Five fatty acid derivatives including three novel compounds were isolated from the mushroom Clitocybe clavipe. Their structures were elucidated by spectral analyses. These compounds inhibited aldehyde dehydrogenase in vitro.

Three of four (75%) vein biopsy samples from four patients (all male, mean onset: age 33.0, mean biopsy: age 59.7) of chronic phase phlebitis migrans showed positive periodontal bacteria DNA under the PCR (polymerase chain reaction) method. Of the 24 cases of Buerger disease (22 males, 2 females, mean onset: age 31.9, mean examination: age 62.6) that were investigated in our vascular laboratory, 65% of the patients suffered from moderate to severe varicose veins. Eight cases had a history of phlebitis migrans and three had an active ulcer or uncontrollable erosion in the foot. The rate of incidence was significantly higher than that of the wellmatched control group. Other findings included one instance of deep vein thrombosis, and one instance of deep vein reflux. We could suggest that some intractable ulcer or erosion cases of Buerger disease may be complicated by superficial vein incompetence or other deep vein insufficiency. We also we need to check Buerger disease patients with duplex for vein reflux and other insufficiencies.

Application of a scoring system based on the detection of both DVT and HITS may be an effective and efficient method of screening for PE after knee arthroplasty.

A mechanism by which acetylcholine (ACh) may elicit vasoconstrictor response in coronary vessels was studied in rat hearts perfused at a constant flow rate. In spontaneously beating hearts, bolus injections of ACh and carbachol (CCh) produced biphasic changes in coronary perfusion pressure (CPP): a transient increase at the initial period followed by a sustained decrease. In KCl-arrested hearts, ACh and CCh produced a monophasic increase in CPP, which was attenuated by either removal of endothelial cells by saponin or cyclooxygenase inhibition by diclofenac sodium. In the spontaneously beating heart, ACh-induced vasoconstriction was almost abolished by atropine (0.1 microM) and was markedly attenuated by an M2 antagonist, methoctramine (0.1 microM), but not by an M1 antagonist, pirenzepine (1 microM). Arecaidine propargyl ester (APE), an M2 agonist, produced coronary artery constriction which was attenuated by methoctramine (0.1 microM) but not by pirenzepine (0.1 microM) in both spontaneously beating and KCl-arrested hearts. McN-A-343, an M1 agonist, increased CPP in both beating and KCl-arrested hearts, but to a lesser degree than APE. These results suggest that the release of vasoconstrictor prostaglandins from endothelial cells contributes to the vasoconstrictor response to ACh in perfused rat coronary vessels, and the response to ACh appears to be mediated, in part, via the M2 subtype of muscarinic receptors.

By using 24 hour urinary creatinine levels, skeletal muscle mass (kg), its rate (%) of body weight and creatinine height index (%) were determined in old Japanese women suffering from walking difficulty in nursing home and compare with those of young university students. Those of old subjects showed approximately 30-50%, 36-44% and 44-46% of young subjects, respectively. It is suggested that these values are important and useful biomarkers for the planning and the achievement of rehabilitation program for the maintaining and restoring skeletal muscle mass and for the careful support by registered care workers to aged persons. J. Med. Invest. 65:122-125, February, 2018.

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Reports of vascular lesion changes in elderly Buerger disease patients are rare. Patients are expected to continue to have typical Buerger disease even after the age of 50. However, after 50, when patients suffer from atherosclerotic risk factors, such as hypertension, diabetes mellitus, or hyperlipidemia, what kind of changes will occur? We will report on 3 cases of hypertension, diabetes mellitus, or hyper lipidemia after or around 50 years of age. As a result, atherosclerosis was present in the iliac or aortic regions in the remaining thromboangiitis lesions below the groin area.

No abstract