Repeated Laparoscopy of 27 Patients with Chronic Non-A,Non-B Hepatitis Showing a Complete Response to IFN Therapy

The laparoscopies and liver histology results of 27 patients with chronic non-A, non-B hepatitis who had a complete response to the longterm administration of IFN-alpha were studied. When comparing the liver surface before IFN therapy, code number 1 using Shimada's classification, i. e., whitish markings, increased from 14.0% to 57.9%, code number 2, i. e., dilated vessels, decreased from 34.9% to 10.6%, code number 4, i. e., reddish markings, decreased from 11.6% to 2.6%, and code number 7, i. e., patchy markings, decreased from 16.3% to 2.6%. Improvement of the liver edge dullness and a decrease of the liver consistency after the IFN therapy were also observed in 40. 7%, and 14. 8% of the patients, respectively. Liver histology after the therapy showed normal liver or liver fibrosis in chronic hepatitis patients, and liver cirrhosis with active hepatitis developed into liver cirrhosis without activity. The hepatitis activity index score decreased significantly after the therapy. The present report seems to be the first which describes detailed changes of the liver surface before and after IFN therapy in patients with chronic non-A, non-B hepatitis who had a complete response to the therapy     

Risk Factors For Duodenal Ulcer Recurrence: Three-year Follow-up during Famotidine Maintenance Therapy

The recurrence-free rate and factors related to recurrence after healing were investigated in duodenal ulcer patients on H₂-blocker maintenance therapy with famotidine. Famotidine maintenance therapy (20 or 40 mg once a day before bedtime) was performed in 488 evaluable patients after endoscopically-proven healing of ulcers (S₁ or S₂). The cumulative recurrence-free rates were 81.1%, 65.1% and 58.2%, respectively, after one, two and three years of maintenance therapy. Among various background factors, those which have been suggested to be closely associated with ulcer recurrence were compared on the basis of their relation to the recurrence-free rate. These factors included a past history of duodenal ulcer, smoking, alcohol use, bulbar deformation, the endoscopic stage of ulcer healing, concomitant drugs and compliance with famotidine therapy. Recurrence correlated most significantly with a past history of duodenal ulcer and with compliance. Compliance was categorized as excellent, good, fair or poor. The recurrence-free rate was significantly lower in patients with excellent compliance than in any other compliance group. A famotidine dose of 40 mg/day (the standard dose), versus the half dose of 20 mg/day, produced no significant difference in the cumulative recurrence-free rate and it was therefore suggested that 20 mg/day of famotidine is comparable to 40 mg/day in its preventive effect on duodenal ulcer recurrence. In addition, because recurrence was more common in patients who had previously experienced recurrence, a past history of ulcer was suggested to be a significant risk factor for ulcer recurrence.     

The Distribution of Tenascin in Rat Embryos with Normal Heart and Cardiovascular Anomalies Induced by Bis-Diamine

The mesenchyme in the truncal ridge and aortico-pulmonary (A-P) septum in the developing heart expresses tenascin (TN), a component of extracellular matrices. We observed immunohistochemically the localization of TN with reference to fibronectin (FN) distribution in rat embryonic hearts at gestation days 12. 13 and 14 and compared the results with those in bis-diamine-induced cardiovascular anomalies. In control rat embryonic hearts, TN was distributed in the dorsal mesocardium and the distal part of the truncal ridge at gestation day 12, and in part of the conal and truncal ridges, A-P septum and proximal wall of aortic arch arteries at gestation days 13 and 14. The conotruncal regions with TN expression may correspond to the areas where cardiac neural crest cells migrate in the heart. In bis-diamine-treated rat hearts showing conotruncal anomalies, TN was localized in incompletely fused and hypoplastic conotruncal ridges, but the intensity and area of staining were decreased suggesting a decreased neural crest cell migration. FN was diffusely distributed in both the normal and anomalous embryonic hearts, including atrioventricular cushion tissue in addition to the region expressing TN. TN was densely distributed in the fusing area of the conal and truncal ridges in comparison to FN, suggesting that TN may be mainly expressed during the time of fusion of conal and truncal ridges to form the A-P septum in the embryonic heart. In conclusion, bis-diamine may cause the poor development of neural crest derived tissue, subsequently bringing about hypoplasia of the A-P septum and truncal and conal ridges.     

The Coordination of Gastrointestinal Hormones and the Autonomic Nerves

We have conducted investigations on the relatinship between gastro-intestinal hormones and the autonomic nervous system. In this paper are described main themes of our investigations where a close association between gastrointestinal hormones and the autonomic nervous system was shown from the functional and morphological points of view.
The "nervism" proposed by Pavlov, where the regulation of various organs in the body was thought to be accomplished wholly by the nervous system was based on the findings on the physiology of the digestive glands. In the meantime, the discovery of secretin from the duodenal mucosa led Bayliss and Starling to propose a chemical co-ordination or a humoral regulatory mechanism in additioin to the nervous system for the regulation of the various organs in the body. It is indeed surprising that the principle of two major regulatory mechanisms in the body was thus developed originally on the basic studies of the exocrine and body was thus developed orginally on the basic studies of the exocrine and endocrine funtion of the digestive system.
Our investigations reported in this paper disclosed the fact that the neural and humoral regulatory mechanisms for gastrointestinal secretions acted not separately but in close association both morphologically and functionally.     

Deletion analyses of SMN1 and NAIP genes in Malaysian spinal muscular atrophy patients

BACKGROUND: The survival motor neuron 1 (SMN1) gene has been recognized to be responsible for spinal muscular atrophy (SMA) because it is homozygously deleted in more than 90% of SMA patients, irrespective of their clinical severity, whereas the neuronal apoptosis inhibitory protein (NAIP) gene is now considered to be a modifying factor of the severity of SMA. In Malaysia, it remains to be elucidated whether deletion of the SMN1 gene is also a main cause of SMA or whether deletion of the NAIP gene is found in the SMA patients. METHODS: To clarify the pathogenesis of SMA in Malaysia, a deletion analysis of the SMN1 and NAIP genes was performed in 24 Malaysian SMA patients. Deletion analysis of exons 7 and 8 of the SMN1 gene was performed according to the method described by van der Steege et al., while deletion analysis of exon 5 of the NAIP gene was performed according to a method described by Roy et al. RESULTS: Homozygous deletion of SMN1 exon 7 and exon 8 were identified in 19 out of 24 patients (79%). As to the NAIP gene, deletion of exon 5 was detected in six out of 24 patients (25%). NAIP gene deletion was correlated with severity of the disease. CONCLUSIONS: Deletion of the SMN1 exon 7 is a major cause of SMA in Malaysia, and NAIP gene deletions are not rare in type I SMA in Malaysia. The lower percentage of the SMN1 gene deletion may be due to the possibility that the present study included some patients without SMN1 gene abnormality and/or some patients with non-deletion type mutations in the SMN1 gene.