Biomedical subjects

K Hayashida

Publications and source records attributed to K Hayashida.

At least 109 records · Page 6Linked to original sources

PubMed1996

Isolation of a cDNA encoding the X enopus homologue of mammalian Cdc25A that can induce meiotic maturation of oocytes.

From a cDNA library of Xenopus laevis (Xl) oocytes, we isolated a cDNA encoding a putative protein phosphatase homologous to mammalian Cdc25A. Sequence analysis predicts that the Xl cdc25A gene product (Xl Cdc25A) consists of 521 amino acid residues and shares overall 55% identity with human Cdc25A. When its mRNA is injected into Xl oocytes, Xl Cdc25A can act as a potent M phase inducer.

Amino Acid Sequence↗

PubMed1996

A simple and secure anchoring system for Caspari's transglenoid multiple suture technique using a biodegradable poly-l-lactic acid button.

To manage a difficulty in tying sutures over the infraspinatus fascia when using Caspari's transglenoid multiple suture technique, we developed a new anchoring system using a biodegradable poly-L-lactic acid (PLLA) button and investigated its clinical efficacy in 28 patients who were followed-up for more than 2 years postoperatively (mean, 26.5 months). Twenty-four patients had Bankart lesions and 4 had detachment of the superior glenoid labrum. The mean age at operation was 22.1 years. The PLLA button measured 8 x 8 x 1.2 mm and had two holes. After multiple sutures were inserted by the routine Caspari technique (mean, 7.3 sutures), the sutures were divided into 2 bundles, passed through the holes in the button, and tied over it on the posterior scapular neck under traction. The arm was immobilized in a Velpeau bandage for 3 weeks after Bankart repair and for 1 to 2 weeks after superior labral repair. The results of Bankart repair were excellent in 13 patients, good in 7, and poor in 4 according to Rowe's rating scale (success rate, 83%), while the outcome of superior labral repair was excellent in 3 and good in 1 according to our own criteria. All 4 patients who showed a poor outcome were contact athletes who developed resubluxation postoperatively. There were no complications, but transient damages to the suprascapular nerve occurred in 2 patients. In conclusion, the PLLA button provided simple and secure suture fixation for the Caspari technique.

Adolescent↗

PubMed1996

High frequency of the MAGE-1 gene expression in hepatocellular carcinoma.

The MAGE-1 gene, originally isolated from a human melanoma cell line, directs the expression of a potential tumor-rejection antigen, MZ2-E. This antigen is recognized by autologous cytotoxic T lymphocytes in association with a major histocompatibility complex class I molecule (HLA-A1), and has provided a basis for specific immunotherapy for melanoma patients. Here we show a high frequency of expression of the MAGE-1 gene in hepatocellular carcinoma (HCC). We examined the expression of the MAGE-1 gene in cell lines originated from hepatoma cells and in tumor and nontumor tissues of livers with HCC by reverse-transcription polymerase chain reaction (RT-PCR) and subsequent Southern blotting. MAGE-1 messenger RNA (mRNA) was expressed in three of four HCC cell lines (75%) and in 16 of 20 (80%) resected HCCs though none was detected in nontumor tissues. The high frequency expression of MAGE-1 gene in HCCs suggests the possibility as a target for tumor-specific immunotherapy for HCC patients.

Adolescent↗

PubMed1996

Reduction of 123I-iomazenil uptake in haemodynamically and metabolically impaired brain areas in patients with cerebrovascular disease.

Iomazenil is a specific ligand for central-type benzodiazepine receptors (BZR). In order to determine the clinical significance of the findings of 123I-iomazenil single photon emission tomography (SPET) in cerebrovascular disease (CVD), we compared the cerebral uptake of 123I-iomazenil with oxygen metabolism measured by positron emission tomography (PET). Depending on the severity of the haemodynamic and/or metabolic impairment based on our institutional criteria [a reduction of < 30.6 ml 100g-1 min-1 in cerebral blood flow (CBF) and an increase of > 0.52 in the oxygen extraction fraction (OEF)], the cortical areas were classified into four groups as follows: Group I, normal CBF and OEF; Group II, normal CBF and increased OEF; Group III, reduced CBF and normal OEF; Group IV, reduced CBF and increased OEF. Seven patients (mean age 65 +/- 7 years) with CVD underwent both PET and 123I-iomazenil SPET within 8 days. The ratios of the mean counts in 14 regions of interest in the cerebral cortices to those in the cerebellar cortices (R/C ratios) were compared with the cerebral metabolic rate of oxygen (CMRO2). The R/C ratios of Group IV were lower than those of Group I (P < 0.005). The R/C ratios correlated with CMRO2 in Group III (r = 0.577, P < 0.01) and in Group IV (r = 0.707, P < 0.005), but not in Groups I or II. These results suggests that reduced uptake in 123I-iomazenil SPET reflects oxidative hypometabolism causing neuronal damage in haemodynamically and metabolically impaired areas in patients with CVD. This information may be valuable when deciding therapeutic approaches.

Aged↗

PubMed1996

Vasoreactive effect of acetazolamide as a function of time with sequential PET 15O-water measurement.

The accurate assessment of vascular flow reserve is crucial for the evaluation of risk among patients with cerebrovascular disease. In six patients with unilateral occlusion of the internal carotid artery and one patient with unilateral occlusion of the middle cerebral artery (mean +/- S.D. age = 68 +/- 3 years), we measured cerebral blood flow (CBF) after the administration of 940 MBq 15O-water using a remotely controlled power injector. Studies were performed at rest, after 10 min, and then 10, 20 and 30 min after the administration of 1 mg acetazolamide to evaluate the vasoreactive effect, as reflected by an increase in CBF. Sixteen regions of interest (ROIs) were drawn over the CBF images. These ROIs were as follows in each hemisphere: Area I, four areas in the cortical middle cerebral arterial territory (superior frontal, frontal, temporal and parietal areas); Area II, four areas of the deep middle cerebral and vertebral arterial territory (occipital area, basal ganglia, thalamus and cerebellum). Taking normalized resting CBF to be 100%, the mean CBF measured 10, 20 and 30 min post-injection using sequential positron emission tomography was as follows: Area I, 141.4 +/- 16.3, 127.7 +/- 15.3 and 128.2 +/- 17.4% for non-occluded sites and 116.3 +/- 22.8, 112.7 +/- 16.4 and 114.9 +/- 17.1% for occluded sites; Area II, 143.4 +/- 14.5, 126.2 +/- 10.4 and 125.0 +/- 12.9% for non-occluded sites and 141.9 +/- 28.9, 126.0 +/- 20.5 and 124.1 +/- 17.1% for occluded sites. A significant difference in mean CBF was noted between the non-occluded and occluded sites in Area I, the most marked difference of 25.1% being observed 10 min after the administration of the acetazolamide. We conclude that for an accurate assessment of vascular reserve in patients with cerebrovascular disease, CBF should be measured 10 min post-administration of the acetazolamide.

Acetazolamide↗

PubMed1996

Effect of cilostazol, a novel anti-platelet drug, on restenosis after percutaneous transluminal coronary angioplasty.

The possible preventive effect of cilostazol, a novel anti-platelet drug, on restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) was examined. One hundred and two consecutive patients, who underwent successful PTCA, were followed for 3 to 6 months. To prevent restenosis, 46 patients (60 PTCA sites) were treated with cilostazol alone (200 mg/day) (cilostazol group) and the remaining 56 (61 PTCA sites) were treated with other anti-platelet drugs and/or warfarin potassium (control group). Restenosis was defined as a more than 50% loss of the initial gain of the coronary diameter achieved by PTCA. Cilostazol did not significantly reduce the patient or lesion restenosis rate; the patient restenosis rate was 32% in the control group and 22% in the cilostazol group (P = 0.24), and the lesion restenosis rate was 30% in the control group and 23% in the cilostazol group (P = 0.44). However, the lesion non-progression rate, which was defined as the incidence of lesions with either no change or regression of coronary stenosis at the PTCA site, was significantly greater with cilostazol (37%) than in the control group (16%) (p < 0.05). Although cilostazol failed to show a significant reduction in restenosis after PTCA, the present results suggest that a further trial with a larger number of patients is needed to confirm its usefulness.

Aged↗

PubMed1996

[Anti-platelet antibody and severe thrombocytopenia during interferon-alpha therapy for chronic active hepatitis C].

We herein report a case of chronic hepatitis C where the patient developed severe thrombocytopenia during interferon therapy. The patient was a 61-year-old woman, who received interferon therapy on April 27, 1993 under the diagnosis of C type chronic active hepatitis. After 4 weeks, her platelet count had decreased to 18,000/microliters and intraoral hemorrhage had begun. Although she received 250 mg of methylprednisolone and 20 U of platelet transfusion three times, her platelet count continued to decrease to 4,000/microliters on both May 28, and on June 3, 1993, and so she was transferred to our hospital on June 4. On her second admission to our hospital, although the platelet-associated IgG (PA-IgG) had increased markedly and the megakaryocytes in her bone marrow had decreased, her platelet count had already increased to 37,000/ microliters, and this gradually returned to a normal level accompanied with a decrease of PA-IgG within one month In this case, although we found immunological abnormalities (high level of IgG, positive ANA and positive anti-smooth muscle antibody) prior to interferon treatment, we could not diagnose the patient as having suffered from autoimmune disease, including autoimmune hepatitis, because she did not satisfy the necessary criteria and because she did not have any symptoms suggesting autoimmune disease. We consider that there may be the possibility that interferon induced only an anti-platelet antibodies that caused the high level of PA-IgG and decreased the production level of platelets within the bone marrow.

Adolescent↗

PubMed1996

Rotenone, a mitochondrial NADH dehydrogenase inhibitor, induces cell surface expression of CD13 and CD38 and apoptosis in HL-60 cells.

We previously demonstrated that the mitochondrial NADH dehydrogenase subunit 2 (ND2) gene was overexpressed in human acute myelogenous leukemia (AML) cells. Since this finding suggested that ND2 gene expression was related to myeloid differentiation, we here investigated the effects of rotenone, a specific NADH dehydrogenase inhibitor, on HL-60 cell growth, differentiation and death. Fifty nM rotenone inhibited the growth of HL-60 cells and caused an increase in the cell population in the G(2) +M phase. In the quantitative comparison of myeloid antigen, the expression of CD13 and CD38 were relatively increased in the rotenone-treated cells. These findings suggest that the inhibition of NADH dehydrogenase changes the cell cycle and induces some specific surface antigens of HL-60 cells. On the other hand, the expression of ND2 gene remained unchanged after the rotenone treatment, suggesting the rotenone-mediated mitochondrial inhibition did not affect the mitochondrial gene expression. Five mu M rotenone strongly inhibited the cellular proliferation. Electron microscopy and an electrophoretic analysis of DNA showed that the majority of the HL-60 cells were induced into typical apoptosis within 24-48 hours. On the basis of this and other studies, we believe that mitochondrial function is directly involved in both cellular differentiation and apoptotic cell death.

ADP-ribosyl Cyclase↗

PubMed1996

Maladaptation of vascular response in frontal area of patients with orthostatic hypotension.

UNLABELLED: To clarify the relationship between abnormalities in cerebral blood flow (CBF) and in blood pressure regulation, we performed 99mTc-HMPAO brain SPECT in association with measurement of plasma norepinephrine and blood pressure in both the upright and supine positions. METHODS: We studied six patients with orthostatic hypotension and six normal patients. No patient had any significant stenosis of the carotid arteries on echocardiography-Doppler ultrasound and no abnormalities on brain MRI or CT. Changes in systolic blood pressure were monitored during the upright test, and 8-ml blood samples were taken at baseline and at 1 and 5 min after the upright position. RESULTS: Systolic blood pressure decreased by a mean of 38 +/- 10 and 9 +/- 3 mmHg in the orthostatic hypotension and normal groups, respectively. Compared with baseline values, plasma norepinephrine levels at 1 and 5 min after the upright test did not increase in the orthostatic hypotension group but did increase significantly in the normal group. In the orthostatic hypotension group, 99mTc-HMPAO brain SPECT showed postural cerebral hypoperfusion in the bilateral frontal areas, of which the mean count ratio of the frontal-to-cerebellar area between the upright and supine positions significantly changed from 0.871 +/- 0.029 to 0.942 +/- 0.067 and from 0.881 +/- 0.035 to 0.954 +/- 0.073 in the right and left areas, respectively. No postural change in CBF was evident in other areas in the orthostatic hypotension group. In the normal group, there were no such changes in CBF, blood pressure and plasma norepinephrine levels during the upright test. CONCLUSION: Postural cerebral hypoperfusion in the frontal areas in the orthostatic hypotension group might relate to maladaptation of the vascular response during the upright test.

Blood Pressure↗

PubMed1996

[Evaluation of remote effect to supratentorial areas in cerebellar infarction: a semiquantitative analysis using 99mTc-HM-PAO SPECT].

We studied 18 patients with unilateral cerebellar infarction to investigate its remote effect to the supratentorial areas with 99mTc-HM-PAO SPECT. Asymmetry indexes (AI) were calculated in the cerebellum and in seven supratentorial areas (thalamus, basal ganglia, superior and inferior frontal areas, temporal area, parietal area and occipital area). Mean AIs of supratentorial areas ranged from -0.64 +/- 2.74% to +1.04 +/- 2.03%. In cerebellar infarction of acute or subacute phase, the mean AI showed larger values (+1.13%) than that of chronic phase (+0.21%), but this difference did not reach statistical significance. There was no significant difference among supratentorial AIs grouped according to cerebellar infarction size. There was also no significant correlation among AIs of cerebellar and the supratentorial areas (r = -0.32 to +0.38). Crossed hemispheric hypoperfusion is thought to be related to the interruption of cerebellocortical tracts. We concluded that the detection of the remote effect to supratentorial areas in cerebellar infarction was difficult with 99mTc-HM-PAO SPECT.

Adult↗

PubMed1996

[Usefulness of 123I-BMIPP scanning for distinction of ischemic from nonischemic dilated cardiomyopathy].

To determine if imaging of blood flow (using 201Tl) and fatty acid (using 123-I-BMIPP) with SPECT can distinguish cardiomyopathy of coronary artery disease from nonischemic dilated cardiomyopathy, 24 patients with severe left ventricular dysfunction were evaluated. The origin of left ventricular dysfunction had been previously determined by coronary angiography to be ischemic (9 patients) or nonischemic (15 patients). Images were visually analyzed by three observers on a graded scale (score 0; normal, 1; mild uptake reduction, 2; severe uptake reduction, and 3; defect) in 20 left ventricular segments revealed higher defect score in ICM compared with NCM for 123I-BMIPP (35.5 +/- 14.4 versus 14.1 +/- 9.3, p <0.0005) and 201Tl (27.6 +/- 14.6 versus 12.1 +/- 7.4, p <0.005). The defect score/segment ratio also revealed higher value in ICM compared with NCM for 123I-BMIPP (2.25 +/- 0.52 versus 1.36 +/- 0.36, p <0.0001) and 201Tl (1.92 +/- 0.51 versus 1.24 +/- 0.42, p <0.005). Myocardium of ICM is more severely damaged than that of NCM. Thus, noninvasive SPECT imaging with 123I-BMIPP is helpful in distinguishing patients with severe left ventricular dysfunction secondary to coronary artery disease from those with nonischemic cardiomyopathy.

Adult↗

PubMed1996

[Significance of 123I-metaiodobenzylguanidine SPECT for detecting left ventricular involvement in patients with arrhythmogenic right ventricular dysplasia].

The right ventricle being primarily involved in ARVD, recent reports indicate the presence of histological and functional abnormalities in the left ventricle for some patients with ARVD. The aim of this study was to evaluate the significance of myocardial sympathetic dysfunction as an early sign of left ventricular (LV) involvement by 123I-MIBG (MIBG) SPECT and to compare the findings with those of 201TlCl (Tl) SPECT, radionuclide left ventriculography, ultrafast computed tomography (UFCT), magnetic resonance imaging (MRI) and echo-cardiography in 10 patients (pts) with ARVD. MIBG defects in LV regions were detected in 9 pts. Seven of the 9 pts showed MIBG defects in LV regions adjacent to RV. The subjects were divided into 2 groups based on left ventriculography, 5 with normal LVEF (> 55%) and 5 with reduced LVEF. In the normal LVEF group, 4 pts showed MIBG defects and 2 pts showed TI defects, and MIBG defects were larger than TI defects (ES: 14 +/- 6 vs. 5 +/- 7, p <0.05). In reduced LVEF group, all of 5 pts showed MIBG and TI defects, and MIBG defects were larger than TI defects (ES: 42 +/- 12 vs. 25 +/- 3, p <0.05). In comparison with normal LVEF group, reduced LVEF group showed larger and more severe MIBG defects (ES: 42 +/- 12 vs. 14 +/- 6, p <0.01, SS: 44 +/- 31 vs. 8 +/- 7, p <0.05). UFCT and MRI showed abnormal findings indicating LV fatty infiltration in only 3 of reduced LVEF group. Thus, MIBG showed abnormal distributions in the left ventricle with the highest frequency in all these modalities. These results suggest that MIBG SPECT provides a sensitive marker for detecting LV involvement in ARVD. Also, the extent of MIBG distribution abnormalities is helpful in assessing the severity of left ventricular involvement in patients with ARVD.

3-Iodobenzylguanidine↗

PubMed1996

Cerebral hypoperfusion in orthostatic hypotension with globally denervated myocardium.

A 57-yr-old woman had frequent syncope when rising from a seated position. Her blood pressure fell from 140/80 mmHg to 60-70/40 mmHg while changing positions. Iodine-123-metaiodobenzylguanidine ([123I]MIBG) did not accumulate in the heart, whereas 201Tl-Cl (201Tl) did. Raise-up 99mTc-hexamethyl-propyleneamine oxime (99mTc-HMPAO) brain SPECT revealed decreased activity in the bilateral frontal areas, and subsequent supine 99mTc-HMPAO brain SPECT revealed filling in these areas, indicating that the cerebral blood flow (CBF) was transiently decreased in the frontal areas more than others in a standing position. The plasma norepinephrine (NE) level of this patient was normal during supine rest, but when she stood up, failure to increase the plasma level of NE uncovered a sympathetic nervous dysfunction. The CBF abnormality in patients with orthostatic hypotension may be due to a "functional" hemodynamic mechanism that induces orthostatic stress. This patient had transient hypoperfusion in the frontal areas when standing, without organic cerebral arterial stenosis. Only CBF in the frontal areas revealed relative hypoperfusion. These regions might be highly susceptible to a change in blood flow. The causes of orthostatic hypotension of this patient were autonomic failure with a disturbance of the sympathetic nerve endings, which was revealed by 99mTc-HMPAO brain SPECT and cardiac [123l]MIBG imaging.

3-Iodobenzylguanidine↗

PubMed1995

HLA DRB4 0101-restricted immunodominant T cell autoepitope of pyruvate dehydrogenase complex in primary biliary cirrhosis: evidence of molecular mimicry in human autoimmune diseases.

We established six T cell clones specific for pyruvate dehydrogenase complex (PDC)-E2 peptides from four different patients with primary biliary cirrhosis using 33 different peptides of 17-20 amino acid residues corresponding to human PDC-E2 as stimulating antigens. The minimal T cell epitopes of these six T cell clones were all mapped to the same region of the PDC-E2 peptide 163-176 (GDLLAEIETDKATI), which corresponds to the inner lipoyl domain of PDC-E2. The HLA restriction molecules for this epitope were all identified as HLA DRB4 0101. The common essential amino acids of this epitope for these T cell clones were E, D, and K at positions 170, 172, and 173, respectively; other crucial amino acids for this epitope differed in each T cell clone. In addition, the alanine-substituted peptides at positions 170 and 173, but not 172, inhibited the proliferation of all T cell clones induced by the original peptide of human PDC-E2 163-176, indicating that amino acid D at position 172 is a critical MHC-binding site for all T cell clones tested. Interestingly, all T cell clones reacted to PDC-E2 peptide 36-49 (GDLIAEVETDKATV), which corresponds to the outer lipoyl domain of human PDC-E2. Furthermore, one T cell clone cross-reacted with exogenous antigens such as Escherichia coli PDC-E2 peptide 31-44/134-147/235-248 (EQSLITVEGDKASM), which has an EXDK sequence. This is a definite demonstration of the presence of molecular mimicry at the T cell clonal level in human autoimmune diseases. It is also considered possible to design peptide-specific immunotherapy based on the findings of T cell autoepitopes in primary biliary cirrhosis.

Adult↗

PubMed1995

Stability and pharmacokinetic studies of a new immunosuppressant, mycophenolate mofetil (RS-61443), in rats.

Mycophenolate mofetil (MPM), a new immunosuppressant, is a morpholinoethyl ester of mycophenolic acid (MPA). The enzymatic and non-enzymatic hydrolysis was studied in an artificial digestive fluid, rat plasma, and tissue homogenates. MPM was chemically stable in the artificial digestive fluid. In rat tissue homogenates and plasma, MPM was rapidly hydrolysed to MPA. The conversion rate of MPM to MPA in various rat tissue homogenates was in the order of liver > kidney > plasma > small-intestine epithelial cells. After the intravenous injection of MPM at 16.7 mg kg-1, the terminal elimination half-life, t1/2 beta, was 4.74 +/- 0.33 (mean +/- SD)h, and the area under the plasma concentration versus time curve, AUC, was 48.78 +/- 6.01 micrograms h mL-1. After intraduodenal (ID) administration of MPM at 16.7 mg kg-1, t1/2 beta was 3.92 +/- 1.05 h, and the AUC was 38.08 +/- 8.30 micrograms h mL-1. The systemic availability of MPA after ID MPM dosing was 1.52 times higher than that after ID administration of MPA. This result supports the usefulness of MPM as an oral prodrug of MPA as a new oral immunosuppressant.

Animals↗

PubMed1995

Establishment and structural analysis of human mAb to the E2 component of the 2-oxoglutarate dehydrogenase complex generated from a patient with primary biliary cirrhosis.

We established one Epstein-Barr virus-transformed B cell hybrid clone producing human mAb of the IgG class to the 2-oxoglutarate dehydrogenase complex (OGDC) for the first time from the peripheral B lymphocytes of a patient with primary biliary cirrhosis (PBC). This mAb, designated mAbM37GO37, specifically bound to OGDC and its dissociation constant with OGDC was calculated to be 3.70 x 10(-10) mol/l. mAbM37GO37 stained murine stomach/kidney cryostat sections in a typical immunofluorescence pattern of antimitochondrial antibody (AMA). Western blotting analysis revealed that mAbM37GO37 reacted with an E2 component of OGDC but not with other components of OGDC nor pyruvate dehydrogenase complex (PDC). Furthermore, mAbM37GO37 completely inhibited the enzymatic activity of OGDC. In order to determine the structure and genetic origin of anti-OGDC autoantibody, we cloned and sequenced the Ig heavy and light chain variable regions of mAbM37GO37. This mAb used the VHIII family member, V3-7, and the V kappa IV family member. The amino acid difference between the expressed V genes of this mAb and respective putative germline genes was concentrated within the complementarity determining regions (CDR) rather than the framework regions (FR). The R:S mutation ratio was high in the CDR and low in the FR. These features suggested that the immune response to OGDC is similar to that to exogenous antigen, and that the heavy and light chain variable regions of the anti-OGDC antibody undergo somatic hypermutation through antigen-driven clonal selection. This human mAb to OGDC, which was established for the first time from a patient with PBC and characterized at the molecular level, would be a valuable tool to study the B cell autoepitopes of OGDC, to clone as yet undetermined full length cDNA encoding OGDC and to dissect the autoimmune response to mitochondrial antigens in PBC.

Adult↗

PubMed1995

I-123 iodoamphetamine lung scanning in patients with ventilation-perfusion mismatching.

I-123 IMP is a nonparticulate agent and becomes trapped by endothelial membranes in the pulmonary capillaries. Using I-123 IMP, the authors studied six patients with ventilation-perfusion mismatch. Three of six patients had pulmonary thromboembolism, and three had pulmonary hypertension. In comparison with conventional perfusion lung scanning using Tc-99m MAA, defect sizes visualized by I-123 IMP were smaller in all patients. I-123 iodoamphetamine is a useful agent for assessing the perfusion of pulmonary arterial microvasculature which Tc-99m MAA fails to penetrate.

Amphetamines↗

PubMed1995

Inferior vena cava occlusion with pulmonary embolism because of complications due to ruptured abdominal aneurysm demonstrated by radionuclide venography.

A 66-year-old man with an abdominal aortic aneurysm confirmed by CT had bilateral swelling of the lower extremities with pain radiating to the back. Radionuclide venography and pulmonary scintigraphy demonstrated occlusion of the inferior vena cava and multiple pulmonary emboli, with a hot spot in the liver. Surgery revealed a ruptured abdominal aortic aneurysm that occluded the inferior vena cava, fistula formation, and extensive thrombosis of the inferior vena cava proximal to the occlusion site. Radionuclide venography was useful in detecting venous obstruction and the collateral formation represented by the hot spot in the liver as complications of the ruptured abdominal aortic aneurysm, and in assessing the improvement of pulmonary embolism by medical therapy.

Aged↗