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Biomedical subjects

F Hartmann

Publications and source records attributed to F Hartmann.

At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

Cell-mediated cytotoxicity in hepatitis A virus infection.

We studied cell-mediated cytotoxicity to hepatitis A virus-infected cells in seven patients with acute type A hepatitis and two controls. Skin fibroblast cultures obtained from the skin biopsies of seven patients after acute hepatitis A virus infection and from two persons without history of current or past hepatitis A virus infection were inoculated with hepatitis A virus. Infection of fibroblast cultures always resulted in an inapparent, persistent infection with production and release of infectious hepatitis A virus. Peripheral blood lymphocytes were collected from the same patients at different times after onset of icterus and were stored in liquid nitrogen. Cytolytic activity of peripheral blood lymphocytes was determined by a microcytotoxicity assay using autologous 51Cr-labeled hepatitis A virus-infected and uninfected target cells. Cytotoxic peripheral blood lymphocytes capable of lysing autologous hepatitis A virus-infected skin fibroblasts were detected in all patients with hepatitis A but were not demonstrable in the controls without antibodies against hepatitis A virus. The clinical course of the hepatitis A virus infection was normal in five patients; and in these patients, cytolytic activity of peripheral blood lymphocytes against hepatitis A virus-infected autologous targets peaked 2 to 3 weeks after onset of icterus. A clinically protracted form of the disease with persistent elevation of aminotransferases for at least 5 months after onset was present in two patients. In these cases, the highest cytolytic activity was demonstrated in peripheral blood lymphocytes collected 8 to 12 weeks after onset of icterus.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMedDate not supplied

Treatment of refractory Hodgkin's disease with an anti-CD16/CD30 bispecific antibody.

A group of 15 patients with refractory Hodgkin's disease were treated in a phase I/II trial with the natural-killer (NK)-cell-activating bispecific monoclonal antibody HRS-3/A9, which is directed against the Fc gamma receptor III (CD16 antigen) and the Hodgkin's associated CD30 antigen. The antibody was given four times every 3-4 days, starting with 1 mg/m2. The treatment was well tolerated and the maximum tolerated dose was not reached at 64 mg/m2. Side-effects were rare and consisted of fever, pain in involved lymph nodes and a maculopapulous rash. Nine patients developed human anti-(mouse immunoglobulin) antibodies. One complete and one partial remission (lasting 5 and 3 months, respectively), three minor responses (1 to 11+ months), and one mixed response were achieved. There was no clear-cut dose side-effect or dose/response correlation. NK cell activity increased in most of the patients treated with 4 mg/m2 or higher doses but lasted no longer than 6 weeks after therapy. Our results encourage further clinical trials with this novel immunotherapeutic approach and emphasize the necessity to reduce the immunogenicity of the antibody to allow retreatment of responding patients.

Adult↗
PubMedDate not supplied

Scintigraphic evaluation of cardiac autonomic innervation.

Alterations in cardiac autonomic neuronal function have become the focus of intense research in various cardiovascular diseases. Both single-photon emission tomography (SPECT) and the positron emission tomography (PET) imaging techniques in combination with radio-labeled neurotransmitters and receptor ligands have become available for the scintigraphic visualization of presynaptic and postsynaptic neuronal function. Several clinical studies have shown changes in tracer distribution in different clinical conditions, such as ischemic heart disease, congestive heart failure, malignant arrhythmias, heart transplantation, and in patients with diabetes. In patients with congestive heart failure, previous in vitro investigations have concentrated on the postsynaptic level of the sympathetic innervation. However, alterations in presynaptic nerve function have been demonstrated with scintigraphic investigations by decreased presynaptic tracer retention. Moreover, correlation between scintigraphic findings and clinical outcome was shown in patients with heart failure, providing important prognostic information superior to conventional risk assessment. In conclusion, scintigraphic evaluation by SPECT and PET allows functional characterization of cardiac presynaptic and postsynaptic neurons. Regional tracer uptake can be used as an index for the integrity of innervation in various diseases. Newer tracer approaches may allow the noninvasive quantification of neuronal function by PET.

Autonomic Nervous System↗
PubMedDate not supplied

Risk stratification and therapeutic decision making in patients with acute coronary syndrome--the role of cardiac troponin T.

Patients with chest pain represent an inhomogeneous group with greatly varying severity of coronary artery disease and cardiac risk. The proper selection of different treatment strategies in these patients requires reliable risk assessment. Patients with definitive myocardial infarction: in patients with ST-segment elevation on ECG, a positive troponin T (cTnT) on admission identifies a group of patients having a threefold higher mortality rate than patients with a negative cTnT test. The differences in risk based on cTnT are found for patients treated with thrombolytic as well as mechanical recanalization therapy. These differences in mortality based on admission cTnT may be explained by more severe coronary artery disease, worse left ventricular function, and less efficient microvascular reperfusion in the cTnT-positive patients. Patients with rest angina: in patients with angina at rest, a positive cTnT value on admission identifies a subgroup having a threefold higher cardiac event rate than cTnT-negative patients. The cTnT-positive patients seem to benefit from treatment with low molecular weight heparin and fibrinogen receptor antagonists, while cTnT-negative patients do not. The differences in risk and response to therapy may be due to more severe coronary artery disease, more critical coronary artery stenoses, and a higher rate of intracoronary thrombus formation in the cTnT-positive versus negative patients. Low risk chest pain patients: in low risk chest pain patients, (i.e. no rest angina, no ECG-changes) cTnT-positive patients on admission have a twofold higher cardiac event rate than cTnT-negative patients. The proper treatment strategy for the low risk cTnT-positive patients remains to be determined. Troponin T versus troponin 1: many of the findings on cTnT also relate to troponin I. However, there is a high interassay variability of troponin I assays, which has to be taken into consideration.

Angina Pectoris↗
PubMedDate not supplied

In vivo metabolism of [4-13C]phenacetin in an isolated perfused rat liver measured by continuous flow 13C NMR spectroscopy.

Continuous flow 13C NMR spectroscopy has been used for the first time to monitor the metabolism of a 13C labeled drug in an isolated liver. Continuous and almost immediate information on the metabolite formation could be obtained using 13C labeled phenacetin without alteration of the biological system. The data are consistent with those observed by conventional techniques (HPLC, aliquot 13C NMR measurements). From the biological point of view the sensitivity of continuous flow 13C NMR spectroscopy is still low (10(-3) M). The results presented demonstrate however that non-invasive and non-radioactive real time monitoring of drug metabolism in intact organs is possible.

Animals↗
PubMedDate not supplied

Neurohumoral activation in percutaneous coronary interventions: apropos of ten vasoactive substances during and immediately following coronary rotastenting.

BACKGROUND: Ischemia, left ventricular dysfunction, endothelial damage and hemodynamic changes during percutaneous coronary intervention can lead to neurohumoral activation. This may partly explain the frequent episodes of coronary spasm, hypotension and bradycardia which occur during the procedure. Rotastenting, by employing the two basic mechanisms for coronary interventions-debulking and dilatation-epitomizes percutaneous coronary interventions in general. We sought to investigate the neurohumoral changes during and immediately following coronary rotastenting. METHODS AND RESULTS: Eighteen patients undergoing elective rotablator atherectomy followed by balloon predilatation and stenting for chronic stable angina were studied. Four femoral vein blood samples were drawn from each patient at the start of the intervention (baseline), and 2 (postdebulking-2), 10 (postdebulking-10) and 60 (postdebulking-60) minutes. respectively, after the first complete passage of the rotablation burr across the whole length of lesion. Levels of 10 neurohormones, namely, endothelin-1, bradykinin, arginine vasopressin, norepinephrine, dopamine, epinephrine, angiotensin II, serum angiotensin-converting enzyme activity. atrial natriuretic peptide and kininogen were estimated in each sample. Endothelin-1 and bradykinin attained their peak levels in the postdebulking-2 samples. and the rise from 0.34+/-0.07 pmol/ml and 235.8+/-17.7 pg/ml to 0.42+/-0.06 pmol/ml and 337.2+/-41.0 pg/ml, respectively, was statistically significant (p<0.05). The level of arginine vasopressin showed a significant (p<0.05) rise from baseline (108.5+/-31.8 pg/ml) to postdebulking-60 samples (136.5+/-39.4 pg/ml). The other neurohormones did not show significant changes. CONCLUSIONS: The results suggest a definite but differential neurohumoral activation during and immediately following rotastenting. These neurohumoral changes may have a role in untoward intra- and postprocedural vasomotor and hemodynamic effects. This study establishes the concept of neurohumoral activation during percutaneous coronary interventions.

Aged↗
PubMedDate not supplied

[LDH- and MDH-isoenzymes in the costo-chondral junction in experimental lathyrismus and under additional medication with 6-methyl-prednisolone and O-(beta-hydroxyethyl)-rutosides].

Several classic studies suggest that experimental lathyrism is not only based on an extracellular distrubance of collagen fibre maturation but on a disturbed cellular energy metabolism. To exemplity this in assessment of skeletal damage the isoenzymes of LDH and MDH on the bone metabolism have been determined. Thus in experimental lathyrism the capacity for glycolysis and for oxidative energy production are significantly diminished in the rib bones and rib cartilage. The resulting reduction of glycoseaminoglycans in the ground substance, thus disturbing the function of the matrix in the formation of collagen fibres. In the bone the lack of mature collagen fibres leads to a mineralisation disturbance because of impaired nucleation function. Thus experimental lathyrism cannot be regarded as a disturbed extracellular collagen metabolism. "Venoruton" could not correct the lathyrogenic disturbance of energy metabolism, but after 3 weeks 6-methyl-prednisolone caused a normalisation of the state of energy metabolism.

Aminopropionitrile↗
PubMedDate not supplied

[Time-dependent flow behavior and fibrinogen content of synovial fluid].

Normal bovine synovial fluid and synovial effusions in human non-inflammatory joint diseases do not show any decrease of viscosity for a long period of time during imposed shear loading, as is required for thixotropy. This observation is based on two different methods of measurement; the "hysteresis loop" method and the recording of the shear stress-time curve. Inflammatory synovial fluids--particularly from patients with rheumatoid arthritis and a high concentration of fibrinogen--form a visible gel after 6 to 20 hours of rest. Those gels show a hysteresis loop typical for thixotropy and a decrease of viscosity with the duration of shear loading. Due to the shearing in the rheometer precipitation occurs and fibrin clots appear. The appearance of fibrin clots induced by mechanical shear loading not known until now, can be discussed with regard to its possible participation in the symptom of morning stiffness, in the formation of rice bodies and in the destruction of joint cartilage in rheumatoid arthritis.

Animals↗
PubMedDate not supplied

[Ulcerative colitis caused by oral gold therapy in rheumatoid arthritis].

We report on a 39-year-old male patient suffering from seropositive rheumatoid arthritis who developed severe colitis during oral gold (Auranofin) therapy. So far, two further cases of colitis during oral, and 28 cases of enterocolitis during parenteral chrysotherapy have been described. The pathomechanism has not been identified. Symptomatic therapy was applied, under which our patient recovered from intestinal discomfort in a few weeks. In differential diagnosis gold induced colitis has to be distinguished both from loose stools occurring during oral gold therapy, most probably caused by an inhibition of NA+K+ ATPase, and from colitis induced by concomitant application of nonsteroidal anti-inflammatory drugs.

Administration, Oral↗
PubMedDate not supplied

[NMR tomography of the knee joint in patients with rheumatic joint diseases].

Twenty patients with rheumatoid gonarthritis were examined in a NMR tomograph with a 0.2 tesla resistive magnet. Synovial effusions were seen in 18 cases and thickening of the synovium in 15 cases. Discrimination between synovial fluid and synovium was gained by different NMR signals from various spin-echo sequences. In demonstrating a thickened synovium NMR tomography enables the depiction of inflammation inside the joint in earlier stages of illness than is possible with bone erosion detection from X-ray photographs.

Adult↗