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Biomedical subjects

M Richter

Publications and source records attributed to M Richter.

At least 217 records · Page 12Linked to original sources

[Inadequate treatment compliance, patient information and drug prescription as causes for emergency hospitalization of patients with chronic heart failure].

UNLABELLED: Causes of decompensation of treated chronic congestive heart failure in patients referred for emergency hospitalization were examined prospectively. 111 consecutive patients (76 +/- 11 years) were interviewed and their records examined on admission. The diagnosed underlying diseases were coronary artery disease (80%), hypertensive heart disease (40%), valvular heart disease (11%), and idiopathic dilated (7%) and alcoholic (5%) cardiomyopathy. The grounds for decompensation of chronic congestive heart failure were: insufficient compliance 47% (n = 52, irregular or not intake of medication [25%], salt [9%] or fluid [7%] excess, stopping medication because of side effects [6%]), uncontrolled hypertension (27%), insufficient diuretic therapy in spite of progressive symptoms (23%), treatment with negative inotropic drugs (21%), acute rhythm disturbances (14%), acute myocardial infarction or unstable angina pectoris (14%), infections (6%). 80% of the patients were treated with diuretics, 34% with digoxin, 31% with ACE-inhibitors. Insufficient basic knowledge about the disease (regular weighing, diet, behavior if symptoms worsen) was found in 78% of patients, complete lack of knowledge concerning the prescribed drugs in 29%. Only 44% were regularly followed by their physicians, 53% had either no regular follow-ups or they were set at too long intervals. CONCLUSIONS: In the majority of patients, one or more avoidable causes leading to decompensation of chronic congestive heart failure can be identified. The main potential for intervention aiming at a reduction of the hospitalization frequency lies in improving patient compliance and state of the art medication by the primary care physician. Equally unsatisfactory is the low frequency of follow-up checks to reassess and renew drug therapy.

Aged↗

Endothelium-dependent relaxation of porcine pulmonary arteries via 5-HT1C-like receptors.

In PGF2 alpha-precontracted pulmonary arteries with intact endothelium, 5-hydroxytryptamine (5-HT, 1.0-100 nmol/l) caused a concentration-dependent reversible relaxation, at higher concentrations the contractile response prevailed. In endothelium-denuded vessels relaxation was absent. 5-HT-induced relaxation of precontracted pulmonary arteries was probably mediated by release of an endothelium-derived relaxing factor (EDRF). Preincubation of the arteries with methylene blue or NG-nitro-L-arginine (200 mumol/l) attenuated the relaxant effect. The 5-HT-induced relaxation was accompanied by an increase in cGMP. Indomethacin (3 mumol/l) did not influence the 5-HT-induced relaxation indicating that eicosanoids are not involved in the relaxant response to 5-HT. The 5-HT1C and 5-HT2 receptor agonist alpha-methyl-5-HT was as potent as 5-HT in inducing relaxation. The rank order of relaxant potency of the agonists investigated was alpha-methyl-5-HT > 5-HT > 5-methoxytryptamine > tryptamine > omega-methyl-5-HT > 5-carboxamidotryptamine > 2-methyl-5-HT > 5,6-dihydroxytryptamine > m-chlorophenylpiperazine > sumatriptan > 8-OH-DPAT. Phentolamine, pindolol and ICS 205-930 did not interfere with the relaxant effect. The 5-HT2 receptor antagonist ketanserin (1 mumol/l) inhibited the contractile response but did not alter vasodilatation. Apart from the blockade of the contractile effects, mesulergine, cyproheptadine and mianserin (0.1-3.0 mumol/l, each) induced a parallel shift to the right of the concentration-response curve for the relaxation induced by alpha-methyl-5-HT or 5-HT. Spiperone (0.3 mumol/l) exerted weak inhibitory effects on relaxation and contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Preservation of vascular access.

Preservation of vascular access is critical in the long-term successful management of hemodialysis patients. Dialysis access abnormalities are the most common cause of hospitalization in this patient group, and access problems can increase the morbidity and cost involved in the care of these patients. Native fistulas are preferable to synthetic grafts because of longer survival and a lower complication rate. Venous outflow stenosis is the most common site of obstruction in a failing graft. The pathophysiology of access failure is poorly understood, but it seems to be related to intimal hyperplasia in the native vessel downstream from the anastomosis. The stimulation of local growth factors by needle puncture may also play a role. An assessment of access adequacy includes careful physical examination, laboratory evaluation, and ultimately, angiography. Measurements of recirculation and venous pressure are commonly used to screen for access dysfunction, and their appropriate use will lower the incidence of graft loss in dialysis units. Treatment is usually either angioplasty or surgery, with some centers having success with thrombolytic therapy. New techniques such as atherectomy and stent placement may prove to be beneficial, but this requires further study.

Angioplasty, Balloon↗

[Atrial-triggered and ventricular-inhibited ventricular VDD pacing with atrial and ventricular single catheter electrodes--the Phymos MPS pacemaker].

Optimal treatment from the haemodynamic aspect in complete atrioventricular block is dual-chamber DDD pacing. It makes possible atrioventricular sequence and adaptability of the frequency of ventricular pacing to the load under the control of the sinoatrial node. DDD pacing calls, however, for an atrial and ventricular electrode on two leads. Italian authors developed in 1984 a pacemaker (PM) PHYMOS (MEDICO ITALIA) which makes possible atrial triggered ventricular VDD pacing by means of a single pass lead with a tripolar electrode. As the first ones in the post-communist countries the authors implanted to six patients a PM PHYMOS MPS. They confirmed that the advantages of the VDD system, as compared with DDD, are the use of a single pass lead. This makes the implantation quicker, simpler and safer and reduces the time of X-ray irradiation and the incidence of electrodes dislocations. Another advantage is the lower incidence of atrial fibrillation and probably also pacemaker mediated tachycardias. The disadvantages of the VDD system are that atrial stimulation is impossible and that the diameter of the single pass lead is somewhat larger. According to data in the literature and the so far small experience of the authors, when the indication is correct--atrioventricular block grade III or II with intact function of the sinoatrial node--the advantages of VDD pacing with a single pass lead, as compared with DDD pacing, predominate over disadvantages.

Aged↗

[Surgical treatment of salivary incontinence in cerebral palsy].

For patients with cerebral palsy, chronic drooling is the result of an abnormality in the cerebral control of orofacial motor functions. Sialorrhea is a troublesome problem for these patients and their attendants. Among various surgical techniques, rerouting of the Stensen's ducts and bilateral excision of the submandibular salivary glands, as described by Wilkie, gives good results. Transposition of the submandibular gland ducts in the tonsillar fossae is an easier procedure but less favorable. We present 19 patients treated by these two methods.

Adolescent↗

Haemostyptic effects of batroxobin with regard to hirudin treatment.

In contrast to thrombin the fibrinogen coagulant effect of the thrombin-like enzyme batroxobin in vitro and in vivo is not inhibited by the specific thrombin inhibitor hirudin. The haemostyptic effect of batroxobin has been studied in rats after bleeding had been induced by corresponding hirudin dosages. Dependent on batroxobin concentration bleeding time was shortened by local application of batroxobin containing solutions. Strong bleeding induced by i.v. injection of 5 mg r-hirudin/kg was stopped almost immediately when a batroxobin concentration of 40 BU/ml was used. Thrombin was less active to stop bleeding after r-hirudin administration than batroxobin.

Animals↗

[Heart contusions: pathological findings and clinical course].

After blunt chest trauma, myocardial contusion is frequently suspected, but diagnostic criteria are difficult to define and commonly accepted recommendations for duration and form of patient monitoring are lacking. We therefore conducted a retrospective review of the hospital records of 50 consecutively hospitalized patients with the diagnosis of myocardial contusion after blunt chest trauma, and analyzed the pathological laboratory, ECG and echocardiography findings as well as the associated injuries and cardiac-related complications. The average injury severity score was 25 +/- 8. Initially 98% of the patients were hemodynamically stable. In 90% there were abnormal enzyme levels consistent with myocardial injury. Typically, the maximum level of CPK-MB, LDH and CPK-MB/CPK (MB-fraction) was found initially and these values declined rapidly. The MB fraction normalized within 8 hours. In 32% of the patients there were the following ECG changes consistent with myocardial contusion transient: ventricular tachycardia (12%), ST/T changes (12%), complete right bundle branch block (10%), atrial fibrillation (4%), first degree AV block (2%). The episodes of ventricular tachycardia were registered within the first 24 hours; in 5 of these 6 patients the admission ECG was normal. An echocardiography was done in 64% of the patients and in 37% showed either a pericardial effusion, regional wall motion abnormalities, a pneumopericardium or an intramyocardial hematoma in the free wall of the right ventricle. One patient died of multiorgan failure during this hospitalization. There were no sudden cardiac deaths. The diagnosis of myocardial contusion is vital in unstable patients but also very important in hemodynamically stable patients, despite its low morbidity. The minimum program we recommend for diagnosis and monitoring should include enzyme levels (CPK, CPK-MB) and ECG controls. Echocardiography may be necessary as well. If during the initial compulsory 24 hour monitoring of ECG and hemodynamics no complications occur, further monitoring is not necessary.

Adolescent↗

H2-forming methylenetetrahydromethanopterin dehydrogenase, a novel type of hydrogenase without iron-sulfur clusters in methanogenic archaea.

A novel hydrogenase has recently been found in methanogenic archaea. It catalyzes the reversible dehydrogenation of methylenetetrahydromethanopterin (CH2 = H4MPT) to methenyltetrahydromethanopterin (CH identical to H4MPT+) and H2 and was therefore named H2-forming methylenetetrahydromethanopterin dehydrogenase. The hydrogenase, which is composed of only one polypeptide with an apparent molecular mass of 43 kDa, does not mediate the reduction of viologen dyes with either H2 or CH2 = H4MPT. We report here that the purified enzyme from Methanobacterium thermoautotrophicum exhibits the following other unique properties: (a) the colorless protein with a specific activity of 2000 U/mg (Vmax) did not contain iron-sulfur clusters, nickel, or flavins; (b) the activity was not inhibited by carbon monoxide, acetylene, nitrite, cyanide, or azide; (c) the enzyme did not catalyze an isotopic exchange between 3H2 and 1H+; (d) the enzyme catalyzed the reduction of CH identical to H4MPT+ with 3H2 generating [methylene-3H]CH2 = H4MPT; and (e) the primary structure contained at most four conserved cysteines as revealed by a comparison of the DNA-deduced amino acid sequence of the proteins from M. thermoautotrophicum and Methanopyrus kandleri. None of the four cysteines were closely spaced as would be indicative for a (NiFe) hydrogenase or a ferredoxin-type iron-sulfur protein. Properties of the H2-forming methylenetetrahydromethanopterin dehydrogenase from Methanobacterium wolfei are also described indicating that the enzyme from this methanogenic archaeon is very similar to the enzyme from M. thermoautotrophicum with respect both to molecular and catalytic properties.

Amino Acid Sequence↗

A tungsten-containing active formylmethanofuran dehydrogenase in the thermophilic archaeon Methanobacterium wolfei.

Methanobacterium wolfei is a thermophilic methanogenic archaeon which requires tungsten or molybdenum for growth. We have found that the organism contains two formylmethanofuran dehydrogenases, one of which is a tungsten enzyme. Indirect evidence indicates that the other formylmethanofuran dehydrogenase is a molybdenum enzyme. The tungsten enzyme was purified and characterized. The native enzyme had an apparent molecular mass of 130 kDa. SDS/PAGE revealed a composition of three subunits of apparent molecular mass 35, 51 and 64 kDa, the N-terminal amino acid sequences of two of which were determined. 0.3-0.4 mol tungsten/mol enzyme was found but no molybdenum. The pterin cofactor was identified as molybdopterin guanine dinucleotide. The purified enzyme exhibited a specific activity of 8.3 mumol.min-1.mg protein-1 and an apparent Km for formylmethanofuran and methylviologen of 13 microM and 0.4 mM, respectively. The optimum temperature for activity was 65 degrees C. At 40-60 degrees C, the rate increased with a Q10 of 1.9; the activation energy of the reaction was 45 kJ/mol. The enzyme was found to require potassium ions for thermostability. The oxygen-sensitive enzyme was not inactivated by cyanide.

Aldehyde Oxidoreductases↗

Caries susceptibility and renal excretion of calcium.

Clearance studies were performed for 2 days in two groups of age-matched young female volunteers: those with low caries prevalence and those with high caries prevalence. Both groups were kept on a low-calcium diet for 1 week and received 0.5 g calcium at the beginning of the second day. In both groups, glomerular filtration rate, urinary flow rate and renal excretions of sodium, calcium, and phosphate were subject to significant circadian variations. In both groups the administration of calcium led to a significant increase in renal excretion of sodium and calcium and a significant decrease in that of phosphate. On the first day, calcium excretion was significantly greater in those with low caries prevalence than in those with high caries prevalence, pointing to altered calcium homeostasis in this group.

Adolescent↗

The interleukin-2 receptor in human monocytes and macrophages: regulation of expression and release of the alpha and beta chains (p55 and p75).

Human monocytes constitutively express the intermediate-affinity interleukin-2 receptor (IL2R) p75, while freshly isolated monocytes lack the low-affinity IL2R p55 (Tac antigen, CD25). Lipopolysaccharide (LPS) upregulates expression of p75 and effectively induces surface expression of CD25 on human monocytes within 18 h, as detected by two-colour FACS analysis on 59.5 +/- 7.6% of cells. IL2-binding studies using biotinylated IL2 reveal the presence of a functional high-affinity receptor on LPS-activated monocytes. Soluble CD25 (sCD25) is not released into supernatants of elutriation-purified monocytes cultured for 24 h with 100 ng/ml LPS. When these monocytes are cultured for up to 7 days in the presence of serum to induce differentiation into macrophages, increasing amounts of sCD25 can be measured in the 24-h supernatants induced with LPS (173 +/- 86 U/ml at day 7), whereas the percentage of CD25+ cells (14.8 +/- 14.1% at day 7) is significantly lower than in monocytes. Thus, the cell surface expression and release of CD25 is differentially regulated in activated monocytes and macrophages.

Humans↗

Cells and mediators involved in immunoglobulin synthesis by human circulating mononuclear cells. IV. B cells synthesize but do not secrete immunoglobulins because of a defect in the non-T non-B (null) cells.

Null cells (non-T and non-B lymphocytes) have previously been demonstrated to be obligatory participants for immunoglobulin synthesis and secretion by normal B cells in culture. Normal null cells have been demonstrated to secrete a factor, human immunoglobulin synthesis/secretion-facilitating factor (HISFF), which can replace the null cells in the culture. In this investigation, the B cells of an 8-month-old male infant and a 46-year-old male adult who presented with a humoral (antibody) immunodeficiency syndrome synthesized immunoglobulin but did not secrete immunoglobulin after culture with pokeweed mitogen and autologous T cells, monocytes, and null cells. In contrast, the patients' B cells synthesized and secreted immunoglobulin after the addition of allogeneic normal null cells or HISFF to the cultures. The same results were obtained with the cells of the infant and the adult patient tested at monthly intervals for 4 months. The results demonstrate that the patients' T cells, B cells, and monocytes functioned normally and that only the patients' null cells were defective. These findings provide an explanation for the absence of immunoglobulin in the circulation of "non(immunoglobulin)secretors," although they possess normal numbers of circulating immunoglobulin-synthesizing B cells. The defect is in the null cell and not in the B cell and consists of the inability of the null cell to secrete HISFF that facilitates the synthesis and secretion of immunoglobulin by the B cell.

Antigens, CD↗