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Vibrio cholerae non-O1 (1148 A) produced β-N-acetylglucosamini-dase and N-acetylglucosamine (GlcNAc) deacetylase intracellularly when grown in chitin or GlcNAc containing medium. It also secreted chitinase only in the chitin-containing medium. The partially purified GlcNAc deacetylase deacetylated GlcNAc but not chitin oligosaccharides, the dimer to hexamer of GlcNAc. We also detected the reaction product by capillary electrophoresis.

This report describes a patient with food-dependent exercise-induced anaphylaxis (FEA). A 25-year-old female has had three episodes of syncopal attack associated with urticaria in the past two years: the attacks have been developed by exercise after taking meals made of wheat flour. She has an allergic predisposition to metals. No abnormal findings were observed in the routine work up for syncope including, ECG, 24-hour Holter ECG, UCG, tilt table test, and EEG examinations. A provocative test for FEA was performed. It included food (sandwich) intake followed by exercise. The serum histamine concentration was elevated to a three times higher than the control value after the provocation. Accordingly, she was diagnosed as FEA and advised not to take wheat flour prior to physical exercise. No syncopal episode has been observed during the 16 months since the diagnosis.

The degree of lung injury in bronchiolo-alveolar lesions may be quantitated from the pulmonary epithelial permeability estimated by 99mTc-DTPA (diethylene triamine penta acetate) aerosol inhalation scintigram. However, significant aerosol deposition sometimes occurs in the central airways and obscures the permeability change in the lung periphery. The radioaerosol deposition pattern and its effect on assessing the pulmonary epithelial permeability was studied. 99mTc-DTPA aerosol scintigraphy was performed in 47 patients with pulmonary fibrosis (PF), 12 patients with chronic obstructive pulmonary diseases (COPD), and 27 non-smoking and 17 smoking healthy volunteers. The scintigraphic images of the lungs were classified into 4 grades, 0; homogeneous distribution, 1; patchy distribution, 2; hot spots with partial defect, and 3; hot spots with little deposition in the lung field. The rate constant was used as a parameter for the permeability. The smokers and patients with PF showed increased kep values of 2.36 +/- 1.21%/min (mean +/- SD) and 2.49 +/- 1.29%/min as compared with the nonsmokers with 0.94 +/- 0.27%/min, respectively. The nonsmokers, smokers and 36 patients with PF were classified as deposition grade 0 or 1, suggesting good aerosol penetration to the lung periphery. All patients with COPD showed either grade 2 or 3 deposition. Aerosol deposition in the central airways can cause underestimation of the permeability because of the thicker lining layer in the bronchus than in the alveolus. In conclusion, the aerosol deposition pattern should be analyzed when the method is applied clinically to assess the permeability of the bronchiolo-alveolar epithelium.

Neutrophils are possibly involved in the pathogenesis of various lung diseases through the release of numerous mediators. In the present study, we studied the regulation of IL-8 gene induction and protein secretion in human blood neutrophils. Northern blot analysis revealed that LPS increased IL-8 mRNA levels in neutrophils, with a maximal fivefold increase by 2 h. IL-8 mRNa levels returned to baseline values within 12 h. In contrast, LPS-stimulated monocytes demonstrated a sustained increase of IL-8 mRNA levels for more than 24 h. TNF-alpha, IL-1 beta, and phorbol myristate acetate also increased IL-8 mRNA levels in neutrophils. Immunohistochemical analysis confirmed that IL-8 was localized within stimulated neutrophils. IL-8 secretion by neutrophils and monocytes was quantified using a specific ELISA for IL-8. Resting neutrophils secreted minimal IL-8 activity. However when cells were stimulated with LPS, TNF-alpha, or IL-1B, neutrophils secreted IL-8. IL-8 secretion was most marked during the first 2 h after stimulation and decreased thereafter. In contrast, monocytes maintained a high rate of IL-8 secretion over 12 h. Although a single monocyte secreted 70-fold more IL-8 than did a single neutrophil after 4 h of incubation, the high abundance of neutrophils in peripheral blood made the neutrophil-secreted IL-8 more significant. During the first 2 h, neutrophils secreted approximately 40% of the IL-8 released by monocytes in the same volume of blood. This ratio decreased to 9% after 12 h. Neutrophil-secreted IL-8 may play an autocrine or paracrine role during the initial stage of inflammation.

To evaluate whether one can predict the course and prognosis of interstitial lung diseases from lung gallium-67 (67Ga) uptake, we studied 31 subjects with sarcoidosis and 28 with idiopathic pulmonary fibrosis (IPF) retrospectively. We quantified the lung 67Ga uptake using posterior scans by Line's method, and calculated a visual index (VI). The normal range of 67Ga uptake was defined as less than 65 VI values, obtained from the 95 percent confidence interval of the control subjects. All subjects with stage I sarcoidosis, having only bilateral hilar lymphadenopathy (BHL) on chest X-ray, revealed normal lung 67Ga uptake. Fifty percent of patients with stage II sarcoidosis, with both BHL and pulmonary involvement on chest X-ray, showed increased lung 67Ga uptake. The patients with increased lung 67Ga uptake showed decreased percent vital capacity and increased alveolar-arterial oxygen tension difference, but none of them showed clinical deterioration during the follow-up period of more than 6 months. Fifty-four percent of subjects with IPF showed increased lung 67Ga uptake. But there was no difference between the subgroups with normal and increased lung 67Ga uptake with respect to the severity of dyspnea, percent vital capacity, arterial oxygen tension, or alveolar-arterial oxygen tension difference. There was also no difference between the two subgroups of IPF in the cumulative percent survival after either the onset of symptoms or the 67Ga scintigram. We conclude that lung 67Ga uptake was not able to predict the clinical course or the prognosis of patients with sarcoidosis and IPF.

Increased vascular permeability in the adult respiratory distress syndrome is due in part to toxic oxygen metabolites. In the present study, we produced lung injury in the isolated rabbit lung with hydrogen peroxide (H2O2) and examined its prevention with isoproterenol. Pulmonary arterial pressure (Ppa) and the fluid filtration coefficient (Kf) were measured as indices of lung injury. Rabbits were divided into two groups, and 7 mmol/l H2O2 was administered in both groups. In one group, isoproterenol (2 micrograms/ml) was administered 10 min before H2O2 injury. Ppa increased transiently after H2O2 administration in the control group but was unchanged in the isoproterenol group. Kf was significantly increased by H2O2 administration in the control group but not in the isoproterenol group. We conclude that H2O2 increases pulmonary vascular permeability and that isoproterenol may protect against H2O2-induced pulmonary injury.

We report 2 cases of renal artery aneurysms in congenital solitary kidneys, which were treated respectively by in situ and ex situ aneurysmectomy. Hyperosmolar intracellular electrolyte solution was valid in preserving renal function during renal ischemia in both cases. The occurrence of an aneurysm in a solitary kidney, ex situ operation and renal preservation during ischemia are discussed.

To clarify the possible risk factors for the development of hypertension, we examined the influences of heredity and environment on blood pressure regulation and whether or not the physiological condition differed in high school students with different levels of blood pressure. A borderline hypertensive (BH) group, consisting of 75 male students with systolic blood pressure (SBP) consistently above 140 mmHg on two separate occasions, was compared to a normotensive (N) group of 84 male students with SBP below 130 mmHg. In the BH group, 43% of students had a family history of hypertension within two generations of relatives, while 18% had one in the N group (p less than 0.05). The BH group was characterized by a gain in weight, a slight increase in 24-hour urinary sodium excretion, a higher heart rate, elevated values of plasma renin and urinary aldosterone, and an elevated sodium concentration in erythrocytes. Nevertheless, urinary excretion of potassium and kallikrein did not differ between the two groups. In each group, students with familial hypertension had a significantly (p less than 0.05) lower 24-hour urinary kallikrein excretion than those without it. Although kallikrein excretion correlated fairly well with aldosterone excretion (r = 0.47, p less than 0.01) or creatinine clearance (r = 0.59, p less than 0.01) in the BH students without familial hypertension, no such correlations were found in those with familial hypertension. These results indicate that the abnormal relationships of aldosterone to kallikrein metabolism and of kallikrein to renal function control may be involved as hereditary factors in the development of hypertension.

Electrolyte concentrations in the erythrocytes, serum and 24-hr urine were measured in 34 untreated essential hypertensives (EH), 32 normotensives with a family history of hypertension (N+), 112 normotensives without a family history of hypertension (N-), 76 senior high school students with high blood pressure (H) and 110 students with normal blood pressure (C). For the measurement of intra-erythrocyte electrolytes, a new method to decrease the trapped plasma was developed and adopted. A new simple method to collect 24-hr urine was devised, too. The results were as follows: 1) The sodium concentration [Na] and the ratio of [Na] to potassium concentration [Na/K] in the erythrocytes were significantly higher in the EH and N+ than in the group of N- (p less than 0.01). 2) There was a positive correlation (r = 0.43) between the [Na/K] in the serum and erythrocytes in the 3 groups. The [Na/K] value in the erythrocytes to a given [Na/K] value in the serum was higher in EH than in the group of N-. 3) When the group of H was compared with C, the Na excretion of the 24-hr urine in the former group was found to be slightly higher, and the [Na/K] of the 24-hr urine and the [Na] and [Na/K] values of the erythrocytes were significantly higher, too. It may therefore be said that an increase in the intracellular [Na] or [Na/K], which may be caused genetically, and an excess of Na intake and an increase of the ratio of Na/K intake are presumed to play an important role in the pathogenesis of essential hypertension.

The protective effect of xanthines against E. coli-induced and cytokine-induced lung injury in guinea-pigs has been demonstrated recently. In the present study, the possible protective effects were examined of an analogue of pentoxifylline, HWA-138, a xanthine derivative, on lung injury in septic guinea-pigs. Three groups of animals were studied over a period of 8 hours: Group I animals--saline control injected intravenously with 3 ml 2% lysine/normal saline followed by a continuous lysine/saline infusion (1 ml/kg/hr); Group II--septic control injected intravenously with 2 x 10(9)/kg Escherichia coli followed by a continuous lysine/saline infusion (1 ml/kg/hr); and Group III--E. coli septicaemia plus HWA-138 continuous infusion (HWA-138 dissolved in lysine/saline) began with a bolus (10 mg/kg) followed by a HWA-138 continuous infusion (3 mg/kg/hr) started 60 minutes before injection of E. coli. Arterial blood pressure and white blood cell counts were monitored serially for 8 hours. Lung water (wet-to-dry ratio) and the concentration ratio of 125I-labelled albumin in bronchoalveolar lavage (BAL) fluid and lung tissue compared to plasma (125I-albumin BAL/plasma, 125I-albumin lung/plasma) were examined. Results demonstrated that an intravenous injection of E. coli caused an increased W/D ratio (p less than 0.01) and an increased 125I-albumin lung/plasma ratio (p less than 0.01). In contrast, the HWA-138-treated group did not demonstrate significantly increased W/D lung ratios (p less than 0.01) and 125I-albumin lung/plasma ratios (p less than 0.05). The data suggest a possible role for HWA-138 in attenuating sepsis-induced lung injury.

We studied the use of single photon emission computed tomography (SPECT) for evaluating lung image and measuring lung tissue volume, in a lung phantom and healthy volunteers. Three conditions of image processing were tested using the phantom, and found out a backprojection method with using a Shepp-Logan filter and a pre-reconstruction smoothing of 3 X 3 pixels to be suited. A lung tissue volume was estimated from the summation of voxels in the region where the SPECT value was greater than an arbitrary threshold level. We changed phantom lung density from 0.34 g/cm3 to 0.58 g/cm3, but there was no significant effect in the estimated volume by the density change. Changes in the lung SPECT images and lung tissue volumes in healthy subjects were studied, after changing the lung volume by applying either continuous negative body-surface pressure (CNP) to the thorax or positive end-expiratory pressure (PEEP). Difference of the lung expansion in the two methods was visualized by the SPECT images. The lung tissue volumes obtained by SPECT were correlated with the functional residual capacity by Helium dilution method (r = 0.91, p less than 0.001). We concluded that lung SPECT could be used clinically to display the distribution of a tracer radio-isotope in the lungs and also used to estimate the lung tissue volume.

Relationships between renal haemodynamics and the renin-angiotensin system were examined in 128 male adolescents with differing predispositions to hypertension. Baseline renal vascular resistance (RVR) was significantly elevated in the normotensive subjects with a positive family history, NT (FH+) group, than in the normotensives with a negative family history, NT (FH-) group, while there were no significant differences in other characteristics between the two groups. The borderline hypertensive subjects with a positive family history, BH (FH+) group, showed an even bigger increase in RVR and also had elevated plasma renin activity (PRA). In the NT (FH+) and BH (FH+) groups RVR correlated significantly with PRA levels. When captopril was given, the increased RVR in the NT (FH+) and BH (FH+) groups decreased, in correlation with baseline PRA, to levels not significantly different from those in the NT (FH-) group, in which no significant changes occurred in RVR. These results suggest that RVR may increase primarily in adolescents genetically predisposed to essential hypertension and that the renin-angiotensin system may play an important role in the mechanism of this increase in RVR.