A chromosomal locus encoding a phosphoserine phosphatase- and a truncated MinD-like protein affects differentiation in Streptomyces azureus ATCC14921.

We isolated BalA1, a representative transformant of thiostrepton-producing strain Streptomyces azureus ATCC14921, which carries an approximately 2.5-kb chromosomal DNA fragment on a high-copy-number plasmid. While strain BalA1 formed little aerial hyphae, its morphological defect was restored by cultivation with S. azureus, S. laurentii, etc. Strain BalA1 strongly inhibited the growth of Bacillus subtilis more than its parent strain, and also inhibited the development of its parent and some Streptomyces strains with thiostrepton resistance. Furthermore, it induced Streptomyces coelicolor A3(2) to produce undecylprodigiosin, at an early stage of growth. The 2.5-kb fragment contained two orfs, orf1 and truncated orf2. The deduced products were somewhat similar to phosphoserine phosphatase-like protein and the N-terminal region of MinD-like protein, respectively. The individual function of orf1 or the function of both orf1 and truncated orf2 seems to induce particular phenotypes or properties in strain BalA1.

[Arachnoid cyst of the middle cranial fossa with extraocular muscle paresis: case report].

Arachnoid cysts in the middle cranial fossa usually present with skull deformity, intracranial hypertension, epilepsy, focal symptoms and delayed mental development. Some cases, however, have neither symptoms nor signs. We have encountered a patient with an arachnoid cyst of the middle cranial fossa with extraocular muscle paresis and who was treated with cyst wall fenestration with good results. An 11-year-old boy presenting with double vision was diagnosed as having an arachnoid cyst in the middle cranial fossa with extraocular muscle paresis. He had no signs of increased intracranial pressure. This patient underwent a cyst membranectomy. Postoperatively this symptom rapidly subsided. Double vision disappeared two months postoperatively. To our knowledge, if those cases associated with increased intracranial pressure signs are excluded, this is the first case reported so far of a middle cranial fossa arachnoid cyst with extraocular muscle paresis. This report illustrates that extraocular muscle paresis can be caused by an arachnoid cyst in the middle cranial fossa and that knowledge of this could be helpful in its early diagnosis and treatment.

An autopsy case of Crow-Fukase syndrome which developed 18 years after the first manifestation of plasmacytoma.

A 57-yr-old woman developed Crow-Fukase syndrome 18 yr after resection of plasmacytoma of the rib. Irradiation applied to the relapsed plasmacytoma and systemic chemotherapy alleviated symptoms and signs, but the tumor relapsed in the unirradiated cervical lymph node and she died of Pseudomonas pneumonia during chemotherapy 3 yr after diagnosis. Biopsy of the lymph node revealed proliferation of IgG-lambda-positive atypical plasma cells while autopsy revealed plasmacytoma remnant in the pleura of the affected side 21 yr before. No amyloid was found on autopsy. Crow-Fukase syndrome can develop long after the origination of plasmacytoma.

[Right ventricular dysplasia: clinical characteristics of five patients].

The purpose of this study was to elucidate the clinical features of right ventricular (RV) dysplasia, a recently described clinical entity characterized by RV myopathic changes and ventricular tachycardia of left bundle branch block morphology. Five cases were reported, in which the diagnosis was established according to the criteria of Marcus. Case 1, a 33-year-old man, was referred to us for evaluation of his paroxysmal ventricular tachycardia of five years duration. Case 2, a 38-year-old man, was admitted because of shock caused by ventricular tachycardia. In both cases, the QRS configurations during ventricular tachycardia were those of the left bundle branch block pattern, and electrocardiograms during sinus rhythm showed T wave inversions in the right precordial leads and late ventricular potentials. Two-dimensional echocardiography, radionuclide angiography and contrast angiography disclosed RV dilatation and dysfunction with normal left ventricular (LV) function. The biopsied myocardium from the right and left ventricles in Case 2 revealed myocytolysis, a paucity of myofibrils and proliferation of collagen fibers. Case 3, a 73-year-old woman began to experience exertional dyspnea since 16 years of age. Her treatment consisted of bed rest, diuretics and digitalis. In December 1983, her New York Heart Association functional class was III, and physical examinations disclosed a Levine III/VI systolic murmur suggestive of tricuspid regurgitation, jugular vein dilatation, hepatomegaly, and pretibial edema. Electrocardiogram showed atrial fibrillation, incomplete right bundle branch block and T wave inversions in the precordial leads. Chest radiograph revealed marked cardiomegaly (cardiothoracic ratio of 92%). Echocardiography, radionuclide angiography and contrast angiography revealed marked RV dilatation, depressed ejection fraction (RV end-diastolic volume index of 342 ml/m2, and RV ejection fraction of 28%). Case 4, a 20-year-old man, was admitted with a chief complaint of palpitation. Case 5, a 19-year-old man, was referred to us for the evaluation of asymptomatic cardiomegaly, and his cardiothoracic ratio was 54%. A 12-lead electrocardiogram showed right bundle branch block and T wave inversions in the right precordial leads. Ambulatory electrocardiography revealed frequent premature ventricular complexes of the left bundle branch block pattern. Echocardiography, radionuclide angiography, and contrast angiography disclosed RV dilatation and dysfunction in both cases, and mild LV dilatation and dysfunction (LV end-diastolic volume index of 149 ml/m2, LV ejection fraction of 48%) in Case 4.(ABSTRACT TRUNCATED AT 400 WORDS)