Transient multiple hepatic nodules with marked infiltration of eosinophils caused by ascariasis.
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Adult↗
Biomedical subjects
M Otsuki
Publications and source records attributed to M Otsuki.
[Posterior cortical atrophy with incomplete Bálint's syndrome].
We report a patient of posterior cortical atrophy (PCA) with progressive memory disturbance and incomplete Bálint's syndrome consisting of optic ataxie (ataxie optique type) and visual inattention without psychic paralysis of fixation of gaze. The patients is a 58-year-old woman who noticed memory disturbance at 53 years old. Neurological deficit at 54 years old was detected only in the domain of memory, and mild diffuse brain atrophy was revealed on MRI. Memory disturbance progressed gradually, and at the age of 58 she was noticed to have visual disorder. Neuropsychological examination revealed severe memory disorder, incomplete Bálint's syndrome, transcortical sensory aphasia, mild ideational apraxia, and severe constructional apraxia. Visual inattention was too severe to evaluate visual acuity and visual field. MRI showed moderate dilatation of bilateral lateral ventricles, especially in their posterior horns, with atrophy of bilateral temporo-parieto-occipital lobes and hippocampus. IMP-SPECT revealed a diffuse decrease of cerebral blood flow in the bilateral temporo-parieto-occipital region, predominantly in the parietal regions. We believe that she is still in the early phase of PCA, and that psychic paralysis of fixation of gaze, visual agnosia will be noted in several years. Our patient represents an example of early stage PCA from neuropsychological and MRI findings.
Ataxia↗
High plasma concentrations of nitrite/nitrate in patients with hepatocellular carcinoma.
OBJECTIVES: Nitric oxide (NO) is considered to play a central role in macrophage or Kupffer cell-induced tumor cytotoxicity. Hepatocytes also produce NO in response to several inflammatory stimuli. Thus, there is a possibility that NO production by hepatic tissue is accelerated in patients with hepatocellular carcinoma (HCC). We, therefore, measured plasma nitrite/nitrate levels as an index of in vivo NO production in patients with HCC. METHODS: Plasma nitrite/nitrate levels were measured using Griess reaction in 95 patients with chronic hepatitis (CH) and compensated liver cirrhosis (LC) with (n = 48) or without HCC (n = 47), as well as 45 healthy control subjects. Possible factors related to nitrite/nitrate levels were evaluated for each subject. RESULTS: Plasma nitrite/nitrate levels in patients with HCC based on CH (mean +/- SD, 71.7 +/- 23.1 microM) and LC (52.4 +/- 20.2 microM) were significantly higher than those without HCC (CH, 31.1 +/- 15.0 microM; LC, 34.6 +/- 16.1 microM) (p < 0.01). Plasma nitrite/nitrate levels in patients with HCC based on CH were significantly higher than those in patients with HCC based on LC (p < 0.05). Simple regression analysis showed that plasma nitrite/nitrate levels significantly correlated with both tumor surface area (r = 0.577, p = 0.001) and tumor volume (r = 0.532, p = 0.003). CONCLUSION: Patients with HCC have elevated plasma nitrite/nitrate levels correlating to tumor volume as well as tumor surface area.
Analysis of Variance↗
Varioliform gastritis and duodenitis associated with protein-losing gastroenteropathy, treated with omeprazole.
A 44-year-old female with varioliform gastritis and duodenitis had gastrointestinal protein loss revealed by 111indium chloride scintigraphy. Treatment with omeprazole, a proton pump inhibitor, for 2 months, followed by famotidine, resulted in clinical improvement with resolution of the gastroduodenal lesions and protein loss. Colonization of the stomach with Helicobacter pylori was found before and after the treatment. The results in this patient suggest that omeprazole can be of value for the treatment of varioliform gastritis associated with protein-losing gastroenteropathy. The role of Helicobacter pylori in the pathogenesis of this disease is unclear.
Adult↗
Case report: primary CD30 (Ki-1)-positive anaplastic large cell lymphoma of the duodenum.
As recently described, Ki-1 anaplastic large cell lymphoma is a distinctive subtype of non-Hodgkin's lymphoma. We report a Ki-1 anaplastic large cell lymphoma of the duodenum in a 62-year-old man. He received modified CHOP therapy and was in complete remission at 18 months. To our knowledge, this is the first report of primary Ki-1 anaplastic large cell lymphoma of the duodenum.
Antineoplastic Combined Chemotherapy Protocols↗
Development of Sjögren's syndrome during treatment with recombinant human interferon-alpha-2b for chronic hepatitis C.
A 63-year-old woman with type C chronic active hepatitis developed Sjögren's syndrome after being treated with recombinant interferon-alpha-2b. After 3 months' interferon-alpha administration, serum levels of gamma-globulin (4.5 g/dl) and titers of antinuclear and anti-SS-A antibodies were greatly increased, anti-SS-B antibody appeared, and the erythrocyte sedimentation rate was elevated. Although no xerostomia was exhibited, the patient experienced conjunctival dryness. Schirmer's test showed reduced lacrimal gland function and a gum test showed reduced salivary gland function. Sialography revealed scattered pools of retained contrast media with a diameter of around 1-2 mm. Based on these findings, a diagnosis of Sjögren's syndrome was made. This present case may provide important information regarding the pathogenesis of Sjögren's syndrome.
Biopsy, Needle↗
Pancreatic cancer and hypercalcemia associated with von Recklinghausen's disease.
A 44-year-old man with von Recklinghausen's disease was admitted to our hospital presenting with left hypochondralgia. Computed tomography showed a large mass at the body and tail of the pancreas, with metastatic liver tumors. Endoscopic retrograde pancreatography revealed an obstruction of the main pancreatic duct at the body. In the course of the illness, the patient's serum calcium concentration increased gradually to 13.6 mg/dl, although bone scan with 99mtechnetium demonstrated no accumulation in the bones. Serum levels of parathyroid hormone related-protein and tumor necrosis factor were also elevated. Based on these findings, he was diagnosed as having pancreatic cancer with liver metastases and humoral hypercalcemia of malignancy associated with von Recklinghausen's disease. Postmortem examination revealed a solid tumor, measuring 6.0 x 6.0 x 8.0 cm, in the body and tail of the pancreas. Histologically, the tumor was moderately differentiated adenocarcinoma. The association of von Recklinghausen's disease with malignant neurogenic neoplasms is well established, whereas the association with non-neurogenic malignant neoplasm is considered to coincidental. Our current case suggests a possible relationship between von Recklinghausen's disease and pancreatic cancer.
Adenocarcinoma↗
Effects of intravenous infusion of amino acids on cholecystokinin release and gallbladder contraction in humans.
We investigated the effect of intravenous infusions of the therapeutically available amino acid solutions Moripron and Morihepamin (Roussel Morishita, Osaka, Japan) on gallbladder contraction and cholecystokinin (CCK) release in healthy male volunteers. Plasma CCK levels were measured by radioimmunoassay, using the antibody OAL-656, which is specific for the aminoterminus of CCK-8 and thus recognizes biologically active forms of all CCKs. The volume of the gallbladder was calculated by ultrasonographic measurements. Intravenous infusion of Moripron at the rate of 3.33 ml/min for 60 min, caused gallbladder contraction, with a peak response of 31.3 +/- 8.6% of the fasting volume at 45-60 min, and a significant increase in plasma CCK concentration, from 1.8 +/- 0.2 pmol/l to a peak of 9.9 +/- 1.5 pmol/l, at 30-45 min. The maximum gallbladder contraction and the peak CCK release during the Moripron infusion were not significantly different from findings after a test meal. There was a close relationship between the peak plasma CCK concentration and the maximal gallbladder contraction during the administration of Moripron, and this agent, even when infused at the rate of 1.67 ml/min, significantly increased plasma CCK levels and gallbladder contraction. Intravenous infusion of Morihepamin had no significant influence on gallbladder volume or plasma CCK levels. The discrepancy in responses appeared to be related to differences in composition between Moripron and Morihepamin, and not to the total dose of amino acid. Intravenous infusions of amino acids appear to have different effects on gallbladder contraction and plasma CCK secretion depending on the amino acids composition. Our findings suggest that an intravenous infusion of Moripron could be used for the prophylaxis of acute acalculous cholecystitis and sludge formation due to reduced biliary motility in patients on total parenteral nutrition.
Adult↗
Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC.
We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
Acute Disease↗
Tryptophan modulates exocrine secretory function in rat pancreatic acini.
We investigated the effect of tryptophan (Trp) on exocrine secretory function, using isolated rat pancreatic acini. Trp inhibited cholecystokinin-octapeptide (CCK-8)-stimulated amylase secretion, causing a downward shift in the dose-response curve. The inhibitory effect of Trp was dose-dependent and was observed only on the sustained secretion, there being no effect on the initial phase of amylase secretion. Trp (10mM) also inhibited amylase secretion in response to carbachol and bombesin, as well as fluoride, a potent activator of guanine-nucleotide binding proteins. Since Ca2+ influx is necessary for sustained secretion, we examined the effect of Trp on Ca2+ influx and efflux. Trp increased the CCK-8-stimulated Ca2+ influx rate without affecting Ca2+ efflux, suggesting that Trp elevates intracellular Ca2+ levels. Increasing intracellular Ca2+ levels with A23187 resulted in the inhibition of CCK-8-stimulated amylase secretion. These results indicate that Trp inhibits CCK-stimulated sustained amylase secretion, in part by increasing Ca2+ influx into acinar cells.
Amylases↗
High-fat hypercaloric diet induces obesity, glucose intolerance and hyperlipidemia in normal adult male Wistar rat.
There is strong evidence that genetic factors contribute to the development of obesity in humans as well as laboratory animals. Another important factor leading to obesity is an increase in energy intake. However, it is difficult to make normal rats obese by controlling daily food intake. There is no report of normal adult male Wistar rats becoming obese and diabetic on a high-fat diet. The aim of the present study was, therefore, to make normal adult Wistar rats obese by infusing high fat and hypercaloric diet through the cannula without disturbing the free movement and to investigate the influence of an increase in the caloric intake on body weight and glucose metabolism. High-fat hypercaloric diet (360 kcal/kg body wt./day; H group) or control diet (180 kcal/kg body wt./day; C group) was continuously infused into the stomach of normal adult male Wistar rats weighing approximately 300 g through gastric cannulas for 27 days. On day 28 after a 24-h fasting, serum concentrations of aspartate aminotransferase, alanine aminotransferase, total cholesterol, triglyceride, phospholipid, and free fatty acids (FFA) were determined, and intragastric glucose loading test (2 g/kg body wt.) was performed. The average weekly body weight gain in the H group was twice as much as that of the C group (40.0 +/- 2.4 vs. 19.4 +/- 1.9 g/week, P < 0.001). Serum levels of triglyceride, phospholipid, total cholesterol, and FFA were significantly elevated in the H group compared to those in the C group. Liver weight in the H group was significantly higher than that in the C group and showed steatosis. Pancreas weight (-13%) as well as protein (-12%), amylase (-53%) and trypsin content (-26%) were all reduced, whereas pancreatic DNA content was significantly increased in the H group compared to those in the C group. Serum glucose and insulin concentrations before and after glucose loading in the H group were significantly higher than those in the C group. Moreover, the insulin response relative to glucose response in the H group was significantly high compared to that in the C group, indicating the presence of insulin resistance. These results indicate that feeding of high-fat hypercaloric diet makes normal Wistar male adult rat obese associated with hyperlipidemia, hyperinsulinemia, and glucose intolerance.
Alanine Transaminase↗
Oral glucose ingestion stimulates cholecystokinin release in normal subjects and patients with non-insulin-dependent diabetes mellitus.
The role of glucose in the regulation of plasma cholecystokinin (CCK) level was investigated in healthy control subjects and patients with non-insulin-dependent diabetes mellitus (NIDDM). Plasma CCK concentration was determined by a specific and sensitive bioassay and by a highly sensitive and reliable double-antibody radioimmunoassay using OAL-656 as an antiserum. In control subjects, ingestion of Trelan G-75 (1,200 mOsm/L,225 mL), which is equivalent to 75 g glucose as metabolic products, caused a rapid and significant increase in plasma CCK bioactivity from 1.3 +/- 0.2 to a peak of 5.8 +/- 0.6 pmol/L and immunoreactive CCK concentration from 1.2 +/- 0.1 to 4.6 +/- 0.6 pmol/L. Ingestion of 75 g glucose in 225 mL water (33.3% solution) increased plasma CCK bioactivity to a similar degree to that observed following Trelan G-75 (peak response, 4.5 +/- 0.4 pmol/L). The same volume of 0.9% NaCl solution or water failed to increase plasma CCK concentration. A smaller dose of glucose (50 b/150 mL water) increased plasma CCK concentration, although the peak level (3.0 +/- 0.5 pmol/L) was less than that observed following 75 g glucose. In patients with NIDDM, Trelan G-75 ingestion increased CCK concentration, but the peak level was lower, albeit insignificantly, than that of normal subjects. When the maximal increment of plasma CCK above the basal value was compared between control and NIDDM subjects, the differences were statistically significant (NIDDM, 3.6 +/- 0.1 pmol/L; control, 5.0 +/- 0.4; P < .01). However, integrated CCK responses to Trelan G-75 in NIDDM (165.8 +/- 15.5 pmol/120 min) were not significantly different from those in control subjects (189.8 +/- 15.9 pmol/120 min). Peak CCK bioactivity occurred within 10 to 30 minutes of ingestion, preceding the increase in glucose and insulin. These results suggest a possible effect of CCK on insulin release in humans, and that the CCK secretory response to glucose in well-controlled diabetic patients is not significantly altered.
Administration, Oral↗
Decreased severity of ethanol withdrawal behaviors in kainic acid-treated rats.
The involvement of kainate (KA)-sensitive regions in ethanol withdrawal behaviors was investigated in male Wistar rats given three intraperitoneal (IP) injections of KA (12 mg/kg) or saline each followed by recovery at 4 degrees C for 5 h and room temperature for 3 days and a final KA or saline injection at room temperature. Some animals received MK-801 (1 mg/kg, IP) 30 min after each injection and one group received saline only. The saline/saline, saline/MK-801, and KA/MK-801 groups displayed typical ethanol withdrawal behaviors 8-12 h after ethanol withdrawal. These behaviors were attenuated in the KA/saline group. Audiogenic seizures could be induced in all treatment groups 12 h after withdrawal. There was severe neuronal degeneration in the hippocampal CA region and the piriform cortex of the KA/saline-treated animals that was reduced by MK-801 treatment. The inferior colliculus remained intact. These results suggest that the N-methyl-D-aspartate receptor mediates KA-induced damage in limbic structures and that these regions may play an important role in typical, but not audiogenically induced ethanol-withdrawal behaviors.
Animals↗
The synergic effects of quinolones and oral cephem antibiotics on Serratia marcescens.
The in-vitro effects of new quinolones and oral cephem antibiotics in various combinations on 26 strains of clinically isolated Serratia marcescens were assessed. The in-vitro activities of ofloxacin and ciprofloxacin in combination with either cefpodoxime or cefcamate were evaluated by the chequerboard titration method. These combinations showed synergistic and additive effects against most of the S. marcescens tested but no antagonism was observed. Time-kill experiments performed with two representative isolates of S. marcescens showed synergic effects with respect to the kill rates, when concentrations of quinolones and beta-lactam antibiotics, exhibiting bacteriostatic effects were combined. Exposure of S. marcescens to ciprofloxacin before the addition of cefpodoxime had no influence on the combination effect. When cefpodoxime was added first, however, the bactericidal effect was reduced. The induction of beta-lactamase by cefmetazole was enhanced by the combination of ciprofloxacin and cefmetazole. These results suggest that the synergic effects observed between new quinolones and cephem antibiotics are due to the stimulation of incorporation of cephems by combination with quinolones.
Anti-Infective Agents↗
Effects of MCI-727 on pancreatic exocrine secretion and acute pancreatitis in two experimental rat models.
The effects of a newly developed compound having antiulcer action, (Z)-2-(4-methylpiperazin-1-yl)-1-[4-(2-phenyl-ethyl)phenyl]-eth anone oxime hydrochloride monohydrate (MCI-727), on pancreatic exocrine secretion were studied in anesthetized rats and evaluated its preventive and therapeutic effects on acute pancreatitis in two experimental rat models. Intraduodenal administration of MCI-727 [25, 50, or 100 mg/kg body weight (wt)] stimulated a dose-dependent increase in pancreatic juice and bicarbonate output without increasing the protein output or plasma cholecystokinin concentration. MCI-727-stimulated pancreatic exocrine secretion was completely abolished by antisecretin serum but not by the cholecystokinin receptor antagonist loxiglumide (50 mg/kg body wt/h) or cholinergic receptor antagonist atropine (100 mu g/kg body wt/h). In rats with acute pancreatitis induced by four subcutaneous injections of 20 mu g/kg body wt cerulein at hourly intervals over 3 h, MCI-727 administered orally at a dose of 100 mg/kg body wt 30 min before the first cerulein injection significantly reduced the increases in serum amylase and lipase activity and pancreatic wet weight and induced improvements in the results of histologic examination. Moreover, when given 30 min before and 90 min after the first cerulein injection, MCI-727 had even more dramatic protective effects on all these parameters. In addition, even when administered immediately after the last cerulein injection, MCI-727 effectively ameliorated all these alterations of acute pancreatitis. However, MCI-727 had no apparent beneficial effects on the biochemical and histologic alterations of acute pancreatitis in the severe form induced by retrograde intraductal injection of 1.0 ml/kg body wt of 4% sodium taurocholate. These findings suggest that oral administration of MCI-727 stimulates pancreatic exocrine secretion by endogenous secretin release and that it has therapeutic as well as preventive effects on mild forms of acute pancreatitis in rats.
Acute Disease↗
Ethanol inhibits CCK-induced enzyme secretion by affecting calcium-pump activity in isolated rat pancreatic acini.
The aim of this study was to clarify the effect of ethanol on stimulus-secretion coupling in pancreatic exocrine secretion. We investigated the effects of 600 mM ethanol on cholecystokinin octapeptide (CCK-8)-stimulated amylase release, cytosolic free Ca2+ concentration ([Ca2+]i) and Ca2+ fluxes using in vitro isolated rat pancreatic acini. Ethanol, given alone, stimulated both the initial and the sustained phases of amylase release. On the other hand, ethanol inhibited only the sustained phase of amylase release stimulated by CCK-8. Ethanol also inhibited amylase release in response to fluoride, a direct activator of guanine nucleotide-binding protein, suggesting that ethanol affects intracellular signal transduction molecules. Ethanol had no influences on the initial rise but increased the sustained rise in [Ca2+]i stimulated by CCK-8 and inhibited CCK-8-stimulated Ca2+ outflux without affecting Ca2+ influx. 8-Bromoguanosine 3':5'-cyclic monophosphate, a membrane-permeable analogue of cGMP regulating membrane Ca(2+)-pump activity in various cells, completely reversed the ethanol-induced inhibition of amylase release and Ca2+ outflux in response to CCK-8 as well as fluoride. Given that Ca2+ plays a critical role in stimulus-secretion coupling in pancreatic exocrine secretion, our results indicate that 600 mM ethanol inhibits CCK-8-stimulated amylase release by inhibiting Ca(2+)-pump activity on the plasma membrane.
Amylases↗
Pharmacological profile of TP-680, a new cholecystokininA receptor antagonist.
1. The pharmacological characteristics of a newly developed serine derivative (R)-1-[3-(3-carboxypyridine-2-yl) thio-2-(indol-2-yl)carbonylamino]propionyl-4-diphenylmethyl- piperazine (TP-680), a cholecystokinin type A (CCKA) receptor antagonist, were studied and compared with those of MK-329 and loxiglumide. 2. TP-680 showed approximately 2 and 22 times greater selectivity for peripheral CCKA receptors relative to brain CCK (CCKB) receptors than MK-329 and loxiglumide, respectively, when IC50 values for inhibition of [125I]-CCK-8 binding in isolated acini and cerebral cortex were compared. 3. TP-680 was approximately 17 times less potent than MK-329, but was 106 times more potent than loxiglumide in inhibiting 100 pM CCK-8-stimulated amylase release from rat pancreatic acini. The antagonism produced by TP-680 was specific for CCK in that the effects of other receptor secretagogues or agents bypassing receptors were not altered. 4. TP-680 caused a parallel rightward shift of the dose-response curve for CCK-8-stimulated amylase release as did MK-329 and loxiglumide. However, in contrast to MK-329 and loxiglumide, TP-680 suppressed the maximal responses of CCK-8-induced amylase release in a concentration-dependent fashion, indicating that TP-680 is an unsurmountable antagonist. 5. Repeated washing of acini after a 30 min treatment with TP-680 restored the responsiveness but not the sensitivity, causing a residual inhibition on the action of CCK-8. 6. The addition of loxiglumide prior to or together with application of TP-680 protected CCK receptors from unsurmountable and irreversible antagonism by TP-680. 7. Our results indicate that TP-680 is a potent and the most selective CCKA receptor antagonist for the pancreas reported to date.
Amylases↗
In vitro and in vivo antibacterial activities of CS-940, a new 6-fluoro-8-difluoromethoxy quinolone.
The in vitro and in vivo activities of CS-940, a new 6-fluoro-8-difluoromethoxy quinolone, were compared with those of ciprofloxacin, tosufloxacin, sparfloxacin, and levofloxacin. The in vitro activity of CS-940 against gram-positive bacteria was nearly equal to or greater than those of the other quinolones tested. In particular, CS-940 was two to eight times more active against methicillin-resistant Staphylococcus aureus than the other quinolones, at the MIC at which 90% of the clinical isolates are inhibited. Against gram-negative bacteria, the activity of CS-940 was comparable to or greater than those of tosufloxacin, sparfloxacin, and levofloxacin, while it was lower than that of ciprofloxacin. The activity of CS-940 was largely unaffected by medium, inoculum size, or the addition of horse serum, but it was decreased under acidic conditions, as was also seen with the other quinolones tested. CS-940 showed potent bactericidal activity against S. aureus, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa. In oral treatment of mouse systemic infections caused by S. aureus, Streptococcus pneumoniae, Streptococcus pyogenes, E. coli, K. pneumoniae, Serratia marcescens, and P. aeruginosa, CS-940 was more effective than ciprofloxacin, sparfloxacin, and levofloxacin against all strains tested. Against experimental pneumonia with K. pneumoniae in mice, CS-940 was the most effective of all the quinolones tested. These results suggest that CS-940 may be effective in the therapy of various bacterial infections.
Animals↗