The Relation of Prostate Tissue Protein Content, Nd : YAG Laser Transmissibility and Thermal Effect on Prostatic Hyperplasia

As our society ages, safe and minimally invasive treatment for the frequent occurrence of prostatic hyperplasia have been sought. We have performed prostatic hightemperature treatment for prostatic hyperplasia with the Prostalase using neodymium : yattriumaluminum garnet (Nd : YAG) laser for patients suffering from a bladder outlet obstruction secondary to benign prostatic hyperplasia (BPH). We used agars which included various densities of protein and skim milk as test materials to determine whether the exothermic mechanism of the Nd : YAG laser irradiation has an effect on protein molecules. By measuring the temperature inside the test materials and the irradiation transmissibility, we verified that in tissues with the same degree of color, the higher the protein content, the stronger the exothermic action of the Nd : YAG laser. In addition, in three human prostates obtained through pathological autopsy, the measurement of the protein content and the temperature inside the prostatic tissue in which prostatic thermal treatment had been performed showed that the exothermic action of the Nd : YAG laser varied according to the protein content: the higher the protein content, the stronger was the exothermic action. The present findings suggest that the temperature inside prostatic tissue reaches at least 60-65邃・with intissues with a protein content more than 23g/100g

Cardio-protective effects of pentraxin 3 produced from bone marrow-derived cells against ischemia/reperfusion injury

AbstractBackgroundInflammation is one of major mechanisms contributing to the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Pentraxin 3 (PTX3), produced in response to inflammatory signals, acts as a humoral arm of the innate immunity. Here we investigated the role of PTX3 produced from bone marrow-derived cells in myocardial I/R injury using PTX3-deficient (PTX3KO) mice.Methods and resultsPTX3KO mice and wild-type littermate (WT) mice were lethally irradiated and injected with bone marrow (BM) cells, generating four types of mice (WTWT-BM, WTPTX3KO-BM, PTX3KOWT-BM and PTX3KOPTX3KO-BM). Six weeks after BM transplantation, the myocardial I/R procedure (45min of left descending coronary artery ligation followed by 48h of reperfusion) was performed. Infarct size was greater in WT and PTX3KO mice with BM from PTX3KO donor (WTPTX3KO-BM and PTX3KOPTX3KO-BM) compared with WT and PTX3KO mice with BM from WT donor (WTWT-BM and PTX3KOWT-BM). Localization of PTX3 was observed in neutrophils and macrophages in WT and PTX3KO mice with BM from WT donor (WTWT-BM and PTX3KOWT-BM), while only in endothelial cells in WT mice with BM from PTX3KO donor (WTPTX3KO-BM). Infiltration of neutrophils and generation of reactive oxygen species (ROS) at ischemic border zones were greater in PTX3KO mice with BM from PTX3KO donor (PTX3KOPTX3KO-BM) than PTX3KO mice with BM from WT donor (PTX3KOWT-BM). Plasma levels and cardiac expressions of interleukin-6 were higher in PTX3KO mice with BM from PTX3KO donor (PTX3KOPTX3KO-BM) than PTX3KO mice with BM from WT donor (PTX3KOWT-BM). However, no significant differences in infarct size, infiltration of neutrophils, generation of ROS and plasma and cardiac levels of interleukin-6 were observed between WT and PTX3KO mice with BM from WT donor and between WT and PTX3KO mice with BM from PTX3KO donor. These results indicated that the lack of PTX3 produced from BM-derived cells, and not from cardiac resident cells, exacerbated myocardial injury after I/R.ConclusionPTX3 produced from bone marrow-derived cells plays a crucial role in cardiac protection against myocardial I/R injury by attenuating infiltration of neutrophils, generation of ROS and inflammatory cytokine

Association of plasma thioredoxin-1 with renal tubular damage and cardiac prognosis in patients with chronic heart failure

AbstractBackgroundThioredoxin-1 (Trx-1) is an abundant 12.5kDa redox protein expressed in almost all eukaryotic cells that protect against the development of heart failure and kidney dysfunction. Plasma Trx-1 levels are considered as a reliable marker for oxidative stress. However, it remains to be determined whether plasma Trx-1 levels can predict cardiac prognosis in patients with chronic heart failure (CHF).Methods and resultsWe measured plasma Trx-1 levels and urinary β2-microglobulin–creatinine ratio (UBCR), a marker for renal tubular damage, in 156 consecutive patients with CHF and 17 control subjects. The patients were prospectively followed for a median follow-up period of 627 days and 46 cardiac events were observed. The patients with cardiac events had significantly higher plasma Trx-1 levels and UBCR levels than the cardiac event-free patients. Multivariate Cox proportional hazard analysis revealed that an elevated Trx-1 level was independently associated with poor outcome in patients with CHF after adjustment for confounding factors (hazard ratio, 1.74; 95% confidence interval, 1.33–2.29; p<0.0001). UBCR was increased with higher plasma Trx-1 levels. Kaplan–Meier analysis demonstrated that the highest Trx-1 tertile was associated with the highest risk of cardiac events.ConclusionPlasma Trx-1 level was associated with renal tubular damage and cardiac prognosis, suggesting that it could be a useful marker to identify patients at high risk for comorbid heart failure and renal tubular damage

Comparison of Mortality between Japanese Peritoneal Dialysis and Hemodialysis Patients: A 5-Year Multicenter Follow-Up Study

To examine the relationship between dialysis modality and prognosis in Japanese patients, we conducted a prospective multicenter observational study. We recruited 83 background-matched peritoneal dialysis (PD) and 83 hemodialysis (HD) patients (average age, 64.9 years; men, 53.6%; diabetic patients, 22.9%; median duration of dialysis, 48 months in all patients) and followed them for 5 years. During the follow-up period, 27 PD patients (16 cardiovascular and 11 non-cardiovascular deaths) and 27 HD patients died (14 cardiovascular and 13 non-cardiovascular deaths). There were 8 PD patients switched to HD, and 6 PD patients received renal transplantation. Kaplan-Meier analysis revealed that the crude survival rate was not significantly different at the end of 5 years (PD 67.5% versus 67.5%, log-rank P = 0.719). The difference in cardiovascular and non-cardiovascular mortalities between PD and HD was not statistically significant. Multivariate Cox analysis showed that the independent predictors for death were age and serum albumin levels, but not the dialysis modality. This study showed that the overall mortality was not significantly different between PD and HD patients, which suggests that dialysis modality might not be an independent factor for survival in Japanese patients

ノウコウソク ノ チリョウ セイセキ ワ ナゼ コウジョウ シナイ ノカ : 10ネンカン ノ ヤマガタケン ノウソッチュウ トウロク データ カラ ノ ヨゴ フリョウ インシ ノ ケントウ

　We studied ten years of stroke data registered with the Yamagata Society on Treatment for Cerebral Stroke（YSTCS）. The subjects included 16,407 cases of acute-phase cerebral infarction that were registered with the YSTCS during the ten years between 2002 and 2011. The cases were divided into two groups: the early phase group（2002-2006）and the late phase group（2007-2011）.　The clinical diagnoses included atherothrombotic cerebral infarction（AT）（n=7,196; 43.9%）, cardiogenic cerebral embolism（CE）（n=4,011; 24.4%）, and lacunar infarction（LI）（n=4,703; 28.7%）. The average age of the early phase group was 72.7±11.43 years, while that of the late phase group was 75.0±11.35 years; the difference was statistically significant. The proportion of CE cases increased in the late phase, while that of LI decreased. This phenomenon was more marked in cases involving patients of ≥80 years of age. In both the early and late phase groups, the AT and CE cases showed a significantly high proportion of poor outcomes. However, when age adjustment was implemented in the late phase group, the treatment outcomes improved across all clinical entities. A multiple logistic regression analysis revealed a significant association between old age, female sex, severe symptoms at onset, CE, a previous history of stroke, and a poor prognosis.　It is clear that developments in medicine have not kept pace with the advancement in the age at onset. The improvement of the outcomes of treatment for cerebral infarction requires further developments in acute-phase therapies and the primary prevention of cardiogenic cerebral embolism, many cases of which are severe

High-mobility group box 1-mediated heat shock protein beta 1 expression attenuates mitochondrial dysfunction and apoptosis

AbstractAimsApoptosis of cardiomyocytes is thought to account for doxorubicin cardiotoxicity as it contributes to loss of myocardial tissue and contractile dysfunction. Given that high-mobility group box 1 (HMGB1) is a nuclear DNA-binding protein capable of inhibiting apoptosis, we aimed to clarify the role of HMGB1 in heat shock protein beta 1 (HSPB1) expression during doxorubicin-induced cardiomyopathy.Methods and resultsMitochondrial damage, cardiomyocyte apoptosis, and cardiac dysfunction after doxorubicin administration were significantly attenuated in mice with cardiac-specific overexpression of HMGB1 (HMGB1-Tg) compared with wild type (WT) -mice. HSPB1 levels after doxorubicin administration were significantly higher in HMGB1-Tg mice than in WT mice. Transfection with HMGB1 increased the expression of HSPB1 at both the protein and mRNA levels, and HMGB1 inhibited mitochondrial dysfunction and apoptosis after exposure of cardiomyocytes to doxorubicin. HSPB1 silencing abrogated the inhibitory effect of HMGB1 on cardiomyocyte apoptosis. Doxorubicin increased the binding of HMGB1 to heat shock factor 2 and enhanced heat shock element promoter activity. Moreover, HMGB1 overexpression greatly enhanced heat shock element promoter activity. Silencing of heat shock factor 2 attenuated HMGB1-dependent HSPB1 expression and abrogated the ability of HMGB1 to suppress cleaved caspase-3 accumulation after doxorubicin stimulation.ConclusionsWe report the first in vivo and in vitro evidence that cardiac HMGB1 increases HSPB1 expression and attenuates cardiomyocyte apoptosis associated with doxorubicin-induced cardiomyopathy. Cardiac HMGB1 increases HSPB1 expression in cardiomyocytes in a heat shock factor 2-dependent manner