Biomedical subjects
Publications and source records attributed to J Shimizu.
An 8-year-old intact male Shih Tzu dog was admitted with acute-onset tetraplegia. Magnetic resonance imaging showed an abnormality of the cervical intramedullary spinal cord. Histopathological examination of a spinal biopsy confirmed the presence of intravascular cartilaginous emboli. This is the first report of an antemortem diagnosis of fibrocartilaginous embolism in a chondrodystrophoid breed dog.
Study of the UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase gene (GNE) revealed that almost all cases of distal myopathy with rimmed vacuoles were caused by GNE mutations. Seven new mutations were identified, including M712T, which is the most common mutation in Jewish hereditary inclusion body myopathy. In addition, a splice-variant characteristic of the skeletal muscle was found, whereas the difference of the expression level between GNE-mutated and -nonmutated patients was not apparent.
AIMS: This study reviews our 30 years experience in the clinical assessment and surgical management of bilateral multiple primary lung cancer (BMPLC). METHODS: Between January 1973 and December 2001, 1906 patients with primary lung cancer underwent surgical resection in Kanazawa University Hospital. Thirty-seven patients (1.9%) who had developed a BMPLC using the criteria of Martini and Antakli. RESULTS: Eighteen patients had synchronous lesions, and 18 patients had metachronous lesions. One patient had synchronous and metachronous lesions. Overall 10-year survival was 56%. The actuarial 5-year survival for bilateral synchronous cancers was 69%, median survival (MST) 90 months (range 8-153 months), and 10-year survival was 47%. The actuarial 5-year survival for second metachronous cancers was 51%, with an MST of 114 months (range 6-192 months). CONCLUSION: Aggressive surgical therapy is effective in patients with a bilateral MPLC if they satisfy the usual criteria of operability. The surgical methods that preserve healthy lung tissue such as sleeve resection and limited resection must be selected in compliance with cancer characters.
BACKGROUND: The most characteristic structural change evident in endobronchial biopsies in asthma, even in mild disease, is subepithelial collagen deposition within the lamina reticularis. This has been associated with progressive loss of lung function and the persistence of airway hyperresponsiveness, and has been linked to airway fibroblast proliferation. A potent fibroproliferative factor in bronchoalveolar lavage fluid in asthma is fibroblast growth factor-2 (FGF-2). FGF-2 is a member of a family of heparin binding growth factors that bind to heparan sulphate proteoglycans (HSPG), an important determinant of FGF-2 activity. This study compared the level of expression and distribution of FGF-2 in relation to HSPG in bronchial tissue from normal and asthmatic subjects. METHODS: The distribution of FGF-2 and HSPG in intact and cleaved forms in endobronchial biopsies from normal and asthmatic subjects was examined using an immunohistochemical approach. A novel ELISA based method was developed to detect solubilisation of FGF-2 following addition of heparin and heparitinase to bronchial tissue slices. RESULTS: Immunohistochemical analysis showed that FGF-2 was co-localised to HSPG in epithelial and endothelial basement membranes. Epithelial FGF-2, but not HSPG, was significantly more abundant in patients with mild asthma than in normal subjects. In vitro experiments indicated that FGF-2 was released from binding sites in the tissue by heparin and heparitinase I. CONCLUSIONS: FGF-2 is bound by HSPG in bronchial tissue. The mast cell, through the release of heparin and endoglycosidase, may make a unique contribution to tissue remodelling in allergic asthma.
Intramyocardial Ca(2+) recirculation fraction (RF) critically determines the economy of excitation-contraction coupling. RF is obtainable from the exponential decay of the postextrasystolic potentiation of left ventricular (LV) contractility. We have shown that RF remains unchanged despite increasing LV volume (LVV) at normothermia, but decreases with increasing temperature at a constant LVV. However, it remains unknown whether the temperature-dependent RF was not due to the simultaneously changed peak LV pressure (LVP) at a constant LVV. We hypothesized that this temperature-dependent RF would be independent of the simultaneous change in LVP. We used nine excised, cross-circulated canine hearts and allowed their LVs to contract isovolumically. During stable regular beats at 500 msec intervals, we inserted an extrasystolic beat at 360 msec interval followed by the postextrasystolic beats (PESs) at 500 msec intervals. We equalized the temperature-dependent peak LVPs of the regular beats at 36 degrees C and 38 degrees C to the peak LVP level of the stable regular beat at 33 degrees C by adjusting LVV. We fitted the same equation: nEmax = a.exp[-(i - 1)/tau(e)] + b.exp[-(i - 1)/tau(s)]cos[pi(i - 1)] + 1, used before to the normalized Emax (maximum elastance) values of PESi (i = 1-6) relative to the regular beat Emax. RF given by exp(-1/tau(e)) decreased by 19% to 38 degrees C from 33 degrees C. The temperature coefficient (Q(10)) of 1/RF was significantly greater than 1.3. The present results indicated a similar temperature dependence of RF and its Q(10) to those we observed previously without equalizing peak LVP. Thus, the temperature-dependent RF is independent of ventricular loading conditions.
We have previously found that the postextrasystolic (PES) potentiation (PESP) of the left ventricular (LV) contractility (Emax) decays typically in transient alternans even in the normally ejecting canine heart. This contradicted the general expectation that arterial pressure (AP) and LV pressure (LVP) usually decay exponentially during PESP. We hypothesized this contradiction to be due to the different cardiodynamic behaviors of AP and LVP from LV Emax during PESP. We tested this hypothesis by measuring AP, LVP, LV volume, Emax, effective arterial elastance (Ea) as an index of afterload, and pulse pressure (PP) during PESP in eight anesthetized open-chest dogs by using the conductance catheter system. We changed Ea by changing the total peripheral resistance (TPR) with methoxamine hydrochloride (iv) and repeated the measurements. Although the Emax alternans patterns during PESP were comparable between the normal and high afterloads, LVP and PP were slightly potentiated and alternated under the normal afterload, whereas LVP and PP were obviously potentiated and alternated under the high afterload. We also simulated the effects of Ea/Emax on the transient alternans of AP and LVP on a computer. Despite the same alternans pattern of Emax, a higher Ea/Emax, which is typical in heart failure, caused a larger PP alternans, whereas a lower Ea/Emax, which is typical in normal hearts, almost eliminated it. These results suggest that a transient alternans of LV contractility during PESP could be overlooked when AP and LVP are monitored in in situ normal hearts.
A 35-year-old female was admitted to our hospital for hysteromyoma. Chest X-ray showed a mass shadow in the left lung field. A thorough examination revealed anomalous systemic arterial supply to the basal segment of the left lung with 2 abnormal arteries. Because the patient had no symptoms, no operation was performed. After 9 months however, the patient had bloody phlegm and chest pain and received an operation. Thus, we propose that the operation for the pulmonary sequestration is to be performed when such a diagnosis is made.
A case of pulmonary hamartoma is reported with clinical, roentgenographical and histopathologic findings. The patient was a 53-year-old woman who had undergone right hemithyroidectomy for thyroid cancer 4 years before. An abnormal shadow, which was a non-clearly demarcated tumor, 2 cm in diameter, in the left middle lung field, was noted on her routine X-ray in February 2001. Physical examination and laboratory data revealed no significant findings, but computed tomography(CT) scans of the chest showed a gathering of small-sized high-density lesions in the nodule. She underwent left S8 segmentectomy on March 21, 2001. The pathology report on the frozen section was pulmonary hamartoma. Histopathologically, the lesion was characterized by a composition of bronchial epithelium, fat tissue and cartilage, with being diagnosed as a chondromatous hamartoma of the lung. The patient's postoperative course was uneventful, and she was discharged with no supportive therapy 14 days after the operation. To date, 14 months after the operation, the patient has been in good condition, without evidence of recurrence or distant metastasis on diagnostic imaging. This case is particularly interesting because a gathering of small-sized pulmonary hamartoma was demonstrated by imaging.
The authors present three novel missense mutations in the UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) gene, the causative gene for hereditary inclusion body myopathy, in Japanese patients with distal myopathy with rimmed vacuoles. Seven out of nine patients had homozygous V572L mutation, one was a compound heterozygote with C303V and V572L mutations, and the remaining patient bore homozygous A631V mutation.
DNA fragmentation and activation of caspase-1, implicating involvement of apoptosis, have been reported in the spinal cord of amyotrophic lateral sclerosis (ALS) patients and transgenic mouse models of ALS. Because BH3-only members of the Bcl-2 family have pro-apoptotic activity, we examined the expression of the BH3-only peptide harakiri (Hrk) in the spinal cord of ALS patients. In situ expression of Hrk mRNA and immunoreactivity against the Hrk peptide were verified in the spinal neurons. In the immunoblot analysis, upregulated Hrk protein migrated at 16 kDa. Heterodimerization of Hrk with Bcl-2 was detected by immunoprecipitation, which suggests the competition of Hrk and anti-apoptotic Bcl-2. These findings suggest that Hrk plays a role in apoptotic events in ALS pathogenesis.
PURPOSE: To determine how interruption of hepatic blood in- or outflow affects the coagulation diameter of microwave coagulation therapy (MCT) in the liver. MATERIALS AND METHODS: Laparotomic MCT at 60 W for 1 minute was performed in 11 Landrace pigs. MCT was performed under six different conditions: without occlusion (Group N; in seven lobes of seven pigs); with occlusion of the hepatic artery (Group A; in five lobes of five pigs); with occlusion of the portal vein (Group P; in five lobes of five pigs); with occlusion of the hepatic artery and portal vein (Group AP; in six lobes of six pigs); with occlusion of the hepatic vein (Group V; in five lobes of four pigs); and with occlusion of the hepatic artery and vein (Group AV; in seven lobes of seven pigs). The maximum diameters for each group were compared. RESULTS: The coagulation diameters (mean +/- SD) were 8.5 mm +/- 2.0, 10.0 mm +/- 1.6, 14.3 mm +/- 2.5, 14.4 mm +/- 2.4, 13.0 mm +/- 0.8, and 14.4 mm +/- 1.5 for Groups N, A, P, AP, V, and AV, respectively. The coagulation diameters for groups P, AP, V, and AV were statistically larger than those for groups N and A (P < .05). There was no significant difference between the coagulation diameters of Groups P, AP, V, and AV. CONCLUSION: The coagulation diameter depends mainly on the portal venous flow. In addition of direct interruption of the portal vein, interruption of the hepatic vein can also result in a substantial increase in the coagulation diameter.
T-cell-mediated dominant control of self-reactive T cells is one mechanism for maintaining immunologic self tolerance. It also hampers the generation of immunity to autologous tumor cells. Abrogation of the control can evoke potent tumor immunity as well as autoimmunity in normal animals. This common regulatory mechanism for autoimmunity and tumor immunity can be exploited to devise a novel immunotherapy against cancer.
The purpose of this study was to investigate whether regional liver damage could be detected by means of enhanced MR imaging with a superparamagnetic iron oxide (SH U 555A) in an ischemia-reperfusion model of rat liver. Ischemic liver damage was induced in the right lobe by vascular clamping for 0 (sham), 30 (I-30), 60 (I-60), and 90 minutes (I-90). There was no significant difference in relative enhancement (RE) between the ischemic and nonischemic lobes in the sham, I-30 and I-60 groups, while RE of the ischemic lobe was significantly lower than that of its nonischemic counterpart in the I-90 group as seen on SH U 555A enhanced proton density spin echo images (P < 0.05). Histological examination revealed that iron deposits were significantly smaller in the ischemic than the nonischemic lobe in the I-90 group (P < 0.05), although there was no significant difference in the number of Kupffer cells. Our results indicate that severe regional liver damage can be evaluated by MR imaging with SH U 555A.
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There is accumulating evidence that T-cell-mediated dominant control of self-reactive T-cells contributes to the maintenance of immunologic self-tolerance and its alteration can cause autoimmune disease. Efforts to delineate such a regulatory T-cell population have revealed that CD25+ cells in the CD4+ population in normal naive animals bear the ability to prevent autoimmune disease in vivo and, upon antigenic stimulation, suppress the activation/proliferation of other T cells in vitro. The CD25+ CD4+ regulatory T cells, which are naturally anergic and suppressive, appear to be produced by the normal thymus as a functionally distinct subpopulation of T cells. They play critical roles not only in preventing autoimmunity but also in controlling tumor immunity and transplantation tolerance.
An 85-year-old man was suffering from right pyothorax caused by methicillin-resistant staphylococcus aureus (MRSA). The empyema cavity was closed by intrathoracic implantation of a free rectus abdominis musculocutaneous (MC) flap using microvascular surgery 2 months after open-window thoracostomy (OWT). Compared with a pedicled MC flap, a free flap has the advantage that it can close a larger empyema cavity since the whole flap can be inserted into the cavity. Although the use of a free MC flap requires a two-stage operation, this method is believed to be more successful for controlling chronic empyema than any other established procedure, including decortication, thoracoplasty or pleuropneumonectomy.
OBJECTIVES: Trends in coronary bypass surgery require less invasive techniques and more conduits. We investigated the ability of direct coronary perfusion from the left ventricle to support regional and global cardiac function. METHODS: A conduit was established between the left ventricle and left anterior descending coronary artery (n = 6) with an interposed Starling resistor that allowed for graded regulation of backward flow. Changes of coronary flow, regional function in the territory of the left anterior descending coronary artery, and reactive hyperemia were studied. In 3 separate dogs, functional tolerance to increased heart rate was tested. In another 3 dogs, left ventricle-left anterior descending and left ventricle-left circumflex coronary artery conduits were established simultaneously (double conduit), and global function was tested. RESULTS: Without flow regulation, flow through the left ventricle-left anterior descending conduit exhibited high peaking (102 +/- 35 mL/min), midsystolic forward flow, and large pandiastolic backward flow (peaking at -47 +/- 22 mL/min). Mean coronary flow and regional function were maintained at 46.0% +/- 7.1% (35.8%-54.2%) and 45.3% +/- 29.1% (-1.8%-74.2%) of their respective normal values. When the Starling resistor was used to regulate backward flow, these values increased to 70.8% +/- 12.5% (56.8%-90.4%) and 70.2% +/- 27.8% (23.6%-107.7%), respectively. Coronary and functional reserve with a left ventricle-left anterior descending conduit were not observed. With the double conduit, global ventricular contractility indexed by end-systolic pressure-volume relation averaged 46% +/- 35% of its normal value. CONCLUSIONS: A left ventricle-coronary artery conduit supplied approximately 45% of normal blood flow and regional function, and both were improved by regulation of backward flow. Therefore, a conduit from the left ventricle to an epicardial vessel could serve as a rapidly deployable means of revascularizing totally occluded coronary vessels for which suitable natural conduits are not available.
We discovered that the coupling beat interval from a slow to a tachycardiac pacing period considerably affected the pattern of the beat-to-beat alternation of the tachycardia-induced sustained contractile alternans. We analyzed the relationship between the coupling interval and the pattern and amplitude of the alternans in the isovolumic left ventricle of canine blood-perfused hearts. The alternans pattern and amplitude varied transiently over the first 30-50 beats and became gradually stable over the first minute in all 12 hearts. We discovered that stable alternans, even under the same tachycardiac pacing, had three different strong-weak beat patterns depending on the coupling interval. A relatively short coupling interval produced a representative sustained alternans of the strong and weak beats. A relatively long coupling interval produced a similar sustained alternans but in a reversed order of even- and odd-numbered beats counted from the coupling interval. However, sustained alternans disappeared after 1-3 specific coupling intervals. We conclude that ventricular pacing rate does not solely determine the pattern and amplitude of sustained contractile alternans induced by tachycardia.