Comparison of mol­ecular structures of cis-bis­[8-(di­methyl­phosphan­yl)quinoline]­nickel(II) and -platinum(II) complex cations

The crystal structures of the complexes (SP-4-2)-cis-bis[8-(dimethylphosphanyl)quinoline-κ2 N,P]nickel(II) bis(perchlorate) nitromethane monosolvate, [Ni(C11H12NP)2](ClO4)2·CH3NO2 (1), and (SP-4-2)-cis-bis[8-(dimethylphosphanyl)quinoline-κ2 N,P]platinum(II) bis(tetrafluoroborate) acetonitrile monosolvate, [Pt(C11H12NP)2](BF4)2·C2H3N (2), are reported. In both complex cations, two phosphanylquinolines act as bidentate P,N-donating chelate ligands and form the mutually cis configuration in the square-planar coordination geometry. The strong trans influence of the dimethylphosphanyl donor group is confirmed by the Ni—N bond lengths in 1, 1.970 (2) and 1.982 (2) Å and, the Pt—N bond lengths of 2, 2.123 (4) and 2.132 (4) Å, which are relatively long as compared to those in the analogous 8-(diphenylphosphanyl)quinoline complexes. Mutually cis-positioned quinoline donor groups would give a severe steric hindrance between their ortho-H atoms. In order to reduce such a steric congestion, the NiII complex in 1 shows a tetrahedral distortion of the coordination geometry, as parameterized by τ4 = 0.199 (1)°, while the PtII complex in 2 exhibits a typical square-planar coordination geometry [τ4 = 0.014 (1)°] with a large bending deformation of the ideally planar Me2Pqn chelate planes. In the crystal structure of 2, three F atoms of one of the BF4 − anions are disordered over two sets of positions with refined occupancies of 0.573 (10) and 0.427 (10).</jats:p

Atrophy of the lower limbs in elderly women: is it related to walking ability?

This study investigated the relationship between walking ability and age-related muscle atrophy of the lower limbs in elderly women. The subjects comprised 20 young women and 37 elderly women who resided in nursing homes or chronic care institutions. The elderly subjects were divided into three groups according to their walking ability. The muscle thickness of the following ten lower limb muscles were measured by B-mode ultrasound: the gluteus maximus, gluteus medius, gluteus minimus, psoas major, rectus femoris, vastus lateralis, vastus intermedius, biceps femoris, gastrocnemius and soleus. Compared to the young group, muscle thicknesses of all muscles except the soleus muscle were significantly smaller in all the elderly groups. There were no significant differences between the fast- and slow-walking groups in the thickness of any muscle. In the dependent elderly group, noticeable muscle atrophy was observed in the quadriceps femoris muscle. The results of this study suggest that the elderly who are capable of locomotion, regardless of their walking speed, show a moderate degree of age-related atrophy, while those who do not walk exhibit more severe atrophy, especially in the quadriceps femoris muscle

Surgical Resection Following Induction Chemoradiotherapy for Locally Advanced Lung Cancer

Fourteen patients with primary bronchogenic carcinoma, including 6 stage IIIA patients and 7 IIIB disease patients, underwent a pulmonary resection following cisplatin-based chemotherapy concurrent with 40 Gy of irradiation. The operations included 10 lobectomies, a bilobectomy, 2 pneumonectomies and a sleeve lobectomy. Dissection of the branches of the pulmonary artery was difficult, and an angioplastic procedure was employed in 2 patients. The average operating time was 306 minutes, and average blood loss was 338g. All patients were managed routinely, without any special measures. No major postoperative complication occurred, and patients were discharged from 11 to 35 days following surgery. Operative mortality rate was 0%. The median survival time was 36 months, and the 2-year survival rate was 68%. There is usually a tremendous amount of fibrosis in the mediastinum and hilum following induction therapy, and therefore, dissection of the adhesion is difficult. However, with meticulous dissection, it is possible to perform a successful operation without fatal complications

Regulation of Oxidative Stress and Cardioprotection in Diabetes Mellitus

Analysis of the Framingham data has shown that the risk of heart failure is increased substantially among diabetic patients, while persons with the metabolic syndrome have an increased risk of both atherosclerosis and diabetes mellitus. Sleep apnea may be related to the metabolic syndrome and systemic inflammation through hypoxia, which might also cause the cardiac remodeling by increased oxidative stress. On the other hand, the renin-angiotensin system is activated in diabetes, and local angiotensin II production may lead to oxidative damage via the angiotensin II type 1 receptor. Basic and clinical data indicate that angiotensin II receptor blockers have the potential to preserve left ventricular function and prevent cardiac remodeling that is exaggerated by oxidative stress in patients with diabetes. Thus, alleviation of oxidative stress might be one possible strategy in the treatment of diabetic patients associated with sleep apnea

DNA-PKcsのリジン3241と3260はゲノムの安定性と放射線抵抗性に重要である

DNA-dependent protein kinase (DNA-PK) is a serine/threonine kinase that plays an essential role in the repair of DNA double-strand breaks (DSBs) in the non-homologous end-joining (NHEJ) pathway. The DNA-PK holoenzyme consists of a catalytic subunit (DNA-PKcs) and DNA-binding subunit (Ku70/80, Ku). Ku is a molecular sensor for double-stranded DNA and once bound to DSB ends it recruits DNA-PKcs to the DSB site. Subsequently, DNA-PKcs is activated and heavily phosphorylated, with these phosphorylations modulating DNA-PKcs. Although phosphorylation of DNA-PKcs is well studied, other post-translational modifications of DNA-PKcs are not. In this study, we aimed to determine if acetylation of DNA-PKcs regulates DNA-PKcs-dependent DSB repair. We report that DNA-PKcs is acetylated in vivo and identified two putative acetylation sites, lysine residues 3241 and 3260. Mutating these sites to block potential acetylation results in increased radiosensitive, a slight decrease in DSB repair capacity as assessed by γH2AX resolution, and increased chromosomal aberrations, especially quadriradial chromosomes. Together, our results provide evidence that acetylation potentially regulates DNA-PKcs.博士（医学）・甲第670号・平成29年6月28日Copyright © 2016 Elsevier Inc. All rights reserved

DNA-PKcsのリジン3241と3260はゲノムの安定性と放射線抵抗性に重要である

DNA-dependent protein kinase (DNA-PK) is a serine/threonine kinase that plays an essential role in the repair of DNA double-strand breaks (DSBs) in the non-homologous end-joining (NHEJ) pathway. The DNA-PK holoenzyme consists of a catalytic subunit (DNA-PKcs) and DNA-binding subunit (Ku70/80, Ku). Ku is a molecular sensor for double-stranded DNA and once bound to DSB ends it recruits DNA-PKcs to the DSB site. Subsequently, DNA-PKcs is activated and heavily phosphorylated, with these phosphorylations modulating DNA-PKcs. Although phosphorylation of DNA-PKcs is well studied, other post-translational modifications of DNA-PKcs are not. In this study, we aimed to determine if acetylation of DNA-PKcs regulates DNA-PKcs-dependent DSB repair. We report that DNA-PKcs is acetylated in vivo and identified two putative acetylation sites, lysine residues 3241 and 3260. Mutating these sites to block potential acetylation results in increased radiosensitive, a slight decrease in DSB repair capacity as assessed by γH2AX resolution, and increased chromosomal aberrations, especially quadriradial chromosomes. Together, our results provide evidence that acetylation potentially regulates DNA-PKcs.博士（医学）・甲第670号・平成29年6月28日Copyright © 2016 Elsevier Inc. All rights reserved