A novel de novo point mutation of the OCT-binding site in the IGF2/H19-imprinting control region in a Beckwith-Wiedemann syndrome patient.

The IGF2/H19-imprinting control region (ICR1) functions as an insulator to methylation-sensitive binding of CTCF protein, and regulates imprinted expression of IGF2 and H19 in a parental origin-specific manner. ICR1 methylation defects cause abnormal expression of imprinted genes, leading to Beckwith-Wiedemann syndrome (BWS) or Silver-Russell syndrome (SRS). Not only ICR1 microdeletions involving the CTCF-binding site, but also point mutations and a small deletion of the OCT-binding site have been shown to trigger methylation defects in BWS. Here, mutational analysis of ICR1 in 11 BWS and 12 SRS patients with ICR1 methylation defects revealed a novel de novo point mutation of the OCT-binding site on the maternal allele in one BWS patient. In BWS, all reported mutations and the small deletion of the OCT-binding site, including our case, have occurred within repeat A2. These findings indicate that the OCT-binding site is important for maintaining an unmethylated status of maternal ICR1 in early embryogenesis.

Analysis of serum chemokine levels in patients with HIV-associated eosinophilic folliculitis.

BACKGROUND: Patients with human immunodeficiency virus (HIV) infection exhibit various skin diseases. HIV-associated eosinophilic folliculitis (EF) and pruritic papular eruption (PPE) are frequently seen. OBJECTIVE: To understand the mechanisms underlying HIV-associated EF and PPE. METHODS: In order to know frequencies of EF and PPE among patients with HIV infection, we first collected HIV(+) patients who visited dermatology clinic in National Center for Global Health and Medicine during February 2007. We next collected 25 serum samples from HIV(+) patients with skin diseases from May 2008 to May 2010. Eight of 25 patients had EF (EF group), four had PPE (PPE group) and others had non-itchy skin problems such as condyloma acuminatum (no itch group). RESULTS: We first confirmed high frequencies of EF (10.7%) and PPE (5.3%) among 75 HIV(+) patients who visited our clinic during one month. We then measured serum levels of CCL11, CCL17, CCL26 and CCL27. Serum CCL17 levels in EF were significantly higher than those of PPE and no itch group. Serum CCL26 and CCL27 levels in EF were higher than those of no itch group. The number of CD4(+) cells in EF was significantly lower than that in no itch group. CONCLUSION: High serum levels of CCL17, CCL26 and CCL27, and low CD4(+) cell counts may account for the development of HIV-associated EF.

Serum apelin levels: clinical association with vascular involvements in patients with systemic sclerosis.

BACKGROUND: Apelin is a bioactive peptide exerting its pro-angiogenic and pro-fibrotic effects in a context-dependent manner through the activation of its receptor APJ, which is ubiquitously expressed on the surface of various cell types. The activation of apelin/APJ signalling appears to be involved in the pathological process of fibrotic disorders, including liver cirrhosis. OBJECTIVE: As an initial step to clarify the role of apelin/APJ signalling in the pathogenesis of systemic sclerosis (SSc), we investigated serum apelin levels and their clinical association in patients with SSc. METHODS: Serum apelin levels were determined by a specific enzyme-linked immunosorbent assay in 56 SSc patients and 18 healthy controls. RESULTS: Serum apelin levels were comparable among three groups, including diffuse cutaneous SSc, limited cutaneous SSc and control subjects (1.77 ± 1.48, 1.63 ± 1.51 and 1.61 ± 0.44 ng/mL, respectively). When we classified SSc patients into three groups according to disease duration, serum apelin levels were elevated in early SSc (<3 years) compared with mid-stage SSc (3-10 years) (1.74 ± 1.26 vs. 1.02 ± 0.52 ng/mL, P < 0.05). Importantly, in late stage SSc (>10 years), the prevalence of severe vascular involvements, including intractable skin ulcers, scleroderma renal crisis and pulmonary arterial hypertension, was significantly higher in patients with elevated serum apelin levels than in those without (100% vs. 20%, P < 0.05). CONCLUSION: Apelin may be associated with altered and activated angiogenesis prior to fibrotic responses in early SSc and with the development of proliferative vasculopathy in late stage SSc.

Serum adiponectin levels inversely correlate with the activity of progressive skin sclerosis in patients with diffuse cutaneous systemic sclerosis.

BACKGROUNDS: Adiponectin has been demonstrated to be one of anti-inflammatory and anti-fibrotic factors, suggesting the potential of this cytokine to be involved in the developmental process of systemic sclerosis (SSc). OBJECTIVE: The aim of this study was to investigate the clinical significance of serum adiponectin levels in patients with SSc. Methods Serum adiponectin levels were determined using enzyme-linked immunosorbent assay (ELISA) in 32 patients with diffuse cutaneous SSc (dcSSc), 28 with limited cutaneous SSc (lcSSc) and 27 healthy controls. No significant difference between these groups existed in terms of gender, age and body mass index. RESULTS: Serum adiponectin levels in dcSSc patients (4.93 ± 6.48 µg/mL) were significantly lower than those in lcSSc patients (9.69 ± 7.61 µg/mL, P < 0.01) and healthy controls (9.36 ± 5.57 µg/mL, P < 0.01). dcSSc patients with disease duration of ≤5 years had significantly decreased serum adiponectin levels (2.15 ± 1.69 µg/mL) than those with disease duration of >5 years (13.29 ± 8.36 µg/mL, P < 0.01), lcSSc patients with disease duration of ≤5 years (8.07 ± 7.98 µg/mL, P < 0.05), lcSSc patients with disease duration of >5 years (10.9 ± 7.34 µg/mL, P < 0.01) and healthy controls (9.36 ± 5.57 µg/mL, P < 0.01). Longitudinal studies in five patients with early dcSSc treated with oral prednisone demonstrated that serum adiponectin levels inversely correlate with the activity of progressive skin sclerosis in dcSSc patients. CONCLUSION: Serum levels of adiponectin may serve as a useful marker to evaluate the activity of progressive skin sclerosis in dcSSc.

Serum Tie2 levels: clinical association with microangiopathies in patients with systemic sclerosis.

BACKGROUND: Tie2 and its ligand, angiopoietins (Ang), regulate the transition between vascular quiescence and angiogenesis. Although defective angiogenesis is one of the major causes of microangiopathies in systemic sclerosis (SSc), the role of Ang/Tie2 signalling in the development of SSc has never been examined. OBJECTIVE: To investigate the clinical significance of the soluble Tie2 domain (sTie2) in serum samples from SSc patients. METHODS: Serum sTie2 levels were determined by a specific enzyme-linked immunosorbent assay in 48 SSc patients and nine normal controls. RESULTS: There was no significant difference in serum sTie2 levels between SSc patients and healthy controls (14.8 ± 3.4 vs. 14.7 ± 1.1 ng/mL). When we set the cut-off value at 16.97 ng/mL (mean + 2SD) based on the data of normal controls, 27% of SSc patients showed elevated serum sTie2 levels. The frequencies of nailfold bleeding and pulmonary arterial hypertension (PAH) were significantly higher in patients with increased serum sTie2 levels than in those with sTie2 levels not elevated (70% vs. 47% and 60% vs. 21%, respectively, P < 0.05). There was also a trend towards the elevation of serum sTie2 levels in SSc patients with PAH compared to those without; however, it did not reach statistical significance (16.7 ± 3.6 vs. 14.2 ± 3.4 ng/mL, P = 0.059). CONCLUSION: Soluble Tie2 domain (sTie2) may be related to the development of vascular abnormalities in SSc, possibly by modulating the Ang/Tie2-mediated angiogenic process. Furthermore, the serum sTie2 levels may serve as a useful marker for SSc-related PAH, contributing to early diagnosis and therapeutic intervention.

Development of a high-hydrous gel phantom for human body communication based on electrical anisotropy.

In this study, we investigated a highly hydrated gel phantom with electrical anisotropy that can be used at 18.375 MHz to 23.625 MHz. This is one of the frequency bands used for human body communication. To achieve the communication, the electrical characteristics of the quadriceps femoris muscle of the rat were measured immediately after sacrifice. These were used to obtain an indicator of electrical characteristics to be satisfied by the phantom. Electrical anisotropy was realized by adding carbon fiber to the phantom and controlling its direction. We were able to develop a high hydrated gel phantom for human body communication with a maximum error of 8.1% assuming its use at 18.735 MHz to 23.625 MHz.

Prevalence of resistant hypertension and associated factors in Japanese subjects with type 2 diabetes.

OBJECTIVE: The prevalence of treatment resistant hypertension (RH) depends on methods used for blood pressure (BP) measurements, goals of BP, and therapeutic efforts in terms of medication and adherence. We focused on diabetic subjects and explored the prevalence of RH in primary care practice. METHODS: In 1737 subjects with type 2 diabetes who continued regular visits, office BP was evaluated by multiple measurements over one year. RH was defined as using more than four antihypertensive drugs or failure to achieve the goal with three antihypertensive drugs from different classes. The RH prevalence was investigated with BP goals <130/80 and 140/90 mmHg. RESULTS: The percentage of subjects who achieved BP goals <130/80 and 140/90 were 70.5% and 93.8% with adherence to medication ≥95%, and the corresponding prevalence rates of RH in treated subjects were 28.4% and 21.8%, respectively. Factors independently associated with RH were age (odds ratio 1.02 [95% CI 1.01-1.04]), body mass index (1.10 [1.06-1.13]), variability in systolic BP (1.06 [1.02-1.09]), triglycerides (2.86 [1.34-6.11]), macroalbuminuria (3.33 [2.03-5.48]), estimated glomerular filtration rate (0.98 [0.97-0.99]), retinopathy (1.91 [1.39-2.61]), and family history of hypertension (1.85 [1.23-2.21]). Worsening albuminuria and glomerular filtration rate enhanced the prevalence of RH in a graded manner. CONCLUSION: Careful estimation of office BP values over one year with a high achievement of BP goals and adequate adherence revealed that the prevalence of RH in type 2 diabetes is high. RH was characterized by accumulation of cardiovascular genetic and environmental risks.

Nucleotide sequence of a cDNA encoding a common precursor of disintegrin flavostatin and hemorrhagic factor HR2a from the venom of Trimeresurus flavoviridis.

The venom of Trimeresurus flavoviridis has three disintegrins that act as platelet aggregation inhibitors by binding to integrin alphaIIb beta3 on platelets through its Arg-Gly-Asp sequence. We isolated the cDNA encoding the flavostatin precursor that is one of the disintegrins in T. flavoviridis venom. The open reading frame consisted of four regions, a pre-peptide region, a metalloprotease region, a spacer region and a disintegrin region, indicating that the flavostatin precursor belongs to the metalloprotease/disintegrin family. Surprisingly, the deduced amino acid sequence of the metalloprotease region was completely consistent with that of hemorrhagic metalloprotease HR2a, which indicated that this metalloprotease released from the flavostatin precursor functions as a hemorrhagic factor. These observations indicated that a disintegrin and a hemorrhagic metalloprotease were synthesized as a common precursor. Thus, our results support the hypothesis that a disintegrin is synthesized as a metalloprotease/disintegrin precursor and matures by cleavage from the precursor molecule.

Intensity-modulated whole pelvic radiation therapy in patients with gynecologic malignancies.

PURPOSE: To evaluate the ability of intensity-modulated radiation therapy (IMRT) to reduce the volume of small bowel irradiated in women with gynecologic malignancies receiving whole pelvic radiotherapy (WPRT). METHODS AND MATERIALS: Ten women with cervical (5) or endometrial (5) cancer undergoing WPRT were selected for this analysis. A planning CT scan of each patient was obtained following administration of oral, i.v., and rectal contrast. The clinical target volume (CTV) was defined as the proximal vagina, parametrial tissues, uterus (if present), and regional lymph nodes. The CTV was expanded uniformly by 1 cm in all directions to produce a planning target volume (PTV). The bladder, rectum, and small bowel were also delineated in each patient. Two plans were created: a standard "4-field box" with apertures shaped to the PTV in each beam's eye view and an IM-WPRT plan designed to conform to the PTV while minimizing the volume of normal tissues irradiated. Both plans were normalized to deliver 45 Gy to the PTV. Isodose distributions and dose-volume histograms (DVH) were compared. RESULTS: The IM-WPRT plan reduced the volume of small bowel irradiated in all 10 patients at doses above 30 Gy. At the prescription dose, the average volume of small bowel irradiated was reduced by a factor of two (17.4 vs. 33.8%, p = 0.0005). In addition, the average volume of rectum and bladder irradiated at the prescription dose was reduced by 23% in both cases (p = 0.0002 and p = 0.0005, respectively). The average PTV doses delivered by the conventional and IM-WPRT plans were 47.8 Gy and 47.4 Gy, respectively. Corresponding maximum doses were 50.0 Gy and 54.8 Gy, respectively. However, on average, only 3.2% of the PTV received greater than 50.0 Gy in the IM-WPRT plans. CONCLUSION: Our results suggest that IM-WPRT is an effective means of reducing the volume of small bowel irradiated in women with gynecologic malignancies receiving WPRT. This approach potentially offers a method for reducing small bowel complications in patients with gynecologic malignancies.

Purification and characterization of a Ca2+ -dependent prothrombin activator, multactivase, from the venom of Echis multisquamatus.

We previously found a novel Ca2+-dependent prothrombin activator, designated as carinactivase-1, in Echis carinatus leucogaster venom [D. Yamada, F. Sekiya, and T. Morita (1996) J. Biol. Chem. 271, 5200-5207]. Of the Viperidae snake venoms examined, the Echis multisquamatus venom had the strongest carinactivase-like activity. We isolated and characterized the carinactivase-like prothrombin activator in E. multisquamatus venom. From 50 mg of E. multisquamatus venom, we isolated 2.3 mg of a Ca2+-dependent prothrombin activator designated as multactivase. Unlike other Echis snake venoms, the E. multisquamatus venom contained no ecarin-like Ca2+-independent prothrombin activator. The structure and function of multactivase are similar to those of carinactivase. Multactivase is composed of a catalytic subunit with metalloprotease activity and a regulatory subunit comprising two homologous polypeptides bound by S-S bridge(s), and it activates prothrombin via recognition of the Ca2+-bound conformation of its Gla domain. We developed a chromogenic assay involving multactivase for normal prothrombin activity in plasma from individuals orally administered anticoagulants. The normal prothrombin activity, as a percentage, measured with multactivase was highly correlated with the prothrombin time. Multactivase is useful for the simple quantification of normal prothrombin in plasma from warfarin-treated individuals.

Improvement by the insulin-sensitizing agent, troglitazone, of abnormal fibrinolysis in type 2 diabetes mellitus.

This study evaluated abnormal fibrinolysis in diabetic patients in terms of the pathophysiological significance and reversibility by oral hypoglycemic agents. Forty-seven patients with type 2 diabetes mellitus were randomly treated for 4 weeks with glibenclamide (n = 23) or troglitazone (n = 24). Before and after treatment, glycemic control, steady-state plasma glucose and insulin (SSPG and SSPI, respectively), and markers of fibrinolysis (tissue plasminogen activator [tPA] and plasminogen activator inhibitor-1 [PAI-1]) were analyzed in each patient. Pretreatment plasma PAI-1 in diabetic patients, but not tPA, was well correlated with the severity of retinopathy assessed by the fluorescence technique. Four weeks of treatment with troglitazone significantly decreased hemoglobin A1c (HbA1c), SSPG, and PAI-1 without an alteration of tPA. The troglitazone-induced decrease in plasma PAI-1 (50.3 v28.8 micromol/L; P < .05) was correlated with HbA1c (8.80% v7.21%, r = .539, P < .01) and SSPG (16.2 v 8.97 mmol/L, r = .562, P < .01) but not with SSPI. In contrast, treatment with glibenclamide for 4 weeks also reduced the HbA1c titer to almost the same extent as troglitazone (1.38% v 1.59%), but did not change the plasma PAI-1 or SSPG titer. These results suggest that an abnormal fibrinolytic state, especially overproduction of PAI-1, may be a pathogenic factor in the development of diabetic complications such as retinopathy, which may be improved by correction of the insulin resistance with troglitazone.

Hydrops fetalis secondary to Bart hemoglobinopathy.

Alpha-thalassemia is the most common cause of hydrops fetalis among Southeast Asians. With the recent influx of Southeast Asian refugees and the rapidly growing Filipino population this will become an increasingly important obstetric problem in the United States. Homozygous alpha-thalassemia, or Bart hemoglobinopathy, is invariably fatal to the fetus and produces significant maternal morbidity. Eighteen cases of homozygous alpha-thalassemia in one hospital are reviewed. This is the largest series reported in the United States. Recommendations are made for antenatal screening, diagnosis, and management of alpha-thalassemia.

CA-1 method, a novel assay for quantification of normal prothrombin using a Ca2+ -dependent prothrombin activator, carinactivase-1.

We established a novel prothrombin assay, designated CA-1 method, for quantification of normal prothrombin in application of a Ca2+ -dependent prothrombin activator, carinactivase-1 (CA-1), found in the venom of Echis carinatus leucogaster. On microplate, thrombin converted from normal prothrombin in plasma sample by CA-1 cleaves a thrombin specific chromogenic substrate, t-butoxy-Val-Pro-Arg-p-nitroanilide and liberates p-nitroaniline. Then, the normal prothrombin level is decided by measuring the velocity of p-nitroaniline liberation. Normal prothrombin levels in plasma from warfarin-treated individuals were highly correlated with coagulant activities assayed by both prothrombin time and thrombotest. CA-1 method is not only a rapid and highly sensitive chromogenic microplate assay for quantification of normal prothrombin in the range of 10-200 ng/100 microl in plasma samples but also suitable for analyses of many samples in a short time. In addition, normal prothrombin levels obtained by CA-1 method are not inhibited by EDTA and heparin, which reduce prothrombin time and thrombotest activities. CA-1 method is a novel assay for monitoring coagulant activity in warfarin-treated individuals.

Prothrombin and factor X activator activities in the venoms of Viperidae snakes.

A Ca(2+)-dependent prothrombin activator, carinactivase-1 (CA-1), was previously found in the venom of Echis carinatus leucogaster. In the present study, the activities of CA-1-like enzymes were screened in the venoms of various Viperidae snakes. The addition of 1 mM Ca2+ ions to the venoms of only Echis snakes in Viperidae produced considerably high prothrombin activator activity, indicating that only the Echis snake venoms contain not only the Ca(2+)-independent prothrombin activator, ecarin, but also Ca(2+)-dependent activator(s). CA-1-like activators and ecarin in the venom of each Echis snake were efficiently separated by Blue Sepharose column chromatography. The venoms of the various Viperidae snakes were also examined for factor X activator activity. The venoms of genera Daboia, Vipera, Cerastes, Echis, Calloselasma and Bothrops contained factor X activator activity in the presence of Ca2+ ions. Cerastes cerastes and Calloselasma rhodostoma venoms also had Ca(2+)-independent factor X activator activity.

Direct evidence for erythropoietin-induced release of endothelin from peripheral vascular tissue.

The effect of recombinant human erythropoietin (r-HuEPO, 0.1 to 2.0 U/ml) on endothelin-1 (ET-1) release was examined in isolated hind legs perfused with Krebs-Ringer solution from normal rats. r-HuEPO increased immunoreactive (ir-) ET-1 release in a dose-dependent fashion; the maximal percent increment in ir-ET-1 release evoked by r-HuEPO (2.0 U/ml) was about +210% over the basal rate of release. However, r-HuEPO showed no effect on release of angiotensin II, thromboxane B2 or vasodilatory prostaglandin I2 from the vasculature. These results not only provide direct evidence that r-HuEPO has the potential to specifically stimulate release of ET-1 from peripheral vascular beds, but, hence, suggest a contributory role of ET-1 in r-HuEPO-induced hypertension in anemic human subjects undergoing r-HuEPO therapy.

Plasma vascular endothelial growth factor in Japanese Type 2 diabetic patients with and without nephropathy.

AIM: To determine whether plasma vascular endothelial growth factor (VEGF) level is elevated in Type 2 diabetic patients with an early stage of diabetic nephropathy. METHODS: We studied 71 Japanese Type 2 diabetic patients with normal serum creatinine level (<100 micromol/l) (age 63.0 [60.3-65.6] years old, diabetes duration 15.6 [14.0-17.3] years, HbA1c 7.36% [7.06-7.66%], mean [95% confidence interval, CI]): normoalbuminuric patients (n=36); microalbuminuric patients (n=21); and proteinuric patients (n=14). Plasma VEGF concentration was measured by a quantitative sandwich enzyme immunoassay technique. RESULTS: Plasma VEGF concentration was not related to the degree of albuminuria: normoalbuminuric patients (25 [13-95] ng/l, median [25th-75th percentile]); microalbuminuric patients (33 [15-120] ng/l); and proteinuric patients (54 [17-107] ng/l). Plasma VEGF level in patients with retinopathy (25 [15-95] ng/l, n=30) was not elevated as compared to those without retinopathy (53 [14-126] ng/l, n=34). Plasma VEGF tended to correlated negatively with diabetes duration (R's=-.217, P=.0690) and HbA1c (R's=-.221, P=.0647), whereas there was no correlation between plasma VEGF level and age, serum creatinine or urinary albumin to creatinine ratio (ACR) of the patients, respectively. Plasma VEGF level in the group of patients with HbA1c equal to or below the median (<7.2%) was significantly higher than that in the group of patients with HbA1c above the median (>7.2%) (P<.05). CONCLUSIONS: The results suggested that Type 2 diabetic patients with microalbuminuria and those with retinopathy are not necessarily associated with an elevation of circulating plasma VEGF concentration. Plausible association between plasma VEGF level and glycemic control remains to be seen.

Determination of plasma prothrombin level by Ca2+-dependent prothrombin activator (CA-1) during warfarin anticoagulation.

BACKGROUND AND AIM OF THE STUDY: The carinactivase-1 (CA-1) test is a new method for monitoring plasma prothrombin levels during warfarin anticoagulation therapy. METHODS: A total of 192 patients were allocated to two groups. Group A patients (n = 42) were controls (no warfarin); group B patients (n = 150) received warfarin. A Ca2+-ion and Boc-Val-Pro-Arg-pNA (a chromogenic substrate for thrombin) were added to 10-fold diluted plasma, after which prothrombin was activated with CA-1. Prothrombin levels were determined by measuring the extent of p-nitoroaniline liberation. RESULTS: The mean prothrombin level was 112.8 +/- 20.0 microg/ml in group A (Gaussian distribution), and 53.3 +/- 19.6 microg/ml in group B. In group B, correlations were found between the CA-1 test and prothrombin levels measured by prothrombin time (PT; r = 0.61, p <0. 01), PT-INR (r = 0.61, p <0.01), Thrombotest (TT; r = 0.57, p <0.01) and Hepaplastin test (HPT; r = 0.69, p <0.01). CONCLUSION: The CA-1 test represents a viable method of monitoring the coagulation system. CA-1 recognized the Gla-domain of prothrombin, and activated prothrombin. The CA-1 test required only 10 microl of diluted blood plasma, and took approximately 30 min to complete. The CA-1 test also measures prothrombin levels, correlates excellently with other tests for coagulation, and compares well with currently available methods for determining the efficacy of warfarin.

[Prostatic tissue and fluid levels of lomefloxacin (NY-198)].

The concentration of Lomefloxacin (NY-198), a new quinolone, in human prostatic tissue and fluid was examined. Lomefloxacin was concentrated in prostatic gland and the mean ratios of prostatic tissue levels to serum levels (P/S) were 1.39-1.83 during 2 to 6 hrs after administration. Concerning prostatic fluid concentrations, there were no significant differences between healthy volunteers and patients with chronic prostatitis. The mean ratios of prostatic fluid levels to serum levels (Pf/S) were 0.36-0.77 during 1 to 4 hrs after administration. The concentration of Lomefloxacin in the prostatic tissue and fluid is high enough to eradicate the majority of pathogens causing bacterial prostatitis.

[Clinico-bacteriological studies on the etiology of bacterial prostatitis. I. The distribution of clinical isolates and bacteria-specific immunoglobulin in EPS].

The distribution of clinical isolates from patients with prostatitis and pathogenicity of the isolates were studied. A new method for measuring the bacteria-specific immunoglobulins in expressed prostatic secretion (EPS) was developed and used for the detection of local immuno-reaction against pathogenic bacteria in the cases with prostatitis. There were no cases with increased antibodies specific for gram-positive cocci (GPC), indicating that the pathogenecity of GPC in bacterial prostatitis was doubtful. On the other hand, specific antibodies against gram negative rods (GNR) were elevated in all cases with acute prostatitis and changes of the antibody titers were correlated well to clinical courses. The present clinico-statistic and immuno-biological studies re-confirmed that E. coli was the main organism in uncomplicated bacterial prostatitis.

[Clinico-bacteriological studies on the etiology of bacterial prostatitis. II. Virulence factors of E. coli in bacterial prostatitis].

The virulence factors of E. coli in bacterial prostatitis were studied using 59 E. coli isolated from uncomplicated prostatitis. O-antigens of prostatitis-derived E. coli belonged to some specific serotypes such as 0-4, 6, 18, 22 and the haemolysin production was positive in 64.4%. With regard to the fimbriae, the majority of the strains had type 1 fimbriae (81.4%). Mannose resistant (MR) fimbriae were also positive in 59.3% and both type 1 and MR fimbriae were positive in 55.9%. Among MR strains, P-fimbriated and S-fimbriated strains were present in 25.7% and 28.6%, respectively, indicating that these two MR fimbriae were not always specific for the prostatitis-derived E. coli. Although the specific adhesion of E. coli onto the human prostatic epithelium mediated by MR-fimbriae was equivocal, that mediated by type 1 fimbriae was observed clearly. Therefore, type 1 fimbriae was thought to be one of the most significant virulence factors in the pathogenesis of prostatitis caused by E. coli.