Biomedical subjects

Hiren P Patel

Publications and source records attributed to Hiren P Patel.

3 recordsLinked to original sources

PubMed2006

The abnormal urinalysis.

The urinalysis is one of the most commonly performed tests in pediatrics, and whether expected or incidental, abnormal findings are common. Understanding the strengths and limitations of the urinalysis allows one to maximize its use as a screening tool while avoiding expensive and unnecessary evaluations. This article reviews the significance of abnormal results on urine dipstick testing and urine microscopy. Causes of false positive and false negative results are summarized. Initial diagnostic considerations of abnormal urinalysis findings are provided where appropriate.

Child↗

PubMed2005

Advances in the pathogenesis and management of hypertensive crisis.

PURPOSE OF REVIEW: This review summarizes recent insights into to the pathophysiology of hypertensive crisis with the emphasis on newly discovered molecular mechanisms underlying hypertension and also updates current therapeutic options for treating hypertensive crisis in children. RECENT FINDINGS: There is growing evidence that the renin-angiotensin system plays a key role in the pathogenesis of hypertensive crises. Recent studies have shown that oxidative stress and factors affecting endothelial function are also important. Treatment of hypertensive crisis still focuses on lowering of blood pressure in an expeditious but safe manner. There is growing experience with IV nicardipine, which is becoming a viable alternative to sodium nitroprusside in children. SUMMARY: Current knowledge of hypertensive crisis emphasizes the need for additional animal and translational studies with the goal of identifying the underlying molecular pathogenesis and developing new therapies to optimize future treatment of hypertensive emergencies.

Antihypertensive Agents↗

PubMed2004

PKD1 intron 21: triplex DNA formation and effect on replication.

Although autosomal dominant polycystic kidney disease is transmitted in an autosomal dominant fashion, there is evidence that the pathophysiology of cystogenesis involves a second hit somatic mutation superimposed upon the inherited germline mutation within the renal tubule cells. The polypurine.polypyrimidine (Pu.Py) tract of PKD1 intron 21 may play a role in promoting somatic mutations. To better characterize this tract and to evaluate its potential to participate in mutagenesis, we investigated the thermodynamics of intramolecular triplex formation by 15 Pu.Py mirror repeat tracts from PKD1 intron 21 by 2D gel electrophoresis. We demonstrate that intramolecular triplexes form with modest superhelical tensions for all the tracts examined. Primer extension studies demonstrated significant polymerase arrest within the Pu.Py tracts in one direction of replication only. We found correlation between polymerization arrest and both the potential length of the triplex and superhelical tension of intramolecular triplex formation. The presence of a Pu.Py tract also led to a replication blockade and double-strand breakage using an SV40 in vitro replication assay with HeLa cell extracts. During DNA replication, the G-rich template of the PKD1 Pu.Py tracts may form a triplex structure with the nascent strand, thereby blocking replication and potentially leading to recombination and mutation.

DNA↗