[Surgical strategy for aortic valve stenosis associated with single ventricle who will be objects of Fontan procedure].
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Publications and source records attributed to S Kasahara.
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To understand the lineage relationship and to define morphological characteristics of each thymocyte subset, we have performed ultrastructural analysis of highly purified thymocyte subpopulations. By flow cytometry, five subpopulations were sorted based on the expression of CD4 and CD8 and on cell size (forward scatter): large and small CD4+8+, CD4-8-, CD4+8-, and CD4-8+ thymocytes. Small CD4+8+ thymocytes were the smallest among lymphoid cells, and had a round and smooth cell outline with condensed nuclei, the cytoplasm was scanty and the cell organelles were not developed, suggesting the majority of this subset might be inactive by morphological criteria. CD4+8- thymocytes appeared to be similar to peripheral CD4+ T cells. The CD4-8- thymocyte subset contained morphologically immature cells in terms of cell size, presence of cell surface villi, and euchromatic appearance of the nucleus. CD4-8+ thymocytes heterogeneous in cell size, nuclear chromatin contents and amount of cytoplasm, could be divided into two distinct types. Type 1 CD4-8+ thymocytes were intermediate in size, and therefore similar to peripheral mature CD8+ T cells. Type 2 CD4-8+ thymocytes were large and irregular in shape (large CD4-8+) with irregular-shaped and euchromatic nuclei. Large CD4-8+ cells were, thus, considered to be at the transitional stage from CD4-8- to CD4+8+. At least two groups of large CD4+8+ cells were ultrastructurally classified by the nuclear chromatin content. Large CD4+8+ cells with heterochromatic nuclei were round with a smooth cell membrane, whereas large CD4+8+ cells with euchromatic nuclei were spherical with projections. Cytological features of heterochromatic large CD4+8+ cells are similar to those of small CD4+8+ thymocytes except for cell size. Euchromatic large CD4+8+ cells could be regarded as active blasts potentially leading to mature cells. Taken together, this is the first report that describes the ultrastructural characteristics of each thymocyte subset highly purified by flow cytometry.
Targeted disruption of two G-protein alpha subunit genes in the chestnut blight fungus Cryphonectria parasitica revealed roles for the Gi alpha subunit CPG-1 in fungal reproduction, virulence, and vegetative growth. A second G alpha subunit, CPG-2, was found to be dispensable for these functions. We now report the cloning and targeted disruption of a C. parasitica G-protein beta subunit gene. The deduced amino acid sequence encoded by this gene, designated cpgb-1, was found to share 66.2, 65.9, and 66.7% amino acid identity with G beta homologues from human, Drosophila, and Dictyostelium origins, respectively, but only 39.7% identity with the Saccharomyces cerevisiae G beta homologue STE4 product. Low stringency Southern hybridization failed to detect any related G beta subunit genes in C. parasitica. Targeted disruption of cpgb-1 resulted in several of the changes previously reported to accompany disruption of the C. parasitica Gi alpha subunit gene cpg-1. These included very significant reductions in pigmentation, asexual sporulation, and virulence. In contrast to results obtained for Gi alpha gene disruption, the reduction in virulence resulting from the disruption of a G beta gene was accompanied by increased, rather than decreased, vegetative growth on synthetic medium. The relevance of these results to mechanisms of fungal virulence is considered.
The reproducibility of coronary vasospasm was assessed in nine patients with complete remission of vasospastic angina by medical treatment by reexamination at intervals of mean [+/-SD] 5.7 +/- 0.9 years. Twenty-one segments were defined as spastic, demonstrating more than 90% narrowing after acetylcholine injection at the initial angiography. The degree of spasticity, type of spasm (diffuse or focal) and coronary artery diameter in these segments at the initial and follow-up studies were compared. Of the 21 segments, 17 (81%) still had some spasticity (> 25%) at the follow-up study and 8 (38%) of these 17 showed spasticity with greater than 90% narrowing. On the other hand, spasm was not reprovoked in 4 (19%) segments. Luminal diameter of the spastic segments decreased significantly at the follow-up study (2.52 +/- 0.83 vs 2.26 +/- 0.62 mm, p = 0.01), but percentage stenosis was not different between the initial and follow-up studies (9.1 +/- 7.2 vs 10.3 +/- 8.0%, NS). The reproducibility of the type of spasm provoked was 83%. Coronary vasospasticity persists to some extent in spite of complete remission of angina by medical treatment, and the type of spasm provoked has high reproducibility. Therefore, the cessation of drug treatment should be done carefully.
A technique with autologous tissue for the correction of type III truncus arteriosus is described. The truncal root was excised as a cylinder that incorporated pulmonary arteries and that was translocated anterior to the ascending aorta. The proximal section of the cylinder was closed and the pulmonary tract was reconstructed with anastomosis of a widely opened distal section to the right ventricle. Autologous pericardium was sutured to the entire surface of the pulmonary tract.
BACKGROUND: This study describes the results of techniques using the autologous truncal wall and part of the pulmonary artery for correction in anticipation of the growth of the pulmonary tract in patients with truncus arteriosus. METHODS: Seven consecutive patients with truncus arteriosus were reviewed. The posterior wall of the pulmonary tract was obtained by anastomosing the lower edge of the truncal arteriotomy to the upper corner of the ventriculotomy from the truncus in types I and II. Anterior translocation of the pulmonary artery was performed in a type III. A pericardial patch with or without a monocusp was placed to complete the right ventricular outflow tract. RESULTS: There were two hospital deaths, one of which was unrelated to a cardiac problem. Postoperative right-to-left ventricular peak pressure ratio was less than 0.55. There was one left pulmonary stenosis due to monocusp adherence in the late postoperative period. The sizes of the pulmonary tract at anastomosis were between 107% and 166% of the normal value between 7 months and 3.8 years of follow-up. CONCLUSIONS: The use of autologous arterial wall instead of a conduit is recommended for the repair of truncus arteriosus to expect growth of the pulmonary tract.
We previously isolated the Saccharomyces cerevisiae HKR1 gene that confers on S. cerevisiae cells resistance to HM-1 killer toxin secreted by Hansenula mrakii (S. Kasahara, H. Yamada, T. Mio, Y. Shiratori, C. Miyamoto, T. Yabe, T. Nakajima, E. Ichishima, and Y. Furuichi, J. Bacteriol. 176:1488-1499, 1994). HKR1 encodes a type 1 membrane protein that contains a calcium-binding consensus sequence (EF hand motif) in the cytoplasmic domain. Although the null mutation of HKR1 is lethal, disruption of the 3' part of the coding region, which would result in deletion of the cytoplasmic domain of Hkr1p, did not affect the viability of yeast cells. This partial disruption of HKR1 significantly reduced beta-1,3-glucan synthase activity and the amount of beta-1,3-glucan in the cell wall and altered the axial budding pattern of haploid cells. Neither chitin synthase activity nor chitin content was significantly affected in the cells harboring the partially disrupted HKR1 allele. Immunofluorescence microscopy with an antibody raised against Hkr1p expressed in Escherichia coli revealed that Hkr1p was predominantly localized on the cell surface. The cell surface localization of Hkr1p required the N-terminal signal sequence because the C-terminal half of Hkr1p was detected uniformly in the cells. These results demonstrate that HKR1 encodes a cell surface protein that regulates both cell wall beta-glucan synthesis and budding pattern and suggest that bud site assembly is somehow related to beta-glucan synthesis in S. cerevisiae.
The patient was a seven-old-boy with univentricular heart of left ventricular morphology with transposition of the great arteries and coarctation of the Aorta. Pulmonary artery banding and coarctactomy (subclavian flap method) were performed as prior surgery during infancy and significant subaortic stenosis (SAS) was not identified before or immediately after Fontan operation. SAS was suspected in an ejection murmur that developed without symptoms two years and five months after Fontan operation. It became clear that the SAS was caused by both restrictive ventricular septal defect and narrowing of outlet chamber (right ventricle). Surgery was performed with myectomy in the outlet chamber, enlargement of ventricular septal defect and a patch enlargement of the right ventricle outflow tract for relief of the SAS. Postoperative pressure gradient across the subaortic component was decreased, however, valve regurgitation remained grade I to II. The mechanisms of SAS after Fontan operation are related to hypertrophy of the subaortic component that incorporates the infundibulum and trabeculae. Careful morphological investigation is essential in patients with risk factors for SAS Mild deterioration of the ventricular compliance due to progressive SAS may result in reduction of the cardiac function and patient's quality of life. Adequate surgical treatment to relieve the SAS is considered essential before and after Fontan operation.
A radical correction involving Vargas's method and a direct anastomosis between the left pulmonary vein (PV) and left atrium (LA) was performed in a 29 day-old infant with supracardiac type Ib total anomalous pulmonary venous return (TAPVR) and an unusual form of the left PV. the left upper and lower PVs drained into a left "common" PV that was just behind the LA, and then into the right pleural cavity. The left common PV was located cephalad to the normal course and received blood from the right lower and upper PVs and drained into the supra-vena cava (SVC). The junction of the SVC and the right PV was slightly stenotic. Vargas's method is a useful technique for Darling's classification Ib TAPVR even in cases without the common PV situated behind the LA. But this patient had a left common PV and it was possible either to anastomose the common PV and LA directly or to perform Vargas's technique. We performed both procedures to prevent left PV obstruction (PVO). Cineangiography performed 2 months after surgery showed that a large amount of blood from the right and left PV drained into the LA through the common PV-LA route. These procedures, which create a dual PV channel, reduce the risk of PVO, so they are useful for radical correction of Darling's Ib type TAPVR.
The relationship between coronary vasospasticity and the development of atherosclerotic lesion was studied in 24 patients with vasospastic angina. All patients had no organic stenosis initially and underwent follow-up coronary angiography at 66 +/- 9 months after the initial examination. The coronary artery diameter was measured with the contour detection method. The spastic and non-spastic sites were identified at the initial coronary angiography with the acetylcholine provocation test. The change of the luminal diameter (delta LD) and the ratio of the change of luminal diameter (% delta LD) were compared at the spastic and the non-spastic sites. The follow-up examination showed significant decreases of coronary artery diameter in both the spastic (2.35 +/- 0.67 vs 2.16 +/- 0.58 mm, p < 0.001) and non-spastic sites (2.66 +/- 0.91 vs 2.54 +/- 0.84 mm, p = 0.02). However, delta LD and % delta LD were not different between the spastic and non-spastic sites (delta LD: -0.19 +/- 0.40 vs -0.12 +/- 0.46 mm, NS; % delta LD: -6.7 +/- 14.8% vs -3.2 +/- 17.0%, NS). In conclusion, coronary vasospasticity does not promote the development of atherosclerotic lesion.
A newborn baby with type II truncus arteriosus and type B interrupted aortic arch was successfully treated by creating a pulmonary tract using autologous flap made from truncal wall without excision of the pulmonary artery and by reconstructing the aortic arch with direct anastomosis. This method provided excellent hemodynamics with wide reconstruction of the pulmonary tract without conduit.
A successful palliative arterial switch operation with arch repair in a 30-day-old infant with tricuspid atresia, ventriculoarterial discordance, subaortic stenosis, coarctation of the aorta, and aortic arch hypoplasia is reported. A concomitant Blalock-Taussig shunt was required because of insufficient pulmonary blood flow through the restrictive bulboventricular foramen. Postoperative arterial oxygen saturation was maintained around 90% and the pressure gradient between the left ventricle and the pulmonary artery was 45 mmHg according to a Doppler echocardiogram. The infant becomes free of subaortic stenosis and is awaiting the subsequent Fontan operation. This alternative palliative operation for neonates and early infants with double inlet ventricle, subaortic stenosis, and arch hypoplasia offers some advantages on the Fontan operation for avoiding pulmonary arterial distortion and subaortic stenosis followed by ventricular hypertrophy.
HM-1 killer toxin secreted from Hansenula mrakii inhibits the growth of Saccharomyces cerevisiae cells by interfering with beta-1,3-glucan synthesis. We found that HM-1 killer toxin killed intact cells but not protoplasts. In addition, cells lacking the functional KRE6 allele (kre6 delta) became resistant to higher concentration of HM-1 killer toxin. As reported by Roemer and Bussey [(1991) Proc. Natl. Acad. Sci. 88 11295-11299], cells lacking functional KRE6 had a reduced level of the cell wall beta-1,6-glucan compared to that in cells harboring the normal KRE6. These results suggest that the cell wall beta-glucan is involved in the action of HM-1 killer toxin. Addition of HM-1 killer toxin with several kinds of oligosaccharides revealed that either beta-1,3- or beta-1,6-glucan blocked the cytocidal action of HM-1 killer toxin whereas alpha-1,4-glucan and chitin did not. Mannan also interfered with HM-1 killer toxin action, but this inhibitory effect was much weaker than that observed with beta-1,3- or beta-1,6-glucans. Thus, it appears that the cell wall beta-glucan interacts with HM-1 killer toxin, and that this toxin-beta-glucan commitment is required for the action of HM-1 killer toxin.
The effectiveness of a 5% potassium nitrate dentifrice as a daily home treatment for dentinal hypersensitivity was evaluated in a double-blind study in 36 Japanese subjects who complained of cold and/or tactile hypersensitivity. The subjects were divided into 2 groups, with 18 being given a 5% potassium nitrate dentifrice (treated group) and the other 18 a vehicle paste (control group). Both groups were instructed to brush their teeth 2 x a day. The hypersensitivity levels of the affected teeth were assessed by 2 stimuli, one tactile and the other cold air, and by the perception of pain. The results of all 3 assessment methods indicated that the potassium nitrate dentifrice significantly decreased the level of hypersensitivity at weeks 4, 8, and 12. In the treated group, a rapid decrease of positive scores for both the cold air stimulus and the subjective symptoms appeared from week 2. Although a significant decrease of the assessment score was also observed in the control group, the reduction rate of the score was much greater in the treated group by all 3 assessment methods at weeks 4, 8, and 12. Complete relief of subjective symptoms throughout the 12 weeks' examination was noted in 67% of the subjects in the treated group, but in only 6% in the control group. These results suggest the usefulness of a 5% potassium nitrate dentifrice in Japanese patients with dentinal hypersensitivity.
A gene whose overexpression can endow Saccharomyces cerevisiae cells with resistance to HM-1 killer toxin was cloned from an S. cerevisiae genomic library. This gene, designated HKR1 (Hansenula mrakii killer toxin-resistant gene 1), contains a 5.4-kb open reading frame. The predicted amino acid sequence of the protein specified by HKR1 indicates that the protein consists of 1,802 amino acids and is very rich in serine and threonine, which could serve as O-glycosylation sites. The protein also contains two hydrophobic domains at the N-terminal end and in the C-terminal half, which could function as a signal peptide and transmembrane domain, respectively. Hkr1p is found to contain an EF hand motif of the calcium-binding consensus sequence in the C-terminal cytoplasmic domain. Thus, Hkr1p is expected to be a calcium-binding, glycosylated type I membrane protein. Southern and Northern (RNA) analyses demonstrated that there is a single copy of the HKR1 gene in the S. cerevisiae genome, and the transcriptional level of HKR1 is extremely low. Gene disruption followed by tetrad analysis showed that HKR1 is an essential gene. Overexpression of the truncated HKR1 encoding the C-terminal half of Hkr1p made the cells more resistant to HM-1 killer toxin than the full-length HKR1 did, demonstrating that the C-terminal half of Hkr1p is essential for overcoming the effect of HM-1 killer toxin. Furthermore, overexpression of HKR1 increased the beta-glucan content in the cell wall without affecting in vitro beta-glucan synthase activity, suggesting that HKR1 regulates beta-glucan synthesis in vivo.
Complete correction without external conduit repair by autologous pulmonary arterial flap was performed for the truncus arteriosus in one neonate and two small infants. In this study, we investigated advantages of postoperative hemodynamics and pulmonary artery growth from the data on truncus arteriosus repaired by the autologous flap technique. Patient in this study was classified as type I or II truncus arteriosus and age ranged from 19 days to 95 days after birth. One of the patients died of unexpected gastric bleeding 25 days after surgery. However, all showed excellent hemodynamics in the early postoperative period. The reconstructed pulmonary tract positioned rather left ward and posterior to the level of the systemic root than the technique with extra cardiac conduit repair. Compression did not occur at the created pulmonary tract and hemodynamics was fairly stable after closure of the chest. The postoperative RVP/LVP ratio ranged among 0.45 to 0.65 and the pressure gradient across the right ventricular out flow tract demonstrated only 10-15 mmHg. The size of the pulmonary arterial flap was sufficient even in type II truncus arteriosus to create right ventricle-to-pulmonary tract. However, the first patient underwent subsequent surgery 20 months after the initial surgery, because of left pulmonary artery stenosis due to intimal tissue overgrowth distal to the outflow patch. Surgical findings revealed that the posterior wall of the pulmonary tract was smooth and well developed. Traction of pulmonary arterial flap toward the right ventricular outflow tract shortens the distance between monocusp and left pulmonary arterial orifice than expected.(ABSTRACT TRUNCATED AT 250 WORDS)
A case of aortic and mitral regurgitation associated with aortitis syndrome was presented. The patient was a 36-year-old female who admitted for palpitation and dyspnea. Left ventriculography showed moderate MR. Aortography showed moderate AR and multiple occlusive lesion of the aortic arch branches. After the inflammation was controlled, aortic and mitral valve replacement was performed. Postoperative course was uneventful. Histologically, aortic and mitral valve showed capillary increase and infiltration of inflammatory cells, mainly lymphocytes.
Two cases of subdural hematoma complicated after open heart surgery were successfully treated during thirty years history of the department. A 45 year-old woman underwent tricuspid valve replacement due to isolated congenital tricuspid insufficiency. On the 27th postoperative day, she was suddenly attacked by headache, and disturbance of consciousness was recognized with gradual deterioration. Brain CT scan showed a subdural hematoma on the right frontal region. Immediate irrigation of the hematoma was performed. Postoperative course was uneventful, and she was discharged without any complications. A 59 year-old woman underwent mitral valve replacement due to mitral re-stenosis. On the 3rd postoperative day, disturbance of consciousness was seen suddenly. Brain CT scan showed a subdural hematoma in the bilateral posterior cranial fossa. Immediate GL-YCEOL drip infusion was started. On the next day consciousness returned without operation and she was discharged without any neurological complications. Both patients did not have head trauma during pre and post operative period. It was important to consider the possibility of a intracranial hematoma, when the disturbance of consciousness was recognized after open heart surgery and/or during anticoagulant therapy.