シンコウセイ ドウミャク コウカセイ ビョウヘン ニ タイシ ショウサイナ ビョウリ ソシキガクテキ ケントウ オ オコナイ エタ コウLp（a） ケッショウ ガッペイ 2ガタ トウニョウビョウ ノ 1レイ

We report a case of type 2 diabetes mellitus showing elevated plasma lipoprotein（a）［Lp（a）］levels with various atherosclerotic lesions. A 54-year-old woman diagnosed as having type 2 diabeteswas treated with oral antidiabetic drugs. She had various atherosclerotic lesions, includingcerebral infarction, occlusion of the middle carotid artery and myocardial infarction, along withdiabetes mellitus, hyperlipemia and hypertension and additionally showed a high level of serum Lp（a）. A high plasma level of Lp（a）is considered to be an independent risk factor for atherosclerosis,and it is associated with the development of cerebral infarction, occlusion of the middlecarotid artery and coronary atherosclerosis. Plasma Lp（a）level is predominantly determined bygenetic factors and is not affected by diet or drugs. Aspirin treatment（100 mg/day）lowered theplasma level of Lp（a）by 60%. Pathological findings of the vascular lesions showed that apolipoprotein（a）［apo（a）］, a major apoprotein component of Lp（a）, was deposited in the tunica media ofthe radial artery with rare atherosclerotic lesions and in the inner rim of the fibrous capsular regionwithin the plaque with a large lipid core of the carotid artery. This suggests that Lp（a）stimulatesthe transformation of vascular smooth muscle cells in the tunica media in the early stage of atherosclerosisand that it is associated with fragility of the atherosclerotic lesion in the progressive stage.Hence, plasma Lp（a）levels should be measured for diabetic patients with various atheroscleroticlesions, and aspirin may need to be given to those who have elevated plasma Lp（a）levels in orderto prevent the development of atherosclerotic complications

Detection and management of cardiomyopathy in female dystrophinopathy carriers

Regular health checkups for mothers of patients with Duchenne muscular dystrophy have been performed at National Hospital Organization Tokushima Hospital since 1994. Among 43 mothers participated in this study, 28 dystrophinopathy carriers were identified. Skeletal and cardiac muscle functions of these subjects were examined. High serum creatine kinase was found in 23 subjects (82.1%). Obvious muscle weakness was present in 5 (17.8%) and had progressed from 1994 to 2015. Cardiomyopathy was observed in 15 subjects (60.0%), including dilated cardiomyopathy-like damage that was more common in the left ventricular (LV) posterior wall. Late gadolinium enhancement on cardiac MRI was found in 5 of 6 subjects, suggesting fibrotic cardiac muscle. In speckle tracking echocardiography performed seven years later, global longitudinal strain was decreased in these subjects, indicating LV myocardial contractile abnormality. These results suggest that female dystrophinopathy carriers should receive regular checkups for detection and treatment of cardiomyopathy, even if they have no cardiac symptoms

トクシマシ イシカイ ノ ジョセイ イシ シエン ジギョウ

In recent years, an increase in the ratio of female physicians in Tokushima Prefecture, with a particularly notable rise among younger generations that has exceeded the national average, has been observed. However, these physicians continue to face severe working environments, and support measures are required for female physicians during childbirth and in the early stages of parenthood. To this end, the Tokushima City Medical Association has been involved in initiatives to support female physicians since ２００８. First, we developed “Net Joy,” a website that provides the information necessary for female physicians to continue their clinical work through a bulletin board system that offers information on topics such as employment and childcare. Furthermore, we have administered questionnaire surveys related to working environments and support systems in clinical training hospitals and compiled a booklet entitled Support Notebook for Female Physicians that is available on the Net Joy website. Since ２０１１, as post-residency training in ultrasound techniques, we have held six separate practical training seminars at the Tokushima University Hospital Ultrasound Examination Center and the Tokushima City Medical Association Hall. Since ２０１４, we have been involved in efforts to enhance its training content and develop it into a long-term program

トクシマシ イシカイ ノ トウニョウビョウ タイサク

Tokushima City Medical Association has founded the committee for the means to prevent diabetesmellitus, because the mortality rate by diabetes mellitus in Tokushima Prefecture remainedranked first for 14 years from 1993 to 2006. It has enlightened a large number of people, such asdiabetic patients and candidates for diabetes, and also healthy citizens in Tokushima for preventingdiabetes mellitus. For this aim, Tokushima City Medical Association has made the home pagenamed Tokushima City Diabetic Network to show clearly the means to prevent diabetes mellitusfor the citizens. By this Web site, the citizens can get a correct knowledge about diabetes mellitus,a useful information about the treatments including exercises, diets and medications, and an informationabout medical institutions by utilizing the search page to receive a proper diabetic treatment.Tokushima City Medical Association held several events, such as Tokushima citizens’extension courses and diabetes forums for the citizens to understand diabetes mellitus clearly.Fortunately, in 2007, Tokushima got out of the first rank of diabetic mortality rate. TokushimaCity Medical Association will continue efforts to prevent diabetes mellitus by approaching the citizensof all ages from various aspects

Microglial SIRP alpha regulates the emergence of CD11c(+) microglia and demyelination damage in white matter

A characteristic subset of microglia expressing CD11c appears in response to brain damage. However, the functional role of CD11c(+) microglia, as well as the mechanism of its induction, are poorly understood. Here we report that the genetic ablation of signal regulatory protein alpha (SIRP alpha), a membrane protein, induced the emergence of CD11c(+) microglia in the brain white matter. Mice lacking CD47, a physiological ligand of SIRP alpha, and microglia-specific SIRP alpha-knockout mice exhibited the same phenotype, suggesting that an interaction between microglial SIRP alpha and CD47 on neighbouring cells suppressed the emergence of CD11c(+) microglia. A lack of SIRP alpha did not cause detectable damage to the white matter, but resulted in the increased expression of genes whose expression is characteristic of the repair phase after demyelination. In addition, cuprizone-induced demyelination was alleviated by the microglia-specific ablation of SIRP alpha. Thus, microglial SIRP alpha suppresses the induction of CD11c(+) microglia that have the potential to accelerate the repair of damaged white matter