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Biomedical subjects

K Kitagawa

Publications and source records attributed to K Kitagawa.

At least 217 records · Page 12Linked to original sources
PubMed1991

Polymorphism of apolipoprotein A-II (apoA-II) among inbred strains of mice. Relationship between the molecular type of apoA-II and mouse senile amyloidosis.

Three types of apolipoprotein A-II (apoA-II) proteins (A, B and C) were predicted from the nucleotide sequence of apoA-II cDNA. Substitution of amino acid residues was noted at four positions (type A: Pro-5, Asp-20, Met-26, Ala-38; B: Pro-5, Glu-20, Val-26, Val-38; C: Gln-5, Glu-20, Val-26, Ala-38). Each type was identifiable by digestion of amplified apoA-II DNA by PCR, using restriction-fragment-length polymorphism of the apoA-II gene for restriction enzymes Cfr13I and MspI. The molecular type of apoA-II was determined among 23 strains of mice including nine of the senescence accelerated mouse series developed in our laboratory. Examination of types of apoA-II and amyloid deposition in the F2 and F3 hybrid mice showed that apoA-II amyloid deposition was present only in the mice homozygous for type C apoA-II and which were 12-17 months of age. The molecular type of apoA-II may be a factor involved in the development of senile amyloidosis in mice.

Aging↗
PubMed1991

'Ischemic tolerance' phenomenon detected in various brain regions.

We investigated the effects of mild and non-lethal ischemic insult on neuronal death following subsequent lethal ischemic stress in various brain regions, using a gerbil model of bilateral cerebral ischemia. Single 10-min ischemia consistently caused neuronal damage in the hippocampal CA1, CA2, CA3 and CA4, layer III/IV of the cerebral cortex, dorsolateral part of the caudoputamen and ventrolateral part of the thalamus. On the other hand, in double ischemia groups, 2-min ischemic insult 2 days before 10-min ischemia exhibited significant protection in the CA1 and CA3 of the hippocampus, the cerebral cortex, the caudoputamen and the thalamus. Five-min ischemic insult 2 days before 10-min ischemia also showed protective effect in the same areas as those of 2-min ischemia except for the CA1 region of the hippocampus, while 1-min ischemic insult exhibited no protective effect in any brain regions. In the immunoblot analysis, both 2- and 5-min ischemia caused increased synthesis of heat shock protein 72 (HSP 72) in the hippocampus, but 1-min ischemia did not. The present study demonstrated that the 'ischemic tolerance' phenomenon was widely found in the brain and also suggested that ischemic treatment severe enough to cause HSP 72 synthesis might be needed for induction of 'ischemic tolerance'.

Animals↗
PubMed1991

Isolation and characterization of the 160,000-Da phosphotyrosyl protein, a putative participant in insulin signaling.

The 160,000-Da protein (pp 160) which is rapidly phosphorylated on tyrosine in response to insulin and thus is a putative participant in signaling from the insulin receptor has been purified to homogeneity from 3T3-L1 adipocytes. Isolation of this protein was accomplished by chromatography on an immobilized monoclonal antibody against phosphotyrosine, followed by gel electrophoresis. Sufficient protein was obtained to allow the determination of the sequences of several peptides, which in turn enabled the development of anti-peptide antibodies that specifically recognize pp 160. Immunoblotting of 3T3-L1 adipocyte lysates, together with the purified pp 160 as a standard, indicate that an insulin-treated 3T3-L1 adipocyte possesses about 230,000 copies of tyrosine-phosphorylated pp160 and that this amount is approximately 25% of the total pp160 in the cell. The number of tyrosine-phosphorylated pp160s per cell is approximately the same as that of insulin receptor beta subunits. These results provide further evidence for a role of pp160 in insulin signaling. Moreover, the availability of purified protein and knowledge of peptide sequences will allow the elucidation of the structure and function of this protein.

Adipose Tissue↗
PubMed1991

Temporal profile of serum albumin extravasation following cerebral ischemia in a newly established reproducible gerbil model for vasogenic brain edema: a combined immunohistochemical and dye tracer analysis.

We investigated the temporal profile of the extravasation of serum albumin in a reproducible gerbil model of unilateral cerebral ischemia, using immunohistochemical and dye-tracer techniques to evaluate albumin accumulation and the occurrence of active extravasation, respectively. After 30 min of cerebral ischemia and subsequent reperfusion, immunostaining for albumin became visible in the lateral part of the thalamus during the first 3 h, and then expanded to other brain regions up to 24 h. At both 24 h and 3 days after reperfusion, massive extravasation of albumin was noted in the whole ischemic hemisphere, and this had decreased again by 7 days after reperfusion. The extent and the degree of albumin immunopositivity were almost the same in all animals examined at each period after reperfusion. The extravasation of Evans blue, which was allowed to circulate for 30 min before death, was limited to the lateral part of the thalamus during the first 6 h of reperfusion. In the circumscribed area of massive albumin extravasation, many neurons were immunopositive for albumin; most of these neurons appeared to be intact and also showed immunostaining for microtubule-associated protein 2. The current investigation clearly demonstrated that (1) albumin extravasation was produced with reliable reproducibility in this model, (2) the lateral part of the thalamus was the region most vulnerable to ischemic blood-brain barrier damage, and (3) many apparently intact neurons in the ischemic region were positive for albumin.

Animals↗
PubMed1991

Asymptomatic constant isolated proteinuria in children.

The clinical features, renal biopsy findings, and subsequent course in 53 children with asymptomatic constant isolated proteinuria were studied retrospectively (1) to determine the prevalence of renal pathologic abnormalities among these children, (2) to identify those clinical characteristics that may enable recognition of children with an increased likelihood of having renal pathologic abnormalities, and (3) to assess the clinical course. All biopsy specimens were examined by light, immunofluorescence, and electron microscopy. Twenty-five patients (47%) had significant glomerular changes (15 had focal segmental glomerulosclerosis, 4 IgA nephropathy, 3 diffuse mesangial proliferative glomerulonephritis without IgA deposition, and 3 membranous glomerulonephritis), and 28 had minimal glomerular changes. There were no differences between the patients with significant glomerular changes and those with minimal glomerular changes with regard to clinical and laboratory findings except for a predominance of boys in the former group. At the latest follow-up, seven patients with significant glomerular changes, but none with minimal glomerular changes, had chronic renal impairment. Because of the high incidence of significant glomerular changes and the high rate of progression to chronic renal impairment, we believe that a renal biopsy is indicated for a child with asymptomatic constant isolated proteinuria.

Adolescent↗
PubMed1991

Hyperthermia-induced neuronal protection against ischemic injury in gerbils.

We investigated the effect of hyperthermic pretreatment before induction of ischemia using a gerbil model of 5-min forebrain ischemia. A single hyperthermic treatment 18 h before ischemia exhibited a partial protective effect, and repetitive hyperthermic pretreatments at 18-h intervals before ischemia showed clear protection against neuronal death in the CA1 area of the hippocampus, whereas single hyperthermic treatment 3, 6, 24, or 50 h before ischemia exhibited little protective effect. This transient and cumulative neuroprotective effect of hyperthermic pretreatment strongly suggested the involvement of stress reactions after hyperthermia in the protective mechanism against ischemic neuronal death.

Animals↗
PubMed1991

Trichilemmal tumor arising in a seborrheic keratosis: analysis of cell kinetics by BrdU staining.

We report a case of a 74-year-old male with a trichilemmal tumor arising in a seborrheic keratosis on the buttock and the results of a cell kinetic study of this tumor using a BrdU staining method. The incidence of trichilemmal tumor arising in a seborrheic keratosis seems to be extremely rare. The labeling index of this tumor was 12.0%; this was a level intermediate between normal epidermis and a variety of hyperproliferative skin diseases such as squamous cell carcinoma, Bowen's disease, and psoriasis vulgaris. DNA replicating cells were present in the germinative layers in normal epidermis and the benign hyperproliferative skin diseases, psoriasis vulgaris. In contrast, DNA replicating cells were found throughout the entire epidermis in premalignant and malignant tumors such as in Bowen's disease and squamous cell carcinoma. In this case, DNA replicating cells were localized mainly in the basal and parabasal cell layers, but also seen in the upper squamous layers. These findings suggest that this trichilemmal tumor had a malignant tendency, though it was slow-growing and relatively benign in nature.

Aged↗
PubMed1991

Detection and typing of multiple genital human papillomaviruses by DNA amplification with consensus primers.

Many types of human papillomavirus (HPV) are associated with genital lesions. In order to develop simple and sensitive diagnostic procedures for HPV infection, we took advantage of the polymerase chain reaction (PCR). We compared the published nucleotide sequences of the L1 region from six genital HPV types and designed a pair of consensus primers for L1 region. The PCR with the consensus primers for L1 region (L1-PCR) could amplify at least nine genital HPV types, 6, 11, 16, 18, 31, 33, 42, 52 and 58, and the amplified HPV DNA could be typed by subsequent restriction mapping. L1-PCR was compared to Southern blot analysis and also to the consensus primer-mediated PCR for E6 region (E6-PCR) described before. Although both our PCR systems are nonradioactive, PCR for E6 region (E6-PCR) described before. Although both our PCR systems are nonradioactive, the sensitivity in detecting HPV DNA was even better than that obtained by using Southern blot analysis. By means of the PCR systems we detected HPV DNA in 100% of cervical condylomas (10/10), 92% of cervical intraepithelial neoplasias (33/36) and 96% of invasive cervical carcinomas (53/55), while we detected HPV DNA in 12% of normal cervices (12/102).

Base Sequence↗
PubMed1991

Hepatocellular carcinomas with excessive copper accumulation: CT and MR findings.

Results of orcein staining and findings obtained with non-contrast-medium-enhanced computed tomography (CT) and magnetic resonance (MR) imaging (T1- and T2-weighted images) were compared for 53 histologically confirmed hepatocellular carcinomas (HCCs). HCCs were 5 cm in the largest diameter. Three lesions with diffuse and strong orcein staining were highly attenuating on nonenhanced CT images. Electron x-ray microanalysis of one of them revealed copper. The high attenuation value at nonenhanced CT may have been due to the abundant copper-binding protein in the cancer cells. The difference between orcein staining results and attenuation patterns at CT was statistically significant (chi 2, P less than .001). It could not be concluded that the paramagnetic effects of copper in HCC had an influence on signal intensity on MR images. The difference between orcein staining results and signal-intensity patterns on T1- and T2-weighted images was not statistically significant.

Adult↗
PubMed1991

[Silent cerebral infarction in the patients with essential hypertension].

Evidence of old cerebral infarction of magnetic resonance imaging (MRI) is common in acute stroke patients without a prior history of stroke. This experience led us to investigate the incidence of silent cerebral infarction (SCI) in the patients with essential hypertension, as well-known major predisposing factor for stroke. The incidence, number, size and localization of SCI on MRI (MARK-J, 0.1 T) and the prevalence of risk factors for stroke were investigated both in 66 hypertensive patients (WHO stage I or II; 63 +/- 9 (mean +/- S.D.) years old) and in 42 age-matched normotensive patients (61 +/- 9 years old). Risk factors selected were as follows: diabetes mellitus, hypercholesterolemia, daily alcohol intake, cigarette smoking, obesity, cardiac disease (arrhythmia and ischemic heart disease), hyperuricemia and high hematocrit. In hypertensive patients, the relationships between the incidence of SCI and hypertensive damages in major organs were also investigated. SCI was found in 45 out of the 108 subjects studied and a total of 216 SCI lesions were detected. All of the SCI lesions were localized in the subcortical white matter or in the basal ganglia. All SCI lesions were smaller than 3 cm in diameter and 201 lesions (93%) were smaller than 1 cm. The incidence of SCI tended to be higher in hypertensive patients (47%) than that in normotensives (33%) and increased significantly with advancing age in hypertensives from 26.9% in the 50s to 86.7% in the 70s, while no significant increase was noted in normotensives.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Mouse senile amyloidosis. ASSAM amyloidosis in mice presents universally as a systemic age-associated amyloidosis.

Amyloid deposition in 11 inbred strains of mice (A/J, SJL/J, DDD, C57BL/6J, B10.BR, C57BL/10, B10A/SgSn, C3H/HeMs, B10A(5R), DBA/2 and C57BL/6Cr5/c) was studied using the peroxidase antiperoxidase (PAP) method and antisera against ASSAM and murine protein AA. Among the 170 mice examined, in 77 (45.3%) from the nine strains other than C3H/HeMs and DBA/2, there was evidence of spontaneous amyloid deposits in routine histological sections. Immunohistochemical studies using 54 mice with amyloid deposition, demonstrated ASSAM deposition in 45 mice (83.3%) in all nine strains, although the incidence and intensity of the deposition differed somewhat between strains. SJL/J and A/J had ASSAM deposits from the age of 8 months and the incidence increased with advancing age. In the other seven strains, ASSAM was first deposited at an older age than in the SJL/J and A/J strains. In A J, C57BL/6J, C57BL/10, B10.BR, B10A(5R) and C57BL/6Cr5/c, protein AA often coexisted with ASSAM. The distribution pattern of the ASSAM deposits was similar to that observed among the SAM strains. Thus, ASSAM is an ubiquitously distributed senile amyloid protein in the mouse. Determination of the molecular type of apoA-II, a serum precursor of ASSAM, among all 11 strains using the polymerase chain reaction (PCR) revealed the SAM-P/1 type apoA-II variant in SJL/J and A/J strains with a high susceptibility to ASSAM deposition. We concluded from this study that amino acid substitution in precursor apoA-II may be responsible for the early onset and severe amyloid deposition in the mouse.

Aging↗
PubMed1991

Inhibitory effect of pentoxifylline and prostaglandin E1 on the release of neutrophil elastase from FMLP-stimulated neutrophils.

We measured the enzymatic and immunologic activities of neutrophil elastase to determine whether pentoxifylline and prostaglandin E1 are useful for inhibiting the enzymatic activity of released neutrophil elastase. Both activities in the medium decrease in the presence of pentoxifylline and prostaglandin E1. These results showed that pentoxifylline and prostaglandin E1 inhibited the release of neutrophil elastase from activated neutrophils, and that they may be useful in the improvement of neutrophil-mediated cellular injury.

Alprostadil↗
PubMed1991

[A case of left lung cancer associated with an aneurysm of the thoracic aorta].

A 61-year-old man was admitted to our hospital because of a left lung cancer. The chest x-ray film showed an irregular mass in the left upper lung field and the ill-defined left upper mediastinal border. A large portion of the aorta seen in the CT section above the aortic arch was understood to be aortic elongation. When a left pneumonectomy was performed, a saccular aneurysm of the distal aortic arch was found and resected under partial aortic clamping. Following the aneurysmectomy mediastinal dissection was performed in the normal way. The patient recovered uneventfully. The pathological specimens showed a pT2N1M0 squamous cell carcinoma with obstructive pneumonia and an arteriosclerotic aneurysm. There was no report of lung cancer associated with aneurysm of the thoracic aorta. In a patient with left lung cancer obliterating the left upper mediastinal border (the "silhouette sign") the aortic arch should be closely examined by MRI and/or angiography.

Aorta, Thoracic↗
PubMed1990

'Ischemic tolerance' phenomenon found in the brain.

We investigated the possibility that neuronal cells given a mild ischemic treatment sufficient to perturb the cellular metabolism acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo. Cerebral ischemia was produced in the gerbils by occlusion of both common carotids for 5 min, which consistently resulted in delayed neuronal death in the CA1 region of the hippocampus. Minor 2-min ischemia in this model depletes high-energy phosphate compounds and perturbs the protein synthesis, but never causes neuronal necrosis, and therefore was chosen as mild ischemic treatment. Single 2-min ischemia 1 day or 2 days before 5 min ischemia exhibited only partial protective effects against delayed neuronal death. However, two 2-min ischemic treatments at 1 day intervals 2 days before 5 min ischemia exhibited drastically complete protection against neuronal death. The duration and intervals of ischemic treatment, enough to perturb cellular metabolism and cause protein synthesis, were needed respectively, because neither 1-min ischemia nor 2-min ischemia received twice at short intervals exhibited protective effects. This 'ischemic tolerance' phenomenon induced by ischemic stress--which is unquestionably important--and frequent stress in clinical medicine, is intriguing and may open a new approach to investigate the pathophysiology of ischemic neuronal damage.

Animals↗
PubMed1990

Insulin regulation of the two glucose transporters in 3T3-L1 adipocytes.

The amounts of the brain type and muscle type glucose transporters (designated Glut 1 and 4, respectively) in 3T3-L1 adipocytes have been determined by quantitative immunoblotting with antibodies against their carboxyl-terminal peptides. There are about 950,000 and 280,000 copies of Glut 1 and 4, respectively, per cell. Insulin caused the translocation of both types of transporters from an intracellular location to the plasma membrane. The insulin-elicited increase in cell surface transporters was assessed by labeling the surface transporters with a newly developed, membrane-impermeant, photoaffinity labeling reagent for glucose transporters. The increases in Glut 1 and 4 averaged 6.5- and 17-fold, respectively, whereas there was a 21-fold in hexose transport. These results indicate that the translocation of Glut 4 could largely account for the insulin effect on transport rate, but only if the intrinsic activity of Glut 4 is much higher than that of Glut 1. The two transporters are colocalized intracellularly: vesicles (average diameter 72 nm) isolated from the intracellular membranes by immunoadsorption with antibodies against Glut 1 contained 95% of the Glut 4 and, conversely, vesicles isolated with antibodies against Glut 4 contained 85% of the Glut 1.

Adipose Tissue↗
PubMed1990

Translocation of the brain-type glucose transporter largely accounts for insulin stimulation of glucose transport in BC3H-1 myocytes.

Insulin-stimulated glucose transport was examined in BC3H-1 myocytes. Insulin treatment lead to a 2.7 +/- 0.3-fold increase in the rate of deoxyglucose transport and, under the same conditions, a 2.1 +/- 0.1-fold increase in the amount of the brain-type glucose transporter (GLUT 1) at the cell surface. It has been shown that some insulin-responsive tissues express a second, immunologically distinct, transporter, namely GLUT 4. We report here that BC3H-1 myocytes and C2 and G8 myotubes express only GLUT 1; in contrast, rat soleus muscle and heart express 3-4 times higher levels of GLUT 4 than GLUT 1. Thus translocation of GLUT 1 can account for most, if not all, of the insulin stimulation of glucose transport in BC3H-1 myocytes. On the other, hand, neither BC3H-1 myocytes nor the other muscle-cell lines are adequate as models for the study of insulin regulation of glucose transport in muscle tissue.

Animals↗