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H P Kohler

Publications and source records attributed to H P Kohler.

At least 19 recordsLinked to original sources
PubMed2005

[Acute chest pain--it's not always the heart! What additional laboratory and diagnostic imaging is needed].

Few diagnostic decisions in medicine have been more heavily researched and debated than the approach to patients with acute chest pain. In addition, the question is which patients with acute chest pain have a presentation benign enough to make discharge from the emergency department safe and appropriate despite the advances in diagnostic tests. There is always the possibility of missed diagnosis which may cause substantial morbidity and mortality. The use of algorithms or protocols is not always sufficient to avoid missed diagnosis and the individual physicians's diagnostic performance and clinical experience is as important as the best algorithm for atypical chest pain! Patients with atypical symptoms are most likely to be mistakenly discharged. This article does mainly focus on diagnostic tests including ECG and biomarkers such as troponin and D-dimer as well as the investigation by helical CT scan in patients with suspected pulmonary embolism. The article also discuss the importance of repeated assessments of biomarkers and the determination of the exact time interval between the first clinical symptoms and the presentation to the emergency department. This time interval can be very crucial for the diagnostic work-up of patients with acute chest pain.

Acute Disease↗
PubMed2005

[Poisoning and drug emergency in practice].

Intoxicated patients make up 5-10% of all patients seen at emergency departments. The management of these patients is not always simple. Many of them are seen after ingestions of relatively non-toxic substances that require minimal medical care, intentional poisoning however often requires the highest standards of medical and nursing care and therefore the admission to an emergency department is mandatory. At admission, the involved substances are often not known since some of the patients are comatose. In such cases, the information from relatives and friends can be very crucial but to get hold of these sometimes essential "hints" is not always easy. Knowledge of the specific toxic agent allows the physician to plan a rational approach to the definitive management of the intoxicated patient after the vital functions have been stabilised. In some cases, very rare intoxications but with typical clinical signs do occur (e.g scromboid fish poisoning, coprinus-syndrome), which needs special diagnostic and therapeutic steps and a great deal of clinical experience. In most cases it is preferable to contact the Poison Control Center for additional advice.

Acute Disease↗
PubMed2002

[Methods for the determination of factor XIII/XIIIa].

Activated factor XIII (FXIIIa) plays an important role in the final stage of the coagulation cascade by covalent crosslinking of fibrin strands. As a transglutaminase FXIIIa catalyses the generation of intermolecular amide bonds between lysine and glutamine residues resulting in a complex three-dimensional clot structure. Enhanced clot stability is supported by covalent binding of cytosceleton factors like actin and myosin. Moreover, the clot is protected against premature lysis by the incorporation of fibrinolysis inhibitors like alpha(2)-antiplasmin and thrombin activatable fibrinolysis inhibitor (TAFI). A covalent crosslinking of the fibrin strands with extra-cellular matrix proteins like fibronectin, vitronectin, collagen and von Willebrand factor (vWF) immobilizes the clot at the site of injury. Moreover FXIII supports the healing process of damaged tissue. In this review assays for determination of FXIIIa activity, FXIII concentration and identification of the FXIIIVal34Leu polymorphism are shown.

Blood Coagulation↗
PubMed2002

[Role of coagulation factor XIII in cardio- and cerebrovascular diseases].

In the final step of the clotting cascade coagulation factor XIII (FXIII) is activated by thrombin. The activated enzyme (FXIIIa) has an important role in the final stage of blood coagulation in cross-linking soluble fibrin to a stable insoluble clot. The role of FXIII in cardio- and cerebrovascular diseases has been investigated recently. The widespread Val34Leu polymorphism in the gene coding for the FXIII subunit A (FXIII Val34Leu) has been shown to protect against myocardial infarction and ischemic stroke, but is also associated with an increased risk for hemorrhagic stroke. Additionally, FXIII Val34Leu is supposed to be protective against pulmonary embolism and deep vein thrombosis. As possible mechanisms for the antithrombotic effect, premature depletion of the mutant protein from circulation and altered fibrin structures of clots cross-linked by the mutant FXIIIa are under discussion. The connection between FXIII and the insulin resistance syndrome also attracts attention, i.e. the interaction between a component of the coagulation cascade and thus a thrombotic risk factor and classical atheromatous risk factors. Therefore, FXIII must be considered as another coagulation factor contributing to complex interactions between genes and environment important for the pathogenesis of cardio- and cerebrovascular and thromboembolic diseases.

Capillary Permeability↗
PubMed2001

Influence of blood coagulation factor XIII and FXIII Val34Leu on plasma clot formation measured by thrombelastography.

Blood coagulation factor XIII (FXIII) plays an important role in the final stage of the blood coagulation process. Thrombelastography (TEG) enables global assessment of the hemostatic function. The present study tested for the first time the specificity and sensitivity of the rotation thrombelastography (ROTEG: rotation thrombelastography) method for the influence of FXIII and the FXIIIVal34Leu polymorphism on thrombelastograms measured in citrated plasma. Three thrombelastographic parameters were determined in (a) citrated pool plasma, (b) FXIII-deficient plasma, (c) different mixtures of both, and (d) in 60 plasma samples genotyped for FXIIIVal34Leu. Thrombelastograms from FXIII-deficient plasma were significantly smaller than those from pool plasma (8 mm vs. 20.9 mm). Increasing amounts of pool plasma added to FXIII-deficient plasma led to an increase in maximum clot firmness (MCF). FXIIIVal34Leu showed an influence on clot formation time (CFT) values, which decreased with increasing number of Leu alleles. The difference between the wild type and the homozygote mutant genotype was statistically significant (median 185.3 vs. 86.0 s, P=.031). ROTEG is a simple but effective method for the investigation of FXIII function in plasma. The ROTEG method has shown to be not only specific for the FXIII influence, as effects exclusively dependent on FXIII could be observed, but also sensitive, as already smallest amounts of FXIII could be detected. Additionally, the impact of a common genetic polymorphism on ROTEG could be shown for the first time.

Amino Acid Substitution↗
PubMed2001

Violence in Bern.

Explore the source record for details and available documents.

Adolescent↗
PubMed2001

DF-analyses of heritability with double-entry twin data: asymptotic standard errors and efficient estimation.

In this paper we establish the asymptotic distribution of DeFries Fulker (1985) regression estimates for heritability and shared environmental influences with double-entry twin data. A simple formula to estimate the covariance matrix of the coefficients in DF-regressions is provided, and applications to simulated data and Danish twin data show that this method can substantially increase the statistical power of the analyses. We also provide an 'efficient DF-analysis' that yields more precise estimates when additional covariates are included among the explanatory variables.

Adult↗
PubMed2001

Biotransformation of various substituted aromatic compounds to chiral dihydrodihydroxy derivatives.

The biotransformation of four different classes of aromatic compounds by the Escherichia coli strain DH5alpha(pTCB 144), which contained the chlorobenzene dioxygenase (CDO) from Pseudomonas sp. strain P51, was examined. CDO oxidized biphenyl as well as monochlorobiphenyls to the corresponding cis-2,3-dihydro-2,3-dihydroxy derivatives, whereby oxidation occurred on the unsubstituted ring. No higher substituted biphenyls were oxidized. The absolute configurations of several monosubstituted cis-benzene dihydrodiols formed by CDO were determined. All had an S configuration at the carbon atom in meta position to the substituent on the benzene nucleus. With one exception, the enantiomeric excess of several 1,4-disubstituted cis-benzene dihydrodiols formed by CDO was higher than that of the products formed by two toluene dioxygenases. Naphthalene was oxidized to enantiomerically pure (+)-cis-(1R,2S)-dihydroxy-1,2-dihydronaphthalene. All absolute configurations were identical to those of the products formed by toluene dioxygenases of Pseudomonas putida UV4 and P. putida F39/D. The formation rate of (+)-cis-(1R,2S)-dihydroxy-1,2-dihydronaphthalene was significantly higher (about 45 to 200%) than those of several monosubstituted cis-benzene dihydrodiols and more than four times higher than the formation rate of cis-benzene dihydrodiol. A new gas chromatographic method was developed to determine the enantiomeric excess of the oxidation products.

Benzene↗
PubMed2001

Transcriptional organization and dynamic expression of the hbpCAD genes, which encode the first three enzymes for 2-hydroxybiphenyl degradation in Pseudomonas azelaica HBP1.

Pseudomonas azelaica HBP1 degrades the toxic substance 2-hydroxybiphenyl (2-HBP) by means of three enzymes that are encoded by structural genes hbpC, hbpA, and hbpD. These three genes form a small noncontiguous cluster. Their expression is activated by the product of regulatory gene hbpR, which is located directly upstream of the hbpCAD genes. The HbpR protein is a transcription activator and belongs to the so-called XylR/DmpR subclass within the NtrC family of transcriptional activators. Transcriptional fusions between the different hbp intergenic regions and the luxAB genes of Vibrio harveyi in P. azelaica and in Escherichia coli revealed the existence of two HbpR-regulated promoters; one is located in front of hbpC, and the other one is located in front of hbpD. Northern analysis confirmed that the hbpC and hbpA genes are cotranscribed, whereas the hbpD gene is transcribed separately. No transcripts comprising the entire hbpCAD cluster were detected, indicating that transcription from P(hbpC) is terminated after the hbpA gene. E. coli mutant strains lacking the structural genes for the RNA polymerase sigma(54) subunit or for the integration host factor failed to express bioluminescence from P(hbpC)- and P(hbpD)-luxAB fusions when a functional hbpR gene was provided in trans. This pointed to the active role of sigma(54) and integration host factor in transcriptional activation from these promoters. Primer extension analysis revealed that both P(hbpC) and P(hbpD) contain the typical motifs at position -24 (GG) and -12 (GC) found in sigma(54)-dependent promoters. Analysis of changes in the synthesis of the hbp mRNAs, in activities of the 2-HBP pathway enzymes, and in concentrations of 2-HBP intermediates during the first 4 h after induction of continuously grown P. azelaica cells with 2-HBP demonstrated that the specific transcriptional organization of the hbp genes ensured smooth pathway expression.

Amino Acid Sequence↗
PubMed2001

Variance effects in the Bongaarts-Feeney formula.

Bongaarts and Feeney have recently proposed an adjusted total fertility rate to disentangle tempo effects from changes in the quantum of fertility. We propose an extension to the Bongaarts and Feeney formula that includes variance effects: that is, changes in the variance of the fertility schedule over time. If these variance effects are ignored, the mean age at birth and the adjusted total fertility rate are biased. We provide approximations for these biases, and we extend the TFR adjustment to fertility schedules with changing variance. We apply our method to the Swedish baby boom and bust, and show that variance effects are important for evaluating the relative contributions of tempo and quantum effects to the fertility change from 1985 to 1995.

Adult↗
PubMed2001

The density of social networks and fertility decisions: evidence from South Nyanza district, Kenya.

Demographers have argued increasingly that social interaction is an important mechanism for understanding fertility behavior. Yet it is still quite uncertain whether social learning or social influence is the dominant mechanism through which social networks affect individuals' contraceptive decisions. In this paper we argue that these mechanisms can be distinguished by analyzing the density of the social network and its interaction with the proportion of contraceptive users among network partners. Our analyses indicate that social learning is most relevant with high market activity; in regions with only modest market activity, however, social influence is the dominant means by which social networks affect women's contraceptive use.

Birth Rate↗
PubMed2001

Behavior genetic modeling of human fertility: findings from a contemporary Danish Twin Study.

Behavior genetic designs and analysis can be used to address issues of central importance to demography. We use this methodology to document genetic influence on human fertility. Our data come from Danish twin pairs born from 1953 to 1959, measured on age at first attempt to get pregnant (FirstTry) and number of children (NumCh). Behavior genetic models were fitted using structural equation modeling and DF analysis. A consistent medium-level additive genetic influence was found for NumCh, equal across genders; a stronger genetic influence was identified for FirstTry, greater for females than for males. A bivariate analysis indicated significant shared genetic variance between NumCh and FirstTry.

Adult↗