Biomedical subjects

Katsunori Yoshida

Publications and source records attributed to Katsunori Yoshida.

At least 19 recordsLinked to original sources

PubMed2006

Polyamines as an inhibitor on erythropoiesis of hemodialysis patients by in vitro bioassay using the fetal mouse liver assay.

The pathogenesis of anemia in patients with chronic renal failure has been greatly attributed to erythropoietin (EPO) deficiency. Recently, however, there has been some thought that uremic inhibitors might suppress the activity of EPO and reduce the maturation of erythropoiesis. Polyamines are well known to be involved in the regulation of cellular proliferation and differentiation. Furthermore, the polyamine levels in the serum or erythrocytes are elevated in chronic hemodialysis patients, and can be lowered immediately by hemodialysis. In the present study, we first measured the polyamines levels (putrescine, spermidine, spermine) by high performance liquid chromatography (HPLC) in 20 chronic hemodialysis patients, and investigated the effects of polyamines on erythropoiesis by in vitro bioassay using fetal mouse liver cells. The direct effects of polyamines in erythroid colony formation in the medium with and without EPO were evaluated. Each polyamine level in chronic hemodialysis patients was higher than in the healthy subjects, and a significant negative correlation was found between polyamines and erythropoiesis. Polyamines inhibited the activity of EPO, but they did not have any direct effect on colony formation of the fetal mouse liver cells. These results suggest that polyamines have inhibitory effects on the proliferation or maturation of erythroid precursor cells and are intimately involved in the pathogenesis of renal anemia in chronic hemodialysis patients.

Adolescent↗

PubMed2005

Acceleration of Smad2 and Smad3 phosphorylation via c-Jun NH(2)-terminal kinase during human colorectal carcinogenesis.

Conversion of normal epithelial cells to tumors is associated with a shift in transforming growth factor-beta (TGF-beta) function: reduction of tumor suppressor activity and increase of oncogenic activity. However, specific mechanisms of this functional alteration during human colorectal carcinogenesis remain to be elucidated. TGF-beta signaling involves Smad2/3 phosphorylated at linker regions (pSmad2/3L) and COOH-terminal regions (pSmad2/3C). Using antibodies specific to each phosphorylation site, we herein showed that Smad2 and Smad3 were phosphorylated at COOH-terminal regions but not at linker regions in normal colorectal epithelial cells and that pSmad2/3C were located predominantly in their nuclei. However, the linker regions of Smad2 and Smad3 were phosphorylated in 31 sporadic colorectal adenocarcinomas. In particular, late-stage invasive and metastatic cancers typically showed a high degree of phosphorylation of Smad2/3L. Their extent of phosphorylation in 11 adenomas was intermediate between those in normal epithelial cells and adenocarcinomas. Whereas pSmad2L remained in the cytoplasm, pSmad3L was located exclusively in the nuclei of Ki-67-immunoreactive adenocarcinomas. In contrast, pSmad3C gradually decreased as the tumor stage progressed. Activated c-Jun NH(2)-terminal kinase in cancers could directly phosphorylate Smad2/3L. Although Mad homology 2 region sequencing in the Smad4 gene revealed a G/A substitution at codon 361 in one adenocarcinoma, the mutation did not correlate with phosphorylation. No mutations in the type II TGF-beta receptor and Smad2 genes were observed in the tumors. In conclusion, pSmad3C, which favors tumor suppressor activity of TGF-beta, was found to decrease, whereas c-Jun NH(2)-terminal kinase tended to induce the phosphorylation of Smad2/3L in human colorectal adenoma-carcinoma sequence.

Adenocarcinoma↗

PubMed2005

Transforming growth factor-beta and platelet-derived growth factor signal via c-Jun N-terminal kinase-dependent Smad2/3 phosphorylation in rat hepatic stellate cells after acute liver injury.

After liver injury, transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF) regulate the activation of hepatic stellate cells (HSCs) and tissue remodeling. Mechanisms of PDGF signaling in the TGF-beta-triggered cascade are not completely understood. TGF-beta signaling involves phosphorylation of Smad2 and Smad3 at linker and C-terminal regions. Using antibodies to distinguish Smad2/3 phosphorylated at linker regions from those phosphorylated at C-terminal regions, we investigated Smad2/3-mediated signaling in rat liver injured by CCl(4) administration and in cultured HSCs. In acute liver injury, Smad2/3 were transiently phosphorylated at both regions. Although linker-phosphorylated Smad2 remained in the cytoplasm of alpha-smooth muscle actin-immunoreactive mesenchymal cells adjacent to necrotic hepatocytes in centrilobular areas, linker-phosphorylated Smad3 accumulated in the nuclei. c-Jun N-terminal kinase (JNK) in the activated HSCs directly phosphorylated Smad2/3 at linker regions. Co-treatment of primary cultured HSCs with TGF-beta and PDGF activated the JNK pathway, subsequently inducing endogenous linker phosphorylation of Smad2/3. The JNK pathway may be involved in migration of resident HSCs within the space of Disse to the sites of tissue damage because the JNK inhibitor SP600125 inhibited HSC migration induced by TGF-beta and PDGF signals. Moreover, treatment of HSCs with both TGF-beta and PDGF increased transcriptional activity of plasminogen activator inhibitor-1 through linker phosphorylation of Smad3. In conclusion, TGF-beta and PDGF activate HSCs by transmitting their signals through JNK-mediated Smad2/3 phosphorylation at linker regions, both in vivo and in vitro.

Adipocytes↗

PubMed2004

TGF-beta and HGF transmit the signals through JNK-dependent Smad2/3 phosphorylation at the linker regions.

Although hepatocyte growth factor (HGF) can act synergistically or antagonistically with transforming growth factor-beta (TGF-beta) signaling, molecular mechanism of their crosstalk remains unknown. Using antibodies which selectively distinguished receptor-regulated Smads (R-Smads) phosphorylated at linker regions from those at C-terminal regions, we herein showed that either HGF or TGF-beta treatment of normal stomach-origin cells activated the JNK pathway, thereafter inducing endogenous R-Smads phosphorylation at linker regions. However, the phosphorylation at their C-terminal regions was not induced by HGF treatment. The activated JNK could directly phosphorylate R-Smads in vitro at the same sites that were phosphorylated in response to TGF-beta or HGF in vivo. Thus, the linker regions of R-Smads were the common phosphorylation sites for HGF and TGF-beta signaling pathways. The phosphorylation induced by simultaneous treatment with HGF and TGF-beta allowed R-Smads to associate with Smad4 and to translocate into the nucleus. JNK pathway involved HGF and TGF-beta-mediated infiltration potency since a JNK inhibitor SP600125 caused the reduction of invasive capacity induced by HGF and TGF-beta signals. Moreover, a combined treatment with HGF and TGF-beta led to a potent increase in plasminogen activator inhibitor type 1 transcriptional activity through Smad3 phosphorylation at the linker region. In contrast, HGF treatment reduced TGF-beta-dependent activation of p15INK4B promoter, in which Smad3 phosphorylation at the C-terminal region was involved. In conclusion, HGF and TGF-beta transmit the signals through JNK-mediated R-Smads phosphorylation at linker regions.

Animals↗

PubMed2004

Association between pentosidine and arteriosclerosis in patients receiving hemodialysis.

BACKGROUND: It has been suggested that advanced glycation endproducts (AGEs) accumulate in arteriosclerotic lesions, playing and important role in the development and progression of arteriosclerosis. A chemical quantification method using high-performance liquid chromatography (HPLC) has been established to determine pentosidine levels in these products. Some studies reported that the abdominal aorta calcification index (ACI), obtained by computed tomography (CT), was useful for noninvasively diagnosing arteriosclerosis and determining its severity. In the present study, we measured the ACI and plasma pentosidine in patients receiving maintenance hemodialysis, and investigated the association between arteriosclerosis and pentosidine. METHODS: In 73 patients receiving maintenance hemodialysis (43 men; 30 women), we determined the ACI, and investigated the association of the ACI with plasma total pentosidine, total cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, serum creatinine, and parathyroid hormone (PTH), as well as the product of serum calcium and serum phosphorus, duration of dialysis, and age. RESULTS: The ACI did not correlate with total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol, serum creatinine, PTH, or the product of serum calcium and serum phosphorus. Age, duration of dialysis, and plasma total pentosidine correlated with the ACI: (y = -33.12 + 0.913x; r = 0.407; P < 0.01), (y = 13.94 + 0.403x; r = 0.488; P < 0.01), and (y = 14.13 + 0.630x; r = 0.365; P < 0.01), respectively. CONCLUSIONS: It is suggested that pentosidine may be associated with arteriosclerotic development in hemodialysis patients. It has been suggested that advanced glycation endproducts (AGEs) accumulate in arteriosclerotic lesions, playing an important role in the development and progression of arteriosclerosis. A chemical quantification method using high-performance liquid chromatography (HPLC) has been established to determine pentosidine levels in these products. Some studies reported that the abdominal aorta calcification index (ACI), obtained by computed tomography (CT), was useful for noninvasively diagnosing arteriosclerosis and determining its severity. In the present study, we measured the ACI and plasma pentosidine in patients receiving maintenance hemodialysis, and investigated the association between arteriosclerosis and pentosidine.

Aged↗

PubMed2004

Metal stent placement for two patients with post-transplantation renal artery stenosis, using intravascular ultrasound imaging.

Post-transplantation renal artery stenosis is recognized at relatively early periods after renal transplantation. We report herein our experience of utilizing transluminal expanded metal stents (Palmaz stent and Wall stent) for post-transplantation renal artery stenosis, and monitoring with intravascular ultrasound (IVUS) imaging. The recipients were a 51-year-old woman (case 1) and a 57-year-old man (case 2), and the grafts were procured from cadaveric donors. Renal function had deteriorated suddenly at 5 months after renal transplantation in case 1 and at 86 months in case 2. The cause of the graft dysfunction was renal arterial stenosis. Color doppler ultrasound imaging and angiography diagnosed post-transplantation renal artery stenosis. The renal artery stenosis was serious, being greater than 90% in both patients. Percutaneous transluminal angioplasty (PTA) was performed, but its effectiveness was not sufficient; therefore, an indwelling endoluminal metallic Palmaz stent and an indwelling Wall stent were placed at the sites of stenosis while monitoring was done with IVUS. No complications were recognized at all. The length and degree of stenosis location became clear by using IVUS, and suitable stents could be selected for the renal artery stenosis. The clinical effect was excellent; the renal function improved to the pre-hospitalization value. We conclude that the Palmaz stent and the Wall stent were useful as a noninvasive strategy for treating post-transplantation renal artery stenosis. This procedure could be performed safely and surely using IVUS.

Female↗

PubMed2004

Prediction of postoperative renal function by preoperative serum creatinine level and three-dimensional diagnostic image reconstruction in patients with renal cell carcinoma.

OBJECTIVES: To investigate retrospectively whether postoperative renal function in patients with renal cell carcinoma can be preoperatively predicted by a combination of the preoperative serum creatinine (sCr) and the renal parenchymal volume (RPV) estimated by three-dimensional image reconstruction of the preoperative diagnostic imaging. METHODS: Of 155 patients who had undergone radical nephrectomy, 76 were eligible for inclusion in our study (group 1). Group 2 was comprised of 26 of 37 patients who had undergone partial nephrectomy. The postoperative RPV in both groups was estimated from the preoperative computed tomography scans or magnetic resonance imaging and were compared with the actual RPV estimated from the postoperative imaging using a three-dimensional image reconstruction program. The postoperative creatinine clearance (Ccr) was predicted from the preoperative Ccr calculated from the sCr level and by the ratio of the postoperative/preoperative RPV. The correlations between the predicted postoperative Ccr and the actual, measured postoperative Ccr were analyzed statistically. RESULTS: In both groups, a statistically significant correlation was found between the postoperative RPV, estimated from the preoperative images and postoperative images. The predicted postoperative Ccr correlated significantly with the actual, measured postoperative Ccr in group 1 (r = 0.86, P <0.0001) and group 2 (r = 0.98, P <0.0001). The postoperatively increased sCr achieved stable levels within 2 to 4 weeks after nephrectomy and showed no statistically significant subsequent changes during 3 years of follow-up. CONCLUSIONS: The present results demonstrated that prediction of the postoperative Ccr, using the preoperative sCr and the postoperative RPV estimated from the preoperative routine diagnostic imaging, is a simple and reliable method for the evaluation of early and medium-term postoperative renal function.

Adult↗

PubMed2004

[A case of intrapelvic retroperitoneal ganglioneuroma].

A 61-year-old man presented with an asymptomatic intrapelvic retrovesical tumor, measuring 8.5 cm in maximum diameter, which was revealed by preoperative diagnostic imaging for transverse colon cancer. When he was referred to our department one year after hemi-colectomy, this tumor showed no change in size, but there was some suspicion of concomitant malignancy because of large tumor size and contrast enhancement in a region adherent to the right seminal vesicle. En-bloc resection of the tumor along with the right seminal vesicle was performed retroperitoneally. The tumor was diagnosed histopathologically as retroperitoneal ganglioneuroma. Herein, we report this rare case of intrapelvic retroperitoneal ganglioneuroma, and present a brief review of the relevant literature including the present case.

Adult↗

PubMed2003

Distortion of autocrine transforming growth factor beta signal accelerates malignant potential by enhancing cell growth as well as PAI-1 and VEGF production in human hepatocellular carcinoma cells.

Resistance to growth inhibitory effects of transforming growth factor (TGF)-beta is a frequent consequence of malignant transformation. On the other hand, serum concentrations of TGF-beta, plasminogen activator inhibitor type 1 (PAI-1), and vascular endothelial growth factor (VEGF) are elevated as tumor progresses. The molecular mechanism of autocrine TGF-beta signaling and its effects on PAI-1 and VEGF production in human hepatocellular carcinoma (HCC) is unknown. TGF-beta signaling involves TGF-beta type I receptor-mediated phosphorylation of serine residues within the conserved SSXS motif at the C-terminus of Smad2 and Smad3. To investigate the involvement of autocrine TGF-beta signal in cell growth, PAI-1 and VEGF production of HCC, we made stable transfectants of human HCC line (HuH-7 cells) to express a mutant Smad2(3S-A), in which serine residues of SSXS motif were changed to alanine. The transfectants demonstrated an impaired Smad2 signaling. Along with the resistance to growth inhibition by TGF-beta, forced expression of Smad2(3S-A) induced endogenous TGF-beta secretion. Moreover, this increased TGF-beta enhanced ligand-dependent signaling through the activated Smad3 and Smad4 complex, and transcriptional activities of PAI-1 and VEGF genes. In conclusion, distortion of autocrine TGF-beta signals in human HCC accelerates their malignant potential by enhancing cell growth as well as PAI-1 and VEGF production.

Amino Acid Motifs↗

PubMed2003

Chromophobe cell renal carcinoma with acquired cystic disease of the kidney in a long-term hemodialysis patient.

We report a rare case of chromophobe cell renal carcinoma found in a 52-year-old female who had received hemodialysis therapy for 13 years. She was diagnosed as having a left renal tumor 7.5 cm in diameter with acquired cystic disease of the kidney (ACDK) by ultrasonographic examination during periodical systemic screening. As abdominal computed tomography scanning and enhanced color Doppler ultrasonography suspected that the hypervascular tumor was renal cell carcinoma, she underwent translumbar nephrectomy in July 2000. The histopathological diagnosis was chromophobe cell carcinoma with pT2 and grade 2 malignancy. Chromophobe cell carcinoma is uncommon among renal tumors with ACDK found in long-term hemodialysis patients.

Biopsy, Needle↗

PubMed2003

Aggressive angiomyxoma in the scrotum expressing androgen and progesterone receptors.

Aggressive angiomyxoma is a rare benign mesenchymal myxoid tumor that arises from the pelvic soft tissues and perineum in relatively young females. This tumor has the ability to infiltrate locally and has a high risk of local recurrence after extirpation, but no potential to metastasize. We report here a rare case of aggressive angiomyxoma that developed in the scrotum of a 47-year-old male. Immunostaining of the resected specimen revealed that the tumor cell nuclei stained strongly and diffusely for androgen receptors (80% of the tumor cells), and moderately and partly for progesterone receptors (20% of the tumor cells). However, staining was negative for estrogen receptors. It is highly suggested that the growth of aggressive angiomyxoma in males may depend on androgen manipulation, contrary to its frequent and close association with estrogen receptor expression, which has been reported in females.

Genital Neoplasms, Male↗

PubMed2003

p38 MAPK mediates fibrogenic signal through Smad3 phosphorylation in rat myofibroblasts.

Hepatic stellate cells (HSCs) spontaneously transdifferentiate into myofibroblast (MFB)-phenotype on plastic dishes. This response recapitulates the features of activation in vivo. Transforming growth factor beta (TGF-beta) plays a prominent role in stimulating liver fibrogenesis by MFBs. In quiescent HSCs, TGF-beta signaling involves TGF-beta type I receptor (TbetaRI)-mediated phosphorylation of serine residues within the conserved SSXS motif at the C-terminus of Smad2 and Smad3. The middle linker regions of Smad2 and Smad3 also are phosphorylated by mitogen-activated protein kinase (MAPK). This study elucidates the change of Smad3-mediated signals during the transdifferentiation process. By using antibodies highly specific to the phosphorylated C-terminal region and the phosphorylated linker region of Smad3, we found that TGF-beta-dependent Smad3 phosphorylation at the C-terminal region decreased, but that the phosphorylation at the linker region increased in the process of transdifferentiation. TGF-beta activated the p38 MAPK pathway, further leading to Smad3 phosphorylation at the linker region in the cultured MFBs, irrespective of Smad2. The phosphorylation promoted hetero-complex formation and nuclear translocation of Smad3 and Smad4. Once combined with TbetaRI-phosphorylated Smad2, the Smad3 and Smad4 complex bound to plasminogen activator inhibitor-type I promoter could enhance the transcription. In addition, Smad3 phosphorylation mediated by the activated TbetaRI was impaired severely in MFBs during chronic liver injury, whereas Smad3 phosphorylation at the linker region was remarkably induced by p38 MAPK pathway. In conclusion, p38 MAPK-dependent Smad3 phosphorylation promoted extracellular matrix production in MFBs both in vitro and in vivo.

Active Transport, Cell Nucleus↗

PubMed2003

[A case of inflammatory myofibroblastic tumor of the retroperitoneum].

Here we report a rare case of inflammatory myofibroblastic tumor of the retroperitoneal space. A 46-year-old woman had had microscopic hematuria for 5 years. Ultrasonographic examination for screening revealed two solid tumors adjacent to the right kidney. These tumors were suspected to be malignant fibrous histiocytoma or liposarcoma by computed tomography and magnetic resonance imaging. She underwent resection of these retroperitoneal tumors and additional right nephrectomy because these tumors were adhered to the kidney and liposarcoma was highly suspected on frozen sections. Histopathologic examination finally revealed that the tumors were inflammatory myofibroblastic tumor arising within Gerota's fasia. She has been followed up for 9 months without any evidence of local recurrence.

Diagnosis, Differential↗

PubMed2002

Serum neopterin monitoring and vitamin E-modified, regenerated hemodialyzer membrane influence on biocompatibility.

The exposure of blood to hemodialysis membranes results in numerous phenomena and/or complications in hemodialyzed patients, which have an influence on the quality of life (QOL) of those patients. A vitamin E-modified regenerated cellulose membrane (E-membrane) was developed to act as a scavenger for reactive oxygen species causing complications in hemodialysis patients. Neopterin (NEOP) is a metabolite derived from guanosine triphosphate with the production and release of NEOP being induced in monocytes and macrophages by cytokines such as interferon-gamma (IFN-gamma). Serum neopterin levels are shown to be a reactive marker of bioincompatibility of dialysis membranes in hemodialysis patients. The following report evaluates the usefulness of serum NEOP as a marker for the biocompatibility of the E-membrane hemodialyzer in a clinical study. In the clinical study, where extracorporeal ultrafiltration strategies with E-membranes were employed, the serum levels of NEOP were lower than those in patients using cellulose triacetate membranes (C-membranes). In the long-term evaluation of the biocompatibility of E- and C-membranes, the increase of serum neopterin levels in the C-membrane was higher than those in the E-membrane. In conclusion, the evaluation of serum neopterin levels during hemodialysis shows that the E-membrane has a good biocompatibility in hemodialyzed patients.

Adult↗

PubMed2002

Differential regulation of TGF-beta signal in hepatic stellate cells between acute and chronic rat liver injury.

During chronic liver injury, transforming growth factor beta (TGF-beta) plays a prominent role in stimulating liver fibrogenesis by myofibroblast-like cells derived from hepatic stellate cells (HSCs). On the other hand, Smad 7 was recently shown to antagonize the TGF-beta-induced activation of signal-transducing Smads (2 and 3). In this study, we investigated the regulatory mechanisms of the TGF-beta signals in rat HSCs during acute liver injury and myofibroblasts (MFBs) during chronic liver injury, focusing on the roles of Smad 2 and antagonistic Smad 7. In acute liver injury, HSC-derived TGF-beta increased plasminogen activator inhibitor type 1 (PAI-1) and alpha2(I) procollagen (COL1A2) transcripts. Smad 2 in HSCs during liver injury and primary cultured HSCs were activated by an autocrine mechanism, because high levels of Smad 2 phosphorylation and induction of PAI-1 transcript by TGF-beta were observed in HSCs. Thereafter, Smad 7 induced by TGF-beta negatively regulated the Smad 2 action. These results indicated that endogenous TGFbeta-mediated Smad 7 in HSCs terminated the fibrotic signals mediated by signal-transducing Smads, and might be involved in the transient response to autocrine TGF-beta signal after acute liver injury. By contrast, Smad 7 was not induced by the autocrine TGF-beta signal, and constitutive Smad 2 activation was observed in MFBs throughout chronic liver injury, although Smad 7 could inhibit the TGF-beta signal requiring Smad 2 phosphorylation by activated TGF-beta receptor in cultured MFBs. This constitutive phosphorylation of Smad 2 by endogenous TGF-beta under a low level of Smad 7 could be involved in the progression of liver fibrosis.

Acute Disease↗

PubMed2002

Non-ischemic nephron-sparing surgery for small renal cell carcinoma: complete tumor enucleation using a microwave tissue coagulator.

OBJECTIVE: To determine the methodological usefulness of non-ischemic complete enucleation for small renal cell carcinomas (RCC) using a microwave tissue coagulator (MTC). METHODS: Fifty-nine patients (61 kidneys) underwent non-ischemic complete tumor enucleation by MTC. Of the 59 patients, 46 had an elective indication and 15 kidneys of 13 patients had an imperative indication. RCC was exposed with minimal peri-renal detachment. The demarcation line, 7-10 mm from the tumor, was coagulated at 8-10 mm intervals with a microwave antenna needle for 30-40 s at 50-60 W. The renal tumor was excised along the coagulated zone with normal surrounding tissue. The enucleation bed was covered with fibrin glue or fat tissue without approximation. RESULTS: The operations were successfully completed in all intended cases. The mean operation time was 160 +/- 43 (median: 160) min and the mean blood loss was 313 +/- 370 (median: 158) ml. No major bleeding or urine leakage from the enucleation bed was observed in 62.2 and 88.5% of cases, respectively. The minor bleeding and urine leakage were controlled easily with absorbable sutures. None of the cases presented with postoperative bleeding or urine leakage from the enucleation bed. Severe impairment of the renal function was not observed in any case evaluated by means of serum creatinine, creatinine clearance and radioisotope examination. The 5-year overall survival rate was 87% without recurrence up to 23.1 +/- 19.5 months of the mean follow-up. CONCLUSION: Non-ischemic complete tumor enucleation using MTC constitutes a simple, reliable and less invasive alternative to ordinary nephron-sparing surgeries for small RCC.

Adult↗

PubMed2002

[Transition zone index in predicting therapeutic efficacy of benign prostatic hyperplasia].

PURPOSE: We studied how transition zone index (TZ index) influenced the therapeutic efficacy of benign prostatic hyperplasia (BPH). In addition, we retrospectively investigated the availability of TZ index in selection of the more effective therapeutic method for BPH. METHOD: One hundred twenty-five patients with symptomatic BPH whose prostate volume (PV) was more than 15 ml by transrectal ultrasonography were investigated. Sixty-nine men underwent transurethral resection of the prostate (TURP) whereas 56 were treated with alpha 1-blocker. Tamsulosin hydrochloride. These patients were evaluated based on TZ index as well as ordinary parameters of BPH; international prostatic symptom score, QOL score, peak flow rate and PV. RESULTS: The patients with TZ index > or = 0.5 showed good therapeutic results in the TURP group. On the other hand, the patients with TZ index < 0.5 showed favorable response in alpha 1-blocker group. Multivariate analysis revealed that TZ index affected the therapeutic efficacy more strongly than the other parameters. CONCLUSION: TZ index had strong influence on therapeutic efficacy of TURP or alpha 1-blocker and seemed to be a useful tool for the selection of BPH therapy.

Adrenergic alpha-Antagonists↗

PubMed2002

[Erectile dysfunction arising from polyarteritis nodosa: a case report].

A 30-year-old male was referred to our department during the examination and treatment for hypertension, because he had not achieved complete erection since the age of 26 years. After detailed examination, he was diagnosed to be suffering from nodal polyarteritis. Since erectile dysfunction persisted, the patient was hospitalized to investigate the cause of erectile dysfunction. Measurement of the penile brachial index (PBI) and cavernous infusion of papaverine hydrochloride strongly suggested the presence of arterial erectile dysfunction. Internal-pudendal angiography revealed multiple microaneurysms in the bilateral internal pudendal arteries, suggesting that nodal polyarteritis caused arterial erectile dysfunction.

Adult↗