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Biomedical subjects

R Frank

Publications and source records attributed to R Frank.

At least 523 records · Page 29Linked to original sources
PubMed1981

Surgical treatment of ventricular tachycardia guided by ventricular mapping in 23 patients without coronary artery disease.

Twenty-three patients with resistant ventricular tachycardia not related to coronary artery disease underwent surgical treatment guided by ventricular mapping. The patients were grouped according to radiological and anatomical findings. Group 1 (13 patients) had arrhythmogenic right ventricular dysplasia. Group 2 (3 patients) had left ventricular aneurysm. Group 3 (2 patients) had nonobstructive myocardiopathy. Group 4 (5 patients) had normal-appearing hearts. At operation all patients underwent ventricular mapping when in sinus rhythm and during ventricular tachycardia. The rationale of operation was ventriculotomy or cryosurgery at the site of origin of ventricular tachycardia or exclusion, resection, or undermining of arrhythmogenic areas where delayed potentials were observed. Four patients died during the perioperative period, 3 of low-output failure and 1 from bleeding. Ventricular tachycardia recurred immediately after operation in 4 patients, 3 of whom died during the perioperative period. Ventricular tachycardia recurred late in 5 patients. Three had only episodic, unsustained runs of tachycardia. Two were well controlled by drugs. All patients with ventricular tachycardia situated over the free wall of the ventricles had inducible ventricular tachycardia and had good surgical results. Three out of 5 patients with ventricular tachycardia situated in the septum had poor surgical results. Septal ventricular tachycardia needs a better surgical approach to the septum and a suitable surgical concept.

Adult↗
PubMed1981

[Systemic mastocytosis with myo-pericardial localization and atrioventricular block].

The case of a 46 year old man with systemic mastocytosis with myocardial and pericardial involvement confirmed histologically after open biopsy is reported. The patient presented with skin, bone and medullary lesions and, in addition, with atrioventricular block and pericardial effusion. The possible mechanisms of the atrioventricular conduction defect are examined in the light of the physiological role of the mastocyte and research into the action of histamine on the myocardium. In particular, the negative dromotropic effect of histamine and fibrosis formation related to the mastocyte's function of connective tissue regeneration are discussed. This case, though rare, should alert the clinician to the possibility of myocardial and pericardial involvement in patients with mastocytosis. Further study into the effects of histamine on myocardium under physiological and pathological conditions is required.

Cardiomyopathies↗
PubMed1981

South African Negroes: isoenzyme polymorphisms (GPT, PGM1, PGM2, AcP, AK, and ADA) and tentative genetic distances.

Data on the genetic polymorphisms of the isoenzyme markers GPT, PGM1, PGM2, AcP, AK and ADA are presented for 7 ethnically defined Negro sub-samples (total n = 847-973, depending on the genetic marker concerned) from South Africa. The results are discussed in terms of previous findings, of the anthropogenetic interrelatedness of the populations concerned and of the factors assumed to have an influence on the distribution of the particular genetic markers. The entire data is subjected to the computation of "genetic distances" using several of the formulae available for this purpose. Some tentative conclusions on these results as well as on the formulae applied are drawn.

Alleles↗
PubMed1980

SO2-particulate interactions: recent observations.

The toxicity of sulfur oxides is discussed briefly. The effects of sulfur dioxide (SO2) are largely confined to the upper airways except during exercise or if the gas is taken up by a carrier aerosol. SO2 may be adsorbed as a monomolecular layer on dry particles, such as elemental carbon, or dissolved in aqueous droplets. Hydrated SO2 forms bisulfite and sulfite ions, which are rapidly oxidized (detoxified) by sulfite oxidase, an enzyme, to form sulfate. SO2 in carrier aerosols (dry or aqueous solutions) may be oxidized to sulfuric acid. The mixture of SO2 (1 ppm) and a droplet of sodium chloride (1 mg/m3) has been shown to be synergistic in guinea pigs. In healthy adults, the same gas-aerosol mixture caused no functional lung changes at rest (two separate studies), but did cause significant changes following moderate exercise. Shortness of breath and wheezing were experiences by about half of the subjects.

Aerosols↗
PubMed1980

The chemical neutralization of inhaled sulfuric acid aerosol.

We hypothesize that gaseous ammonia (NH3) released into respiratory airways can neutralize inhaled acidic particles and alter or mitigate their toxicity. To test this hypothesis, we have examined the relationship between respiratory NH3 and the chemical neutralization of inhaled sulfuric acid (H2SO4) aerosol in the surgically isolated upper airways of anesthetized dogs. With air entering via the mouth, the NH3 concentration measured at the larynx, ranged between 30 and 225 parts per billion (ppb). The extent of neutralization at this point ranged from 8%-70% (n = 16) for the 0.5-micrometer particles and 7%-22% (n = 16) for the 1.0-micrometer particles. With air entering via the nose, the laryngeal NH3 concentrations ranged between 50 and 220 ppb. Neutralization values were between 15%-65% (n = 8) for 0.5-micrometer particles, and between 16%-18% (n = 3) for 1.0-micrometers particles. For both routes of entry, the extent of neutralization was correlated with the laryngeal NH3 concentration. We conclude that the chemistry of acidic particles is significantly altered by respiratory NH3 during inhalation. The extent of neutralization is related to both the NH3 concentration in the airway and the size of the particle entering the airway. The extent of neutralization per ppb of laryngeal NH3 is related to the route of entry, being greater for the mouth than the nose.

Aerosols↗
PubMed1980

Composition and properties of trypsin-cleaved elongation factor Tu.

Native elongation factor Tu from Escherichia coli, EF-Tu, is initially attacked by trypsin at three adjacent sites in the primary structure. These are arginine-44, arginine-58, and lysine-56. The rates of hydrolysis at the two arginine residues are about the same but that at the lysine residue is much slower. The products of the tryptic digestion have been analysed by Edman degradation and polyacrylamide gel electrophoresis. The peptide from alanine-45 to arginine-58 is eventually excised and does not complex with the remaining polypeptides (fragments A and D). The loss of this peptide does not lead to a concomitant loss of activity in stimulating polyphenylalanine synthesis. The latter is closely correlated with the further hydrolysis of the remaining fragment (A + D) complex. This complex resembles native EF-Tu in its ability to stimulate both polyphenylalanine synthesis and the binding of aminoacyl-tRNA to 70-S ribosomes, but does not form so stable a ternary complex with aminoacyl-tRNA and GTP as the native protein.

Amino Acid Sequence↗
PubMed1980

Intracardiac conduction defects in dystrophia myotonica. Electrophysiological study of 12 cases.

Twelve patients with dystrophia myotonica had cardiac electrphysiological study for conduction disturbances (five cases) or for syncope (seven cases). Conduction disturbances were found in each case, being intranodal in two cases, intra-Hisian in three cases, or diffuse in seven cases. These findings are in agreement with those previously reported, and may be related to the high incidence of sudden death in these patients. Pacemakers are advocated in symptomatic patients, and in some asymptomatic patients with severe and diffuse lesions.

Adolescent↗
PubMed1980

Antigenuria in St. Louis encephalitis.

Patients with St. Louis encephalitis may have urinary tract symptoms when they develop manifestations related to involvement of the central nervous system. During 1976, 12 patients with St. Louis encephalitis were studied for the presence of antigenuria, and compared to controls. Although virus isolation attempts were negative indirect immunofluorescence, electron microscopy, and immune electron microscopy demonstrated the presence of viral antigen in urine. Further study of antigenuria in St. Louis encephalitis is needed to delineate the pathophysiology of the lower urinary tract symptoms and to determine whether this phenomenon might furnish the basis for a rapid diagnostic test for the disease.

Antibodies, Viral↗
PubMed1980

[Attenuated nodal response. Apropos of 30 cases].

In a population of 600 consecutive patients undergoing endocavitary electrophysiological study to assess nodal conduction, 40 had an atriohisian Wenckenbach point of over 200/mn. In 30 cases, vagal stimulation with ATP (10 to 40 mg IV) provoked an increase in atrioventricular conduction, with lengthening the AH interval by over 100 p. 100 or transient atrioventricular block. This increase allowed elimination of an accessory atriohisian pathway which could give similar high Wenckenbach points, but which do not show decremental conduction. In all our cases, the conduction passed through the artrioventricular node (AVN) whose response to rapid atrial stimulation was attenuated compared to normal. The parameter of this attenuated nodal response varied from case to case, but in general, the intervals were shorter than normal. The AH interval was less than 50 ms in 22 cases (N = 70 +/- 20 ms). The effective nodal refractory period was shorter than the functional atrial refractory period in 20 cases. The shortest atrial cycles transmitted 1/1 to the ventricles ranged from 230 to 300 ms (274 +/- 33 ms) (N = 375 +/- 40 ms). The functional structure of the AVN was studied by the lengthening of the AH interval with heart rate : 5 types were distinguished : 10 patients had progressive lengthening of AH interval greater than 100 ms (Type I) as in a normal AVN; 5 had progressive lengthening of AH interval of less than 50 ms (Type II), 5 had progressive lengthening of AH which then remained stable for a number of heart rates before lengthening again (Type III); 3 had an initial moderate lengthening of the AH interval which then became more rapid (Type IV) and 7 had no change in AH until 120/mn and then a progressive lengthening was observed (Type V). Two functional groups could also be identified depending on whether the lengthening was progressive, suggesting a single nodal pathway (Types I and II) or on whether differing increases were observed related to the atrial rate, suggesting two (Types IV and V) or even three (Type III) atrionodal or intranodal pathways with different refractory periods. Of these 30 patients, only 14 had documented supraventricular tachycardia, 13 being atrial fibrillation and the other a junctional tachycardia. Attenuated nodal behavior does not seem to be a direct cause of supraventricular arrhythmias but these arrhythmias were not tolerated as well because of the special properties of the atrioventricular node.

Adenosine Triphosphate↗