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Hareyama H.,Sapporo City General Hospital | Ito K.,Sapporo City General Hospital | Uchida A.,Sapporo City General Hospital | Hayakashi Y.,Sapporo City General Hospital | And 3 more authors.
Annals of Surgical Oncology | Year: 2012

Background: Lower extremity lymphedema (LEL) is a serious complication caused by lymphadenectomy in patients with gynecologic malignancies. In this study, we evaluated the effect of preserving the circumflex iliac lymph nodes (CILNs), i.e., the most caudal external iliac lymph nodes, for the prevention and reduction of LEL by comparing two groups of patients, one in which CILN were removed and the other in which CILNs were preserved. Methods: We retrospectively reviewed 329 patients with gynecologic malignancies who had undergone abdominal complete systematic pelvic and para-aortic lymphadenectomy. The patients were divided into nonpreserved (n = 189) and preserved (n = 140) groups, depending on whether CILNs were removed. Primary outcome measures included the incidence and severity of LEL. Results: The incidence of LEL was significantly lower in the preserved group than in the nonpreserved group (P < 0.0001). The frequency of LEL was also significantly lower in the preserved group than in the nonpreserved group regardless of the range of pelvic and para-aortic lymphadenectomy (P < 0.0001). LEL in the overwhelming majority of cases in the preserved group was mild, and no patients experienced severe LEL. Further, the incidence of cellulitis was 0% in the preserved group, while it was 12.7% in the nonpreserved group (P < 0.0001). Lymphoscintigraphy revealed collateral pathways from the preserved CILN along the iliac and large abdominal vessels. Conclusions: This method of lymph node preservation is a simple and extremely effective approach for preventing/reducing LEL after pelvic and para-aortic lymphadenectomy for patients with gynecologic malignancies. © 2011 Society of Surgical Oncology. Source

Cho K.Y.,Hokkaido University | Miyoshi H.,Hokkaido University | Kuroda S.,University of Toyama | Yasuda H.,Sapporo Asabu Neurosurgical Hospital | And 5 more authors.
Journal of Stroke and Cerebrovascular Diseases | Year: 2013

Background: Proinflammatory (M1) macrophages and anti-inflammatory (M2) macrophages have been identified in atherosclerotic plaques. While these macrophages have been speculated to be related to plaque vulnerability, there are limited studies investigating this relationship. Therefore, we examined the association between macrophage phenotype (M1 versus M2) and plaque vulnerability and clinical events. Methods: Patients undergoing carotid endarterectomy received an ultrasound of the carotid artery before surgery. Plaques were processed for analysis by immunohistochemistry, Western blotting, and real-time polymerase chain reaction studies. Medical history and clinical data were obtained from medical records. Results: Patients were divided into 2 groups: those suffering from acute ischemic attack (symptomatic, n = 31) and those that did not present with symptoms (asymptomatic, n = 34). Ultrasound analysis revealed that plaque vulnerability was greater in the symptomatic group (P=.033; Chi-square test). Immunohistochemistry revealed that plaques from the symptomatic group had a greater concentration of M1 macrophages (CD68-, CD11c-positive) while plaques from the asymptomatic group had more M2 macrophages (CD163-positive). This observation was confirmed by Western blotting. Characterization by real-time polymerase chain reaction studies revealed that plaques from the symptomatic group had increased expression of the M1 markers CD68 and CD11c, as well as monocyte chemoattractive protein-1, interleukin-6, and matrix metalloproteinase-9. In addition, more M1 macrophages expressed in unstable plaques were defined by ultrasound analysis, while more M2 macrophages were expressed in stable plaques. Conclusions: Our data show that M1 macrophage content of atherosclerotic plaques is associated with clinical incidence of ischemic stroke and increased inflammation or fibrinolysis. We also show the benefits of using ultrasound to evaluate vulnerability in the plaques. © 2013 by National Stroke Association. Source

Kusumi I.,Hokkaido University | Boku S.,Kobe University | Takahashi Y.,Sapporo City General Hospital
Psychiatry and Clinical Neurosciences | Year: 2015

The original definition of atypical antipsychotic drugs (APD) was drugs that are effective against positive symptoms in schizophrenia with no or little extrapyramidal symptoms (EPS). However, atypical APD have been reported to be more effective for cognitive dysfunction and negative symptoms in schizophrenia than typical APD, which expands the definition of 'atypicality'. This article provides a critical review of the pharmacology of atypical APD, especially from the viewpoint of receptor binding profiles and neurotransmitter regulations as well as neuroprotection and neurogenesis. A variety of serotonin (5-HT) receptors, such as 5-HT2A/2C, 5-HT1A, 5-HT6 and 5-HT7 receptors, may contribute to the mechanisms of action of 'atypicality'. The dopaminergic modulations, including a low affinity for dopamine D2 receptors and a partial D2 receptor agonistic action, and glutamatergic regulations may also be involved in the pharmacological backgrounds of 'atypicality'. Atypical APD, but not typical APD, may facilitate cortical neuroprotection and hippocampal neurogenesis, which might be a part of the action mechanisms of atypical APD. The facilitation of cortical neuroprotection and hippocampal neurogenesis induced by atypical APD might be mediated by an increase in the Ser9 phosphorylation of glycogen synthase kinase-3β (GSK-3β). The stimulation of 5-HT1A receptors and/or the blockade of 5-HT2 receptors, which is characteristic of atypical APD, might increase Ser9 phosphorylation of GSK-3β. Moreover, atypical APD increase brain-derived neurotrophic factor (BDNF) levels. BDNF increases Ser9 phosphorylation of GSK-3β and has neuroprotective and neurogenic effects, as in the case of atypical APD. These findings suggest that GSK-3β might play a role in the action mechanisms of atypical APD, in both the 5-HT-dependent and BDNF-dependent mechanisms. © 2014 The Authors. Psychiatry and Clinical Neurosciences © 2014 Japanese Society of Psychiatry and Neurology. Source

Osawa T.,Sapporo City General Hospital
[Hokkaido igaku zasshi] The Hokkaido journal of medical science | Year: 2013

Nephron-sparing surgery (NSS) has become the standard treatment for small renal cell carcinoma because of its comparable oncological outcome and superior patient survival compared to total nephrectomy. However, the precise chronological course of recovery from initial kidney damage and the factors responsible for it remain unknown. Seventy-one patients who underwent NSS were enrolled. To elucidate the chronological changes in kidney function that occur after NSS, the estimated glomerular filtration rate (eGFR) was calculated at different two points, the early (7 days after surgery) and late time points (more than 12 months after surgery), and compared with the preoperative eGFR. Perioperative factors were applied to a multivariate regression model to investigate the factors that most affect patient recovery from nephron damage. eGFR was decreased at the early time point but had partially recovered at the late time point. Male gender, ischemic time, and tumor size were found to be significant predictors of the initial drop in eGFR. The only significant factor that prevented later functional recovery was the presence of DM. Several perioperative factors significantly influence early kidney damage; however, the presence of DM is the only factor affecting the risk of long-term chronic kidney damage. Source

Sakuraba M.,Sapporo City General Hospital
Kyobu geka. The Japanese journal of thoracic surgery | Year: 2013

We performed retrospective analysis of 22 cases who received pulmonary resection of metastases originated from renal cell carcinoma between 1997 and 2011. Patients comprised 18 men and 4 women with a mean age of 63 years (range, 39~79). The total pulmonary resection was 30 times, lobectomy was performed 5 times and wedge resection was 25 times. The 5-year overall survival was 35% and 10-year overall survival was 26%. Prognostic factors were histology of renal cell carcinoma (G1, 2 group vs. G3 group; 2-year survival rate was 69% and 20% respectively, p=0.023) and disease-free interval (less than 24 months vs. more than 24 months; 5-year disease-free survival rate was 22% and 75% respectively, p=0.019) in univariate analysis. Only disease-free interval showed significant difference (p=0.037) in multivariate analysis. This study demonstrated that aggressive surgical resection of pulmonary metastasis from renal cell carcinoma leads to the good prognosis, especially in cases with a long disease-free interval. Source

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