Clinical and Demographic Characteristics of Patients (n = 604) and controls (n = 468).

<p>HDL  =  high-density lipoprotein cholesterol; LDL  =  low-density lipoprotein cholesterol; CHO =  cholesterol; TG  =  Triglyceride; BMI  =  body mass index; APO = apolipoprotein; GLU = fasting blood-glucose; UA = uric acid.</p><p>Clinical and Demographic Characteristics of Patients (n = 604) and controls (n = 468).</p

The association between polymorphisms of ICAM-1 gene and coronary atherosclerosis.

<p>* Fisher Exact test. Significant values (p<0.05) are in bold.</p><p>cases: n = 604; missing, n = 0; controls, n = 468; missing, n = 0.</p><p>The association between polymorphisms of ICAM-1 gene and coronary atherosclerosis.</p

Haplotypes of ICAM-1 gene and risk of coronary atherosclerosis.

<p>Haplotypes of ICAM-1 gene and risk of coronary atherosclerosis.</p

Relationship between ICAM-1 polymorphisms and risk factor of coronary atherosclerosis in coronary stenosis patients.

<p>rs5491 A/T, rs281428 C/T, rs281432 C/G, rs5498 A/G, rs281437 C/T.</p><p>CHO =  cholesterol; TG  =  Triglyceride; HDL  =  high-density lipoprotein cholesterol; LDL  =  low-density lipoprotein cholesterol; APO = apolipoprotein; UA = uric acid; GLU = fasting blood-glucose.</p><p>The data were analyzed by ANOVA and shown as mean value.</p><p>Relationship between ICAM-1 polymorphisms and risk factor of coronary atherosclerosis in coronary stenosis patients.</p

Hypertention or smoking and ICAM-1 gene polymorphisms (n = 604).

<p>*Fisher Exact Test.</p><p>Hypertention or smoking and ICAM-1 gene polymorphisms (n = 604).</p

Pleurospermum camtschaticum Hoffm.

原著和名: オホカサモチ科名: セリ科 = Umbelliferae採集地: 青森県 下北郡 東通村 尻屋 (陸奥 下北郡 東通村 尻屋)採集日: 1972/6/11採集者: 萩庭丈壽整理番号: JH004982国立科学博物館整理番号: TNS-VS-95498

The autophagy-inducing kinases, ULK1 and ULK2, regulate axon guidance in the developing mouse forebrain via a noncanonical pathway

<p>Mammalian ULK1 (unc-51 like kinase 1) and ULK2, <i>Caenorhabditis elegans</i> UNC-51, and <i>Drosophila melanogaster</i> Atg1 are serine/threonine kinases that regulate flux through the autophagy pathway in response to various types of cellular stress. <i>C. elegans</i> UNC-51 and <i>D. melanogaster</i> Atg1 also promote axonal growth and defasciculation; disruption of these genes results in defective axon guidance in invertebrates. Although disrupting ULK1/2 function impairs normal neurite outgrowth in vitro, the role of ULK1 and ULK2 in the developing brain remains poorly characterized. Here, we show that ULK1 and ULK2 are required for proper projection of axons in the forebrain. Mice lacking <i>Ulk1</i> and <i>Ulk2</i> in their central nervous systems showed defects in axonal pathfinding and defasciculation affecting the corpus callosum, anterior commissure, corticothalamic axons and thalamocortical axons. These defects impaired the midline crossing of callosal axons and caused hypoplasia of the anterior commissure and disorganization of the somatosensory cortex. The axon guidance defects observed in <i>ulk1/2</i> double-knockout mice and central nervous system-specific (<i>Nes-Cre</i>) <i>Ulk1/2</i>-conditional double-knockout mice were not recapitulated in mice lacking other autophagy genes (i.e., <i>Atg7</i> or <i>Rb1cc1</i> [RB1-inducible coiled-coil 1]). The brains of <i>Ulk1/2</i>-deficient mice did not show stem cell defects previously attributed to defective autophagy in <i>ambra1</i> (autophagy/Beclin 1 regulator 1)- and <i>Rb1cc1</i>-deficient mice or accumulation of SQSTM1 (sequestosome 1)⁺ or ubiquitin⁺ deposits. Together, these data demonstrate that ULK1 and ULK2 regulate axon guidance during mammalian brain development via a noncanonical (i.e., autophagy-independent) pathway.</p