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B Lauer

Publications and source records attributed to B Lauer.

At least 37 records · Page 2Linked to original sources

Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis.

OBJECTIVES: The study evaluates the clinical course and the development of systolic and diastolic left ventricular function in patients with chronic myocarditis with or without autoantibodies against cardiac myosin. BACKGROUND: Patients with myocarditis often show autoantibodies against cardiac myosin. The clinical and pathophysiologic significance of these antimyosin autoantibodies (AMAAB) is yet unknown. The results from studies comparing the clinical course and the development of left ventricular function in patients with chronic myocarditis with or without AMAAB are not yet available. METHODS: Thirty-three patients with biopsy proven chronic myocarditis underwent analysis of AMAAB, right and left heart catheterization and left ventriculography at baseline and after six months. Left ventricular volumes and ejection fraction as well as the time constant of left ventricular relaxation "tau" and the constant of myocardial stiffness "b" were determined at baseline and at follow-up. RESULTS: In 17 (52%) patients, AMAAB could be detected at baseline. After six months, AMAAB were still found in 13 (76%) initially antibody-positive patients. No initially antibody-negative (n = 16) patient developed AMAAB during follow-up. Clinical symptoms improved slightly in antibody-negative patients and remained stable in antibody-positive patients. Left ventricular ejection fraction developed significantly better in antibody-negative patients (+8.9 +/- 10.1%) compared with antibody-positive patients (-0.1 +/- 9.4%) (p < 0.012). Stroke volume (SV) and stroke volume index (SVI) also improved in antibody-negative patients (SV: +20 +/- 31 ml; SVI: +10 +/- 17 ml) compared with antibody-positive patients (SV: -14 +/- 43 ml; SVI: -8 +/- 22 ml) (SV: p < 0.015; SVI: p < 0.016). Left ventricular end-diastolic and end-systolic volumes and the time constant of left ventricular relaxation "tau" did not change significantly different in antibody-positive and antibody-negative patients. The constant of myocardial stiffness "b" improved significantly in antibody-negative patients (-6.1 +/- 10.8) compared with antibody-positive patients (+7.3 +/- 22.6) (p < 0.040). Analyzing only the persistently antibody-positive patients yielded essentially the same results. CONCLUSIONS: Antimyosin autoantibodies are associated with worse development of left ventricular systolic function and diastolic stiffness in patients with chronic myocarditis.

Adult↗

Molecular characterization of two genes from Streptomyces tendae Tü901 required for the formation of the 4-formyl-4-imidazolin-2-one-containing nucleoside moiety of the peptidyl nucleoside antibiotic nikkomycin.

The genes nikQ and nikR were identified by sequencing DNA of the nikkomycin biosynthetic gene cluster from Streptomyces tendae Tü901/8c. The nikQ gene encodes a P450 cytochrome, and the predicted NikR gene product shows 48-56% sequence identity with uracil phosphoribosyltransferases from eukaryotic organisms. The nikQ and nikR genes were inactivated separately by insertion of a kanamycin-resistance cassette. Inactivation of the nikQ gene abolished synthesis of nikkomycins containing 4-formyl-4-imidazolin-2-one as the base (nikkomycins X and I), whereas production of nikkomycins containing uracil (nikkomycins Z and J) was not affected. Nikkomycin X and I production could be restored by feeding 4-formyl-4-imidazolin-2-one to the nikQ mutants, indicating that NikQ is responsible for its formation from L-histidine. Disruption of the nikR gene resulted in formation of decreased amounts of nikkomycins X and I, whereas nikkomycins Z and J were synthesized at wild-type levels. A fluorouracil-resistant nikR mutant lacking uracil phosphoribosyltransferase (UPRTase) activity did not synthesize nikkomycins X and I and accumulated 4-formyl-4-imidazolin-2-one in its culture filtrate, whereas formation of nikkomycins Z and J was unimpaired. The mutant was complemented to nikkomycin X and I production by nikR expressed from the mel promoter of plasmid pIJ702. The nikR gene expressed in Escherichia coli led to the production of UPRTase activity. Our results indicate that NikR converts 4-formyl-4-imidazolin-2-one to yield 5'-phosphoribosyl-4-formyl-4-imidazolin-2-one, the precursor of nikkomycins containing this base.

Aminoglycosides↗

A putative enolpyruvyl transferase gene involved in nikkomycin biosynthesis.

The nikO gene encoding a putative enolpyruvyl transferase has been identified within the Streptomyces tendae Tü901/8c nikkomycin gene cluster. nikO encodes a deduced protein of 471 amino acid residues which exhibits significant sequence similarity to UDP-N-acetylglucosamine enolpyruvyl transferase and 5-enol-pyruvylshikimate 3-phosphate synthase from various origin. The nikO gene was inactivated by inserting a kanamycin resistance cassette; the mutant did not produce biologically active nikkomycins I, J, X, and Z nor the nucleoside moieties, nikkomycins C(x) and C(z), but accumulated the novel component RT 2.0. RT 2.0 has been isolated from culture filtrate and its structure was determined by using mass spectrometry and NMR analyses as ribofuranosyl-4-formyl-4-imidazolone which represents a novel nucleoside. The putative activity of the nikO gene product in nikkomycin biosynthesis will be discussed.

Alkyl and Aryl Transferases↗

[Percutaneous myocardial laser revascularization (PMR), a new therapeutic procedure for patients with refractory angina pectoris].

In patients with severe angina pectoris due to coronary artery disease, who are not candidates for either percutaneous coronary angioplasty or coronary artery bypass surgery, transmyocardial laser revascularization (TMR) often leads to improvement of clinical symptoms and increased exercise capacity. One drawback of TMR is the need for surgical thoracotomy in order to gain access to the epicardial surface of the heart. Therefore, a catheter-based system has been developed, which allows creation of laser channels into the myocardium from the left ventricular cavity. Between January 1997 and November 1999, this "percutaneous myocardial laser-revascularization" (PMR) was performed in 85 patients at the Herzzentrum Leipzig. In 43 patients, only one region of the heart (anterior, lateral, inferior or septal) was treated with PMR; in 42 patients two or three regions were treated in one session. 12.3 +/- 4.3 (range 4-22) channels/region were created into the myocardium. Six months after PMR, the majority of patients reported significant improvement of clinical symptoms (CCS class at baseline: 3.3 +/- 0.4; after 6 months: 1.6 +/- 0.9) (p < 0.001) and an increased exercise capacity (baseline: 349 +/- 138 s; after 6 months: 470 +/- 193 s) (p < 0.05); however, thallium scintigraphy failed to show increased perfusion in the PMR treated regions. PMR seems to be a safe and feasible new therapeutic option for patients with refractory angina pectoris due to end-stage coronary artery disease. The first results indicate improvement of clinical symptoms and increased exercise capacity; evidence of increased perfusion in the laser-treated regions is still lacking.

Adult↗

Catheter-based percutaneous myocardial laser revascularization in patients with end-stage coronary artery disease.

OBJECTIVES: This study evaluates the feasibility and safety of a catheter-based laser system for percutaneous myocardial revascularization and analyses the first clinical acute and long-term results in patients with end-stage coronary artery disease (CAD) and severe angina pectoris. BACKGROUND: In patients with CAD and intractable angina who are not candidates for either coronary artery bypass grafting (CABG) or percutaneous transluminal coronary angioplasty (PTCA), transmyocardial laser revascularization (TMR) has been developed as a new treatment that results in reduced angina pectoris and increased exercise capacity. However, surgical thoracotomy is required for TMR with considerable morbidity and mortality. METHODS: A catheter-based system has been developed that allows creation of laser channels in the myocardium from within the left ventricular cavity. Laser energy generated by a Holmium: YAG (Cardiogenesis Corporation, Sunnyvale, California) laser was transmitted to the myocardium via a flexible optical fiber capped by an optic lens. The optical fiber was maneuvered to the target area under biplane fluoroscopy through a coaxial catheter system permitting movement in three dimensions. RESULTS: Thirty-four patients with severe CAD not amenable to either CABG or PTCA and refractory angina pectoris (Canadian Cardiologic Society [CCS] Angina Scale Class III-IV) were included in the study. Ischemic regions were identified by coronary angiography and confirmed by thallium scintigraphy. The percutaneous myocardial revascularization (PMR) procedure was successfully completed in all patients. In 29 patients, one vascular territory of the left ventricle and in 5 patients, two vascular territories were treated. Eight to fifteen channels were created in each ischemic region. Major periprocedural complications were limited to an episode of arterial bleeding requiring surgical repair. There was one death early after PMR, due to a myocardial infarction (MI) in a nontreated region. Clinical follow-up at 6 months (17 patients) demonstrated significant improvement of angina pectoris (CCS class before PMR: 3.0+/-0.0, six months after PMR: 1.3+/-0.8, p<0.0001) and increased exercise capacity (exercise time on standard bicycle ergometry before PMR: 384+/-141 s, six months after PMR: 514+/-158 s, p<0.05), but thallium scintigraphy failed to show improved perfusion of the laser treated regions. CONCLUSIONS: Percutaneous myocardial revascularization is a new safe and feasible therapeutic option in patients with CAD and severe angina pectoris not amenable to either CABG or PTCA. Initial results show immediate and significant improvement of symptoms and exercise capacity but evidence of improved myocardial perfusion is still lacking.

Aged↗

[Acute hantavirus infection caused by a genetically newly identified viral strain. Severe and complicated course of hemorrhagic fever with renal syndrome (nephropathia epidemica)].

HISTORY AND CLINICAL FINDINGS: A 49-year-old patient, a hobby hunter, fell ill acutely with joint and limb pain, abdominal pain, nausea and subfebrile temperatures. At hospitalization, the patient was in bad general condition, showing ascites and lid edema, and acute renal failure was diagnosed. INVESTIGATIONS: Laboratory tests revealed marked thrombocytopenia (15,000/ml), leucocytosis, elevated levels of creatinine, blood urea nitrogen and liver enzymes, respectively. Blood gas analysis showed metabolic acidosis. Chest X-ray showed an interstitial fluid accumulation, abdominal ultrasound disclosed ascites and enlarged kidneys as in acute renal failure. Immunologic tests verified the diagnosis of an acute hantavirus infection, by use of specific molecular biology techniques a previously unknown virus strain was identified. TREATMENT AND COURSE: Hantavirus infections in western Europe usually show a benign course. However, in the present case, acute progressive pulmonary failure developed despite effective dialysis so that mechanical ventilation was necessary for several weeks. Dialysis had to be carried out for 17 days. As a complication a severe ulcero-destructive tracheobronchitis developed, caused by Aspergillus fumigatus. After several weeks, both renal and pulmonary function had returned to normal. CONCLUSION: Hantavirus infections may lead to severe and complicated courses also in western Europe. By use of new immunologic and molecular biology techniques a specific diagnosis is possible.

Diagnosis, Differential↗

Molecular characterization of co-transcribed genes from Streptomyces tendae Tü901 involved in the biosynthesis of the peptidyl moiety of the peptidyl nucleoside antibiotic nikkomycin.

Six genes (nikA, nikB, nikD, nikE, nikF, and nikG) from Streptomyces tendae Tü901 were identified by sequencing the region surrounding the nikC gene, which encodes L-lysine 2-aminotransferase, previously shown to catalyze the initial reaction in the biosynthesis of hydroxypyridylhomothreonine, the peptidyl moiety of the peptidyl nucleoside antibiotic nikkomycin. These genes, together with the nikC gene, span a DNA region of 7.87 kb and are transcribed as a polycistronic mRNA in a growth-phase dependent manner. The sequences of the deduced proteins NikA and NikB exhibit significant similarity to those of acetaldehyde dehydrogenases and 4-hydroxy-2-oxovalerate aldolases, respectively, which are involved in meta-cleavage degradation of aromatic hydrocarbons. The predicted NikD gene product shows sequence similarity to monomeric sarcosine oxidases, and the deduced NikE protein belongs to the superfamily of adenylate-forming enzymes. The nikF gene and the nikG gene encode a cytochrome P450 monooxygenase and a ferredoxin, respectively. Disruption of any of the genes nikA, nikB, nikD, nikE and nikF by insertion of a kanamycin resistance cassette abolished formation of the biologically active nikkomycins I, J, X, and Z. The nikA, nikB, nikD, and nikE mutants accumulated the nucleoside moieties nikkomycins Cx and Cz. In the nikD and nikE mutants nikkomycin production (nikkomycins I, J, X, Z) could be restored by feeding with picolinic acid and hydroxypyridylhomothreonine, respectively. The nikF mutant exclusively produced novel derivatives, nikkomycins Lx and Lz, which contain pyridylhomothreonine as the peptidyl moiety. Our results indicate that the nikA, nikB, nikD, nikE, nikF, and nikG genes, in addition to nikC, function in the biosynthetic pathway leading to hydroxypyridylhomothreonine, the putative activities of each of their products are discussed.

Aldehyde Oxidoreductases↗

Initial results of laser-based percutaneous myocardial revascularization for angina pectoris.

Results of a 30-patient pilot study of a recently developed percutaneous myocardial revascularization approach are described. The feasibility and positive safety profile of percutaneous myocardial revascularization are clearly demonstrated, with no mortality associated with the treatment or in the immediate post-treatment period and an incidence of only 1 major complication.

Aged↗

[Cardiac troponin T in the diagnosis and follow up of suspected myocarditis].

BACKGROUND AND OBJECTIVE: Results of routine laboratory tests for demonstrating myocardial damage in patients suspected of having myocarditis are often negative. This study was undertaken to ascertain (1) whether measuring Tropinin T (cTnT) in these patients can sensitively determine myocardial cell death, (2) to what extent this correlates with the findings of endomyocardial biopsy, and (3) whether measurement of cTnT can provide noninvasive assessment of the course of myocarditis. PATIENTS AND METHODS: 80 consecutive patients (52 men, 28 women) with clinically suspected myocarditis were investigated. The main clinical symptoms were heart failure (n = 45), angina pectoris (n = 25) or cardiac arrhythmias (n = 10). In most patients the symptoms had developed in temporal relation to a viral infection. Coronary heart disease was excluded in all by coronary angiography. Interventricular septal endomyocardial biopsies were examined histologically and immunohistologically. cTnT was measured with a highly sensitive sandwich-immunoassay. RESULTS: An increased level of cTnT (> 0.1 ng/ml) was demonstrated in 28 of the 80 patients (35%). Myocarditis was diagnosed histologically in only 5 patients, but immunohistologically in 26 of 28 (93%) with a raised cTnT level and in 23 of 52 (44%) with a normal cTnT level. The cTnT level was more frequently elevated in patients with a brief rather than a long history of myocarditis. After 6 months the cTnT level was elevated in only 4 of 28 patients with myocarditis, but the myocardial biopsy showed persisting myocarditis in 14 patients. CONCLUSION: Measurement of cTnT is a very sensitive way of demonstrating myocardial cell damage in patients clinically suspected of having myocarditis. Immunohistological analysis can often provide positive results even if the histological findings are unremarkable. The sensitivity in diagnosing of cTnT is greatest when the patient is tested shortly after the onset of symptoms.

Acute Disease↗

[Biphasic course of left ventricular dysfunction in a 22-year-old female with acute myocarditis].

HISTORY AND CLINICAL FINDINGS: Two days before admission a 22-year-old woman developed general fatigue, nausea, headache and retrosternal pain. Physical examination was unremarkable. INVESTIGATIONS: Erythrocyte sedimentation rate was increased to 20/48, C-reactive protein to 3.3 mg/dl, and there was evidence of myocardial damage (creatine kinase 609 U/l, creatine kinase-MB 42 U/l, troponine T 8.39 ng/ml); ST-segment elevations in I, II, III, aVF and V-V6 of the ECG. Echocardiography revealed clearly thickened myocardium, moderate but haemodynamically not significant pericardial effusion, as well as impaired left ventricular function. Antimyosin scintigraphy was very abnormal. Cardiac catheterization confirmed the left ventricular dysfunction, rise of left ventricular enddiastolic pressure to 17 mm Hg, and a markedly reduced cardiac output of 2.4 l/min. Myocardial biopsy showed severe myocarditis with marked myocytolysis and considerable lymphocytic infiltrations. Enteroviral RNA was demonstrated in the myocardium by polymerase chain reaction. TREATMENT AND COURSE: The haemodynamics became normal within only 3 days. Myocardial biopsy after 6 months was unremarkable histologically and immunohistologically, and left ventricular function was also normal. However, while after a further 12 months myocardial biopsy remained normal and no virus was demonstrated, there was definite, though moderate, impairment in left ventricular function, indicating a dilated cardiomyopathy. INTERPRETATION: Even when histological and immunohistological evidence of healing of an acute viral myocarditis has been achieved, with complete normalization of left ventricular function, a dilated cardiomyopathy may subsequently develop. The pathophysiological mechanism of this occurrence remains unknown.

Acute Disease↗

[Myocardial infarct caused by dissection of the anterior interventricular ramus after blunt thoracic trauma--a case report].

A 23 year old man, having experienced sudden retrosternal pain, radiating to both hemithoraces, with dyspnea at rest was admitted to another hospital. The physical examination of heart and lung was unremarkable, but the patient showed discrete signs of a respiratory infection. Because of the young age and the history of a respiratory infection, the differential diagnosis perimyocarditis was favored and an appropriate treatment was begun. Five days later the patient was transferred to our center for cardiac catheterization and further treatment. After admission the patient was reported to be hit by a football shortly before the onset of symptoms. The electrocardiogram and chemical values showed the signs of myocardial damage with extensive myocardial necrosis. In the coronary arteriography a dissection of the proximal left anterior descending artery of a length of about 2 cm was seen; in the levocardiogram anterior akinesis was verified. Because of the already completed myocardial infarction, the short distance of the lesion to the left main coronary artery, and the restored flow in the left anterior descending, a non-invasive treatment was preferred. A control coronary arteriography five days later showed solely an irregularity of the vessel wall, the coronary dissection was not further demonstrable.

Adult↗

[Antimyosin scintigraphy for diagnosis and follow-up of patients with clinically suspected myocarditis].

Antimyosin-scintigraphy is believed to have a high specificity but a low sensitivity for the diagnosis of myocarditis when histological analysis of endomyocardial biopsy is used as the reference method. However, the histological evaluation itself seems to have a low sensitivity for the diagnosis of myocarditis. Therefore, immunohistological techniques have been developed for the detection of lymphocytic infiltrates and increased expression of HLA antigens in the myocardium. The present study compares the results of antimyosin-scintigraphy with histological and immunohistological analysis of the endomyocardial biopsy. 65 patients with clinically suspected myocarditis underwent antimyosin-scintigraphy and histological and immunohistological analysis of the endomyocardial biopsy. Myocarditis could be diagnosed histologically in only 9/36 (25%) patients with a positive antimyosin scan but additional immunohistological analysis revealed lymphocytic infiltrates in 31 (86%) of these patients. In 29 patients with a normal antimyosin scan, histological analysis showed evidence of myocarditis in 3 (10%) patients; additional immunohistological evaluation disclosed lymphocytic infiltrates in 17 (59%) patients. With immunohistological analysis of the endomyocardial biopsy as the reference method, antimyosin-scintigraphy has a high sensitivity but a lower specificity for the diagnosis of myocarditis. Detection of autoantibodies against human cardiac myosin in patients with myocarditis is associated with a significantly lower incidence of positive antimyosin scans in these patients. Antimyosin-scintigraphy was repeated after six months in 14 patients with myocarditis. Histological and immunohistological evaluation of the endomyocardial biopsy now showed persistent myocarditis in 3/8 patients with a positive antimyosin scan and in 5/6 patients with a normal antimyosin scan.

Adult↗

Antimyosin scintigraphy and immunohistologic analysis of endomyocardial biopsy in patients with clinically suspected myocarditis--evidence of myocardial cell damage and inflammation in the absence of histologic signs of myocarditis.

OBJECTIVES: This study compares the results of antimyosin scintigraphy in patients with clinically suspected myocarditis with histologic and immunohistologic findings in the endomyocardial biopsy. BACKGROUND: In patients with clinically suspected myocarditis, antimyosin scintigraphy often demonstrates myocardial cell damage but histologic evaluation of the endomyocardial biopsy often fails to show evidence of myocarditis. Recently developed immunohistologic techniques appear to be more sensitive for the detection of myocardial inflammation than histologic analysis alone. Studies comparing antimyosin scintigraphy and immunohistologic analysis of the endomyocardial biopsy in patients with clinically suspected myocarditis are not yet available. METHODS: Sixty-five patients with clinically suspected myocarditis underwent antimyosin scintigraphy. Antimyosin antibody uptake was correlated with histologic and immunohistologic findings in the endomyocardial biopsy. RESULTS: Antimyosin scintigraphy showed evidence of myocardial cell damage in 36 (55%) of the 65 patients and was negative in 29 (45%) patients. Histologic analysis of the endomyocardial biopsy revealed myocarditis in nine patients: six had a positive and three had a negative antimyosin scan, respectively. Thirty (83%) of 36 patients with evidence of myocardial cell damage on antimyosin scintigraphy were histologically negative for myocarditis. Immunohistologic analysis showed evidence of myocarditis in 31 (86%) of 36 patients with a positive antimyosin scan and also in 17 (59%) of 29 patients with a normal scan (p < 0.047). CONCLUSIONS: Antimyosin scintigraphy often shows myocyte injury in patients with clinically suspected myocarditis. Histologic analysis of the endomyocardial biopsy alone is often negative, but additional immunohistologic analysis of the endomyocardial biopsy frequently provides evidence of myocardial inflammation in these patients. With immunohistologic analysis as the reference method, antimyosin scintigraphy has a high specificity but a lower sensitivity for the detection of myocarditis.

Adult↗

Transmyocardial laser revascularization using the Holium-YAG laser for treatment of end stage coronary artery disease.

OBJECTIVE: Transmyocardial Laserrevascularization (TMLR) is a treatment for end-stage coronary artery disease, that is not eligible for surgery or PTCA. The experience with TMLR using the Holium YAG laser is presented. METHODS: Transmyocardial Laserrevascularization (TMLR) was performed in 28 patients with end stage coronary artery disease, using a new Holium YAG Laser. All patients were refractory to a maximum of medical treatment. In 16 patients TMLR was used as the sole therapy with a mean of 28 +/- 4 laser created channels (group A). In 12 patients TMLR was combined with coronary artery bypass graft surgery with a mean of 17 +/- 2 channels and 1.3 +/- 0.2 grafts (group B). Preoperative and postoperative examination included angina classification, exercise test and thallium scan. RESULTS: Postoperative demographics were as follows: (a) age 55-71 years (mean 63.9 +/- 6.5 years); (b) Canadian Cardiovascular Society Angina Scale (CCS) mean 3.3 +/- 0.5; (c) ejection fraction 35-71% (mean 54 +/- 13.7%). All patients had an peri- and postoperative course without major complications and a duration of hospitalization of 8.2 +/- 1.9 days. Minor complications were a clinically silent myocardial infarction n = 1, atrial arrhythmia n = 2 and pneumothorax n = 2. A follow-up at 3-12 months was completed in 23 patients (82%). Only one patient died 5 months after surgery (cardiac related death). In all remaining patients CCS had improved with a mean of 1.6 +/- 0.3, P < 0.01. The exercise tolerance test (bicycle) improved in 17 patients with a mean 26.5 +/- 6.5 watt, P < 0.01. The ejection fraction did not significantly improve. The repeated thallium scan did not show an improvement of perfusion in the lasered area to a significant level. Subjective benefit from the treatment was confirmed by 21 patients. CONCLUSION: Based on these results it is concluded that TMLR with the Holium-YAG laser is a safe therapy for the treatment of end stage coronary artery disease. The postoperative clinical results are comparable to that achieved with the CO2-laser in terms of reducing angina symptoms and improving exercise tolerance and quality of life. However. relief of symptoms is not correlated to objective findings of cardiac function.

Adult↗

Cardiac troponin T in patients with clinically suspected myocarditis.

OBJECTIVES: The present study investigated whether myocyte injury can be assessed sensitively by measurement of serum levels of cardiac troponin T (cTnT) in patients with clinically suspected myocarditis and whether cTnT levels may predict the results of histologic and immunohistologic analysis of endomyocardial biopsy specimens. BACKGROUND: Conventionally used laboratory variables often fail to show myocyte injury in patients with clinically suspected myocarditis, possibly because of a low extent of myocardial injury in these patients. Sensitive variables for myocyte injury have not yet been investigated. METHODS: Eighty patients with clinically suspected myocarditis were screened for creatine kinase (CK) activity, MB isoform of CK (CK-MB) activity and cTnT. Endomyocardial biopsy specimens were examined histologically and immunohistologically. RESULTS: cTnT was elevated in 28 of 80 patients with clinically suspected myocarditis, CK in 4 and CK-MB in 1. Histologic analysis alone of the endomyocardial biopsy specimen revealed evidence of myocarditis in only five patients, all with elevated cTnT levels. Twenty-three of 28 patients with elevated cTnT levels had histologically negative findings for myocarditis. Additional immunohistologic analysis revealed evidence of myocarditis in 26 (93%) of 28 patients with elevated cTnT levels and in 23 (44%) of 52 patients with normal cTnT levels. Mean cTnT levels were higher in patients with myocarditis proved histologically or immunohistologically, or both, than in patients without myocarditis (0.59 +/- 1.68 vs. 0.04 +/- 0.05, p < 0.001). CONCLUSIONS: Measurement of serum levels of cTnT provides evidence of myocyte injury in patients with clinically suspected myocarditis more sensitively than does conventional determination of cardiac enzyme levels. Myocardial cell damage may be present even in the absence of histologic signs of myocarditis. Additional immunohistologic analysis often shows lymphocytic infiltrates in these patients. Elevated levels of cTnT are highly predictive for myocarditis in this group.

Adolescent↗

Egg-cumulus-oviduct interactions and fertilization.

In this communication we approach the events leading to fertilization in mammals by examining the triangle of egg, sperm and oviductal cell taking account of the local physiology and focussing on auto/paracrine interactions. The expression of growth factors and extra-cellular matrix (ECM)-components in bovine ovarian granulosa- and theca-cells, the oocyte-cumulus complex (OOC) and oviductal epithelium, as well as some of the corresponding secreted proteins can be detected through the estrous cycle. Components of the insulin-like (IGF), fibroblast (FGF) and transforming (TGF) growth factor systems, and also metalloproteinase 1 (MMP1) and urokinase (uPA) are found to be modulated in these cells prior to fertilization. Different expression levels between the cell types are found, each representative of a specific reaction window within that particular stage of the cycle. Our findings support the concept that most of the observed tissue in the reproductive tract is dependent upon on the effects of gonadotropins or steroids, but that the fine-regulation is conveyed by, for example, growth factors and ECM-components. We suggest a sophisticated, auto/paracrine and species-specific crosstalk of growth factors and ECM components between the different cell types involved, enabling fertilization and development of the embryo at the right time and in the right location.

Animals↗