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This study suggests multiple susceptibility loci for comitant strabismus. The loci at chromosomes 4q28.3 and 7q31.2 show a significant evidence of linkage.

We report five cases of blunt cardiac rupture seen in our hospital during the last 6 years. All these patients sustained blunt chest trauma due to motor vehicle or motorcycle accidents, and all had vital signs on arrival at the emergency department. We suspected cardiovascular injuries from the findings of echocardiography and CT scans, and all five cases were operated on 2-6 h after injury. Four had a median sternotomy, and one had a lateral thoracotomy. During the operations, we found that two patients had pericardium injuries and all five patients had right chamber injuries, which included multiple, ventricle, and large venous injuries in three patients. The tears were repaired using simple suture or ligation techniques for all patients, with cardiopulmonary bypass in three patients. One patient died during the operation, and four patients survived, therefore the survival rate was 80%. We believe that patients with cardiac rupture who are alive when they reach hospital can often be saved by prompt diagnosis and immediate, adequate surgical repairs.

Intraoperative and perioperative administration of low-dose landiolol has a preventive effect on the appearance of atrial fibrillation after CABG surgery.

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Aim: To identify ARIX gene polymorphisms in patients with congenital superior oblique muscle palsy and to find the relation between the ARIX gene and congenital superior oblique muscle palsy. Methods: The three exons of the ARIX gene were sequenced by genomic DNA amplification with polymerase chain reaction (PCR) and direct sequencing in 15 patients with superior oblique muscle palsy (13 with congenital and two with acquired palsy) and 54 normal individuals. PCR products cloned into plasmids were also sequenced. A family with father and a daughter each having congenital superior oblique muscle palsy was also involved in this study. Results: Four patients with congenital superior oblique muscle palsy carried heterozygous nucleotide changes in the ARIX gene. One patient with the absence of the superior oblique muscle had T7C in the 59-UTR of the exon 1 and C-44A in the promoter region, both of which were located on the same strand. Another unrelated patient with congenital superior oblique muscle palsy had C76G in the 59-UTR of the exon 1 and C-9A in the promoter region on the same strand. G153A in the 59-UTR of exon 1 was found in common in two affected members of a family with congenital superior oblique muscle palsy. This G153A in the 59-UTR of exon 1 was also present in four unrelated normal individuals. No other heterozygous nucleotide changes were found in normal individuals. Conclusions: The nucleotide change (G153A) in the 59-UTR of exon 1 co-segregated with congenital superior oblique muscle palsy in one family. Four other nucleotide changes in the exon 1 or the promoter region were found only in patients with congenital superior oblique muscle palsy. These nucleotide polymorphisms may be one of the risk factors for the development of congenital superior oblique muscle palsy.

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