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M H Qari

Publications and source records attributed to M H Qari.

5 recordsLinked to original sources
PubMed2005

High throughput coagulation analyzers review.

The increasing no. of ordered coagulation screening tests has led to a remarkable improvement in the efficiency of automated coagulation testing, and appearance of a new generation of high throughput analyzers ensuring accuracy and precision, and reducing the strain and human error. The earliest analyzers operated mechanically, using the hook to detect the clot in the cuvette are now replaced with more sophisticated analyzer that simultaneously uses the clotting, chromogenic, and immunological principles, to provide a versatile test menu covering antigenic and functional aspects of coagulation. The armamentarium of coagulation testing is complimented with tools like; automated platelet function analyzer, flowcytometer, and molecular techniques including the polymerase chain reaction, and lately the microarrary (biochip) technology. This review addresses the principle of operation and distinctive features of various automated high throughput coagulation analyzers, their impact on improving efficiency, eliminating preanalytical and postanalytical handling thus maximizing productivity and return on investment.

Automation↗
PubMed1998

Mutation of p16, p21 or cyclin dependent kinase 4 is rare in acute lymphoblastic leukaemia.

Homozygous deletion of the p16 tumour suppressor gene (at frequencies ranging from 14% to 29%) have been implicated in the pathogenesis of acute lymphoblastic leukaemia (ALL) by several studies. We investigated the prevalence of this deletion in a group of 46 Arab patients with common ALL. Deletion of p16 was assessed in a multiplex PCR which amplified a 405 bp fragment from exon 2 of the p16 gene, and a 242 bp fragment of the ApoE lipoprotein gene which served as an internal control. Homozygous deletion of p16 in tumour cells could be readily detected in samples containing >75% blasts. Surprisingly, none of the cases in our study showed homozygous deletion of the p16 gene. We also investigated the possibility of other genetic alterations in the p16 gene or mutation in the p21 and CDK4 (not previously reported in ALL) genes which are part of the same signal transduction pathway. A heterozygous G --> A transition at nucleotide position 273 of the p16 gene was present in one patient, but did not result in an amino acid change. A C --> A transversion at codon 88 of the p21 gene, which results in replacement of a phenylalanine with a leucine at position 63, was detected in one patient. In another patient a G --> C transversion in exon 2 at codon 82 (5'-untranslated region of the CDK4 gene) was detected. Results of this study showed mutation of p16, p21 or CDK4 to be rare events in Arab ALL patients.

Cyclin-Dependent Kinase Inhibitor p21↗
PubMed1995

The Sebastian platelet syndrome. Report of the first native Saudi Arabian patient.

Sebastian platelet syndrome is an hereditary thrombocytopenia with giant platelets and inclusion bodies in the granulocytes consisting of dispersed filaments, clusters of ribosomes and a few segments of rough and smooth endoplasmic reticulum at the ultrastructural level, similar to those observed in Fechtner syndrome (a variant of the Alport syndrome)--Sebastian platelet syndrome lacks the additional clinical features such as high frequency deafness, congenital cataract, and chronic interstitial nephritis. Here we report the fourth case worldwide and the first of an Arabian ancestry.

Blood Platelets↗
PubMed1994

Immunophenotyping of childhood acute lymphoblastic leukemia in Saudi Arabia: second look.

Geographical variations in the incidence of disease are of considerable theoretical and practical importance. It has been claimed that the distribution of acute lymphoblastic leukemia (ALL) phenotypes in Saudi Arabia is different from that recorded in the Western literature. One hundred and twelve (112) patients under 15 years of age, diagnosed as ALL between January 1992 and May 1994 had immunophenotypes performed on their blast cells. Common ALL (cALL) together with pre-B-ALL, formed 86.5% of the total; B-cell 3%, T-cell 6% and null cell 4.5%. These figures are not significantly different from the Western literature. A previous claim from this institution in 1990, that both null and B-cell ALL were significantly increased compared with elsewhere, is not supported by the present figures. Age and sex distribution, and FAB classification, L1 77%, L2 20% and L3 3%, were also of the same order as described elsewhere and, in particular, there was no increase in the frequency of L3 subtype.

Adolescent↗