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Biomedical subjects

T Kondoh

Publications and source records attributed to T Kondoh.

At least 199 records · Page 11Linked to original sources
PubMed1989

[Diagnosis and treatment of fibrous adhesion into upper joint compartment of the TMJ. Part 2. Arthroscopic findings and arthroscopic sweeping and lysis].

A fibrous adhesion into upper joint compartment of the TMJ is indicated by a secondary pathological condition of the disk displacement. A fibrous adhesion increases resistance to motion in the joint because condyle translation disrupted. The treatment for this condition is too difficult. On this paper, we presented to arthroscopic findings of 4 cases of the fibrous change and fibrous adhesion into upper joint compartment of the TMJ (1) and arthroscopic sweeping as the treatment procedure (2). On these cases, we compared double contrast arthrotomographic findings with arthroscopic findings (3). (1) On the arthroscopic findings, banddle like fibrous adhesion, wide areal fibrous adhesion, and wide areal fibrous change of the articular surfaces were observed. These findings varied to case by cases. (2) The arthroscopic sweeping and lysis performed on this four cases. The clinical symptoms prior to arthroscopic surgery, improved post surgically in all cases. (3) The fibrous lesions in the upper joint compartment was presumed by double contrast arthrotomography that demonstrated by arthroscopy.

Arthroscopy↗
PubMed1989

[The effect of bilateral vagal blockade on respiration].

Although respiratory regulation has been extensively studied so far, the relation between the vagal nerves and respiratory reflex in man is still open to controversy. This paper describes the effect of bilateral vagal blockade on respiration. 1) Dyspnea due to unilateral bronchial occlusion. This type of dyspnea is caused by extreme depression of the intrabronchial pressure on the occluded side and is accompanied by a rapid increase in respiratory rate and a rapid decrease in tidal volume. This type of dyspnea is relieved by blockade of the ipsilateral cervical vagal nerve. 2) Animal experiments on bilateral lung transplantation, heart-lung transplantation and bilateral cervical vagal blockade. The respiratory changes induced by CO2 inhalation, low O2 inhalation, respiratory stimulant. Loss of blood or fever stimulation in the manipulated dogs were compared with those in normal controls. CO2 inhalation alone produced differences in the respiratory rates and tidal volumes between the two groups. The tidal volume increase under CO2 inhalation was suppressed by the inflation reflex but other afferent vagal nerves seemed to be closely associated with the increased respiratory rate. 3) Vagal nerve reflex in humans. Blockade of the bilateral cervical vagal nerves in an awake state resulted in irregular PETCO2 in cases that had been stable and sometimes produced a pattern of Cheyne-Stokes respiration. Inhalation of 5% CO2 restored the regular rhythm of respiration and enhanced the response to CO2. When subjected to bilateral vagal blockade in an awake state, the patient expressed an unbearbly uneasy dyspneic sensation as if he were pulled into a bottomless abyss. This was demonstrated by the unstable FRC level.

Animals↗
PubMed1989

[A case of primary malignant lymphoma of the brain associated with acute hydrocephalus].

A case of primary cerebral malignant lymphoma associated with hydrocephalus is reported. The patient was a 54 year-old male who enjoyed good health until the onset of headache and vomiting 4 weeks before admission. His consciousness was alert and neurological examination revealed severe papilloedema with retinal hemorrhage. No lymph node or abdominal tumor enlargement were noted. CT scan and MR images revealed no abnormal lesion except mild ventriculomegaly. CSF study revealed mild elevation of protein and sugar and cell count was 66/3. CSF cytology revealed atypical lymphoid cell with irregular nuclear contour and large nucleolus. Immunological marker studies of the tumor cell revealed increasing of anti J-5 (CD10), anti B-4 (CD19) and OKT-IA1. The patient was treated by a whole brain irradiation and chemotherapy after V-P shunt. It is 12 months since the operation, and the patient's condition is still good.

Acute Disease↗
PubMed1988

Complex glycerol kinase deficiency: molecular-genetic, cytogenetic, and clinical studies of five Japanese patients.

Five male Japanese patients with complex glycerol kinase deficiency (CGKD) and their relatives were studied clinically, cytogenetically, and molecular-genetically. All patients had muscular dystrophy or muscle weakness, mental retardation, congenital adrenal hypoplasia, and glycerol kinase deficiency. High-resolution GTG-banded chromosomes showed a microdeletion in the Xp21 region in all four patients examined and in all five mothers. Southern hybridizations, after digestions by restriction endonucleases, with various cloned DNAs (D2, 99-6, B24, C7, L1-4, cDMD13-14, J66-HI, P20, J-Bir, ERT87-30, ERT87-15, ERT87-8, ERT87-1, XJ-1.1, 754, cx5.7, and OTC-1) that are located around Xp21 also showed a deletion in the genome of all patients and mothers. Although the deletion differed in size among patients, a segment commonly absent was located between the genomic sequences corresponding to L1-4 and cDMD13-14. This finding indicated that the gene coding for glycerol kinase (GK) is located within this segment. A comparison of the clinical manifestations of the present five patients and reported CGKD or Duchenne muscular dystrophy (DMD) patients with DNA deletion suggests the existence of a certain gene responsible for gonadotropin deficiency (GTD). The result of the present study and results of previous studies suggest that genes for ornithine transcarbamylase (OTC), DMD, and GK and putative genes responsible for congenital adrenal hypoplasia (AHC) and GTD are arranged from telomere to centromere as pter--GTD--AHC--GK--DMD--OTC--cen.

Adolescent↗
PubMed1988

Origin of the extra chromosome in trisomy 18. A study on five patients using a restriction fragment length polymorphism.

The parental origin of an extra chromosome in five patients with trisomy 18 was traced using a restriction fragment length polymorphism (RFLP) of the human prealbumin (PA) gene, localized to 18p11.1-q12.1, as a genetic marker. MspI digests of the genomic DNAs of the five patients, their parents and normal controls were hybridized with the PA-cDNA. Densitometric analysis on the gene dose of the polymorphic fragments of these patients revealed that three had originated from a maternal meiotic error. The other two patients were uninformative for the parental origin of trisomy 18. Our results indicate that nondisjunctional errors leading to trisomy 18 may occur predominantly at the maternal meiosis, consistent with the results of previous studies on the parental origin of trisomies 21 and 13.

Chromosomes, Human, Pair 18↗
PubMed1988

Prenatal DNA analysis in four embryos/fetuses at risk of 21-hydroxylase deficiency.

Prenatal diagnosis of 21-hydroxylase deficiency (21-OHD) in two unrelated embryos and two fetuses was attempted with the Southern hybridization method using the 21-hydroxylase (21-OHase) complementary DNA as a probe. The two embryos whose genomic DNA was extracted from their chorionic villi both had four TaqI fragments (3.7 kb, 3.2 kb, 2.4 kb and 2.3 kb) identical to those of their respective parents and normal controls, while the DNA from each proband of these two families lacked with the 3.7 kb and the 2.3 kb fragments corresponding to the functional 21-OHase gene (21-OHase B gene). These findings indicated that none of the embryos examined were deletion homozygotes for the 21-OHase B gene. In the two fetuses, only amniotic fluid cells were available for prenatal diagnosis. The results of Southern hybridization analysis were uninformative since all family members, including the probands and fetuses, had all four TaqI fragments. Linkage studies between 21-OHD and human leukocyte antigen (HLA) haplotypes and those between the disease and restriction fragment length polymorphisms of the 4th complement gene revealed that the fetus of one family was normal. The other fetus could not be diagnosed because a recombination between the class I HLA and the 21-OHD loci had occurred in this family.

Adrenal Hyperplasia, Congenital↗
PubMed1988

Acute subdural hematoma associated with nontraumatic middle meningeal artery aneurysm: case report.

A rare case of acute subdural hematoma from rupture of a nontraumatic aneurysm of the middle meningeal artery is described. The subdural hematoma was evacuated and the aneurysm was removed. The literature on nontraumatic aneurysm of the middle meningeal artery is reviewed. The importance of cerebral angiography in the patient with an unexplained subdural hematoma is emphasized.

Acute Disease↗
PubMed1988

Tetrodotoxin sensitivity of high K+-induced 86Rb efflux in the duodenal circular muscle of pigs.

The 86Rb efflux by high K+ was measured simultaneously during the mechanical responses in pig duodenal circular muscle using a superfusion technique. A slightly higher K+ (17.7-23.6 mM) simultaneously induced tetrodotoxin (TTX)-sensitive relaxation and 86Rb efflux. Much higher K+ (47.2-143.4 mM) contracted and also increased the 86Rb efflux markedly, but the extent of TTX-sensitive efflux remained the same as the one at 17.7-23.6 mM K+, indicating that the TTX-insensitive efflux was contraction-related. The former efflux may lead to hyperpolarization linked to relaxation.

Animals↗
PubMed1988

Fatal intracranial hemorrhage after balloon occlusion of an extracranial vertebral arteriovenous fistula. Case report.

A patient is presented who developed a fatal hemorrhage immediately after balloon occlusion of an extracranial vertebral arteriovenous fistula. The fistula was associated with marked retrograde flow not only from the contralateral vertebral artery but also from the carotid artery system through the posterior communicating artery and the basilar artery. The bleeding appeared to be caused by acute hemodynamic effects following abrupt occlusion of the long-standing fistula. A gradual staged occlusion or trapping procedure should be considered for the treatment of such vertebral arteriovenous fistulae.

Adult↗
PubMed1988

[Clinical and hemodynamic effects of lipo PGE1 in cerebral infarction].

Prostaglandin (PG) E1 is a potent vasodilator on the peripheral vessels and also has an inhibitory action of platelet aggregation. Lipo PGE1, the lipid emulsified PGE1 has much longer half life time in the circulation than PGE1 which is rapidly inactivated in the lung. The purpose of this investigation was to study the clinical and hemodynamic effect of Lipo PGE1 on the 15 patients with acute or subacute focal cerebral ischemia. Of these patients, five had evidence of internal carotid artery occlusion, and ten had either occlusion or severe stenosis of middle cerebral artery. Lipo PGE1 containing 15 micrograms of PGE1 was administered within 12 days of onset of ischemic events. Before the first Lipo PGE1 administration, regional cerebral blood flow (rCBF) of the affected middle cerebral artery (MCA) territory was 41.8 +/- 8.4 ml/100 g/min and on the non-affected side was 60.0 +/- 9.4 ml/100 g/min. Immediately after the Lipo PGE1 treatment, rCBF of the MCA region was increased by 6% on the affected side and by 11% on the non-affected side. rCBF of the affected MCA territory was increased more than 15% in five cases (Group 1) and was changed less than +/- 15% in seven cases (Group 2) by the first Lipo PGE1 treatment. Lipo PGE1 was administered every 8 hours for 10 to 14 days in these 12 cases. By the continuous Lipo PGE1 treatment, rCBF of the affected MCA territory increased by 18% in the Group 1 and by 3% in the Group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Lipo prostaglandin E1 administration in the acute stage following subarachnoid hemorrhage].

Prostaglandin (PG) E1 is a potent vasodilator on the peripheral vessels and also has an inhibitory action of platelet aggregation. Thus it is expected that PGE1 may be used for the treatment of cerebral vasospasm due to aneurysmal subarachnoid hemorrhage (SAH). Lipo-PGE1, lipid emulsified PGE1 less destroyed in the lung, has much longer half life time in the circulation than PGE1 which is rapidly inactivated in the lung. A pilot study, examining the clinical effect of Lipo-PGE1 on cerebral vasospasm, was performed. Of 27 patients with a ruptured anterior circulation aneurysm, who were operated on at acute stage, 12 were treated with Lipo-PGE1 and hypervolemic therapy (Lipo-PGE1 treated group) and 15 with hypervolemic only (control group). After the aneurysm was clipped, Lipo-PGE1, containing 15 micrograms of PGE1 was administered every 8 hours for 2 weeks. The appearance and severity of symptomatic vasospasm were less in the Lipo-PGE1 treated group than the control, and the outcome of the Lipo-PGE1 treated patients with or without vasospasm improved significantly at 1 month follow-up examination. The cerebral blood flow (CBF) measurements were performed three times, at first (1st), second to third (2nd) and fourth to sixth (3rd) week after SAH. In the Lipo-PGE1 treated group, the 1st CBF measurement was done before administration of Lipo-PGE1 started and the 2nd examination was performed after the completion of administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Proglumide peptides and CCK antagonistic action in hog duodenal circular muscle.

New proglumide peptides were synthesized and their inhibitory activity against the cholecystokinin (CCK)-induced relaxation was tested in duodenal circular muscles of hogs in order to locate the active moiety. Isotonic tension is reported as a percentage of the relaxation induced by CCK-4 (4.23 microM) or by Ca-free EGTA (2 mM). In R1-CONHCH(CH2CH2CO-R2)CON(CH2CH2CH3)2, P2-II(R1 = PhCH2O, R2 = Phe33-NH2), its D isomer and P3-I (R1 = Ph, R2 = Asp32-Phe33-NH2) had potent antagonistic activity (IC50 = 47.9 (32.4-72.4) microM, 25.1 (10.0-61.7) microM and 186 (141-240) microM, respectively). Benzotript, from another group of CCK antagonists had an IC50 of 52.5 (40.7-67.6) microM. P2-II (49 microM) or its D isomer (19.6 microM) antagonized non-competitively, and P3-I (168 microM) and benzotript (58.4 microM) antagonized competitively the CCK-4-induced relaxation. P3-I (84 or 168 microM) also antagonized competitively the CCK-8-induced relaxation. The amino acids of Tyr27, Trp30 and Phe33, separately, play important roles for agonist activity for relaxation. Tyr27 is the main relaxing group, Trp30 an antagonistic one and Phe33 is another relaxing one. In the proglumide skeleton, N,N-dipropylglutaramic acid acts like Trp30. Agonist, partial agonist and antagonist activities are exerted by these three groups and bulky substituents.

Animals↗
PubMed1987

[Surgical resection of pulmonary metastases from colorectal carcinoma].

Twelve patients with pulmonary metastases of recurrent colorectal carcinoma underwent pulmonary resection at National Ohkura Hospital. The Cumulative five-year survival rate was 60 per cent. No correlation was found between the disease-free interval and survival following thoracotomy. There was a statistically significant difference in survival rates corresponding to Duke's classification of the primary lesion. Patients with solitary lesions had a better survival rate than patients with multiple lesions. We believe that the surgical treatment of pulmonary metastases in a select group of patients, i.e., those with solitary pulmonary lesions, will prolong survival and be curative in a number of patients.

Aged↗
PubMed1986

Full and partial relaxing CCK-C-terminal fragments in hog duodenal circular muscle.

The essential active moieties in the cholecystokinin (CCK) ligand for relaxing duodenal circular muscles of pigs were investigated. The decrease in isotonic tension from the normal tone was expressed as a percentage of the relaxation obtained with Ca2+-free EGTA (2 mM) solution. Inhibition was expressed as a percentage of the relaxation induced by CCK-C-terminal tetrapeptide (CCK-4, 4.23 microM) without antagonists. Amino acid sequences from CCK-(27-28) to CCK-(27-31) increased the potency. CCK-(27-30) or CCK-(27-31) attained the same extent of relative intrinsic activity as CCK-8. The amino acid sequence from Tyr27, CCK-(27), to Trp30, CCK-(30), is another prerequisite for relaxation, in addition to the sequence of CCK-4. Newly synthesized CCK-(27-30)-R derivatives with increasingly bulky substituents (R = H, ethyl, phenyl, n-butyl and allyl) were changed from full agonists to partial agonists. Phenyl, n-butyl and allyl derivatives of CCK-(27-30)-R, in particular, had a mixed agonist and antagonist action. CCK-(27-30)-allyl antagonized competitively the CCK-4-induced relaxation (IC50 = 123 (75.9-200) microM).

Animals↗