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Biomedical subjects

M Aoki

Publications and source records attributed to M Aoki.

At least 451 records · Page 25Linked to original sources
PubMed1995

Effect of an antihypertensive drug on brain angiotensin II levels in renal and spontaneously hypertensive rats.

1. Although numerous studies suggest that brain angiotensin (AII) may play an important role in the regulation of blood pressure, it is still unclear what factors may influence brain AII. In this study, we hypothesized that brain AII is influenced by circulating factors. To investigate the role of blood pressure and plasma AII in brain AII level, we studied the effect of an antihypertensive drug on brain AII in two-kidney, one-clip (2K1C) and spontaneously hypertensive (SHR) rats. 2. Hydralazine (20 mg/kg per day) and vehicle (water) were given to 2K1C rats between 2 and 6 weeks after operation and SHR for 4 weeks. In addition, vehicle was applied to sham operated rats and Wistar-Kyoto (WKY) rats. Brain and plasma AII was measured by a highly sensitive radioimmunoassay coupled with high performance liquid chromatography. 3. Hydralazine treatment effectively lowered blood pressure to the same level of sham-operated and WKY rats. 2K1C rats showed significantly higher plasma AII than sham rats, but hydralazine treatment did not show any change in plasma AII. Brain AII in the hypothalamus region of 2K1C rats showed a significantly higher level than sham rats. Interestingly, hydralazine treatment diminished this increase in brain AII. In contrast, SHR showed higher brain AII levels in the hypothalamus, brainstem and cerebellum than in WKY rats, whereas there was no significant change in plasma AII concentration between SHR and WKY rats. In contrast to the results found in 2K1C rat experiments, hydralazine treatment failed to decrease brain AII levels despite lowered blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1995

Anti-CD18 attenuates deleterious effects of cardiopulmonary bypass and hypothermic circulatory arrest in piglets.

Cardiopulmonary bypass (CPB) and hypothermic circulatory arrest induce leukocyte and platelet activation and cytokine production as part of the inflammatory response to bypass. These events are thought to be responsible for producing at least some of the morbidity of bypass. We studied the effects of a monoclonal antibody to a specific leukocyte adhesion integrin, CD18, on the deleterious effects of CPB and circulatory arrest in piglets using techniques from infant heart surgery. Seventeen immature piglets were subjected to CPB, cooling, 1 hour of circulatory arrest at 15 degrees C, and subsequent reperfusion and rewarming. Nine piglets received anti-CD18 monoclonal antibody (group MAb), and eight randomly selected control piglets received none (group C). Monoclonal antibody to leukocyte integrin CD18 significantly decreased deleterious effects of CPB and hypothermic circulatory arrest in our immature animal model. This study suggests that antiadhesion therapy that alters fundamental leukocyte/endothelial interactions during open heart surgery may be protective against some deleterious effects of bypass and circulatory arrest in infants.

Animals↗
PubMed1995

Glutathione S-transferases as a cefpiramide binding protein in rat liver.

To clarify the intrahepatical transport mechanism of cefpiramide, we investigated effects of various agents mainly excreted into the bile by several different mechanisms on the biliary excretion of cefpiramide in rats. Sulfobromophthalein, indocyanine green, bilirubin and probenecid, known to be bound to glutathione S-transferases (GST) (EC 2.5.1.18) in liver cytosol, reduced the biliary excretion of cefpiramide, while neither secretory IgA, which is transported via vesicles in the liver, nor colchicine, which inhibits movements of vesicles, had any effect on the excretion of cefpiramide. Propranolol and metoprolol, metabolized by mixed function oxidases, had no effect on the biliary excretion of cefpiramide. In the chromatography of liver cytosol, the amount of sulfobromophthalein or benzylpenicillin bound to the GST fraction decreased in the presence of cefpiramide or probenecid. The study showed that cefpiramide was transported in the liver without relation to mixed function oxidases or vesichle-mediated transporting system, but in relation to GST which binds cefpiramide, sulfobromophthalein, benzylpenicillin and probenecid, indicating an important role of GST in the cefpiramide excretion into the bile.

Animals↗
PubMed1995

[Useful abdominal ultrasonography for diagnosis of Fitz-Hugh-Curtis syndrome: two case reports].

Recently, Chlamydia trachomatis infection in sexually active women has increased. C. trachomatis cause pelvic inflammation. A few of these patients develop Fitz-Hugh-Curtis syndrome (FHCS). Clinical symptoms of FHCS include pain of sudden onset in the right upper quadrant mimicking acute biliary disease. Diagnosis of FHCS has been weighed upon laparoscopic findings. Since FHCS is a benign disorder which responds to appropriate antibiotics, non-invasive diagnostic method would be expected. We report here two cases of FHCS, diagnosed by a high serum antibody titer against C. trachomatis and clinical manifestations. Both cases showed small effusion in the pelvic cavity detected by ultrasonography, one of them was associated with small effusion in the right perirenal space suggesting perinephritis. Detection of small effusion intra abdominal cavity or pelvic space could be useful for non-invasive diagnosis of FHCS.

Adult↗
PubMed1995

[Clinical efficacy of lomefloxacin (100 mg or 300 mg) single-dose therapy in female acute uncomplicated cystitis].

Female acute uncomplicated cystitis responds relatively well to antimicrobial chemotherapy. In particular, new quinolones are suited for use as antimicrobial agents in single-dose therapy of female acute uncomplicated cystitis since they have a long serum half-life and express potent antimicrobial activity against the causative microbes of this infection. Lomefloxacin (LFLX) is one such new quinolone which shows a long serum half-life, expresses potent antimicrobial activity against Escherichia coli (E. coli) and maintains an effective urinary drug concentration for approximately three days after a single administration. The authors carried out a comparative investigation of the clinical efficacy of single doses of 100 mg and 300 mg of LFLX in the treatment of female acute uncomplicated cystitis. The clinical efficacy rates with these doses, evaluated on the 3rd day after administration, were 98.2% (56/57 cases) for the 100mg-LFLX dose and 100% (62/62 cases) for the 300-mg LFLX dose. When the evaluation was performed on the 7th day after administration, the clinical efficacy rates were 91.3% (42/46 cases) for the 100-mg LFLX dose and 95.8% (46/48 cases) for the 300-mg LFLX dose. In addition, the microbial eradication rates were 73.7% (42/57 cases) for the 100-mg LFLX group and 75.8% (47/62 cases) for the 300-mg LFLX group on the 3rd day after administration, and 71.7% (33/46 cases) for the 100-mg LFLX group and 83.3% (40/48 cases) for the 300-mg LFLX group on the 7th day after administration. Although there were no statistically significant differences between the two LFLX dosage groups for these parameters at either of the evaluation times, the rates for the 300-mg LFLX dose were slightly superior. The investigators judged the efficacy of the LFLX treatment as having been insufficient in 12 patients, and urological examinations performed on six of those cases determined that there were mild underlying diseases in four cases, such as stenosis of the urethral meatus. On the basis of the findings described above, it is clear that a single 100-mg dose of LFLX provided sufficient clinical efficacy in the treatment of female acute uncomplicated cystitis, but the efficacy of the 300-mg dose of LFLX was even better. In addition, it was surmised that performance of detailed urological examinations provides an opportunity to detect mild underlying diseases that may be the cause of the intractability in female acute uncomplicated cystitis cases showing an insufficient response to treatment with antimicrobial agents such as LFLX.

Acute Disease↗
PubMed1995

[An autopsy case of fungal (Mucor) cerebral aneurysm].

An autopsy of rupture of Mucor cerebral aneurysm, not diagnosed during the patient's life, was experienced. A 63-year-old female was admitted to our hospital with the chief complaint of disturbance of consciousness and high fever. Her past histories were diabetes mellitus, liver cirrhosis and nasal sinusitis. The remarkable findings on admission were moderate inflammatory data, high blood sugar level in serum and ascites. Brain CT film revealed a non-enhanced low-density area in the frontal region. The cerebrospinal fluid showed bloody color and white blood cell counts were 3300/microliter (mostly neutrophils). Under our suspected of bacterial encephalomeningitis, intravenous cefotaxime and ampicillin therapy was started immediately. Cultures of cerebrospinal fluid for bacteria were negative. The disturbance of her consciousness gradually improved under general treatment. However, her conscious level suddenly became a coma on the 6th hospital day and she died on the 9th hospital day. An autopsy revealed Mucor at the site of the rupture of the cerebral aneurysm.

Aneurysm, Infected↗
PubMed1995

[Long-term monitoring of female acute uncomplicated cystitis cases after lomefloxacin single-dose therapy].

Female acute uncomplicated cystitis responds relatively well to antimicrobial chemotherapy, but this is also a disease which shows a high frequency of recurrence. However, there have been no published reports regarding long-term monitoring of the course of this disease after therapy has been administered. Accordingly, using primarily a questionnaire, the authors carried out long-term monitoring (for a mean of 242 days) of the natural course of cases of female acute uncomplicated cystitis after single-dose therapy with lomefloxacin (LFLX), a new quinolone antimicrobial agent. The subjects of this study were female patients diagnosed as having acute uncomplicated cystitis with pain upon urination, pyuria (> or = 10 WBCs/hpf) and bacteriuria (> or = 10(4) cfu/ml). LFLX was orally administered as a single dose of 100 mg or 300 mg, and the therapeutic efficacy was evaluated on the 3rd and 7th days thereafter. In principle, the evaluation of cure was performed on the 7th day after LFLX administration, and monitoring was conducted to detect early recurrence during the next 7 days (i.e., through the 14th day after treatment). Then the subjects were monitored for late recurrence during a mean follow-up period of 242 days by means of a questionnaire. Confirmation of recurrence was carried out to the greatest extent possible. It was possible to carry out long-term monitoring of the natural course of 101 cases of female acute uncomplicated cystitis in which the clinical efficacy on the 3rd day after LFLX treatment had been evaluated as good or excellent.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1995

Transient decrease in high blood pressure by in vivo transfer of antisense oligodeoxynucleotides against rat angiotensinogen.

The renin-angiotensin system plays an important role in blood pressure regulation. Angiotensinogen, which is mainly produced in the liver, is a unique component of the renin-angiotensin system, because angiotensinogen is only known as a substrate for angiotensin I generation. It is unclear whether circulating angiotensinogen is a rate-limiting step in blood pressure regulation. Recent findings of genetic studies and analyses suggest that the angiotensinogen gene may be a candidate as a determinant of hypertension. To test the hypothesis that angiotensinogen may modulate blood pressure, we transfected antisense oligonucleotides against rat angiotensinogen into the rat liver via the portal vein using liposomes that contain viral agglutinins to promote fusion with target cells, a technique that has been reported to be highly efficient. Transfection of antisense oligonucleotides resulted in a transient decrease in plasma angiotensinogen levels in spontaneously hypertensive rats from day 1 to day 7 after the injection, consistent with the reduction of hepatic angiotensinogen mRNA. Plasma angiotensin II concentration was also decreased in rats transfected with antisense oligonucleotides. Moreover, a transient decrease in blood pressure from day 1 to day 4 was observed, whereas transfection of sense and scrambled oligonucleotides did not result in any changes in plasma angiotensinogen level, blood pressure, or angiotensinogen mRNA level. Overall, our results demonstrate that transfection of antisense oligonucleotides against rat angiotensinogen resulted in a transient decrease in the high blood pressure of spontaneously hypertensive rats, accompanied by a decrease in angiotensinogen and angiotensin II levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Ischemic delayed neuronal death. A mitochondrial hypothesis.

BACKGROUND: A brief period of global brain ischemia causes cell death in hippocampal CA1 pyramidal neurons days after reperfusion in rodents and humans. Other neurons are much less vulnerable. This phenomenon is commonly referred to as delayed neuronal death, but the cause has not been fully understood although many mechanisms have been proposed. SUMMARY OF REVIEW: Hippocampal CA1 neuronal death usually occurs 3 to 4 days after an initial ischemic insult. Such a delay is essential for the mechanism of this type of cell death. Previous hypotheses have not well explained the reason for the delay and the exact mechanism of the cell death, but a disturbance of mitochondrial gene expression could be a possibility. Reductions of mitochondrial RNA level and the activity of a mitochondrial protein, encoded partly by mitochondrial DNA, occurred exclusively in CA1 neurons at the early stage of reperfusion and were aggravated over time. In contrast, the activity of a nuclear DNA-encoded mitochondrial enzyme and the level of mitochondrial DNA remained intact in CA1 cells until death. Immunohistochemical staining for cytoplasmic dynein and kinesin, which are involved in the shuttle movement of mitochondria between cell body and the periphery, also showed early and progressive decreases after ischemia, and the decreases were found exclusively in the vulnerable CA1 subfield. CONCLUSIONS: A disturbance of mitochondrial DNA expression may be caused by dysfunction of the mitochondrial shuttle system and could cause progressive failure of energy production of CA1 neurons that eventually results in cell death. Thus, the mitochondrial hypothesis could provide a new and exciting potential for elucidating the mechanism of the delayed neuronal death of hippocampal CA1 neurons.

Animals↗
PubMed1995

Variable clinical symptoms in familial amyotrophic lateral sclerosis with a novel point mutation in the Cu/Zn superoxide dismutase gene.

We report a novel missense point mutation in exon 4 of the Cu/Zn superoxide dismutase (SOD) gene of affected members of a Japanese kindred segregating familial amyotrophic lateral sclerosis (FALS) through at least three successive generations. The mutation, which is predicted to cause the replacement of isoleucine at codon 104 by phenylalanine (I104F), is associated with a significant reduction in Cu/Zn SOD enzyme activity but results in a highly variable clinical phenotype. Age at onset varied from 6 to 55; the initial symptoms occurred in either the lower or upper extremities in different family members. The duration of the disease varied from 3 to 38 years. Two subjects, aged 59 and 34, remained asymptomatic until their death from other causes, although their offspring carrying the same mutation have already developed clinical evidence of the disease. These results suggest that FALS from this novel I104F mutation shows considerable clinical variation.

Adult↗
PubMed1995

Analysis of spinocerebellar ataxia type 1 (SCA1)-related CAG trinucleotide expansion in Japan.

Spinocerebellar ataxia type 1 (SCA1) is a neurodegenerative disorder caused by expansion of a CAG trinucleotide repeat. We analyzed CAG repeat expansion in 25 families in the northeast of Japan with hereditary ataxia of Menzel type. Twenty of 38 patients in 12 families had expanded allele for SCA1. The number of CAG repeats correlated with the age at onset. Although the relationship between anticipation and the number of CAG repeats in successive generations was not ascertainable, there was a tendency to paternal bias for the accelerated age at onset. Study of the number of CAG repeats in various tissues showed no differences in the repeat length in lymphocytes, muscle, or brain; sperm, however, showed an obvious expansion. This may be a clue to a possible mechanism for the molecular basis of paternal anticipation of the disease. The SCA1 gene was transcribed from both wild and mutated alleles in muscles of affected individuals, but the repeat length was the same for both the muscle cDNA and the lymphocyte genomic DNA. These results suggest that, in the area of Japan where SCA1 is prevalent, 48% of families with spinocerebellar degeneration have SCA1 mutation.

Adult↗
PubMed1995

Alteration of bone status with ascorbic acid deficiency in ODS (osteogenic disorder Shionogi) rats.

Rats with hereditary defects in ascorbic acid (AsA) synthesis (ODS rats) subjected to AsA-deficiency for 3 weeks showed reductions of plasma alkaline phosphatase and dry and ash weights of the tibia, but no body weight alteration. In accordance with the chemical changes, bone loss and decrease of bone formation by AsA deficiency but not by malnutrition were observed in contact microradiographs of the tibia and by a tetracycline double labeling technique, respectively. The mechanical properties of femora measured by a three point-bending procedure were also altered by AsA deficiency for 3 weeks and showed decreases of 59% in toughness, 32% in strength, 32% in ductility and 22% in stiffness. The biomechanical changes by AsA deficiency were greater than the chemical changes in bone, indicating the usefulness of measuring mechanical properties as a sensitive method for the evaluation of the bone status. The second moment of the area of the femur was not changed by AsA deficiency. These results suggest that AsA deficiency in ODS rats causes marked bone loss and reduction in bone formation, which is accompanied by a greater reduction in biomechanics of the femur without causing macroarchitectural changes.

Animals↗
PubMed1995

[Age-related changes in the retina of WBN/Kob rats--a pathological study].

Male rats of the WBN/Kob strain, which are known to spontaneously develop diabetes with aging, were examined for histopathological changes in the retina. Five rats (10 eyes) each of WBN/Kob and Wistar/ST as a control were used, and the thickness of the retinal layers, both the central region and the peripheral region of the retina, were measured on weeks 1, 2, 3, 5, 9, 13, 17, 23, 27, 36, 45, 54, 67 and 80 after birth. The rod and cone cell layer in WBN/Kob rats was under-grown, and its thickness decreased 71.7% in the central zone and 59.3% in the peripheral zone of the retina compared with that of the control. In the central and peripheral retina, the rod and cone cell layer, outer nuclear layer and outer plexiform layer, as well as the inner plexiform layer in the central retina, gradually decreased in thickness from 5-45 weeks of age. In the central and peripheral parts of the retina, the number of nuclei decreased in accordance with the thinning of the nuclear layer. The thinned layers showed only cell loss. The rod and cone cell layer of the peripheral retina was thinner than that of the central retina. We obtained the following findings in the retina of male WBN/Kob rats. First, the rod and cone cell layer is undergrown compared with that of the control. Second, the first change occurred in the rod and cone cell layer. Third, the thinning of the rod and cone cell layer appeared at 5 weeks of age, and thinning with aging was slow. And finally, the thinning of the peripheral retina was more severe than that of the central retina. From the above findings, it seems that retinal changes in WBN/Kob rats are similar to the retinal degeneration of rds mice (retinal degeneration slow mice) and that WBN/Kob rats provide a useful animal model for human retinopathy.

Aging↗
PubMed1995

Vasospastic angina pectoris associated with apical hypertrophic cardiomyopathy.

As the chest symptoms and electrocardiographic changes of hypertrophic cardiomyopathy are occasionally very similar to those of angina pectoris, there are some difficulties in the diagnosis and treatment of cases of ischemic heart disease associated with hypertrophic cardiomyopathy. Here we report a case of vasospastic angina pectoris associated with hypertrophic cardiomyopathy diagnosed by coronary spasm provocation test performed by intracoronary administration of acetylcholine. In the treatment of such cases, beta blockers, which have the effect of decreasing the oxygen demand of the heart and the potential to induce coronary spasm, must be administered carefully.

Acetylcholine↗
PubMed1995

Characterization of the LIM/homeodomain gene islet-1 and single nucleotide screening in NIDDM.

Islet-1 (Isl-1) is a unique transcription factor that binds to the enhancer region of the insulin gene. To evaluate this gene in non-insulin-dependent diabetes mellitus (NIDDM), a full-length human Isl-1 cDNA was isolated and the genomic structure was characterized. The cDNA [2,395 bp plus additional poly(A) residues] contained an open reading frame from an initiator methionine at nucleotide 240 to an opal stop codon at nucleotide 1,286 (GenBank accession number UO7559), encoding a predicted protein of 349 amino acids (39 kDa). From their ends, 23 additional clones were sequenced, revealing 15 incomplete cDNAs and 8 intron-containing partially processed precursors. As determined by Northern blotting and reverse transcriptase-polymerase chain reaction analysis, Isl-1 was most abundantly expressed as a 2.4-kb mRNA in human islets, with a restricted pattern of expression in other adult human tissues. Analysis of genomic clones revealed that Isl-1 is encoded by six exons, varying in size from 168 bp (exon 5) to 1,230 bp (exon 6). Exons 2 and 3 each encode a LIM domain, while the homeodomain is completely contained within exon 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1995

Posterior pituitary hematoma in a case of posttraumatic diabetes insipidus. Case report.

A 28-year-old man presented with diabetes insipidus (DI) 10 days after basilar skull fracture without brain injury. Magnetic resonance (MR) imaging revealed a hematoma in the posterior lobe of the pituitary gland but no lesions in the hypothalamus or pituitary stalk. The patient's DI continued for 2 months at which time transsphenoidal surgery was performed to decompress the cystic hematoma with persistent mass effect. The DI attenuated shortly after the surgery and the patient became completely free from DI 5 months later. Although hemorrhage into the posterior lobe is one of the frequent pathological changes in fatal head-injury victims and secondary DI in these cases has usually been thought to be acute and transient, the true incidence and natural course of the posterior pituitary hemorrhage and subsequent DI in nonfatal head-injury patients are totally unknown. In this article, the authors present the first demonstration on MR imaging of a posterior pituitary hematoma in a patient with head injury. The authors propose that serial MR imaging is an important diagnostic tool in patients with posttraumatic DI because some of them may harbor pituitary hematoma and because decompression surgery may prevent transition to permanent DI, especially in cases when the mass effect is persistent due to a cystic change in the hematoma.

Acute Disease↗
PubMed1995

Work of flexion after flexor tendon repair according to the placement of sutures.

Tendon repairs comparing dorsal or volar placement of sutures were done on 36 flexor profundus tendons from 9 canine cadaveric paws. Three suture techniques were used. Work of flexion as a measure of resistance to tendon gliding was measured in the following groups: Groups 1 and 2: 4-strand Savage technique with 5-0 core suture, dorsal or volar placement; Groups 3 and 4: 4-strand Savage technique with 4-0 core suture, dorsal or volar placement; and Groups 5 and 6: tendon splint technique, dorsal or volar placement. The increase in work of flexion values were 11.3%, 14.1%, 12.2%, 37%, 20.5%, and 92.7% for Groups 1 through 6, respectively. The increase in work of flexion value in Group 4 was significantly greater than that in Group 3, and the value in Group 6 was significantly greater than Group 5. These data suggest that the work of flexion after tendon repair was influenced by the location of the suture material; volar location of suture material significantly increased the work of flexion value.

Animals↗