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There is little definitive evidence to guide the use of prophylactic antibiotics for prostate brachytherapy. The purpose of this study is to evaluate the incidence of postimplant infections in patients who receive antimicrobial prophylaxis with pazufloxacin (PZFX). A total of 84 patients who underwent prostate brachytherapy received a single intravenous dose of PZFX at 500 mg perioperatively for 1 day. No postimplant antibiotic medication was prescribed. Urinalysis, plasma white blood cell (WBC) count, and C reactive protein (CRP) levels were evaluated before the implantation, on the day after implantation, and on the 7th and 28th days after brachytherapy. None of the 84 patients (0.0%) developed a symptomatic urinary tract infection or had febrile infectious complications after brachytherapy. There were statistically significant elevations in the levels of erythrocytes, leukocytes, bacteria in urine, plasma WBC and CRP postoperatively, but these values did not exceed the normal range or were only slightly elevated on the day after brachytherapy (day 1) and on day 7. All laboratory examinations had returned to the normal range on day 28. Single-dose therapy with fluoroquinolone helps to prevent infections after prostate brachytherapy.

The purpose of this study was to investigate the effects of water exercise at a day service facility and the effects of water exercise frequency on health-related quality of life (HRQL). Participants (n = 30) were randomly separated into three groups: two indicating exercise frequency, at once-weekly or twice-weekly, and a control group. One-hour exercise intervention sessions were carried out once or twice a week, accordingly, for 24 weeks. The water exercise session comprised a warm-up on land, activities of daily living (ADL) exercises, stretching, strength training, and relaxation in water. HRQL was evaluated using the Medical Outcomes Survey Short-Form 36 (SF-36) questionnaire, and ADL disability was assessed using the Functional Independence Measure. Significant differences were found between pre- and 6 months in both the once- and twice-weekly groups in HRQL (p

Sporadic cases have developed pulmonary toxicity after receiving chemotherapy and granulocyte colony-stimulating factor (G-CSF). However, because such cases received chemotherapy that alone frequently causes pulmonary toxicity, the role of G-CSF in this toxicity has been unclear. CHOP therapy (cyclophosphamide, doxorubicin, vincristine and prednisolone) only slightly induces pulmonary toxicity. However, we observed a considerable incidence of this toxicity in non-Hodgkin's lymphoma subjects receiving CHOP therapy and G-CSF (6 out of 52 subjects, 11.5%). In this cohort, among various characteristics, including the dose and interval of CHOP therapy, only the mean peak leucocyte count (MPLC) with each therapy cycle was associated with development of this toxicity (MPLC > or = 23.0 x 10(9) l(-1), 6 out of 29 cases; MPLC < 23.0 x 10(9) l(-1), 0 out of 23 cases; P = 0.020). These findings suggest that the effect of G-CSF is the main determinant of the pulmonary toxicity in these cases. Because the toxicity was associated with a large MPLC and did not recur in cases readministered G-CSF, an idiosyncratic reaction to G-CSF is unlikely to be the pathogenesis of this toxicity. Thus, lowering the G-CSF dose seems to be useful in the prevention of this toxicity. In all six cases, the time course of manifestation of the toxicity was the same, and early application of high-dose corticosteroid led to cure. This knowledge will be helpful in the care of similar cases. Images Figure 2

Autoantibody against erythrocytes has occasionally been observed in patients with de novo acute myelocytic leukemia (AML). However, it is not clear whether this autoantibody in AML patients induces frank hemolysis (autoimmune hemolytic anemia, AIHA), as seen in lymphoid neoplasms. We present two de novo AML patients who showed hemolysis due to antiglobulin test-positive and test-negative AIHA, respectively. AIHA should be considered as one cause of anemia in de novo AML patients, and blood transfusions should be given carefully in such cases to avoid harmful hemolysis.

Background The Vav family of Rho/Rac guanosine nucleotide exchange factors comprises three members in mammalian cells. Vav3 enhances androgen receptor (AR) activity during progression to androgen independence in prostate cancer. We examined Vav3 small interfering RNA (siRNA) effects on cell proliferation and apoptosis in docetaxel-treated LNCaP cells under chronic hypoxia (LNCaPH). Methods We examined individual and combined effects of Vav3 siRNA (si-Vav3) and docetaxel on cell growth and apoptosis under chronic hypoxia by cell proliferation, flow cytometric, DNA fragmentation, and immunoblot analyses. To clarify the molecular basis of si-Vav3- and docetaxel-induced apoptosis, we analyzed alterations in phosphatidylinositol 3-kinase (PI3K)/Akt, extracellular signal-regulate kinase (ERK), c-jun N-terminal kinase (JNK), and AR pathways using kinase inhibitors in LNCaPH cells. The effects of si-Vav3/atelocollagen complex alone or in combination with docetaxel were assessed on xenografts in nude mice by tumor growth delay. Results Vav3 overexpression was observed in LNCaPH compared with the expression under normoxia. Interrupting Vav3 signaling using siRNA enhanced docetaxel-induced cell growth suppression compared with that induced by docetaxel alone by inhibition of Akt and ERK phosphorylation, resulting in AR phosphorylation inhibition. In addition to increased B-cell lymphoma 2 (Bcl-2) phosphorylation through JNK signaling in response to docetaxel, si-Vav3 enhanced docetaxel-induced apoptosis, as characterized by the accumulation of sub-G1 phase cells and DNA fragmentation, through Bcl-xL/Bcl-2-associated death promoter (Bad) dephosphorylation, resulting in increased caspase-9, caspase-3, and cleaved poly(ADP-ribose) polymerase activation. Xenograft tumor growth was slightly inhibited by si-Vav3/atelocollagen complex injection and combined use of si-Vav3/atelocollagen complex and docetaxel produced a greater effect than docetaxel alone. Conclusions Interrupting Vav3 signaling enhances docetaxel-induced apoptosis in LNCaP cells under chronic hypoxia by inhibiting the PI3K/Akt, ERK, and AR signaling pathways. Therapy targeting Vav3 in combination with docetaxel may have practical implications for managing castration-resistant prostate cancer.

Response-oriented individualized induction chemotherapy (ROIIC) has been reported to achieve a high complete remission (CR) rate in acute myeloid leukemia (AML). In ROIIC, drug dose is modified for each patient to achieve hematologic target points, based on the concept that this achievement, not a preset drug dose, increases the likelihood of attaining CR. However, the existing target points lack objectivity, therefore prohibiting worldwide use of ROIIC. In addition, the achievement of these target points does not statistically relate to CR, which contradicts the concept of ROIIC. To solve these problems, we evaluated various parameters of 117 AML cases treated by ROIIC to identify the factors relating to CR. Of 117 AML subjects, 75 achieved CR with ROIIC and most cases achieving CR did so with one ROIIC course. Not the administered dose of drugs but several hematologic parameters at the end of ROIIC correlated significantly with CR. A total of four parameters, all related to the leukemic cell mass, were independent predictive factors of CR. A formula consisting of these parameters predicted CR cases with high sensitivity (98%) and non-CR cases with high specificity (96%). Based on this formula, an objective target point (a bone marrow blast mass ratio between before and after ROIIC of below 0.15), valid for dose modification during ROIIC, was established. These results validate the concept of ROIIC and enable objective dose modification in ROIIC and universal application of this therapy. Further, the formula predicting non-CR cases at the end of ROIIC is useful for deciding early therapeutic intervention for such cases.

We investigated the effect of high-dose intravenous gamma globulin therapy on the plasma level of macrophage-colony stimulating factor (M-CSF) level in 13 patients with chronic idiopathic thrombocytopenic purpura. M-CSF and interleukin-6 levels were determined by enzyme-linked immunosorbent assay. The mean +/- S.D. level of M-CSF in the patients was 1235 +/- 439 U/ml, and the level in 8 patients was higher than the mean + S.D. (903.6 U/ml) in normal controls. All 8 patients had steroid-refractory disease. M-CSF levels were significantly correlated with the serum levels of interleukin-6 (r = 0.66, P < 0.05). Interleukin-6 levels were also significantly raised in the high M-CSF group compared with the normal M-CSF group (P < 0.05). In the whole patient population, M-CSF levels decreased, but not significantly, after intravenous gamma globulin, while interleukin-6 decreased significantly. However, in the patients with high pretreatment M-CSF levels, both M-CSF and interleukin-6 decreased significantly after treatment (M-CSF, 4 weeks, P < 0.05; IL-6, 1 week, P < 0.05, 4 weeks, P < 0.01). These findings suggest that high-dose intravenous gamma globulin causes thrombocytosis by the decrease of M-CSF levels in idiopathic thrombocytopenic purpura.

To determine the prevalence of the myelodysplastic syndromes (MDS) in Japan, we conducted a nationwide survey in 1991. The survey included the sex, birth date and type of MDS of the patients from all (n = 2315) hospitals with 200 beds or more and 188 hospitals randomly selected from 7526 hospitals (1/40) with 199 beds or less. The point prevalence of MDS was estimated to be almost 3000 as of September 1, 1991, and it was 3.4 per 100,000 men of 15 years old or older and 2.1 per 100,000 women of 15 years old or older. Refractory anemia (RA) was most common (51%) followed by RA with excess of blasts (RAEB; 18%) and RAEB in transformation (RAEB-t; 14%). RAEB, RAEB-t and chronic myelomonocytic leukemia (CMML) showed a high male/female ratio (3.0 or higher) although the sex ratio of other types was almost 1.0.