Reversal of Ga-67 'bone scan' with vitamin B12 therapy in a patient with pernicious anemia.
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Biomedical subjects
Publications and source records attributed to H Okazaki.
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Infection by a baculovirus (Bombyx mori nuclear polyhedrosis virus, BmNPV) in silkworm (Bombyx mori) larvae is highly efficient as an expression system for the production of useful proteins. However, the amount of the protein of interest expressed tends to decrease in the later stages of infection presumably due, in part, to a proteinase produced in the larval haemolymph. The N-terminal amino acid sequence of a proteinase purified from the haemolymph of BmNPV-infected larvae was identical to the internal amino acid sequence of the viral cysteine proteinase gene of BmNPV, suggesting that the cysteine proteinase in the haemolymph originated from the BmNPV gene. We constructed a mutant virus (CPd) which had a deletion in the cysteine proteinase gene. No proteinase activity corresponding to this proteinase was detected in the haemolymph of silkworm larvae infected with CPd. The firefly luciferase and the human growth hormone genes were separately introduced into CPd under control of the polyhedrin promoter. These constructs produced these proteins very efficiently, because of a greatly reduced degree of degradation of these proteins. A BmNPV vector system using CPd enhances the stability of foreign expressed proteins, especially for those that are cysteine proteinase-sensitive.
We performed femoral lengthening for post-traumatic femoral shortening in 14 patients (10 men). The mean age was 26 (17-33) years. The callotasis method was employed using an Orthofix or Hifixator monolateral external fixator. The average length gained was 6 (3-13) cm, equal to 16 (7-36)%. The mean narrowing ratio of the hip joint space during lengthening was 9 (0-26)% and the narrowing persisted at the final follow-up. Cases with narrowing greater than 5% had a longer time between the development of the shortening and the lengthening than the others (p = 0.03). Our findings indicate that femoral lengthening for posttraumatic femoral shortening should be done as early as possible to prevent the development of joint space narrowing during the lengthening procedure.
Extracranial internal carotid artery aneurysm is rare. Most cases are due to spontaneous or traumatic dissection of the cervical internal carotid artery. Here we report a case of surgically treated extracranial internal carotid artery (ICA) aneurysm. A 74-year-old man noticed a pulsatile mass just below the left mandibular angle. Intravenous digital subtraction angiography revealed multiple aneurysms in the systemic arteries, including the aortic arch, abdominal aorta and left extracranial ICA. It was decided to treat the aneurysms of the aortic arch and of the abdominal aorta conservatively. Cerebral angiography, however, showed a saccular aneurysm which projected latero-posteriorly at the C2 level of the left extracranial ICA. Although the patient had no previous ischemic event, we decided to treat this aneurysm surgically in view of the risk of cerebral ischemia caused by intraaneurysmal thrombus formation or rupture of the aneurysm by neck injury. The operation was performed under mild hypothermal general anesthesia. Electroencephalography was carried out during the operation. A skin incison was made from the anterior border of the sternocleidomastoid muscle to the pretragal region to expose the parotid gland. This skin incision, elevation of the parotid gland and division of the digastric muscle were useful for exposing the distal portion of the extracranial ICA. After trapping of the aneurysm, it was punctured and collapsed by aspiration and the dome was excised at its neck. The ICA was then reconstructed by suturing the cut neck of the aneurysm. Patency of the ICA was confirmed by postoperative angiography. The postoperative course was smooth except for hoarseness, which was caused by damage to a minor branch of the vagus nerve during exposure of the aneurysmal dome.
A 44-year-old woman was admitted to our hospital complaining of dyspnea. A chest X-ray film obtained on admission showed bilaterally shrunken lungs, and peripheral bundle-like and linear shadows. A chest CT scan revealed marked thickening of bronchovascular bundles and low lung volumes. Mild dryness of the mouth, and the results of a Rose-Bengal test, Schirmer test, and sialography led to the diagnosis of primary Sjögren's syndrome. Corticosteroid pulse therapy was followed by slight improvement. To determine the pathological diagnosis and to plan further therapy, video-assisted thoracoscopic lung biopsy was done. Examination of the biopsy specimen revealed alveolitis and infiltration of lymphocytes, which suggested active interstitial pneumonia. Therapy with corticosteroids and the immunosuppressant azathioprine was followed by marked improvement.
A 60-year-old woman presented with stiff-person syndrome (SPS). Treatment with diazepam controlled her painful spasms initially. Two and one-half years after the onset of SPS, new spells of paroxysmal leg jerking and apnea developed. A spell was recorded with simultaneous video and polygraphic techniques that revealed simultaneous firing of motor unit potentials in several muscles (paraspinal, internal hamstring, and abdominal muscles). Apnea was associated with arterial oxygen desaturation. An increase in the dose of diazepam decreased the number and severity of these episodes. Seventeen months later, the patient began to taper the diazepam dose. Shortly thereafter, she had a cardiorespiratory arrest and subsequently died. Autopsy showed small chronic inflammatory foci in the pancreas (some associated with islets) and findings of diffuse encephalomyelitis characterized by perivascular cuffing in the spinal cord, brainstem, thalamus, hippocampus, and amygdala and a dense mononuclear infiltrate in the anterior horns of the lumbar and cervical cord, with relative preservation of axons and myelin. Cell typing showed this infiltrate was polyclonal and reactive. There have been rare cases of SPS associated with encephalomyelitis reported previously. Although the prolonged course in our patient suggested that SPS may have preceded encephalomyelitis, the more likely explanation is that the patient had an unusually long course of encephalomyelitis alone.
The effect of basic fibroblast growth factor (bFGF) applied locally into the bone under physiological conditions was investigated. An aqueous solution containing 0 microgram (vehicle), 100 micrograms or 400 micrograms recombinant human bFGF was percutaneously applied through a needle into the right ilium in rabbit, and the ilia were harvested 4 weeks after the application. Compared with vehicle-treated animals, bone mineral density measured by dualenergy X-ray increased in the 400 micrograms bFGF group. The width of trabeculae in the bFGF-treated groups was greater than in the vehicle group. These results showed that bFGF applied locally into the bone under physiological conditions affected bone formation, and suggested that such an application might have potential for increasing bone.
We have reviewed 28 tibial lengthenings in 14 patients with achondroplasia at an average age of 15 years, and compared the effectiveness of physiotherapy and an orthosis in preventing an equinus deformity. Physiotherapy of 15 min a day was ineffective even when the patients were able to walk. An orthosis worn for 16 h a day prevented equinus deformity up to at least 50% of lengthening, and the difference from physiotherapy was significant at more than 30% of lengthening.
Measurement of serum HCV-RNA is a useful index for evaluating the antiviral effect of interferon therapy in chronic hepatitis C. In the present study, we investigated whether the detection of hepatic HCV-RNA after interferon treatment, using a polymerase chain reaction assay, predicted long-term response to therapy in patients with chronic hepatitis C. Thirty-three patients underwent liver biopsies before and after interferon therapy. Histology and clinical courses were compared after treatment. Before therapy, serum and hepatic HCV-RNA was detected in specimens from 32 (97%) and 33 (100%) patients, respectively. Serum HCV-RNA became undetectable in samples from 22 (67%) patients; however, in 10 of these patients (45%), serum HCV-RNA levels relapsed after therapy. Hepatic HCV-RNA became undetectable in 14 patients after therapy and the serum aminotransferase concentration remained within normal limits during and following (24-92 weeks) therapy in 12 of these patients (86%). All 11 patients with detectable hepatic HCV-RNA also had serum HCV-RNA and elevated aminotransferase concentrations refractory to therapy. The absence of hepatic HCV-RNA at the end of interferon treatment thus predicted a long-term complete response to therapy with a sensitivity of 100%, a specificity of 90% and an accuracy of 94%. We conclude that hepatic rather than serum HCV-RNA is a more useful index for the prediction of the long-term efficacy of interferon therapy.
The reversibility of right ventricular function in patients with mitral stenosis associated with secondary tricuspid regurgitation (TR) is as yet undetermined. We assessed the right ventricular systolic performance by cardiac catheterization before and 19 months after surgery in 18 patients who underwent DeVega's tricuspid annuloplasty plus mitral valve replacement (MS plus TR group) and in 9 with mitral valve replacement for isolated mitral stenosis (MS group). After surgery, the right ventricular systolic pressure decreased significantly in both groups (both p < 0.01). In the MS plus TR group, the postoperative right ventricular end-diastolic and end-systolic volume indices (RVEDVI and RVESVI, respectively) were significantly decreased compared with the respective preoperative values (both p < 0.001). No significant difference was noted between the groups with regard to the right ventricular peak-systolic pressure/end-systolic volume index ratio (RVPSP/ESVI) either before or after surgery. Various left ventricular indices were comparable between the groups both before and after surgery. Linear regression analysis revealed significant correlations between RVEDVI and the RVPSP/ESVI, and between RVPSP and the RVPSP/ESVI both before and after surgery. These results indicate that right ventricular systolic performance in patients with MS plus secondary TR became comparable to those that in patients with isolated MS after surgery, and that this was probably due to nearly equivalent right ventricular contractility before surgery.
Radiofrequency (RF) catheter ablation of the slow AV nodal pathway was attempted in 34 patients with common type of AV nodal reentrant tachycardia (AVNRT). Radiofrequency energy of 18-32 watts was applied for 30-60 seconds at sites exhibiting atrial-slow pathway potentials or slow potentials. These potentials were recorded at the mid or posterior septum, anterior to the coronary sinus ostium. A mean of two radiofrequency applications successfully eliminated AVNRT in all patients. The incidence of junctional ectopy was significantly higher during 34 effective applications of radiofrequency energy than during 36 ineffective applications (100% versus 17%). Thus, the recording of atrial-slow pathway potentials or slow potentials, and the development of junctional ectopy can be used as a marker for successful ablation. Slow AV nodal conduction was eliminated in 22 patients and persisted without inducible AVNRT in 12. None of the patients had recurrences of AVNRT over a mean follow-up interval of 12 months, and all had preserved AV conduction. Long-term follow-up studies with an electrophysiological method confirmed that the ablation was effective. Transient AV block was observed in only 1 patient, and no major complications were noted. Thus, radiofrequency catheter ablation of the slow AV nodal pathway is highly effective and safe, with a low rate of complication, for the treatment of common type of AVNRT.
To clarify the role of microvessels in the development of pulmonary hypertension of acute lung injury, we induced lung edema by oleic acid (OA) in ten artificially perfused cat lungs and measured microvascular pressure. Pulmonary artery pressure (Ppa) and pressure of 30-50 microns arteriole (Parteriole) increased from 19.2 +/- 1.4 and 15.7 +/- 1.0 cmH2O before to 30.5 +/- 5.0 cmH2O and 22.7 +/- 2.4 cmH2O after edema, respectively. Pressure of 30-50 microns venule (Pvenule) and venous occlusion pressure (Pvo) did not change significantly after edema. Double occlusion pressure (Pdo) which represents pulmonary microvascular pressure increased from 14.5 +/- 0.6 to 17.7 +/- 2.0 cmH2O. Pressure gradient in the artery, i.e., between Ppa and Parteriole and in the microvessels, i.e., between Parteriole and Pvenule increased when lung became edematous. Pressure gradient in vein, i.e., between Pvenule to left atrium was not affected by edema. Pdo was in the midst of Parteriole and Pvenule in both edematous and non-edematous lung. In acute lung injury, increase of microvascular resistance was followed by an increase of arterial resistance and caused pulmonary hypertension.
We examined the callus formation during leg lengthening in 7 achondroplastic patients who underwent 3 bilateral femoral and 4 bilateral tibial lengthenings. Bone mineral content and bone mineral density (BMD) in the lengthened callus space were evaluated every 1 or 2 weeks for 10 weeks after the start of distraction using dual energy X-ray absorptiometry. The mean rate of callus mineralization in femurs (0.64 g/wk) was higher than in tibias (0.22 g/wk). The mean BMD at 10 weeks after the start was 0.35 g/cm2 in the femur and 0.14 g/cm2 in the tibia. Different rates of callus formation in different kinds of long tubular bones have not been reported previously.
Our surgical experiences in 9 patients who required steroid treatment for systemic diseases before, during and after the open heart surgery were reviewed. Subjects included 3 patients with systemic lupus erythematodes, 3 with aortitis syndrome, 1 with Behçet disease and 1 with rheumatoid arthritis. Cardiovascular lesion was aortic valve regurgitation in 2, Stanford A aortic dissection in 1 and ischemic heart disease in 3 patients. Duration of morbidity for systemic diseases before the surgery ranged between 0 nd 102 months, with a mean of 36 months. Steroid treatment was continued for 4 to 216 months (mean 70+/-76 months) before the surgery at a dose of 5-40 mg per day for conversion into prednisolone. In principal, methylprednisolone was given during the surgery, and the prednisolone was given at a dose of 20-140 mg per day on the day of operation or on the first postoperative day. Surgical procedures included a aortic valve prosthesis with Dacron cloth skirt implantation in 1 patient, surgical angioplasty of the left main coronary ostium in 1 and internal thoracic arteries grafting in 2 patients. Hospital mortality was 1 patient due to low cardiac output syndrome. Acute renal failure occurred in 2 patients with systemic lupus erythematodes, and wound complication was observed in 2 patients. In our experience, appropriate treatment for systemic diseases, timing of surgery and continuation of steroid treatment at an appropriate dose during and after the surgery seemed very important such as surgical procedure in order to prevent postoperative complications such as periprosthetic leakage and failure of anastomosis.
It has been reported that the high flow and pressure perfusion produced the brain damage during selective cerebral perfusion. This time we studied the mechanism of this brain damage with mock circulation. We made the mock circulation system of brain with the hard shell reservoir as cranium, and with the triple soft bags as brain tissue, involving into reservoir. We designed the control group that intracranial pressure (ICP) was 0 mmHg at pump off, and the increasing intracranial pressure (IICP) group that ICP was 10 mmHg at pump off. We measured the flow-pressure relationship in the control and IICP group, and then stenosis in outflow. In results, the flow and pressure in both the inflow and outflow side increased significantly (p < 0.001) in control groups, as pump flow increased. The changes of the flow and pressure in IICP group showed a same tendency to the control group. Moreover, both the inflow volume into bag and the outflow volume from bag decreased as pump flow increased stepwisely. The pressure in both inflow and outflow side increased significantly and the volume of the inflow side in IICP group showed a tendency to decrease, compared with the control. The stenosis in the outflow side produced the significant increase in the pressure of both inflow and outflow side, and intracranium, with the same pump flow as the control without stenosis. In conclusion, the high flow perfusion produced the increase of the several pressure in intracranial and extracranial vessels. Moreover, the high flow perfusion produced the decrease of the intracranial blood volume cerebral blood flow. The high flow perfusion does not necessarily contribute to the cerebral tissue perfusion. The stenosis at the side of venous return produced relative high perfusion. This result suggests that the venous return should be taken care of during the selective cerebral perfusion.
BACKGROUND: The purpose of this study was to evaluate the protective effects of a neuroselective calcium antagonist, nimodipine on spinal cord ischemia during and after thoracic aortic cross-clamping. METHODS: Thirty adult dogs underwent 60 minutes of thoracic aortic cross-clamping via a left thoracotomy. The dogs were randomized into 3 groups (n = 10) and received either intravenous control (normal saline), sham (polyethylene glycol) or nimodipine solution during a period of 150 minutes. Spinal cord perfusion (SCP) was directly monitored using a laser doppler flowmeter. After 48 hours, neurologic status was assessed using Tarlov scores and the spinal cords evaluated histologically for evidence of ischemia (grades 1-4: severe to mild ischemia). RESULTS: Twenty-six dogs survived the operation. Proximal (carotid) blood pressure increased 30-40% and cerebrospinal fluid (CSF) pressure increased 50% during cross-clamping for all 3 groups. The SCP decreased predictably during cross-clamping in all dogs but after unclamping, the nimodipine group had significantly less hyperperfusion than the saline and sham control groups (30 min after unclamping, control: 74.1 +/- 12.6 ml/min, sham: 51.8 +/- 4.15 ml/min, nimodipine: 33.1 +/- 3.9 ml/min, p = 0.04). This hyperperfusion phenomenon correlated with adverse neurologic (Tarlov score) outcome (p = 0.01). Paraplegia rates were 78% (control), 70% (sham) and 71% (nimodipine) (p = NS). The histologic grades of the spinal cords from those dogs which received nimodipine tended to correspond to better tissue preservation (control: 1.72 +/- 0.49, sham: 1.75 +/- 0.46, nimodipine: 2.14 +/- 0.56, p = NS). CONCLUSIONS: Nimodipine used as single agent therapy failed to show a statistically significant clinical neurologic benefit. However, nimodipine significantly decreased postischemic reperfusion hyperemia in the spinal cord as measured by laser doppler flowmetry. This reduced hyperperfusion, which significantly correlated with functional outcome, may be responsible for dampening neural cell damage. Thus, nimodipine should be considered as an adjunct to a multimodality approach in the prevention of spinal cord ischemia during thoracic and thoracoabdominal aortic reconstructions.
Femoral lengthening has been associated with narrowing of the joint space at the hip. We have studied the joint space before lengthening in 20 patients with a short femur due to a femoral-shaft fracture (15) or distal femoral epiphyseal injury (5). Their mean age at injury was 16 years (3 to 27) and the mean shortening was 5.4 cm (1.1 to 14). We found that the hip joint space of the shortened femur was significantly narrower (p < 0.001) than that on the normal side, with a mean narrowing ratio of 15.5% (-5 to +43). The narrowing ratio was directly related to the period spent non-weight-bearing (p < 0.001), but not to the amount of femoral shortening. We have shown that the joint space of the hip in patients with post-traumatic femoral shortening was narrowed even before femoral lengthening had been started.
To determine the role of interstitial lung disease (ILD) in the outcome of polymyositis-dermatomyositis (PM/DM), we studied 41 patients who had radiographic evidence of ILD among 51 patients with PM/DM. The patients were divided into 3 groups according to therapy: progressive, no change, or improved. Those classified as progressive had significantly higher rates of skin and lung symptoms, milder muscle symptoms, and lower levels of muscle enzymes than the other 2 groups, and none was positive for the anti-Jo-1 autoantibody. Nine patients with DM died of respiratory failure; they had low serum creatine kinase levels, no anti-Jo-1 antibodies, and a rapidly progressive course before death. Autopsy findings were obtained in 7 patients, and all had diffuse alveolar damage as the main pulmonary histological finding. A subgroup of patients with PM/DM-ILD have a poor prognosis, and ILD in PM/DM is an important prognostic factor.