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An essential mission of life cycle management (LCM) is to manage the life time of a target system by understanding its states. Since LCM is becoming digitalized and various data throughout a product life cycle can be collected, a data-driven approach such as machine learning has been used. However, a data-driven approach has some drawbacks: a large volume of required data and so called “black box” problem of reasoning results. This paper proposes a model-based approach for condition-based maintenance, where deterioration simulation is executed. The deterioration simulation enables to examine all possible state changes when each part is deteriorated.

Protein separation was performed using the high-speed countercurrent chromatograph (HSCCC) at both synchronous and nonsynchronous type-J planetary motions. The partition efficiency was evaluated with two different column configurations, eccentric coil and toroidal coil, on the separation of a set of stable protein samples including cytochrome C, myoglobin and lysozyme with a polymer phase system composed of 12.5% (w/w) polyethylene glycol 1000 and 12.5% (w/w) dibasic potassium phosphate. Better peak resolution was obtained by the eccentric coil than by the toroidal coil using either lower or upper phase as the mobile phase. The peak resolution was further improved using the eccentric coil by the nonsynchronous type-J planetary motion with the combination of 1066 rpm of column rotation and 1000 rpm of revolution.

Most pandalid shrimps exhibit protandric hermaphroditism, and detailed information on ovarian development of pandalid species is important for a better understanding of vitellogenesis in crustacean species. In the present study, we characterized ovarian development under light and electron microscopy and examined the hemolymph vitellogenin levels in the coonstriped shrimp, Pandalus hypsinotus under laboratory conditions. To measure vitellogenin levels, a time-resolved fluoroimmunoassay (TRFIA) was developed after purification of vitellin and production of the anti-vitellin antiserum. The TR-FIA showed wide assay range (0.98-2000 ng/ml), high sensitivity (0.5 ng/ml), and low assay variability (0.9- 6.4% of intraassay coefficients, 1.4-5.1% for interassay coefficients). Female P. hypsinotus had non-vitellogenic ovaries in March after the eggs attached to the abdomen hatched, and started yolk accumulation in the ovaries during April-October. During yolk accumulation, yolk globules appeared and increased in the ooplasm. After yolk accumulation, gonadosomatic index (GSI) reached 8.3-8.5 just before oviposition. Females spawned and were ovigerous during June-July of the next year. Hemolymph vitellogenin levels were low (0.006 ± 0.008 mg/ml, mean ± SD) before the yolk accumulation, and became significantly higher (2.66 ± 0.93 mg/ml) during yolk accumulation (GSI, 2-8). Just before oviposition, levels declined to low levels (0.040 ± 0.012 mg/ml). Vitellogenin levels were significantly correlated to GSI during the yolk accumulation. The obtained results show that the process of vitellogenesis during the female phase of P. hypsinotus is similar to other crustacean species that do not change sex. [ABSTRACT FROM AUTHOR]

The current study was undertaken to compare the organ protective effects of an angiotensin-converting enzyme inhibitor, temocapril, with those of an angiotensin II type 1 receptor antagonist, CS-866 (olmesartan medoxomil), alone or combined, in the remnant kidney model of rats. Eight-week-old spontaneously hypertensive male rats were subjected to five-sixths nephrectomy. At the age of 10 weeks, the rats were randomly allocated to groups that received two doses of CS-866 (CS-L, 3 mg/kg/day; CS-H, 10 mg/kg/day), temocapril (TEM, 10 mg/kg/day), CS-866 (3 mg/kg/day) plus temocapril (10 mg/kg/day), or a vehicle alone (untreated control group). Systolic blood pressure (SBP) and urinary protein excretion (UprotV) were measured every 2 weeks. When the rats were 18 weeks old, biochemical measurement and histologic examination were performed. All the drug treatments significantly reduced SBP, UprotV, glomerular sclerosis index (GSI), relative interstitial volume (RIV), and heart weight. The hypotensive effects were on the order of combination therapy > CS-H TEM > CS-L. Correlational analysis was based on the values for SBP and UprotV derived from the average of values obtained when the rats were 12 to 18 weeks of age. UprotV, GSI, and RIV were found to be highly correlated with SBP among the individual rats pooled from all the groups, and the correlation was maintained among the group means. A similar correlation was found between heart weight and SBP. The results suggest that the organ protective effects of temocapril, CS-866, and combination therapy are closely related to the magnitude of their antihypertensive effects.

Patients with chronic renal failure are restricted to mild physical activity and tend to a lack of exercise. However, there have been few reports regarding the influence of chronic exercise on the progression of renal disease. Similarly, there are few animal models concerned with the effect of exercise training on improving renal function. Therefore, we assessed the renal effects of moderate chronic treadmill exercise in a remnant kidney model of spontaneously hypertensive rats (SHR) with chronic renal failure. We also assessed the effects of exercise and antihypertensive therapy on renal function.

The insulin resistance state is common in humans and animals with chronic renal failure. We investigated the effects of troglitazone, an insulin sensitizer, on blood pressure and nephropathy in the remnant kidney model of spontaneously hypertensive rats (SHR).

Inhibition of neutral endopeptidase (NEP) in the kidney was studied ex vivo after oral administration of candoxatril (UK79300), an NEP inhibitor, to rats to study the time course and dose response by quantitative in vitro autoradiography by using the NEP inhibitor 125I-SCH47896 as a radioligand. In control rats, high NEP binding was demonstrated in the deep proximal tubule. After oral administration of candoxatril (10 mg/kg), kidney NEP binding was rapidly decreased and recovered gradually over a period of 24 h. The inhibition was maximal at 1 h (13.3 ± 2.5% of control). Increasing doses of candoxatril administered to rats produced progressive inhibition of NEP binding in the kidney. A dose of 100 mg/kg inhibited kidney NEP binding to 2.6 ± 0.2% of the control value at 1 h after administration. Candoxatrilat (UK73967), an active metabolite of candoxatril, given intravenously inhibited kidney NEP binding also in a time- and dose-dependent manner. This inhibition of NEP activity at the tissue level may be important in the actions of NEP inhibitors.

To assess the renal benefits of cicletanine (CIC) in diabetic rats with renal impairment.

Abstract A 61‐year‐old woman with chronic lymphocytic leukaemia (CLL) was found to have multiple pulmonary nodules on an annual chest radiograph 4 months after recovery from chickenpox. To exclude the metastatic carcinoma, an open lung biopsy was performed. Histological examination disclosed isolated necrotic nodules surrounded by some lymphocytes and a few giant cells. These histological findings were compatible with healed varicella pneumonia and the DNA of varicella‐zoster virus (VZV) was detected by polymerase chain reaction (PCR) method. We report a case of asymptomatic pulmonary involvement of VZV infection in a patient with CLL.

It is well known that angiotensin-converting enzyme inhibitors attenuate progressive ventricular enlargement or hypertrophy after myocardial infarction and that cardiac angiotensin-converting enzyme activity is increased in the rat model of myocardial infarction. In this study, to determine whether the beneficial effects of angiotensin-converting enzyme inhibition on cardiac hypertrophy after myocardial infarction are due to a reduction in ventricular afterload or to inhibition of cardiac angiotensin-converting enzyme, we used sodium loading during angiotensin-converting enzyme inhibition. The rat model of myocardial infarction was treated with a vehicle, 1% saline, as drinking fluid, perindopril (2 mg/kg/day), or 1% saline as drinking fluid plus perindopril (2 mg/kg/day) for 6 weeks. Perindopril reduced blood pressure, prevented cardiac hypertrophy, and inhibited cardiac angiotensin-converting enzyme. The effects of perindopril on blood pressure and cardiac hypertrophy were abolished by sodium loading, which did not alter the degree of cardiac angiotensin-converting enzyme inhibition. Thus the actions of perindopril on cardiac hypertrophy depend more on blood pressure reduction than on cardiac angiotensin-converting enzyme inhibition in the rat model of myocardial infarction.

To assess the potential of the kallikrein-kinin and renin-angiotensin systems in mediating the cardio- and renoprotective effects of angiotensin converting enzyme (ACE) inhibitors in rats with chronic renal failure.

A severe case of arteriosclerosis was observed in a female Japanese bantam (Gallus gallus) associated with Marek's disease (MD) infection. The hen, showing clinical, macroscopic and microscopic evidence of MD infection, harbored arteriosclerosis in the aorta and large arteries characterized by an extremely thickened intima and marked luminal occlusion. Proliferating cell nuclear antigen (PCNA) immunostain-ing showed many labeled nuclei in the thickened intima, and less frequent positivity in the media. This is the first report on avian arteriosclerosis in natural MD infection.

We examined the role of bradykinin in the onset andor the maintenance of blood pressure and renal blood flow in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by using a competitive antagonist of bradykinin Arg—Pro-Hyp-Gly—Thi–Ser–Dphe–Thi—Arg; Hyp, L-4-hydroxyproline; Thi, β-(2-theinyl-L-alanine) The intravenous injection of the bradykinin antagonist (25, 50 and 100 µg) produced an increase in mean arterial pressure in all rats treated with tap water, 1 NaCI and DOCA 1 NaCI. However, the magnitude of the increase in mean arterial pressure was significantly lower in the DOCA-hypertensive rats than in the two groups of rats drinking tap water and 1 NaCI after 4 and 6 weeks, but there was no significant difference after 2 weeks. The bradykinin antagonist induced a decrease in renal blood flow in all rats. However, the extent of the fall in renal blood flow was reduced in the DOCA-hypertensive rats compared with the control rats drinking tap water. These results suggest that endogenous bradykinin is depressed in the established phase of hypertension in DOCA-hypertensive rats. It is also suggested that endogenous bradykinin may counteract the elevation of vascular resistance in the early stages of this model.

To assess the renal benefits of a specific angiotensin II receptor antagonist, losartan, in diabetic rats with renal impairment.

The effects of cicletanine, a new antihypertensive agent, on the prostaglandin-kallikrein system and the reninangiotensin system were studied. A single oral dose of 200 mg cicletanine or placebo was administered to 9 healthy male volunteers, with samples of blood and urine obtained before and 2 hours after drug administration. Cicletanine increased the urine flow, urinary excretion of sodium, and fractional excretion of sodium by 47%, 115%, and 104%, respectively. While the excretion of 6-keto-prostaglandin-F1a was enhanced significantly, urinary excretion of thromboxane-B2, prostaglandin-E2, and kallikrein were unchanged. Cicletanine also did not alter plasma renin activity, plasma aldosterone concentration, or creatinine clearance. These observations suggest that cicletanine may suppress sodium reabsorption at the nephron, and it may stimulate prostacyclin generation with no effect on that of thromboxane-A2. Thus cicletanine may be beneficial in the management of cardiovascular disorders in which the equilibrium between prostacyclin and thromboxane is disturbed.

1. The effects of prolonged chlorothiazide treatment of left ventricular failure on cardiac hypertrophy, circulating vasoactive hormones and exchangeable body sodium were examined in rats with chronic myocardial infarction induced by left coronary artery ligation. Chlorothiazide therapy commenced either immediately or 2 weeks after infarction. For 4 weeks, the rats were given either chlorothiazide (50 mg day−1 kg−1) in their drinking water or drinking water alone. 2. Cardiac weight increased in untreated rats with infarction in comparison with sham-operated controls, indicating the presence of chronic left ventricular dysfunction, although exchangeable body sodium, plasma renin activity, plasma vasopressin and plasma osmolality remained unchanged. 3. Chlorothiazide raised haematocrit and plasma renin activity equally in rats with and without infarction, although exchangeable body sodium, plasma vasopressin and plasma osmolality were not changed by the treatment. Plasma atrial natriuretic peptide was 2-fold higher in rats with infarction and this response was not affected by chlorothiazide treatment. Chlorothiazide therapy did not prevent or reverse cardiac hypertrophy. 4. Chronic diuretic therapy in this experimental model of heart failure did not reduce extracellular sodium, plasma vasopressin or the extent of ventricular hypertrophy, possibly because the condition was associated with activation of the renin—angiotensin system.

To examine the effect of ZD7155, an angiotensin II receptor antagonist, on blood pressure, heart rate and occupancy of tissue angiotensin II receptor in two-kidney, one-clip Goldblatt hypertensive rats.

Urinary porphyrin analyses were carried out in five patients with porphyria cutanea tarda and in a control group of 44 individuals. Quantitative analysis revealed that the mean value of coproporphyrin was 67.3 μg/l (range 13.1–189.1 μg/l) in 44 normal individuals and the mean value of uroporphyrin was 9.7 μg/l (range 5.0 to 13.7 μg/l) in 11 of 44 controls, but not detectable in the remainder. Four of the five patients with porphyria cutanea tarda, however, had markedly elevated coproporphyrin and uroporphyrin levels. Urinary porphyrin pattern analysis was carried out using one dimentional thin layer chromatography. The pattern in controls revealed that the mean value of coproporphyrin was 85.5%, while the other fractions consituted less than 6.0%. In the porphyria cutanea tarda group, however, hepta‐carboxyl porphyrin and uroporphyrin were predominant in two; all five fractions appeared in roughly equal amounts in one; and in the remaining two, coproporphyrin was decreased to a value of only about 50%.

Aortoesophageal fistula occurring as a complication of a thoracic aortic aneurysm is difficult to repair because of the contaminated surgical field. We report the case of a 67-year-old man in whom an aortoesophageal fistula developed secondary to a dissecting thoracic aortic aneurysm. We performed in situ graft repair of the aneurysm, then covered the site with omentum and resected the esophagus to prevent graft infection. About 5 months later, the esophagus was reconstructed subcutaneously using an ascending colon pedicle. The patient recovered well and has resumed leading a normal life.

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Renal papillary collecting tubule (RPCT) hormone responsiveness was compared between cultured RPCT cells from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Unstimulated cells from 4-week-old SHR produced less prostaglandin E2(PGE2) and cyclic (c)AMP than comparable cells from WKY, while cells from both strains synthesized similar amounts of PGE2after stimulation with arachidonate, A23187 or bradykinin and similar amounts of cAMP after stimulation with vasopressin or PGE2. There was no difference in basal or stimulated levels of cyclic (c)GMP between the strains. In RPCT cells from 16-week-old rats, basal levels of cAMP, cGMP and PGE2were significantly lower than those from 4-week-old rats, but they did not differ between the strains. These results suggest that RPCT cells of SHR and WKY at the post-weaning period may differ in the metabolism of PGE2and cAMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.

J Thorac Cardiovasc Surg 2003;125:1158-9

For Abstract see ChemInform Abstract in Full Text.