is important for intestinal tumorigenesis. Multiple intestinal neoplasia mice (a model for human familial adenomatous polyposis) were crossed with cyclin D1 knockout (Ccnd1(-/-)) mice. Despite the absence of cyclin D1, intestinal tumors still developed. However, Ccnd1(-/-) multiple intestinal neoplasia mice developed significantly fewer tumors than Ccnd1(+/-) or Ccnd1(+/+) mice (P = 0.003). We conclude that cyclin D1 is not essential for intestinal tumorigenesis, but it may act as a modifier gene.

Animals↗
PubMed2002

Age-related radiological imaging in children with acute pyelonephritis.

Accurate diagnosis of acute pyelonephritis (APN) using clinical and laboratory parameters is often difficult in children. The aims of this retrospective study were twofold. Firstly, to correlate the clinical and laboratory manifestations of APN with the results of the dimercaptosuccinic acid (DMSA) renal scan in different age groups. Secondly, to compare the DMSA renal scan, renal ultrasonography (RUS), and voiding cystourethrography (VCUG) in patients with clinical APN. The DMSA renal scan was utilized as the gold standard for renal involvement. We determined the sensitivity of these tests in febrile urinary tract infections (UTI) in three age groups: group I less than 2 years; group II 2-8 years; group III older than 8 years. During the period January 1992 through December 1998, 222 children presented with a febrile UTI. All patients had a DMSA renal scan, 208 had contrast VCUG, and 163 had RUS. The clinical and laboratory manifestation of pyelonephritis correlated better with a positive DMSA renal scan in the older children than in the younger children; 85% of the DMSA renal scans were positive in group III; 69% in group II; 48% in group I (P<0.001). Vesicoureteral reflux detected by contrast VCUG was more prevalent in the younger age groups. Although high grades of reflux (grade IV-V) correlated better with a positive DMSA renal scan, it did not reach a level of statistical significance (P>0.05). RUS did not correlate with a positive DMSA renal scan in any age group.

Acute Disease↗