Biomedical subjects

H Yoshida

Publications and source records attributed to H Yoshida.

At least 901 records · Page 50Linked to original sources

PubMed1997

Cholecystokinin peptides stimulate pancreatic secretion by multiple signal transduction pathways.

In an attempt to examine the structure-activity relationship of the cholecystokinin (CCK) peptide, we examined the structural motif of CCK truncated peptides responsible for rat pancreatic acinar amylase secretion and signal transduction. CCK-6 (Met28-Gly29-Trp30-Met31-Asp32-Phe33 -NH2), CCK-5 [CCK-(29-33)], and CCK-4 [CCK-(30-33)] caused monophasic amylase secretion with EC50 values of 3, 20, and 30 nM, respectively. CCK-7 [Tyr(SO3H)27 plus CCK-(28-33)] evoked biphasic secretion with an EC50 of 0.7 pM, whereas CCK-3 [CCK-(31-33)] had no effect, suggesting the importance of Tyr(SO3H)27 and Trp30. Whereas CCK-7 [Tyr(SO3H)27/ Met28] evoked biphasic amylase secretion, CCK-OPE [Tyr(SO3H)27/Nle28] and CCK-6 (Met28) caused monophasic secretion. Thus Tyr(SO3H)27/Met28 appears to be required for biphasic secretion. CCK-8-OH and CCK-5-OH did not cause amylase secretion and Ca2+ spiking, suggesting the importance of Phe33 amidation. Similar to CCK-8, CCK-6 and CCK-4 caused Ca2+ oscillations at low doses and large Ca2+ transients at high doses. In contrast, similar to JMV-180 and CCK-OPE, CCK-5 elicited Ca2+ oscillations at all concentrations. Phospholipase C (PLC) inhibitor inhibited amylase secretion induced by high doses of CCK-6 and CCK-4 but not by CCK-5. Protein tyrosine kinase (PTK) inhibitor only inhibited the action of high doses of CCK-4. Neither PLC inhibitor nor PTK inhibitor affected amylase secretion evoked by low doses of CCK-6, CCK-5, and CCK-4. In contrast to its actions on JMV-180 and CCK-OPE, phospholipase A2 (PLA2) inhibitor had no effect on the action evoked by all CCK short peptides. CCK-6, CCK-5, and CCK-4 caused a 2.1- to 3.2-fold increase in intracellular inositol 1,4,5-trisphosphate levels over basal. None of these CCK short peptides increased intracellular arachidonic acid levels. CCK-6 and CCK-5 did not stimulate PTK activity, whereas CCK-4 evoked a 3.2- to 5.3-fold increase over basal. We conclude that Tyr(SO3H)27, Trp30, and Phe33-CONH2 of the CCK peptide are key amino acids in evoking amylase secretion. At low doses, CCK-6, CCK-5, and CCK-4 utilize some yet to be identified pathways to evoke Ca2+ oscillations and amylase secretion. At high doses, CCK-6 and CCK-4 utilize PLC but not PLA2 pathways. CCK-4 possesses the minimal essential amino acids to fully activate the PTK pathway.

Aminobenzoates↗

PubMed1997

Targeting deletion of angiotensin type 1B receptor gene in the mouse.

We null mutated the mouse angiotensin type 1B (AT1B) receptor gene (Agtr1b) by gene targeting. To identify the specific cell types carrying high Agtr1b gene transcriptional activities, the AT1B coding exon was replaced with a reporter gene, lacZ. In 6- to 8-wk-old Agtr1b -/- mice, high AT1B transcriptional activity was observed in adrenal zona glomerulosa cells and the testis, including mature and immature spermatic cells, whereas low activity was detected homogeneously in anterior pituitary cells and choroidal plexus vessel walls. A similar pattern was observed in Agtr1b +/- mice with less intensity. Microscopically, the anterior pituitary, heart, adrenal, zona glomerulosa, kidney, and the testis of Agtr1b -/- mice were intact and were indistinguishable from those of Agtr1b +/+ mice. Systemic blood pressure was comparable in Agtr1b -/- and Agtr1b +/+ mice. Moreover, plasma aldosterone level was comparable between the two mouse groups. No compensatory enhancement of AT1A mRNA was found in the kidney and adrenal gland of Agtr1b -/- mice. The observed absence of the abnormal phenotypes in Agtr1b -/- mice, which have been described for homozygous angiotensinogen null mutant mice, indicates that 1) AT1A receptors can take over the role of AT1B receptors in Agtr1b -/- mice or 2) functionally significant non-AT1, non-AT2 receptor(s) may exist for the action of angiotensin.

Aldosterone↗

PubMed1997

Effects of protein tyrosine kinase inhibitors on the replication of herpes simplex virus and the phosphorylation of viral proteins.

The effect of protein tyrosine kinase (PTK) inhibitors on the replication of herpes simplex virus (HSV) was examined. Tyrphostins AG17, AG213, AG490, and AG555, and herbimycin A all inhibited the plaque formation of HSV type 1 (HSV-1) in Vero cells, but AG17, AG490, and AG555 exhibited a more selective antiviral effect. In the presence of 0.4 microM AG17, the virus production 24 h after infection was decreased to 7.7% of the untreated control level. Even if the treatment was started 12 h after the initiation of infection, the viral titer was reduced by 82.4%, compared with the untreated control level. In HSV-1-infected cells ICPs 6, 17/18, 19/20, and 25 were tyrosine-phosphorylated proteins. The synthesis and phosphorylation of these proteins were inhibited by AG17, and suppression of ICP 19/20, which were identified as the UL47 gene products, was the greatest. In contrast, the in vitro autophosphorylation of viral proteins was not affected by this PTK inhibitor. These results indicate that tyrphostin may represent a novel class of inhibitors of HSV-1, and that the viral proteins which have phosphorylated tyrosine residues and are suppressed by AG17 most significantly are the products of the UL47 gene, the tegument proteins VP13/14.

Amino Acid Sequence↗

PubMed1997

Selective breeding for high serum IgA levels from noninbred ddY mice: isolation of a strain with an early onset of glomerular IgA deposition.

An outbred mouse strain known as ddY has been reported to spontaneously develop, late in life, mesangioproliferative glomerulonephritis with a severe glomerular immunoglobulin A (IgA) deposition that mimics human IgA nephropathy. However, the incidence of the disease in this strain is not very high, probably due to its heterogeneous genetic background. Therefore, we attempted to isolate a strain with a high incidence and an early onset of the disease through selection for high serum IgA from the outbred ddY mice. The selection procedure was successful in increasing the serum IgA level of the selected line and proved effective both in increasing the incidence and in accelerating the onset of the disease. We propose to designate this line of mice 'HIGA', denoting a line with high serum IgA levels. More than half of the mice from the HIGA strain showed a moderate to severe glomerular IgA deposition as early as 25 weeks of age. The severe deposition observed was comparable to that occasionally seen in the original nonselected ddY strain after 40 weeks of age. Thus, we have succeeded in generating a mouse model of IgA nephropathy with a high incidence and an early onset of glomerular IgA deposition. Using light microscopy, progressive and marked mesangial matrix accumulation was shown to develop in HIGA mice. However, they showed only mild proteinuria (100-300 mg/dl) and did not show hematuria.

Aging↗

PubMed1997

Reversal of anemia by erythropoietin therapy retards the progression of chronic renal failure, especially in nondiabetic patients.

Therapy with human recombinant erythropoietin (EPO) has been accepted as effective for renal anemia in dialysis patients. However, studies in rats have shown that correcting anemia with EPO may affect the progression of renal dysfunction. In humans, however, the effect of EPO on residual renal function is a matter of controversy. We, therefore, investigated whether the long-term administration of EPO to predialysis patients influences residual renal function. Anemic patients at the predialysis stage with a serum creatinine (Cr) concentration ranging from 2 to 4 (average 2.9) mg/dl and a hematocrit (Ht) of less than 30% were randomly assigned to two groups which consisted of anemic patients not treated with EPO (group I, untreated anemic controls, n = 31) and anemic patients treated with EPO (group II, treated anemics, n = 42). Patients with nonsevere or moderate anemia (Ht > 30%) with a Cr ranging from 2 to 4 (average 2.6) mg/dl were also recruited as nonanemic controls (group III, untreated nonanemic controls, n = 35). Blood pressure was controlled to the same degree among the three groups by combined treatment with calcium antagonists and angiotensin-converting enzyme inhibitors. All patients were kept strictly on a low-protein (0.6 g/kg/day) and a low-salt (7 g/day) diet. The degree of control of dietary protein and blood pressure and the frequency of angiotensin-converting enzyme inhibitor administration were comparable among the three groups. The primary end point for each patient was a doubling of the baseline Cr which yielded cumulative renal survival rates which were plotted against time. Ht rose significantly from 27.0+/-2.3 to 32.1+/-3.2% in group II (n = 42, p < 0.001) with a rate of increase of 0.4+/-0.06%/week. However, it declined from 27.9+/-1.8 to 25.3+/-1.9% in group I (n = 31, p < 0.001) and from 35.9+/-3.5 to 32.2+/-3.9% in group III (n = 35, p < 0.001). Cr doubled in 26 patients (84%) in group I as compared with 22 (52%) in group II and 21 (60%) in group III. The cumulative renal survival rates in groups II and III were significantly better than that in group I: p = 0.0003 (group I vs. group II) and p = 0.0024 (group I vs. group III). However, there was no difference in the renal survival rate between groups II and III (p = 0.3111). The better survival rate obtained in group II was attributable to the better survival rate for the nondiabetic patients in this group. The present study suggests that anemia, per se, is a factor in the progression of end-stage renal failure and that reversal of anemia by EPO can retard the progression of renal failure, especially in nondiabetic patients, provided that blood pressure control, rate of increase in Ht, and dietary protein restriction are appropriate.

Adult↗

PubMed1997

Beneficial effects of alcohol withdrawal on LDL particle size distribution and oxidative susceptibility in subjects with alcohol-induced hypertriglyceridemia.

LDL subclass pattern B, reported to have a higher prevalence in hypertriglyceridemics (HTGs), is considered to be associated with an increased risk for coronary artery disease, and the small dense LDL characteristic of this pattern is susceptible to oxidative modification. Alcohol is considered one of the most frequent causes of increases in plasma triglyceride (TG) levels. We investigated the effects of alcohol withdrawal on LDL subclass distribution and oxidizability in drinkers with different plasma TG levels. Thirty-seven male subjects with relatively heavy alcohol-consumption habits were divided into four groups; normotriglyceridemic (NTG)/withdrawal (n = 11), NTG/control (n = 8), hypertriglyceridemic (HTG)/withdrawal (n = 10), and HTG/control (n = 8). Both withdrawal groups abstained form alcohol for 4 weeks, while the control subjects maintained their usual intake of alcohol. Peak LDL particle diameter (PPD) was smaller in the combined HTG groups than in the combined NTG groups before abstinence, although PPD increased significantly (P < .01) from 25.5 to 26.1 nm in the HTG/withdrawal group. Before abstinence, lag times preceding LDL oxidation in the combined HTG groups were shorter than in the combined NTG groups; after withdrawal, lag time was prolonged significantly (P < .01) from 49.9 to 57.3 minutes in the HTG-withdrawal group. No significant changes in PPD and lag time were observed in the other three groups. Significant correlations (P < .05) were observed between the change (delta) in the lag time and delta TG and between delta lag time and delta PPD. We conclude that in alcohol-induced HTG subjects, alcohol withdrawal has beneficial effects on the LDL profile by shifting the particle size from smaller to larger and decreasing its susceptibility to oxidation.

Adult↗

PubMed1997

Vitamin E/lipid peroxide ratio and susceptibility of LDL to oxidative modification in non-insulin-dependent diabetes mellitus.

The presence of conventional risk factors cannot sufficiently account for the excess risk of atherosclerosis in patients with non-insulin-dependent diabetes mellitus (NIDDM). Oxidative modification of LDL has been implicated in the pathogenesis of coronary atherosclerosis. Thirty-five patients with NIDDM, 20 nondiabetic, hypertriglyceridemic subjects (HTG-control), and 21 diabetic, normotriglyceridemic subjects (NTG-control) were enrolled in this study. Oxidative susceptibility of LDL was determined by monitoring formation of conjugated dienes. Mean lag time of LDL oxidation and vitamin E/lipid peroxide of LDL was lower in patients with NIDDM (43.2 +/- 3.9 minutes and 1.6 +/- 1.3) than in HTG-control (48.8 +/- 3.2 minutes and 2.3 +/- 1.2, respectively) and NTG-control subjects (54.2 +/- 6.1 minutes and 3.0 +/- 1.8, respectively). Mean LDL particle size in patients with NIDDM and HTG-control subjects (24.4 +/- 0.9 and 24.7 +/- 0.7 nm, respectively) was smaller than in NTG-control subjects (25.9 +/- 1.0 nm). Multiple stepwise regression analyses ascertained that the vitamin. E/lipid peroxide of LDL is a major determinant of LDL oxidation lag time. These results suggest that LDL in patients with NIDDM is more susceptible to oxidative modification primarily because of a reduced level of vitamin E/lipid peroxide of LDL. The enhanced susceptibility of LDL to oxidation may be a pivotal factor underlying the increased incidence of vascular disease in patients with NIDDM.

Adult↗

PubMed1997

A mutation in plasma platelet-activating factor acetylhydrolase (Val279-->Phe) is a genetic risk factor for stroke.

BACKGROUND AND PURPOSE: Platelet-activating factor (PAF) is a phospholipid with multiple actions that include thrombosis and inflammation. It is inactivated by a plasma enzyme, PAF acetylhydrolase. Deficiency of this enzyme in plasma is caused by a missense mutation in the gene (Val279-->Phe). We have studied a possible association of this mutation with the risk of stroke. SUBJECTS AND METHODS: We studied 120 consecutive patients with cerebral thrombosis. The control group consisted of 134 patients matched for age and sex with minor complaints but without stroke. Genomic DNA was analyzed for the mutant allele by a specific polymerase-chain reaction. Plasma PAF acetylhydrolase activity was determined by the method of Stafforini et al. RESULTS: The prevalence of the mutant gene was 43.4% in stroke patients (39.2% heterozygotes and 4.2% homozygotes), which was significantly higher than the 25.4% in control subjects (22.4% heterozygotes and 3.0% homozygotes) (chi 2 = 9.22, P < .01). The prevalence was slightly higher in stroke patients without hypertension than those with hypertension, but the difference was not significant. The patients with family histories of stroke had a slightly higher but not a significant prevalence of the mutant gene as compared with those without family histories of stroke. Plasma PAF acetylhydrolase activity was higher in patients than in control subjects, in normal subjects, or patients with a heterozygous genotype. CONCLUSIONS: These results suggest that plasma PAF acetylhydrolase deficiency may be a risk factor for stroke. This may explain the relatively high prevalence of stroke in Japan, as the mutation is more common among Japanese than Caucasians.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed1997

PDGFR alpha expression during mouse embryogenesis: immunolocalization analyzed by whole-mount immunohistostaining using the monoclonal anti-mouse PDGFR alpha antibody APA5.

We investigated the cells that express platelet-derived growth factor receptor alpha (PDGFR alpha) during mouse embryogenesis. PDGFR alpha expression has been identified by in situ hybridization or immunohistochemistry using polyclonal antibodies on tissue sectins. Because no immunostaining study using whole-mount specimens has been published to date, we established a new monoclonal antibody (MAb), APA5, for this purpose. Our results differed in that APA5 stained only the paraxial mesoderm, whereas other investigators concluded that most if not all mesodermal cells expressed PDGFR alpha. Moreover, we did not find PDGFR alpha expression in embryonic erythrocytes, which have been previously suggested to express PDGFR alpha. On the basis of our present results, we wish to revise the proposed PDGFR alpha expression as follows. At the pregastrulation stage, PDGFR alpha is expressed only in primitive endoderm, particularly that in the ectoplacental cone. On gastrulation, it is expressed at high levels in the paraxial mesoderm. This expression continues after its differentiation into the somite. Along with the differentiation and migration of the sclerotome, PDGFR alpha + cells begin to become distributed throughout the embryonal mesenchyme. During organogenesis, particularly intense staining is detected in regions of epithelial and mesenchymal interaction, such as the tooth bud and bronchi. In addition to mesodermal derivatives, the developing lens, apical ectodermal ridge, glial precursor, cardiac valves, and choroid plexus express PDGFR alpha. Our results with whole-mount immunostaining show that PDGFR alpha is abundantly expressed and may play important roles during embryogenesis.

Animals↗

PubMed1997

A novel method for induction and detection of anaphylactic reaction using the mouse abdominal wall (AW method).

We found that an antigen-specific anaphylaxis was induced by antigen challenge to the abdominal wall, ear auricle, or subcutaneous tissue in mice sensitized 9 days previously with antigen and adjuvant. The anaphylactic reaction was detected by vascular permeability at the injected site 7 minutes after challenge, which was the best time for estimation. A novel method (AW method) for induction and detection of the anaphylactic reaction in mice was established using the abdominal wall as the challenge site. This method could detect the anaphylactic response in mice 1 to 3 weeks after sensitization. The increase in vascular permeability was completely inhibited by administration of diphenhydramine.

Abdominal Muscles↗

PubMed1997

Relationship between the metabolic chiral inversion and chemical structure of 4-phenyl-4-oxobutanoic acids, derivatives of anti-rheumatic agent KE-298.

The relationship between metabolic chiral inversion and chemical structure of various 4-phenyl-4-oxobutanoic acids (4-OBA), derivatives of anti-rheumatic agent KE-298 [2-acetylthiomethyl-4-(4-methylphenyl)-4-oxobutanoic acid], was investigated in rats. Chiral inversion occurred with the thio-alkyl group, whereas the thio-acyl group played no role in the inversion of 4-OBA. A 2-methylene moiety was required for the inversion. When the 4-carbonyl moiety was removed, chiral inversion was significantly decreased, which provided an affinity for the intramitochondrial medium chain fatty acid CoA ligase. In addition, the distance between the chiral center and the carbonyl moiety was also an important factor for chiral inversion. While a sulfur atom was not indispensable for the chiral inversion, the existence of the sulfur atom influenced its affinity to the long chain fatty acid CoA ligase.

Animals↗

PubMed1997

[Activation of skin cells by inorganic compounds].

It has been known that the stimulation of skin cells by physiologically active substances is accompanied by the quantitative and qualitative alterations of the glycosaminoglycans (GAGs) in skin. This phenomenon make it possible to evaluate the activity of test substances for the stimulation of skin cells. The purpose of our study is to elucidate the effectiveness of inorganic compounds for the stimulation of skin cells. (1) The cultured skin cells including keratinocytes and fibroblasts, (2) the cultured model skin constituted of collagen gel, fibroblasts and keratinocytes, and (3) the mouse damaged skin were used in the present study. The results obtained from these studies demonstrate that inorganic substances commonly have a possibility to activate cyclic AMP-dependent protein kinase (A-kinase), and the A-kinase activation results in an increase in GAGs. These findings brought the scientific basis for the effectiveness of the Japanese traditional balneotherapy for damaged skin.

Animals↗

PubMed1997

Effects of long-term antihypertensive therapy on physical fitness of men with mild hypertension.

This study was conducted to investigate the effects of long-term administration of a calcium-channel antagonist (nifedipine) and a beta-blocker (acebutolol) on physical fitness in men with mild hypertension. All subjects underwent symptom-limited treadmill stress testing and routine echocardiographic studies. Twenty-two subjects who had either a causal diastolic blood pressure of more than 105 mmHg or a left ventricular mass index (LVMI) of 125 g/m2 or more during follow-up were assigned to receive medical therapy. The other 31 men who did not meet either criterion were continuously followed-up without medication. Among the 22 treated men, the age-adjusted treadmill time (normalized treadmill time, TMTn) significantly decreased before the initiation of medication, while 31 untreated men showed no change in TMTn throughout the study. The 22 treated subjects were subsequently divided into two groups; 13 were given nifedipine and 9 were given acebutolol. All treated subjects were followed-up for more than 3 years. After treatment, the two groups showed similar reductions in blood pressure and LVMI, but a different outcome for TMTn: TMTn increased from 104 +/- 8% to 115 +/- 16% in subjects given nifedipine (p < 0.05) and decreased from 106 +/- 12% to 99 +/- 10% (p < 0.01) in those given acebutolol. Thus, the physical fitness of subjects who required medication significantly deteriorated without medication; their physical fitness improved after treatment with a calcium-channel antagonist and deteriorated after treatment with a beta-blocker.

Acebutolol↗

PubMed1997

Indomethacin enhances the cytotoxicity of VCR and ADR in human pulmonary adenocarcinoma cells.

The ability of anti-inflammatory agents to modulate cellular sensitivity to anticancer drugs was investigated for pulmonary carcinoma cells in vitro. We examined the drug sensitivity of two pulmonary adenocarcinoma cell lines (76-2, 77-4) in the presence of two drugs, an anticancer drug and an anti-inflammatory agent, for 72 hr by the 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay with 96 well plates. Anticancer drugs used for screening test were cyclophosphamide (CPM), mitomycin C (MMC), adriamycin (ADR), 5-fluorouracil (5FU), vindesine (VDS), cisplatin (CDDP), cytarabine (Ara C), methotrexate (MTX), etoposide (VP-16), and vincristine (VCR). Anti-inflammatory agents examined as modulators to anticancer drugs were aspirin, mefenamic acid, ibuprofen, sulindac, piroxicam, phenacetin, dicrofenac, ketoprofen, tolmetin and indomethacin. Screening tests showed indomethacin to be the most effective modulator, resulting in more than a 3-fold increase in cytotoxicity of VCR as compared with that produced by VCR alone. Study of each of the ten anticancer drugs in combination with indomethacin showed VCR to be the most effective anticancer drug in this combination. In 76-2 cells, the concentration of VCR producing 50% growth inhibition (IC50) for VCR alone and VCR in combination with 2 micrograms/ml indomethacin were 1.58 +/- 0.16 and 0.52 +/- 0.1 ng/ml respectively, which represents a 3-fold decrease. In 77-4 cells, the IC50 for VCR alone and VCR in combination with 2 micrograms/ml indomethacin were 2.86 +/- 0.2 and 0.52 +/- 0.11 ng/ml respectively, which represents a 3.8-fold decrease. Our studies indicate that clinically achievable concentrations of indomethacin may be useful in modulating VCR resistance in human pulmonary adenocarcinoma cells, so that combined use of VCR and indomethacin may be of potential clinical significance in the treatment of lung cancer.

Adenocarcinoma↗

PubMed1997

Endoscopic retrograde cholangiopancreatography (ERCP) in biliary tract disease of infants less than one year old.

We performed a total of 75 examinations with endoscopic retrograde chlangiopancreatography (ERCP) in 73 infants aged from 8 days to 300 days (mean 71 days) between 1977 and 1995. ERCP examination was performed with a prototype duodenoscope and was successful in 47 of 52 examinations in biliary atresia, 9 of 11 in neonatal hepatitis, all 4 in paucity of intra-hepatic bile duct, 4 of 5 in congenital biliary dilatation, 1 of 2 in duodenal stricture, and 1 case of in postoperative jaundice of hepatoblastoma. In 46 infants with biliary atresia, excluding one in whom the findings could not be evaluated due to poor x-ray image quality, we distinguished the following four patterns of ERCP findings: Pattern 1, only the pancreatic duct could be demonstrated and no bile duct was visualized (76%); Pattern 2, only a part of the distal common bile duct with the pancreatic duct was visualized (2%); Pattern 3, the entire length of the common bile duct with the pancreatic duct was visualized without the gallbladder and the common hepatic duct (4%); and Pattern 4, the common bile duct and the gallbladder with the pancreatic duct were visualized without the common hepatic duct (18%). In all of these 46 patients, laparotomy, an operative cholangiogram, and histological evaluation of the biliary duct were performed. In 9 neonates with neonatal hepatitis, the biliary tract was opacified and biliary atresia was excluded. Laparotomy was thus avoided in these neonates. There was no complication caused by either ERCP or by anesthesia.

Anesthesia↗

PubMed1997

Acute renal failure after binge drinking of alcohol and nonsteroidal antiinflammatory drug ingestion.

A case of reversible acute renal failure (ARF) following binge drinking together with the transient use of a nonsteroidal antiinflammatory drug (NSAID) is described. After binge drinking. the patient experienced hyperdipsia, and the volume of his urine decreased. Subsequently, he took an NSAID to relieve systemic joint pain associated with low grade fever, and then he had complete anuria. One day after taking the NSAID, he visited our hospital, and was found to have severe renal dysfunction accompanied by severe liver damage (blood urea nitrogen and creatinine concentrations were 57 and 5.4 mg/dl, respectively). The impaired renal function progressed over the first three hospital days, as reflected by an elevated creatinine concentration to 11.6 mg/dl. Nine treatment sessions of hemodialysis were, therefore, required to recover the loss of renal function. The present case suggests that binge drinking may be a potential risk factor for ARF in the presence of NSAIDs.

Acute Kidney Injury↗

PubMed1997

Systemic sclerosis associated with diabetes insipidus.

A rare case of systemic sclerosis that preceded the development of diabetes insipidus is reported. This 25-year-old man presented with Raynaud's phenomenon and ulceration of the tip of the right thumb. The diagnosis of systemic sclerosis was based on findings of proximal scleroderma, sclerodactyly, serological abnormalities, and skin abnormalities verified histologically. Partial central diabetes insipidus was later diagnosed after the sudden appearance of polyuria and polydipsia. Coexistence of systemic sclerosis with diabetes insipidus suggests that diabetes insipidus in this patient might have occurred via an autoimmune mechanism.

Adult↗

PubMed1997

A method to estimate the transient interstitial osmolarity change upon application of osmotic stress in perfused rat submandibular gland.

Transient osmolarity changes in the interstitium of perfused rat submandibular glands were estimated by measurement of the interstitial Cl- concentration ([Cl-]ECF) with an Ag-AgCl electrode upon application of osmotic stress by the addition or subtraction of NaCl. A simple model was used to describe the interstitial osmolarity changes upon the application of osmotic stress. The measured [Cl-]ECF values and interstitial osmolarities were fit well by an exponential function derived from the model. The good fit of the theoretical curve indicates that this model describes adequately the changes in interstitial osmolarity after switching the perfusate osmolarity to a new value.

Animals↗