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Biomedical subjects

M Printz

Publications and source records attributed to M Printz.

11 recordsLinked to original sources
PubMed1996

Guidelines of the National Heart, Lung, and Blood Institute Working Group on Blood Drawing, Processing, and Storage for Genetic Studies.

The guidelines presented here are intended for epidemiologic investigators who wish to store blood samples for genetic studies, either by extracting DNA directly from white blood cells or from immortalized cell lines. Recommended procedures for blood drawing and for processing samples are described. Protocols for freezing and storage of both white blood cells and extracted DNA are provided. Although the extraction of DNA and immortalization of cell lines should be conducted in collaboration with an experienced laboratory, a summary of the available methods with appropriate references is given, and a method for the extraction of DNA from clotted blood is referenced. In addition, criteria for selecting study subjects for whom immortalized cell lines are preferable to merely extracting DNA are presented. Finally, the use of alternative sources of genetic material, including cheek swabs and dried blood spots, is described briefly.

Blood Preservation↗
PubMed1996

A genetic linkage map of the rat derived from recombinant inbred strains.

We have constructed a genetic linkage map in the rat by analyzing the strain distribution patterns of 500 genetic markers in a large set of recombinant inbred strains derived from the spontaneously hypertensive rat and the Brown-Norway rat (HXB and BXH recombinant inbred strains). 454 of the markers could be assigned to specific chromosomes, and the amount of genome covered by the mapped markers was estimated to be 1151 centimorgans. By including a variety of morphologic, biochemical, immunogenetic, and molecular markers, the current map integrates and extends existing linkage data and should facilitate rat gene mapping and genetic studies of hypertension and other complex phenotypes of interest in the HXB and BXH recombinant inbred strains.

Animals↗
PubMed1995

Recombinant retroviral vector interferes with the detection of amphotropic replication competent retrovirus in standard culture assays.

Many protocols for gene therapy employ recombinant retroviral vectors, which are replication-defective retroviruses engineered to serve as gene delivery vehicles. The use of retroviral vectors for human gene therapy requires careful screening of vector-producing cell lines and culture supernatants to ensure the absence of replication competent retrovirus (RCR) in clinical products. In this study we have examined several different culture assays routinely used to test for the presence of RCR. Results indicate that cocultivation of a vector-producing cell line with a permissive cell line can reproducibly detect a low level of contaminating RCR. RCR was detected less frequently in direct tests of cell-free culture supernatants from a contaminated vector-producing line. Further studies revealed that recombinant retroviral vector can interfere, to varying degrees, with the detection of low-level RCR in culture supernatants when a marker rescue assay, an extended mink S+L- assay or a PG-4 S+L- assay is used. Interference can be partially overcome by culturing the vector preparation with a permissive cell line for several days before testing on the indicator cell line. The interference phenomenon we have observed may also occur in other culture assays routinely used for the detection of RCR.

Animals↗
PubMed1992

On the role of renal alpha-adrenergic receptors in spontaneously hypertensive rats.

We tested the hypothesis that a genetically determined increase in renal alpha-adrenergic receptor density might be a pathophysiologically important factor in the spontaneously hypertensive rat model of genetic hypertension. In a first study, we compared renal alpha 1 and alpha 2-adrenergic receptor density with systolic blood pressure in 45 rats of an F2 generation of Wistar-Kyoto x spontaneously hypertensive rat hybrids but were unable to detect significant cosegregation between either receptor density or blood pressure. In a second study, we determined renal alpha 1- and alpha 2-adrenergic receptor density in Wistar-Kyoto and spontaneously hypertensive rat kidneys that were transplanted into an F1 generation of Wistar-Kyoto x spontaneously hypertensive rat hybrids. Although Wistar-Kyoto kidneys lowered blood pressure in these animals and spontaneously hypertensive rat kidneys increased blood pressure, renal alpha-adrenergic receptor densities were similar in membranes from both types of kidneys. Since rat kidney coexpresses alpha 1A- and alpha 1B-adrenergic receptors, we also investigated whether differential regulation of these two subtypes might conceal ongoing alterations. The alpha 1A/alpha 1B-adrenergic receptor ratio, however, was similar in Wistar-Kyoto rats, spontaneously hypertensive rats, and F1 rats transplanted with a kidney from either strain. Taken together these data do not support the hypothesis that genetically determined alterations of renal alpha-adrenergic receptor numbers play an important role in the development of elevated blood pressure in the spontaneously hypertensive rat.

Animals↗
PubMed1992

Tau syndrome (thrombocytopenia and absent ulnar) with mental retardation and facial dysmorphy.

A girl with pancytopenia (hemoglobin 9 g. 2,000 PMN. 75,000 platelets) was examined at 23 years of age. She had microcephaly, facial dysmorphy, skeletal deformities (kypho-scoliosis, club feet, club hands) and mental retardation. Puberty was normal, Roentgenograms showed bilateral agenesia of the distal part of the ulna with dislocation of the head of the radius. No other skeletal parts were absent. The condition is probably due to an autosomal recessive gene, the parents being second cousins.

Abnormalities, Multiple↗
PubMed1988

Regulatory role of vasoactive peptides in subcutaneous skin microcirculation of the hamster.

The microcirculatory effects of vasoactive peptides on arteriolar diameter were determined in the dorsal skin-fold preparation of conscious Syrian hamsters and related to arterial blood pressure (MABP). (5 Ile)-angiotensin II (ANG II), (8 Arg)-vasopressin (AVP), vasoactive intestinal polypeptide (VIP), atrial natriuretic factor (ANF), and substance P (SP) were administered intravenously as bolus injections in picomolar concentrations. The diameters of subcutaneous A3 arterioles (15-40 microns) at bifurcation sites were determined via a microscope video system and stored in a digital memory. When spontaneous rhythmic vasoconstrictions and dilations (vasomotion) were present, the diameter oscillations were analyzed by means of the Prony Spectral Line Estimator. ANG II caused sustained arteriolar contraction at increased MABP, but did neither induce nor modulate vasomotion. Both ANF and VIP slightly reduced MABP and had no effect on microcirculatory parameters. SP led to a significant dilation of subcutaneous arterioles in the hamster skin with concomitant drop in MABP, but did not influence arteriolar vasomotion. Physiological concentrations of AVP, as determined in the plasma by radioimmunoassay, caused a marked contraction of the arterioles and evoked a mild pressor response. In addition, AVP induced or greatly enhanced vasomotoric activity. This study therefore provides evidence that endogenous vasoactive peptides play an important role in regulation of skin peripheral resistance by altering arteriolar diameter in a tonic or even dynamic way.

Angiotensin II↗
PubMed1983

The brain angiotensin system: subcellular localization and interferences with converting enzyme inhibitors.

Renin is stored in synaptosomes of rat brain, separately from cathepsin D and intraneuronal angiotensin II (ANG II) has been demonstrated with the electron-microscope. Although the subcellular localization of other components of the renin-angiotensin system (RAS) have still to be investigated, these data suggest possible intracellular synthesis of ANG II in the brain. Brain ANG II is biochemically identical to the plasma peptide and corresponds to (IIe) 5-ANG II. The peptide level is unchanged after bilateral nephrectomy, and angiotensin I (ANG I) accumulation is observed in nephrectomized animals following brain angiotensin converting enzyme blockade. The significantly greater accumulation of ANG I and reduction of ANG II in stroke prone spontaneously hypertensive Wistar-Kyoto rats (WKY) indicates a higher synthesis and turnover rate of ANG II in SHR. Most converting enzyme inhibitors (CEI) penetrate the brain after chronic oral treatment. Part of their blood pressure lowering action may therefore be explained by an inhibition of the brain RAS.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Changes in control of renin release in congestive heart failure in dogs: response to acute and chronic vasodilator therapy.

Neural control of renin secretion is an important physiologic mechanism, but alterations in the central nervous system feedback and control of renin release in heart failure have not been investigated. Accordingly we studied conscious dogs after volume overload (arteriovenous fistula) or chronic myocardial infarction. Acute infusion of nitroprusside was used to test the renin response to arterial hypotension and decreased central blood volume. Hydralazine and prazosin administration were used to test the response to chronic vasodilator administration. After 4 weeks of volume overload or 3 weeks after myocardial infarction, the renin response to a graded hypotensive stimulus was blunted. After 7 days of hydralazine or prazosin administration, plasma renin activity remained elevated and blood volume increased from baseline values. Our results indicate a decrease in the neural feedback control of renin release after chronic volume overload or myocardial infarction. However, chronic vasodilator administration still resulted in sustained augmented renin secretion and an increase in blood volume.

Animals↗