Long-term follow-up of exercise tolerance after coronary bypass grafting]

Six hundred forty-eight serial graded exercise tests were performed on 400 patients up to 10 years after coronary bypass graftings (CABG). The maximal attained exercise tolerance, over 10 METS, were observed in 60% of patients and the negative response to exercise test in 43% of patients. The positive response in various parameters were observed at the following rates: graft occlusion-30% vs graft patent-46% (p less than 0.01); incomplete revascularization-39% vs complete revascularization-22% (p less than 0.01); and less than or equal to 8 METS 4-45% vs greater than or equal to 10 METS-28% (p less than 0.01), respectively. However, no significant difference was observed among number of vessels diseased, number of graftings, and presence of old myocardial infarction. The maximal attained stage of exercise, over 10 METS, in various parameters were at the following rates: less than or equal to 59 years old-70% vs greater than or equal to 60 years old-44% (p less than 0.01); male-63% vs female-32% (p less than 0.01); and graft patent-63% vs graft occlusion-50% (p less than 0.05), respectively. The serial analysis of exercise test demonstrated that improved exercise tolerance appears to persist for at least 5 years after CABG. However, the patients in complete revascularization had a tendency to increase the rate of positive response. In conclusion, the completeness of revascularization as well as graft patency was the main factor limiting exercise tolerance, and correlates with the extent and the duration of improvement after CABG.     

Important role of serotonin in the antitumor effects of recombinant human tumor necrosis factor-alpha in mice

The possible involvement of chemical mediator(s) in the induction of the antitumor effects of recombinant human tumor necrosis factor-alpha (rTNF-alpha) on Meth A fibrosarcoma (Meth A) in mice was studied. On day 7 after intradermal implantation of Meth A in mice, rTNF-alpha caused tumor necrosis and inhibited the tumor growth. Ketanserin, cyproheptadine, and spiperone [serotonin (5-HT) receptor blockers] inhibited or attenuated the antitumor effects of rTNF-alpha, but the other types of receptor blockers tested (histamine H1 and H2, adrenaline alpha and beta, dopamine, and acetylcholine receptor blockers) did not. The large i.v. doses of 5-HT caused tumor necrosis and inhibited tumor growth in mice when given i.v. on day 7 but not when given on day 3 after Meth A implantation, which effects closely resemble those of rTNF-alpha. Its anti-tumor effects were completely inhibited by the 5-HT receptor blockers. 5-HT, like rTNF-alpha, showed no cytotoxicity against in vitro cultured Meth A cells. The results suggest that 5-HT is, at least in part, important for the induction of antitumor effects of rTNF-alpha on Meth A in mice.     

Musculoskeletal conditions of acute leukemia and malignant lymphoma in children

We retrospectively reviewed 16 patients who presented to hospitals with orthopaedic complaints. Twelve patients experienced initial symptoms in the extremities and four patients had back pain. The leukocyte count was elevated in one patient, decreased in two patients, and normal in 13 patients. On radiographic examination, osteopenia was observed in 10 patients, osteolytic lesions were observed in five, and pathologic fractures were observed in five. Because the initial presentation of patients with leukemia often involves the musculoskeletal system, orthopaedists need to recognize the symptoms of this disease to avoid misdiagnosis and to expedite the initiation of appropriate potentially lifesaving treatment.     

Hemochromatosis with mutation of the ferroportin 1 (IREG1) gene

The HFE, H ferritin, TFR2, and ferroportin 1 genes of a Japanese patient diagnosed as having hemochromatosis were amplified by PCR and sequenced. A novel mutation in the ferroportin 1 was found in the patient. It was located in the noncoding region of the ferroportin 1; nucleotide 117 adenine was changed to guanine, 7 nucleotides downstream the iron responsive element (IRE) region. This mutation was not found in the patient's son or daughter, or in 50 healthy individuals. It was suggested that the mutation in the ferroportin 1 may be related to hemochromatosis of this patient.     

MR imaging of normal perivascular space expansion at midbrain

BACKGROUND AND PURPOSE: A previous investigation of the MR imaging findings in the midbrain reported expanded perivascular (PV) spaces in only the ponto-mesencepalic junction (PMJ) in 20% of healthy subjects, whereas pathologically expanding PV spaces have been reported at the mesencephalo-diencephalic junction (MDJ) as multi-lobulated, cystic lesions with signal intensity compatible with that of CSF that cause aqueductal stenosis. To clarify the anatomical distinctions between normally expanded and pathologically expanding PV spaces, we defined their distribution in the normal midbrain by using high-spatial-resolution MR imaging. METHODS: Heavily T2-weighted MR imaging was performed in 115 adult subjects with neurologic complaints without cerebral disease. Histologic studies were performed from two normal midbrain blocks. RESULTS: Expanded PV spaces were visible at the PMJ in 87% of subjects and at the MDJ in 63% of subjects. On axial images, ovoid or linear lesions with signal intensity compatible to CSF were present behind the cerebral peduncle at both the PMJ and MDJ. These areas varied from less than 1 mm to 5 mm (maximum diameter on coronal sections). Histologic studies confirmed the distribution of expanded PV spaces, as noted on MR images. CONCLUSION: This study, by using high-spatial-resolution MR imaging, revealed that expanded PV spaces were visible at the PMJ and MDJ. Our finding of expanded PV spaces normally present at the MDJ may be related to pathologically expanding PV spaces, which should be kept in mind as a differential diagnosis for intraparenchymal cystic lesions in the midbrain with signal intensity compatible to CSF.     

Surgery for acute aortic dissection concomitant with preceding axillofemoral bypass to prevent malperfusion of visceral organs and limb ischemia

A 52-year-old man was admitted with sudden onset of epigastralgia. Abdominal X-ray showed dilated intestine and computed tomography (CT) revealed extended type A aortic dissection. Marked abdominal distention and weak pulse of right femoral artery were recognized so malperfusion of visceral organs due to narrowing true lumen compressed by thrombosed false lumen was suggested. In the operation, right axillo-right femoral bypass was established preceding to median sternotomy. This graft was used as an arterial perfusion site of cardiopulmonary bypass, and replacement of the ascending aorta was performed under hypothermic circulatory arrest and retrograde cerebral perfusion. Sign of malperfusion of visceral organs was showed for several days after the operation but it disappeared without further intervention. Axillofemoral inflow of cardiopulmonary bypass may be effective procedure in these cases.     

Induced reactivity of intestinal CD4(+) T cells with an epithelial cell lectin, galectin-4, contributes to exacerbation of intestinal inflammation

Inflammatory bowel disease is an immune-mediated intestinal inflammatory condition that is associated with an increase in autoantibodies that bind to epithelial cells. However, it is unknown whether the epithelial cell-derived products that are recognized by such autoantibodies are involved in the pathogenic process. Through a combined antigen-screening approach utilizing humoral and cellular immune responses, we identify herein an epithelial lectin, galectin-4, that specifically stimulates IL-6 production by CD4(+) T cells. Interestingly, the reactivity of CD4(+) T cells to galectin-4 is precisely elicited under intestinal inflammatory conditions. The galectin-4-mediated production of IL-6 is MHC class II independent and induced by PKCtheta-associated pathway through the immunological synapse. The galectin-4-mediated stimulation of CD4(+) T cells is shown to exacerbate chronic colitis and delay the recovery from acute intestinal injury. These studies identify the presence of an immunogenic, endogenous lectin in the intestine and dissect the biological role of lectin/CD4(+) T cell interactions under inflammatory conditions.