ÜBER DIE IDIOPATHISCHE KARDIOMYOPATHIE – PATHOLOGISCHE UNTERSUCHUNG VON 16 FÄLLEN –

The present study consists of 16 cases of idiopathic cardiomyopathy ranging between 7 to 68 years of age. All cases demonstrated moderate degree of dilatatory hypertrophy of both ventricles with some having mural thrombosis. Over-all distribution of scar and degeneration of heart muscle cells was considered to be the characteristic features of idiopathic cardiomyopathy. A variety of transitional changes between myocardial degeneration and collagenous scars were found in the younger age group, and fall-off of myocardium was interpreted to result in scar formation. Hypertrophy of heart muscle cells is a compensatory phenomenon following partial fall-off of muscle cells. Vacuolar changes, deposition of waxlike substance and bizarre nuclei found in the hypertrophic muscle cells are in general not characteristic for this condition.
One must be careful in differentiating idiopathic cardiomyopathy and mitral insufficiency having multiple scars and of rheumatic nature from both clinical and pathologic standpoints.
Endocardial fibroelastosis should not be included in the entity of idiopathic cardiomyopathy, since the role played by the myocardium in the pathologic process is much less in endocardial fibroelastosis. ACTA PATH. JAP. 20: 153–169, 1970.     

Comparative Study on Inclusion Complexation of Maltosyl-β-cyclodextrin,Heptakis(2,6-di-O-methyl)-β-cyclodextrin and β-Cyclodextrin with Fucosterol in Aqueous and Solid State

Abstract— The complexation of fucosterol with three kinds of β-cyclodextrin (β-CyD) was investigated in aqueous solution and in the solid state. The solubility of fucosterol increased significantly on its complexation with maltosyl-β-CyD and heptakis(2,6-di-O-methyl)-β-CyD (DM-β-CyD), while no appreciable increase was observed when complexed with β-CyD. The stability constant of complexation with β-CyD estimated from solubility determinations was greater for a 1:2 complex than for a 1:1 complex. On the other hand, 1:1 complexation of fucosterol with maltosyl-β-CyD or DM-β-CyD was greater than 1:2 complexation. The solid complexes were obtained in molar ratios of 1:2 and 1:3 for β-CyD and maltosyl-β-CyD complexes, respectively. The inclusion behaviour of fucosterol with maltosyl-β-CyD was compared with β-CyD in the solid state using DSC, powder X-ray diffractometry and CP/MAS ¹³C NMR. Maltosyl-β-CyD showed different inclusion behaviour compared with β-CyD, and produced an amorphous structure of fucosterol on complex formation. The dissolution rate of fucosterol-maltosyl-β-CyD complex was significantly faster than other complexes due to its high aqueous solubility and amorphous structure.     

Biopharmaceutics: Cytotoxicity of Absorption Enhancers in Caco-2 Cell Monolayers

This study was performed to evaluate the utility of absorption enhancers with reference to mucosal cell cytotoxicity. Overall assessment of the damage to plasma, lysosomal and nuclear membranes by three absorption enhancers, sodium deoxycholate, sodium caprate and dipotassium glycyrrhizinate, was performed on Caco-2 cell monolayers. The cytotoxicities of sodium deoxycholate (0.02–0.1% w/v), sodium caprate (0.1–0.5% w/v) and dipotassium glycyrrhizinate (0.5–2% w/v) were evaluated by the trypan blue-exclusion test, the protein-release test, the neutral-red assay, the DNA-propidium iodide staining test and the test for recovery of transepithelial electrical resistance (TEER) up to 24 h after treatment with each enhancer. Sodium dodecyl sulphate (SDS; 0.1% w/v), a potent surfactant, was used as positive control. SDS at this level was significantly cytotoxic whereas dipotassium glycyrrhizinate was not cytotoxic in any tests. Results from the trypan blue-exclusion and protein-release tests showed that high concentrations of sodium caprate (0.5% w/v) and sodium deoxycholate (0.1% w/v) were significantly cytotoxic to the plasma membrane. The neutral-red assay, an indicator of damage to lysosomal membranes, revealed that 0.5% (w/v) sodium caprate had no effect whereas the uptake of neutral red was slightly increased by treatment with 0.1% (w/v) sodium deoxycholate, implying that the compound had cell-growth-enhancing activity. Nuclear-membrane damage, as evaluated by the DNA-propidium iodide staining test, was severe in cell monolayers treated with 0.5% (w/v) sodium caprate compared with that induced by 0.1% (w/v) sodium deoxycholate. In the TEER recovery test, TEER failed to recover 24 h after treatment with 0.5% (w/v) sodium caprate and 0.1% (w/v) SDS, but recovered after treatment with 0.1% (w/v) sodium deoxycholate. The recovery of TEER might be related to nuclear membrane damage and cell-growth-enhancing activity. These results indicate that of the three classes of enhancer, dipotassium glycyrrhizinate was not cytotoxic and that high concentrations of sodium caprate and sodium deoxycholate could damage plasma and nuclear membranes.     

Gastric vascular ectasia treated by endoscopic mucosal resection

An 80‐year‐old woman consulted our hospital complaining of general weakness. She had iron deficiency anemia, and upper gastrointestinal endoscopy revealed a small lesion accompanying a small amount of fresh bleeding in the stomach. Close observation of the lesion revealed that it was composed of a local assembly of dilated microvessels. The diagnosis of this patient was gastric vascular ectasia causing anemia. Endoscopic ultrasonography demonstrated that the lesion involved the mucosal and submucosal layers of the stomach, and that there were no large vessels inflowing to or outflowing from the lesion. In the present case, we attempted endoscopic mucosal resection (EMR). The lesion was completely resected by only one procedure of EMR without complications such as bleeding. After the endoscopic treatment, iron deficiency anemia improved. Follow‐up endoscopy performed 1 year later revealed that there was no residual or recurrent lesion. Although there have not been any published reports describing the use of EMR for gastric vascular ectasia, EMR may be a useful endoscopic treatment for this condition.