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Biomedical subjects

M Jorgensen

Publications and source records attributed to M Jorgensen.

At least 19 recordsLinked to original sources
PubMed2007

Analysis of interval-censored data from circular migrant and non-migrant sexual partnerships using the EM algorithm.

In epidemiological studies where subjects are seen periodically on follow-up visits, interval-censored data occur naturally. The exact time the change of state (such as HIV seroconversion) occurs is not known exactly, only that it occurred sometime within a specific time interval. Methods of estimation for interval-censored data are readily available when data are independent. However, methods for correlated interval-censored data are not well developed. This paper considers an approach for estimating the parameters when data are interval-censored and correlated within sexual partnerships. We consider the exact event times for interval-censored observations as unobserved data, only known to be between two time points. Dependency induced by sexual partnerships is modelled as frailties assuming a gamma distribution for frailties and an exponential distribution on the time to infection. This formulation facilitates application of the expectation-maximization (EM) algorithm. Maximization process maximizes the standard survival frailty model. Results show high degree of heterogeneity between sexual partnerships. Intervention strategies aimed at combating the spread of HIV and other sexually transmitted infections (STI)s should treat sexual partnerships as social units and fully incorporate the effects of migration in their strategies.

Adolescent↗
PubMed2000

New methods for detection of potential endocrine disruptors.

It has been hypothesized that recent adverse trends in humans are linked to an increased exposure to potential endocrine disrupting agents. These include widely used compounds that mimic the action of sex hormones, including bisphenol A, phthalates and parabens. Since the chemical structure is not sufficient to determine whether a chemical will act as an oestrogen, there is a need for assays that can determine whether a compound interferes with the endocrine systems. The Environmental Protection Agency has recently suggested a testing scheme, composed of an initial screening followed by a more comprehensive investigation of chemicals that are positive in the screening. The screening will use several short-term assays to screen many thousands of compounds for potential endocrine disrupting properties. However, none of these tests determines compound-induced effects on the expression of endogenous genes, which is the cause of the adverse effects. We propose to use a precise quantification of the expression levels of endogenous oestrogen-regulated genes to test whether a chemical has oestrogenic properties, and describe how an endogenous gene expression assay can be established and conducted. Furthermore, different applications of such an assay are discussed: in cell cultures; in experimental animals; or, optimally, directly in blood samples from exposed humans.

Animals↗
PubMed1997

Effect of dexamethasone on voltage-gated Ca2+ channels and cytosolic Ca2+ in rat chromaffin cells.

The present study examined whether the synthetic glucocorticoid dexamethasone (DEX) can modulate voltage-gated Ca2+ channel (VGCC) activity, and as a consequence agonist-induced increases in cytosolic Ca2+, in cultured rat adrenal medullary chromaffin (RAMC) cells. Exposure to 1 microM DEX for 48 h significantly increased peak VGCC current (delta +140%). DEX treatment also significantly potentiated the increases in cytosolic Ca2+ in response to submaximal stimulatory concentrations of KCl (delta +64%) and nicotine (delta +32%). The Ca2+ channel agonist BAY K-8644 increased both VGCC current (delta +109%) and potentiated the KCl-stimulated increase in cytosolic Ca2+ (delta +35%) to a comparable extent to that seen with DEX. These data suggest that DEX treatment increases VGCC activity, and that this increased Ca2+ influx leads to potentiation of agonist-induced increases in cytosolic Ca2+ in RAMC cells.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

Mechanism of atrial natriuretic peptide release with increased inspiratory resistance.

Elevated plasma atrial natriuretic peptide (ANP) levels and concomitant increases in renal sodium and water excretion are often encountered in respiratory diseases associated with increased airway resistance such as obstructive sleep apnea. The present study utilized an anesthetized rat model to determine the principal mechanism(s) responsible for stimulation of ANP release in this clinical syndrome. A 10-minute increase in external resistive loading, which reduced peak tracheal pressure to -15 to -17 mm Hg produced a significant increase in both central venous pressure and right atrial transmural pressure. This maneuver subsequently resulted in significant transient increases in glomerular filtration rate; urine flow; urinary Na+, K+, and Cl- excretion; and urinary cyclic guanosine monophosphate (cGMP) excretion, which was taken as an index of increased circulating levels of ANP. Similar changes in renal function and cGMP excretion occurred when arterial PO2 was lowered to a degree equivalent to that seen with increased resistive loading. Lowering arterial PO2 also significantly increased mean central venous pressure and right atrial transmural pressure. Conversely, the resistive loading-induced changes in renal function and cGMP excretion did not occur when the reduction in arterial PO2 was prevented by breathing a high O2 gas mixture during the resistive loading. Additionally, O2 supplementation prevented the increases in both mean central venous pressure and right atrial transmural pressure caused by increased resistive loading. These data indicate that the elevated ANP release that results from an acute increase in external resistive loading is not caused by a decrease in intrathoracic pressure but rather suggest that the elevated ANP release is primarily caused by an increased right atrial transmural pressure resulting from hypoxia-induced pulmonary vasoconstriction.

Airway Resistance↗
PubMed1996

Multiple strain colonization and metronidazole resistance in Helicobacter pylori-infected patients: identification from sequential and multiple biopsy specimens.

Helicobacter pylori strain diversity was investigated in infected persons by collection of multiple biopsies before and after therapy failure. It was demonstrated by random amplification of polymorphic DNA polymerase chain reaction that patients may be infected with a mixed population of H. pylori strains. Most patients were colonized with a predominant strain accompanied by up to 5 variant strains. The use of antimicrobials resulted in an altered distribution of the strains present, but the predominant strain usually remained. Patients may be infected with a mixed population of metronidazole-sensitive and -resistant strains at one time, with metronidazole-based therapy selectively enriching for a resistant population.

Biopsy↗
PubMed1996

Typing multidrug-resistant Staphylococcus aureus: conflicting epidemiological data produced by genotypic and phenotypic methods clarified by phylogenetic analysis.

An outbreak of an unusual tetracycline-sensitive, rifampicin- and ciprofloxacin-resistant, methicillin-resistant Staphylococcus aureus (MRSA) strain at a large teaching hospital was investigated. Two typing methods, phage typing and restriction fragment length polymorphism (RFLP) by pulsed-field gel electrophoresis (RFLP-PFGE), gave conflicting results which were clarified by phylogenetic analysis. Phage typing identified all the "epidemic-associated" strains as identical, while RFLP-PFGE further divided these strains into four pulsotypes. Phylogenetic analysis showed these four pulsotypes were related genetically and also recognized a second strain of MRSA causing a continuing cross-infection problem. Variation in the RFLP-PFGE pattern was shown to occur following lysogenization of phage-sensitive MRSA. These results indicate that in analyzing outbreaks caused by subgroups of clonal organisms like MRSA, it is necessary to use at least two typing methods and that conflicts between these could be resolved by phylogenetic analysis.

Bacterial Typing Techniques↗
PubMed1991

Changes in C-reactive protein and erythrocyte sedimentation rate after hip fractures.

Serial measurements of C-reactive protein (CRP) levels and erythrocyte sedimentation rates (ESR) were performed during the week after operation in 140 patients with hip fractures. There was no selection, and patients with minor or major complications before or after operation were included. In uncomplicated cases, the ESR was variably raised during the first week, whereas the CRP showed a distinct pattern with a rapid increase on the second day; it then decreased by the 7th day. In cases with early postoperative bronchopneumonia and deep wound infection, the CRP was high, but minor infections did not influence the usual levels. Complications had no effect on the ESR during the 1st week.

Aged↗
PubMed1981

Acquired vitamin K-dependent carboxylation deficiency in liver disease.

gamma-Carboxyglutamic acid residues on prothrombin are synthesized from glutamic acid on a prothrombin precursor in the liver through a vitamin K-dependent carboxylase. In the absence of vitamin K or in the presence of vitamin K antagonists, an inert form of prothrombin - abnormal prothrombin - circulates in the blood. We have developed specific immunoassays for native and abnormal human prothrombin. The prothrombin concentration in our normal subjects was 108 +/- 19 microgram per milliliter. The abnormal-prothrombin concentration varied over four orders of magnitude between the limits of detection in normal plasma and the level in patients with cirrhosis (0 to 5 microgram per milliliter), acute hepatitis (0 to 33 microgram per milliliter), or vitamin K deficiency (32 to 100 microgram per milliliter) and in those treated with sodium warfarin (12 to 65 microgram per milliliter). These studies indicate that abnormal prothrombin is not a component of normal plasma but appears in a variety of hepatic and nutritional disorders characterized by impaired hepatic vitamin-K-dependent carboxylation.

Adult↗