We rotated the nucleus up to 270 degree and dislocated it into anterior chamber through the diameter of capsulorhexis after hydrodissection by using the planned extracapsular cataract extraction. And later on we delivered the nucleus with hydroexpression using the irrigating Vectis or with rotation using a lens spatuala. As a result of this procedure, the nucleus was safely delivered in all cases without zonular rupture and vitreous prolapse.
Anterior Chamber ; Capsulorhexis* ; Cataract Extraction* ; Cataract* ; Prolapse ; Rupture

For the purpose of correction of high myopia, we had implanted Worst-Fechner Biconcave Lens (Ophtec B.V., Groningen, Holland) in the 10 phakic eyes which were more myopic than -8.0 D. We examined postoperative visual acuity and complications. Postoperative uncorrected visual acuity was from 0.3 to 1.0. Cataract, glaucoma, chronic iridocyclitis and macular edema or retinal detachment did not occur and during the iris fluorescein angiography of 4 eyes there was no leakage of dye at the fixation site of iris by haptic of the lens. But all patients complained of glare. In the 3 eyes which were followed up for 12 months, corneal endothelial cell loss occurred continuously and the endothelial cell loss was 17.2% at the central cornea and 19.5% at the paracentral cornea. Therefore, long term follow up is necessary.
Cataract ; Cornea ; Corneal Endothelial Cell Loss ; Endothelial Cells ; Fluorescein Angiography ; Follow-Up Studies ; Glare ; Glaucoma ; Humans ; Iridocyclitis ; Iris ; Macular Edema ; Myopia* ; Retinal Detachment ; Visual Acuity

A pacemaker-induced venous obstruction is relatively common, but is rare in cases where chronic venous occlusion has developed and progressed after the removal of permanent pacemaker leads. We report a case of permanent pacemaker implantation following percutaneous balloon venoplasty in a patient with innominate vein stenosis. The patient had a history of permanent pacemaker implantation, using a right subclavian approach, with lead extraction due to infective endocarditis 6 years earlier. Although the epicardial leads were re-implanted, once more the ventricular lead broke. When we tried to implant a new pacemaker, using a left subclavian endovascular approach, extensive venous stenoses of the innominate, right internal jugular and subclavian veins were found. As it was impossible to advance the standard pacemaker lead; therefore, percutaneous balloon venoplasty of the innominate vein was performed, and a DDD-R pacemaker successfully implanted.
Angioplasty, Balloon ; Brachiocephalic Veins* ; Constriction, Pathologic* ; Endocarditis ; Humans ; Pacemaker, Artificial ; Subclavian Vein ; Venous Thrombosis

We evaluated pseudophakia in high myopic patients whose an axial lenght were 26mm and over. Cataract surgery was performed with ECCE and posterior chamber intraocular lens implantations from May 1986 to May 1991 on 69 patients (80 eyes). The results were as follows; 1. Most myopic patients were good candidates for posterior chamber intraocular lens implantation regardless of axial length. 2. Posterior chamber intraocular lens implantations in high myopia were a good refractive surgery. 3. The theoretical formula had better predictabilized than the empirical formula in apredictive accuracy.
Cataract ; Humans ; Lens Implantation, Intraocular* ; Lenses, Intraocular* ; Myopia* ; Pseudophakia ; Refractive Surgical Procedures

BACKGROUND: Through a genome-wide search using the genetic markers(RFLP genetic markers), the familial hypertrophic cardiomyopathy(FHCM) with an autosomal dominant mode of inheritance has been firstly detected to be genetically linked to chromosome 14q1. The subsequent studies have shown that the point mutations at the exons encoding for the head and head /rod junction of the cardiac beta myosin heavy chain(beta-MHC) are the most frequent type of mutation in the FHCM families genetically implicated with a linkage to beta-MHC, whereas the alpha/beta-MHC hybrid gene and a large deletion at the 3' region of beta-MHC gene were also rarely detected. With the other families genetically implicated with the chromosomes 1,11,15,16 and 18, FHCM also manifests locus heterogeneity, a phenomenon in which abnormalities at different genes are involved in different families. In addition, a korean FHCM family with 403Arg-->Gln mutation of beta-MHC gene has been previously found by an american research group. METHODS: For clinical diagnosis, echocardiography and electrocardiography were performed on the individual members of a korean FHCM family. The microsatellite markers(MYO-I,MYO-II) located in the beta-MHC gene region were amplified by PCR(polymerase chain reaction) and the polymorphism was analyzed for the possible linkage to the phenotypic expression of FHCM. Independently, the same PCR products of the exons 13 and 23 were digested with the specific restriction enzymes for the presence of the most frequently reported point mutations of beta-MHC gene (403 and 908 amino acid mutations). Single strand conformation polymorphism(SSCP) of the exon 13 and 23 of the beta-MHC gene was also analyzed of the mobility shift expected if any point mutation is present at these two exons. RESULTS: The inheritance pattern of HCM(hypertrophic cardiomyopathy) in the family is considered as autosomal dominant. In this family(KU 101), one of the microsatellite markers(MYO-II) indicated the possible cosegregation between the allele was also present in the 32-year-old brother of the proband, who reveals no clinical signs of the disease. The other microsatellite genetic marker(MYO-I) was uninformative, without giving the discriminating power to verify the linkage to beta-MHC gene. In the analysis for two common mutations of beta-MHC gene by PCR-RFLP and PCR-SSCP, no evidence was found for 403 and 908 amino acid mutations and any point mutation in the exons 13 and 23. CONCLUSIONS: Based on the linkage analysis using microsatellite genetic markers, there was a possibility that the disease could be linked to an abnormality in the beta-MHC gene of the chromosome 14q1.
Adult ; Alleles ; Cardiomyopathy, Hypertrophic, Familial* ; Diagnosis ; Echocardiography ; Electrocardiography ; Exons ; Genetic Markers ; Head ; Humans ; Inheritance Patterns ; Mass Screening* ; Microsatellite Repeats ; Point Mutation ; Polymerase Chain Reaction ; Population Characteristics ; Siblings ; Ventricular Myosins* ; Wills

BACKGROUND: Through a genome-wide search using the genetic markers(RFLP genetic markers), the familial hypertrophic cardiomyopathy(FHCM) with an autosomal dominant mode of inheritance has been firstly detected to be genetically linked to chromosome 14q1. The subsequent studies have shown that the point mutations at the exons encoding for the head and head /rod junction of the cardiac beta myosin heavy chain(beta-MHC) are the most frequent type of mutation in the FHCM families genetically implicated with a linkage to beta-MHC, whereas the alpha/beta-MHC hybrid gene and a large deletion at the 3' region of beta-MHC gene were also rarely detected. With the other families genetically implicated with the chromosomes 1,11,15,16 and 18, FHCM also manifests locus heterogeneity, a phenomenon in which abnormalities at different genes are involved in different families. In addition, a korean FHCM family with 403Arg-->Gln mutation of beta-MHC gene has been previously found by an american research group. METHODS: For clinical diagnosis, echocardiography and electrocardiography were performed on the individual members of a korean FHCM family. The microsatellite markers(MYO-I,MYO-II) located in the beta-MHC gene region were amplified by PCR(polymerase chain reaction) and the polymorphism was analyzed for the possible linkage to the phenotypic expression of FHCM. Independently, the same PCR products of the exons 13 and 23 were digested with the specific restriction enzymes for the presence of the most frequently reported point mutations of beta-MHC gene (403 and 908 amino acid mutations). Single strand conformation polymorphism(SSCP) of the exon 13 and 23 of the beta-MHC gene was also analyzed of the mobility shift expected if any point mutation is present at these two exons. RESULTS: The inheritance pattern of HCM(hypertrophic cardiomyopathy) in the family is considered as autosomal dominant. In this family(KU 101), one of the microsatellite markers(MYO-II) indicated the possible cosegregation between the allele was also present in the 32-year-old brother of the proband, who reveals no clinical signs of the disease. The other microsatellite genetic marker(MYO-I) was uninformative, without giving the discriminating power to verify the linkage to beta-MHC gene. In the analysis for two common mutations of beta-MHC gene by PCR-RFLP and PCR-SSCP, no evidence was found for 403 and 908 amino acid mutations and any point mutation in the exons 13 and 23. CONCLUSIONS: Based on the linkage analysis using microsatellite genetic markers, there was a possibility that the disease could be linked to an abnormality in the beta-MHC gene of the chromosome 14q1.
Adult ; Alleles ; Cardiomyopathy, Hypertrophic, Familial* ; Diagnosis ; Echocardiography ; Electrocardiography ; Exons ; Genetic Markers ; Head ; Humans ; Inheritance Patterns ; Mass Screening* ; Microsatellite Repeats ; Point Mutation ; Polymerase Chain Reaction ; Population Characteristics ; Siblings ; Ventricular Myosins* ; Wills

No abstract available.
Craniocerebral Trauma* ; Head* ; Protons*

no abstract available.

Spontaneous renal allograft rupture is an uncommon complication of renal transplantation, but it represents a life-threatening emergency that requires prompt recognition and treatment. The incidence of spontaneous renal allograft rupture is variable and range between 3.6 and 9.6 percent of all transplants. In the majority of cases the rupture is associated with acute rejection episodes and with renal vein thrombosis. Most frequently, the allograft rupture occurs within the first 2 weeks of transplantation. in addition, most ruptures reported have occurred in cadaveric renal allograft. Debate on the management of such allograft salvage versus transplant nephrectomy. It appears that the recent trend is toward performing surgical repair of the graft if the rupture is secondary to rejection and oo evidence of renal vein thrombosis ; otherwise, graft nephrectomy be done. We report a case of spontaneous renal allograft rupture due to renal vein thrombosis occurred in a 21-year-old woman 6 days after transplantation. Unusual severe localized pain, swelling over at allograft site, and hypotension, a triad frequently seen in renal allograft rupture, were present. Management by graft nephrectomy was inevitable because of the patient's downhill course.
Allografts* ; Cadaver ; Emergencies ; Female ; Humans ; Hypotension ; Incidence ; Kidney Transplantation ; Nephrectomy ; Renal Veins ; Rupture ; Rupture, Spontaneous* ; Thrombosis ; Transplants ; Young Adult

BACKGROUND: Myocardial contrast two-dimensional echocardiography(MC-2DE) has been known to have the real time capabilities for repeat in vivo assessment of ischemic risk areas and for evaluation of the myocardial perfusion. The aims of this investigation are (1) to evaluate the feasibility of MC-2DE for the delineation and quantitation of the area at risk. (2) to determine the relationship between the extent of the echocontrast defect area(EDA) during reperfusion and the size of myocardial infarction as determined by post-mortem tissue examination, and (3) to observe serial changes in the time echo-intensity characteristics of MC-2DE during coronary occlusion and reperfusion. METHODS: Myocardial contrast echocardiographic images were made by injecting bolus 5mL of two-syringe-agitated mixture of sodium meglumine ioxaglate(Hexabrix(R)) and normal saline(2 : 3 by volume) into the aortic root before and during coronary occlusion of the left anterior descending coronary artery, distal to the first diagonal branch and during reperfusion on eight open-chest dogs. Two-dimensional echocardiographic short axis views were obtained at four anatomic levels : the apex, the low papillary muscle, the high papillary muscle and the mitral valve. The changes in EDA and echo-intensity with its wash-out half time(WHT) at the high papillary muscle level during coronary occlusion and reperfusion were measured every 15 minutes. The total EDA was measured by planimetry at 3 minutes after coronary occlusion and at 60 minutes after reperfusion. Evans blue or methylene blue were used for the measurement of the anatomic area at risk and triphenyl-tetrazolium chloride(TTC) for the measurement of the infarct area. RESULTS: The EDA measured 30 minutes after coronary occlusion(19.6%) was smaller than that at 3 minutes after coronary occlusion(24.0%, p<0.01). Then EDA at 3 minutes occlusion was strongly predictive of the anatomic extent of area at risk(EDA=0.48 Area at risk+16.95, r=0.84, p<0.05). The EDA at 60 minutes after reperfusion, which showed an irregular margin and was located within the subendocardium of the area at risk, also correlated well with the infarct area(IA)(EDA=0.78 IA+3.32, r=0.82, p=0.09). The peak echo-intensity in the ischemic area during coronary occlusion was significantly low(14.2+/-6.5 vs 73.8+/-31.7 in the non-ischemic area, p<0.01) and the WHT was delayed more in the ischemic area than in the non-ischemic area(23.2+/-2.8 sec vs 8.1+/-3.3sec, p<0.01). During the period of reperfusion, WHT in the previously ischemic area was markedly delayed compared to that in the non-ischemic area (p<0.01), although the peak echo-intensity in the ischemic area at 3 minutes after reperfusion increased modestly compared to that in the non-ischemic area(80.9+/-22.8 vs 72.7+/-8.4), suggesting the impairment in the transit of microbubbles is probably due to microvascular damage after reperfusion. There were no adverse hemodynamic or electrocardiographic effects after injection of the contrast agent. CONCLUSIONS: These findings suggest that myocardial contrast echocardiography was useful as a non-invasive technique, first, to delineate the area at risk in vivo during coronary occlusion and, after reperfusion, the infarct area, and secondly, to evaluate indirectly the state of myocardial perfusion during coronary occlusion and reperfusion.
Animals ; Axis, Cervical Vertebra ; Coronary Occlusion* ; Coronary Vessels ; Dogs ; Echocardiography* ; Electrocardiography ; Evans Blue ; Hemodynamics ; Meglumine ; Methylene Blue ; Microbubbles ; Mitral Valve ; Myocardial Infarction ; Papillary Muscles ; Perfusion* ; Reperfusion* ; Sodium