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Tanaka Y.,Kanazawa University | Nishi T.,Kanazawa University | Takase K.,Kanazawa University | Yoshita Y.,Komatsu Municipal Hospital | And 4 more authors.
Circulation | Year: 2014

Background - : Dispatcher-assisted cardiopulmonary resuscitation (DA-CPR) attempts to improve the management of out-of-hospital cardiac arrest by laypersons who are unable to recognize cardiac arrest and are unfamiliar with CPR. Therefore, we investigated the sensitivity and specificity of our new DA-CPR protocol for achieving implementation of bystander CPR in out-of-hospital cardiac arrest victims not already receiving bystander CPR. METHODS AND RESULTS - : Since 2007, we have applied a new DA-CPR protocol that uses supplementary key words. Fire departments prospectively collected baseline data on DA-CPR from January 2009 to December 2011. DA-CPR was attempted in 2747 patients; of these, 417 (15.2%) did not experience cardiac arrest. The sensitivity and specificity of the 2007 protocol versus estimated values of the previous standard protocol were 72.9% versus 50.3% and 99.6% versus 99.8%, respectively. We identified key words that may be useful for detecting out-of-hospital cardiac arrest. Multiple logistic regression analysis revealed that the occurrence of cardiac arrest after an emergency call (odds ratio, 16.85) and placing an emergency call away from the scene of the arrest (odds ratio, 11.04) were potentially associated with failure to provide DA-CPR. Furthermore, at-home cardiac arrest (odds ratio, 1.61) and family members as bystanders (odds ratio, 1.55) were associated with bystander noncompliance with DA-CPR. No complications were reported in the 417 patients who received DA-CPR but did not have cardiac arrest. CONCLUSIONS - : Our 2007 protocol is safe and highly specific and may be more sensitive than the standard protocol. Understanding the factors associated with failure of bystanders to provide DA-CPR and implementing public education are necessary to increase the benefit of DA-CPR. © 2014 American Heart Association, Inc.

Misaki K.,Kanaza wa University | Uchiyama N.,Kanaza wa University | Nitta H.,Komatsu Municipal Hospital | Hamada J.-I.,Kanaza wa University
Neurologia Medico-Chirurgica | Year: 2010

A 65-year-old man presented with a hyperplastic anomalous anterior choroidal artery (AChA) associated with a ruptured internal carotid artery aneurysm at the origin of a perforating artery manifesting as sudden onset of headache and vomiting. The aneurysm was too small for endovascular embolization, so we performed open surgery via the left pterional approach. Aneurysm clipping with preservation of the perforator was impossible, so we clipped the aneurysm neck and sacrificed the perforator. We also performed dome clipping because dome puncture resulted in continuous bleeding. Head computed tomography obtained 3 days after the operation showed cerebral infarction at the territory of the sacrificed perforator, but the patient suffered no neurological deficits. This case of internal carotid artery aneurysm with a perforating artery arising from the aneurysm dome shows that sacrifice of the perforator may be necessary to prevent rebleeding.

Narimoto K.,Kanazawa University | Mizokami A.,Kanazawa University | Izumi K.,Kanazawa University | Mihara S.,Municipal Tsuruga Hospital | And 6 more authors.
International Journal of Urology | Year: 2010

Objectives: To analyze the clinical effects of flutamide as a second-line anti-androgen for combined androgen blockade in patients with castration-resistant prostate cancer (CRPC) initially treated with bicalutamide as a first-line anti-androgen. Methods: Our study population consisted of 16 patients with CRPC who were treated with flutamide (375 mg daily) as second-line hormonal therapy. Dehydroepiandrosterone (DHEA), androstenedione, androstenediol, testosterone and dihydrotestosterone were measured to investigate the relationship between plasma androgens and outcome following treatment. Furthermore, adrenal androgen levels in a medium of adrenal cancer cell line were also measured. Results: Second-line hormonal therapy using flutamide resulted in a reduction of the prostate-specific antigen (PSA) level in 14 (87.5%) of 16 patients. A PSA decline greater than 50% was observed in 8 (50%) of the 16 patients. The duration of median responsiveness was 6.25 months. PSA elevation of baseline androstenediol level was a predictive factor of PSA responsiveness. The lower DHEA group improved the duration of responsiveness to flutamide. In vitro, 3 μmol/L flutamide suppressed DHEA, androstenedione and androstenediol synthesis compared with bicalutamide in a medium of adrenal cancer cell line. Conclusions: Our data show that flutamide suppresses the adrenal androgens in comparison with bicalutamide. The responsiveness and response duration of flutamide can be predicted in patients with a higher baseline androstenediol level and a lower DHEA level. Metabolites from adrenal androgens contribute to the progression of prostate cancer. © 2010 The Japanese Urological Association.

Mabuchi H.,Kanazawa University | Nohara A.,Kanazawa University | Noguchi T.,Kanazawa University | Kobayashi J.,Kanazawa University | And 12 more authors.
Atherosclerosis | Year: 2014

Backgrounds: Familial hypercholesterolemia (FH) is an autosomal dominant disease characterized by hypercholesterolemia, tendon xanthomas, and premature coronary heart disease. FH is caused by mutations of "FH genes," which include the LDL-receptor (LDLR), apolipoprotein B-100 (APOB) or proprotein convertase subtilisin/kexin type 9 (PCSK9). We evaluated the usefulness of FH gene analysis for diagnosing homozygous FH (homo-FH), particularly in cases caused by gain-of-function (g-o-f) mutations in PCSK9 (PCSK9 E32K). Objectives: To evaluate the frequency of homo-FH caused by PCSK9 E32K compared with FH due to other genetic causes and to report the phenotypic features of homo-FH caused by PCSK9 E32K. Methods: Genomic DNA was prepared from white blood cells, and LDLR and PCSK9 mutations were identified using the Invader assay method. Results: Of the 1055 hetero-FH patients, 62 patients (5.9%) carried the PCSK9 E32K mutation, while in the 82 alleles of 41 homo-FH patients, 13 (15.9%) had double mutations of LDLR allele and PCSK9 E32K mutation. Mean plasma total cholesterol (TC) (9.93±2.95mmol/L, mean±SD) in true homo-FH cases with PCSK9 E32K or double hetero-FH cases with PCSK9 E32K and LDLR mutations were significantly lower than those in true homo-FH (18.06±4.96mmol/L) and compound heterozygous cases with LDLR mutations (14.84±1.62mmol/L). Mean plasma TC concentrations in the 59 hetero-FH cases with PCSK9 E32K (7.21±1.55mmol/L) were significantly lower than those (8.94±1.53mmol/L) in the hetero-FH by LDLR mutations. Conclusions: FH caused by PCSK9 g-o-f mutations is relatively common in Japan and causes a mild type of homo- and hetero-FH compared with FH caused by LDLR mutations. © 2014 Elsevier Ireland Ltd.

Hayashi K.,Kanazawa University | Konno T.,Kanazawa University | Tada H.,Kanazawa University | Tani S.,Kanazawa University | And 10 more authors.
Circulation: Arrhythmia and Electrophysiology | Year: 2015

Background - Few rare variants in atrial fibrillation (AF)-associated genes have been functionally characterized to identify a causal relationship between these variants and development of AF. We here sought to determine the clinical effect of rare variants in AF-associated genes in patients with lone AF and characterized these variants electrophysiologically and bioinformatically. Methods and Results - We screened all coding regions in 12 AF-associated genes in 90 patients with lone AF, with an onset of 47±11 years (66 men; mean age, 56±13 years) by high-resolution melting curve analysis and DNA sequencing. The potassium and sodium currents were analyzed using whole-cell patch clamping. In addition to using 4 individual in silico prediction tools, we extended those predictions to an integrated tool (Combined Annotation Dependent Depletion). We identified 7 rare variants in KCNA5, KCNQ1, KCNH2, SCN5A, and SCN1B genes in 8 patients: 2 of 8 probands had a family history of AF. Electrophysiological studies revealed that 2 variants showed a loss-of-function, and 4 variants showed a gain-of-function. Five of 6 variants with electrophysiological abnormalities were predicted as pathogenic by Combined Annotation Dependent Depletion scores. Conclusions - In our cohort of patients with lone AF, 7 rare variants in cardiac ion channels were identified in 8 probands. A combination of electrophysiological studies and in silico predictions showed that these variants could contribute to the development of lone AF, although further in vivo study is necessary to confirm these results. More than half of AF-associated rare variants showed gain-of-function behavior, which may be targeted using genotype-specific pharmacological therapy. © 2015 American Heart Association, Inc.

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