A new hypothesis for the origin of metastases is presented. It assumes that a cancer-transformed gene in a primary tumour is incorporated in its identical form via a virus-vector function into biologically potent recipient cells in other organs, such as stem cells, multipotent cells or cells in an early phase of division. The origin of metastases may thus possibly occur via a genetic pathway.

A 67-year-old man fell from the second floor of his home and was impaled on an iron pipe used for a garden stake. The pipe was 2 cm in diameter and had entered his left buttock to his anus. A plain abdominal X-ray film showed that the tip of the pipe was located in front of the 4th lumbar vertebra, so the penetration distance was 30 cm. An emergency operation was performed for hemorrhagic shock. Laparotomy revealed massive intra-abdominal bleeding, injuries of the sigmoid and transverse mesocolon, superior rectal artery, and the first part of the duodenum. Because of suspected lower rectal injury, division of the upper rectum, closure of the rectal stump, and sigmoidostomy were performed. Gauze packing into the pelvic cavity was performed for uncontrollable bleeding. All the gauze was postoperatively removed from the drain wound without laparotomy. Six months after the operation, he underwent a second operation including anastomosis of the descending colon and lower rectum, which allowed him to live a normal daily life.

Selective IgA deficiency (SIgAD) is the most common type of primary immunoglobulin deficiency. Most individuals with SIgAD are asymptomatic. However, some patients are associated with allergic and autoimmune disease. SIgAD is included in the list of differential diagnoses of eosinophilia. We experienced a patient who initially presented with abdominal pain and eosinophilia. A >1-year follow-up revealed SIgAD, and we had difficulty differentiating it from Churg-Strauss syndrome (CSS) or hypereosinophilic syndrome (HES). A 66-year-old Japanese male presented with a history of recurrent abdominal pain. A diagnostic work-up revealed eosinophilia, eosinophilic gastritis, eosinophilic pneumonia, and SIgAD over 1 year of clinical observation. He also suffered from asthma and sinusitis. Anti-neutrophil cytoplasmic antibody was negative and vasculitis was not detected in the obtained tissue specimens of stomach, lung, nose and skin. The patient showed no evidence of drug ingestion, parasitic infections, or malignant neoplasms. Although we cannot rule out prevasculitic CSS and idiopathic HES, the whole clinical picture in this patient can be explained most consistently by SIgAD.

Radial head dislocation associated with plastic bowing of the ulna is classified as a Monteggia equivalent lesion. This injury in children can be treated by closed reduction, but manipulative reduction may not completely correct plastic bowing of the ulna. We encountered two cases of incomplete reduction in which the radial head was reduced in a supination position, but redislocated during rotation from neutral to a pronation position. The patients were treated conservatively using an adjustable hinged elbow splint. Plain radiography at 6 weeks after incomplete closed reduction showed that the radial head was reduced in all positions from supination to pronation; thus, both patients had good outcomes. Our method is non-invasive and may be an option for treatment of incomplete reduction of radial head dislocation with acute plastic bowing of the ulna.

Surface-based bone hemangiomas are uncommon, mostly occurring in long bones of the lower extremities. Radiographic surface-based bone hemangioma images may present various features that provide a diagnostic challenge. We report a case of surface-based hemangioma of the radius that posed radiological diagnostic difficulties. The tumor size was small and the cortical reaction was subtle. MRI findings were nonspecific and angiography was useful in the assessment of painful but less obvious surface-based bone hemangioma. The patient's pain improved following surgery and no tumor recurrence was observed at 3 years after surgery.

Exposure of the mitral valve is of critical importance in mitral valve surgery. The mitral valve is located near the interatrial groove. As we accumulated experience and learned from embryology, we found that a more central left atriotomy was advantageous, and was made possible by interatrial groove dissection using an ultrasonic scalpel. This crucial finding prompted us to report the technique.

We sought to investigate the effects of the left internal mammary artery anastomosed to the left anterior descending artery for improving mid-term outcome in patients with severe left ventricular dysfunction. Twenty consecutive coronary artery bypass grafts performed by a single surgeon for less than 35% ejection fraction patients were reviewed retrospectively from April 2000 to November 2008. There was one perioperative death (5.0% mortality). The mean survival was 55 months with an actual 5-year survival rate of 75%. Echocardiography showed the ejection fraction improved to 10.7 +/- 0.32% (p < 0.01). The strongest correlation was observed between both the flow and the pulsatile index of the left internal mammary artery measured intraoperatively by transit time flow meter and the postoperative ejection fraction improvement (R2=0.737 and 0.639, respectively). We reappraised the mid-term beneficial effects of the internal mammary artery anastomosed to the left anterior descending artery in patients with severe left ventricular function.

Autologous chondrocyte implantation (ACI) is a method of cartilage repair. To improve the quality of regenerated tissue by ACI, it is essential to identify surface marker expression correlated with the differentiation status of monolayer expanded human articular chondrocytes and to define the index for discriminating dedifferentiated cells from monolayer expanded human articular chondrocytes. Normal human articular chondrocytes were cultured in monolayer until passage 4. At each passage, mRNA expression of collagen type I, II, and X and aggrecan was analyzed by real-time quantitative PCR, and the surface marker expression of CD14, CD26, CD44, CD49a, CD49c, CD54, and CD151 was analyzed by fluorescence-activated cell sorting (FACS). The ratios of mRNA levels of collagen type II to I (Col II/Col I) represented the differentiation status of chondrocytes more appropriately during monolayer culture. The surface marker expression of CD44, CD49c, and CD151 was upregulated according to the dedifferentiation status, whereas that of CD14, CD49a, and CD54 was downregulated. The most appropriate combination of the ratio of Col II/Col I was CD54 and CD44. Cell sorting was performed using a magnetic cell sorting system (MACS) according to CD54 and CD44, and real-time quantitative PCR was performed for the cell subpopulations before and after cell sorting. The expression of collagen type II and aggrecan of the chondrocytes after MACS was higher than that before sorting, but not significantly. The mean fluorescence intensity (MFI) ratio of CD54 to CD44 could be an adequate candidate as the index of the differentiation status.

Several genome-wide association studies (GWAS) have revealed that single nucleotide polymorphisms (SNPs) of ABCG2 and SLC22A12 were strongly associated with serum uric acid (SUA), but those of methylene tetrahydrofolate reductase (MTHFR) were not. However, there were several studies indicating the association with MTHFR C677T polymorphism. This study examined the association with the polymorphism, taking into account the genotypes of ABCG2 Q126X and SLC22A12 W258X. Subjects were 5,028 health checkup examinees of Seirei Preventive Health Care Center (3,416 males and 1,612 females) aged 35 to 69 years, who participated in the Japan Multi-Institutional Collaborative Cohort Study (J-MICC Study). Hyperuricemia was defined as SUA equal to 7 mg/dL or over. The genotype frequency was 35.9% for CC, 48.1% for CT, and 16.0% for TT, being in Hardy-Weinberg equilibrium (p=0.90). Among 4,425 participants with ABCG2 126QQ and SLC22A12 258WW who were not under medication for hyperuricemia, the mean SUA was 5.6 mg/dL, 5.6 mg/dL, and 5.7 mg/dL, respectively. When 114 participants with ABCG2 126QQ and SLC22A12 258WW under medication for hyperuricemia were included in hyperuricemia cases, the sex-age adjusted odds ratio (OR) of hyperuricemia was not significant; OR=1.00 (95% confidence interval, 0.89-1.24) for CT genotype and OR=0.98 (0.84-1.32) for TT genotype, relative to CC genotype. The present study indicated no association between SUA and MTHFR C677T genotype, after the influences of ABCG2 Q126X and SLC22A12 W258X were removed.

Glucocorticoids are widely administered for the treatment of various disorders, although their long-term use results in adverse effects associated with glucocorticoid excess. We investigated the pathophysiological roles of glucocorticoid receptors (GRs) and mineralocorticoid receptors (MRs) in the cardiac changes induced by exogenous corticosterone in rats. Corticosterone or vehicle was injected twice daily in rats from 8 to 12 weeks of age. The effects of the GR antagonist RU486, the MR antagonist spironolactone, or both agents on corticosterone action were also determined. Corticosterone induced hypertension, left ventricular (LV) fibrosis, and LV diastolic dysfunction. Neither RU486 nor spironolactone affected corticosterone-induced hypertension, whereas spironolactone, but not RU486, attenuated the effects of corticosterone on LV fibrosis and diastolic function. Corticosterone also increased cardiac oxidative stress and inflammation in a manner sensitive to spironolactone but not to RU486. The corticosterone-induced LV atrophy was not affected by either RU486 or spironolactone. Our results implicate MRs in the cardiac fibrosis and diastolic dysfunction, but not MRs or GRs in the cardiac atrophy, induced by corticosterone. Neither MRs nor GRs appear to contribute to corticosterone-induced hypertension.