It has been established that there is glucose intolerance in the patients with obstructive jaundice. However, the interaction of insulin and glucagon receptors of hepatic plasma membranes in rats with obstructive jaundice has not been studied. Mechanical cholestasis in rats was induced by double ligation and excision of the common bile duct. Sham-operated rats were referred to as their controls. After 7 days, plasma membranes of rat liver were prepared according to the method of Lesko. As marker enzyme for the plasma membrane, Na^+, K^+-ATPase activity was assayed. The bindings of insulin and glucagon to liver plasma membranes were measured. Specific bindings of ^<125>I-insulin and ^<125>I-glucagon with hepatic plasma membrane in rats with bile duct excision decreased. Kinetic studies by the Scatchard plot analysis of these results revealed decrease in insulin binding affinity and number of glucagon receptors. Activities of Na^+, K^+-ATPase also decreased in bile duct excised rats. These results suggest that alterations in receptors of insulin and glucagon are involved in mechanisms of glucose intolerance in human obstructive jaundice.

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There are many reports on the mechanisms of action of prolactin using mammary tissues. Some of them suggest that prolactin might regulate intracellular calcium concentration. Therefore, the authors examined whether prolactin causes an influx of calcium into mouse mammary cells or not. Since changes in the activity of ATPase in plasma membrane and acceleration of the turnover of phosphatidylinositol might be considered as some of the mechanisms of an influx of calcium into mammary cells, these phenomena were also studied. No significant differences were observed between the group treated with prolactin and the control group in all experiments conducted. Based on the present experimental data, it is considered that prolactin does not cause an influx of calcium into mammary cells.

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In Esherichia coli, most of cellular proteins are synthesized at constant rate through a cell cycle. However, there are a class of proteins such as β-galactosidase encoded by lacZ gene which are synthesized at a specific stage of the cycle. These cell-cycle dependent proteins are found in cytoplasm as well as outer and cell membrane. The previous studies have indicated that synthesis of these cell-cycle dependent proteins is regulated by both gene products of divE and dnaJ, although the precise mechanism is not determined. In order to obtain the molecular mechanism of the regulation, we tried to construct a fusion gene in which the promoter of cell-cycle dependent operon is replaced by that of cell-cycle independent one. The ptrp-lacZ fusion gene plasmid we constructed has regulator regions of tryptophan operon (cell-cycle independent) upstream of lacZ gene (cell-cycle dependent). We determined the nucleotide sequence of ptrp-lacZ and transduced it into bacteria to confirm that its hybrid β-galactosidase protein is synthesized under the control of tryptophan promoter. In the divE mutant which has a temperature sensitive defect of cell-cycle dependent protein synthesis, the chimeric β-galactosidase encoded by the hybrid gene was almost normally synthesized at the non-permissive temperature, in contrust to synthesis of intact β-galactosidase. We examined the in vitro DNA directed β-galactosidase synthesis using λ-dlac and ptrp-lacZ DNA as templates. It was found that the S-30 fraction obtained from the dnaJ mutant grown at permissive temperature had a normal level of β-galactosidase synthesizing activity wheares the S-30 fraction prepared from cells exposed to nonpermissive temperature lost its activity when λdlac DNA as a template. On the other hand, the synthesis of tryptophan promoter mediated chimeric β-galactosidase occurred at normal rates with both S-30 fractions. These results indicate that the temperature sensitive defect in divE and dnaJ mutants has a promoter specificity and resides on transcriptional step of protein synthesis.

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In order to study the pathogenesis of pulmonary fat embolism (PFE), the author investigated the temporal sequence of morphological changes using 92 rabbits divided into three groups : In the first group, triolein (300mg/kg) was infused into the marginal ear vein and in the second group both the triolein (300mg/kg) and tissue thromboplastin (1 mg/kg) were injected simultaneously into the separate ear veins. In the third group, oleic acid (100mg/kg) was used in the similar way. In the first group, fat emboli appeared in the interalveolar capillaries and pulmonary leukostasis occurred in the lumen of small arteries with edema in the perivascular connective tissue. In the second group, fatty acid was histochemically demonstrated in the capillary, essentially with the similar findings as seen in the first group. Furthermore, "intra-alveolitis" and thrombi in small arteries were also manifested. Although neither fat embolism nor pulmonary leukostasis was found in pulmonary vessels in the third group, intense hemorrhagic "intra-alveolitis" with necrosis of the interalveolar septum occurred at first. Then, the intraalveolar lesions were replaced by granulomas with calcium deposits and foreign body giant cells, resulting in formation of the localized fibrous foci. So far, the fatty acid has been considered playing an important role upon the pathogenesis of PFE. From this series of study, the author has realized that the pulmonary leukostasis caused by embolization of fat droplets and the thrombi induced by tissue thromboplastin should not be disregarded as the important factors for the occurrence of PFE.

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Bacteroides fragilis KHM027, which is resistant to penicillins, cephalosporins and oxyiminocephalosporins was examined for the presence of β-lactam antibiotics resistance plasmid. Plasmid DNA isolated by Kado's DNA extraction method was analyzed by agarose gel electrophoresis. This strain was found to harbor four different sizes of plasmid DNA. Two different sizes of the β-lactam antibiotics resistance plasmid were isolated by genetic transformation of Escherichia coli K-12 strain HB101. These plasmids were designated as pBFSK1 and pBFSK2. The molecular sizes of these were 2.6kb for pBFSK1 and 5.8kb for pBFSK2. Genetic and physical analyses were used to characterize the pBFSK1. The major objectives of this study on molecular genetics were to : (1) construct a physical map of the plasmid by restriction endonuclease cleavage studies, (2) map the bla gene region by insertion mutation method, and (3) observe the stability of plasmid in four different E. coli K-12 strains (HB101, JC1569, λ984, C600). Results from restriction endonuclease digestion by a combination of standard approaches, each one site of PstI, EcoRI recognition sequence and two sites of DraI, PvuII recognition sequence were mapped on the pBFSK1 molecule. The putative bla gene region was mapped over the PstI site by insertion mutation of β-lactam antibiotics resistance phenotype. 50 single colonies from each E. coli strain transformed by pBFSK1, were analysed to observe the stability of plasmid. This plasmid pBFSK1 was harbored extremely stable in each E. coli cells. Resistance pattern of each transformants suggests that the bla gene of pBFSK1 is an oxyiminocephalosporinase (CXase) form. Usually, the CXase gene is encoded on chromosome DNAs. It is very interesting that the CXase gene is encoded on the plasmid pBFSK1.

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Identical twins, 23 years in age, were seen to our clinic with chief complaints of multiple tumor nodes palpable in the right breast. When the older and younger sister were examined in 1984, three tumor nodes were found in the right breast with a maximal diameter of 5.2cm and 5.5cm for each case. Under the diagnosis of fibroadenomata, tumor resectomies were done when the pathological diagnosis of fibroadenoma and/or fibroadenoma with tubular adenoma were given. Borderline malignancy was identified in the tumor nodes of the older sister. The sisters were confirmed as the identical twins by means of HLA analysis and blood typing. This gives us a suggestion that the genetic factors should be considered as a cause for the development of neoplasm, especially in case of fibroadenoma mammae.

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Lectin binding sites in the normal human esophageal epithelium were studied by light and electron microscopy using lectins as a probe. Lectins used were concanavalin A (ConA), wheat germ agglutinin (WGA), Ricinus communis agglutinin (RCA), Dolichos biflorus agglutinin (DBA), peanut agglutinin (PNA), soybean agglutinin (SBA), and Ulex europeus agglutinin-1 (UEA-1). For light microscopy, specimens were obtained by autopsy from 37 patients without esophageal disease and malignancy in the upper gastrointestinal tract. The ABC method with biotinyl lectins was employed. ConA diffusely stained all the layers of the esophageal epithelium. WGA and RCA stained the plasma membrane of the cells in all the layers. In some cases, the middle and the superficial layers were intensely stained with WGA, whereas the basal layer was intensely positive for RCA reaction. PNA, SBA and UEA-1 preferentially stained the middle layer. No positive staining for DBA was seen. The specificity of each lectin reaction was confirmed with appropriate cytochemical control experiments. For electron microscopy, specimens obtained by endoscopic biopsy were fixed, frozen-sectioned and incubated with HRP-labeled lectins. Positive reaction for these lectins was found in the plasma membrane, especially along the desmosomes, and also in the Golgi membranes of the epithelial cells. In addition, ConA staining was seen in the nuclear envelope and endoplasmic reticulum also. These results suggest that cell surface sugar residues change during the course of the cellular differentiation from the basal to the superficial layer of the human esophageal epithelium.

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A 71 year-old man was admitted for the closer examination of hypoproteinemia, which was noted at the age of 54. On admission lower limbs were edematous. Serum protein was 4.1g/dl and albumin 2.0g/dl. Urinalysis and liver function tests were negative. The half life of ^<131>I-albumin is shortened to 6.1days. Protein-losing enteropathy was suspected and intestinal clearance of α_1-antitrypsin (α_1-AT) was determined. Fecal content of α_1-AT and α_1-AT clearance rate were 1422mg/day and 569ml/day respectivity, which were remarkably high. These findings suggested plasma protein was leaking into the intestinal tract. Roentogenological study of the jejunum revealed coarse mucosal pattern and biopsy showed dilatation of lymphatic vessels. Lymphography demonstrated no abnormality. Diagnosis of primary proteinlosing enteropathy was done. Measurement of α_1-AT clearance was useful in establishing the diagnosis.

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A 56 years old male with a chief complaint of dyspnea on admission was diagnosed as cardiac tamponade associated with pulmonary adenocarcinoma of lower differentiation type through the subsequent examination. As far as we surveyed only several similar cases of cardiac tamponade with pulmonary carcinoma have been reported in Japan. However, these cases do not include the case like the present one in which CA 19-9 was so high as over 10000U/ml, so that this case was considered as an extremely rare case.

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A 60-year-old female with 7 years history of generalized sarcoidosis and betamethasone therapy developed apparent proteinuria and slight intermittent glucosuria with minor abnormalities of urinary sediments. Oral GTT showed NIDDM. Urinalysis, blood chemistry, serology, and lymphocyte subsets were suggestive of membranous glomerulonephritis with generalized sarcoidosis and steroid-induced hyperglycemia. She died from cardiac arrhythmia 13 years later after the diagnosis of sarcoidosis and autopsy finidings of the kidney revealed diabetic glomerulosclerosis without granulomatous lesions. Although both diabetes mellitus and sarcoidosis are fairly common diseases in America and Europe, no report of diabetic nephropathy has yet been described on a patient with sarcoidosis. Thus, we report the renal histopathology of this case with her clinical course and laboratory data in detail.

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A case of Bartter's syndrome associated with acquired cytomegalovirus (CMV) infection and hydrocephalus was described. A 185 days old boy was admitted to our department for electrolytic disturbances (hypokalemia, hyponatremia, hypochloremia), failure to thrive and progressive ventricuromegaly. He was born at 27 weeks of gestation weighing 1200g. He developed IRDS and was mechanically ventilated for 15 days. No intracranial hemorrahge was found by cranial echography. CMV was cultured in urine at 60 days. Hypokalemia was revealed from 110 days. On admission, his weight was 2150g. Shunt operation was done, however electrolytic disturbances were not improved. Plasma renin activity, aldosterone, angiotensin II were elevated, and metabolic alkalosis was recognized. He was diagnosed as Bartter's syndrome. He was treated with Aldacton-A succsessfully for maintaing serum K without supplement. But at 293 days, he died of purulent meningitis. Renal autopsy specimen showed moderate hyperplasia of the juxtaglomerular cells, tubular hydropic degeneration, and interstitial nephritis.

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Basic principal of our unit about nutritional and repiratory managements of extremely premature infant is discribed. Strict breast milk feeding is indicated during 3-4 weeks after birth and then premature formula is given alternating with breast milk. Sufficient calories for growth will be 120 Cal/kg/day, however total water intake is restricted to 150ml/kg/day until one's body weight becomes 1500 grams. Multivitamin syrup (Popon S) is administered from 2-3 weeks after birth, Iron syrup (Incremin) is given when one's body weight reaches 2000 grams. Intrvenous hyperalimentation will not be indicated actively at this point. Heart and repriratory rate monitoring is indicated for all the exstremely premature infant and infant of less than 34 weeks gestation in order to recognize apneic spells. Low dose oxygen and aminophylline are administered under transcutaneous oxygen monitoring. Continuouse positive airway pressure is indicated when PaCO_2 is more than 60 mmHg under 60% oxygen administration. Mechanical ventilation is indicated when PaCO2 is less than 50 mmHg and/or PaCO_2 is more than 60 mmHg under 100% oxygen therapy and apnea. Administrating oxygen must be fully moistured and warmed. During oxygen therapy. transcutaneous Po_2 and/or blood gases must be monitored.

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