Purpose: To investigate the effectiveness of acotiamide on lower urinary tract dysfunction by using a rat model of neurogenic underactive bladder induced through pelvic nerve crush (PNC) injury. Methods: Bilateral PNC injuries were performed on 8-week-old female Sprague-Dawley rats (PNC group); the sham surgery group was used as control (control group). Two weeks after surgery, awake cystometrography (CMG) was performed, and acotiamide (10 or 100 mg/kg) was subcutaneously administered to the control and PNC groups. Subsequently, CMG parameter values obtained before and after treatment were compared. Results: In baseline CMG, compared to control group, PNC group revealed statistically significant elevations in the intercontraction intervals (ICIs), number of nonvoiding contractions, baseline pressure, threshold pressure, bladder capacity, voided volumes, and postvoid residual. However, contraction amplitudes and voiding efficiency were significantly decreased. In the control group, compared with the baseline values, 10-mg/kg acotiamide resulted in statistically significant elevations in contraction amplitudes. Treatment with 100-mg/kg acotiamide led to statistically significant elevations in contraction amplitudes and decreases in ICI and bladder volume. In the PNC group, there were no statistically significant changes noted in CMG parameters after treatment with 10-mg/kg acotiamide (n=6). Compared with the baseline values, the administration of 100-mg/kg acotiamide significantly decreased ICI (1,025±186 seconds vs. 578±161 seconds; P=0.012), bladder capacity (1,841±323 µL vs. 871±174 µL, respectively; P=0.0059) and postvoid residual (223±46 µL vs. 44±22 µL, respectively; P=0.023), and increased contraction amplitudes (22.09±1.76 cm H2O vs. 43.84±6.87 cm H2O, respectively; P=0.012) and voiding efficiency (0.87±0.02 vs. 0.94±0.03, respectively; P=0.029). Conclusions Acotiamide showed effectiveness in the treatment of underactive bladder, possibly through activation of bladder afferent and detrusor activities.

Purpose: To investigate the effectiveness of acotiamide on lower urinary tract dysfunction by using a rat model of neurogenic underactive bladder induced through pelvic nerve crush (PNC) injury. Methods: Bilateral PNC injuries were performed on 8-week-old female Sprague-Dawley rats (PNC group); the sham surgery group was used as control (control group). Two weeks after surgery, awake cystometrography (CMG) was performed, and acotiamide (10 or 100 mg/kg) was subcutaneously administered to the control and PNC groups. Subsequently, CMG parameter values obtained before and after treatment were compared. Results: In baseline CMG, compared to control group, PNC group revealed statistically significant elevations in the intercontraction intervals (ICIs), number of nonvoiding contractions, baseline pressure, threshold pressure, bladder capacity, voided volumes, and postvoid residual. However, contraction amplitudes and voiding efficiency were significantly decreased. In the control group, compared with the baseline values, 10-mg/kg acotiamide resulted in statistically significant elevations in contraction amplitudes. Treatment with 100-mg/kg acotiamide led to statistically significant elevations in contraction amplitudes and decreases in ICI and bladder volume. In the PNC group, there were no statistically significant changes noted in CMG parameters after treatment with 10-mg/kg acotiamide (n=6). Compared with the baseline values, the administration of 100-mg/kg acotiamide significantly decreased ICI (1,025±186 seconds vs. 578±161 seconds; P=0.012), bladder capacity (1,841±323 µL vs. 871±174 µL, respectively; P=0.0059) and postvoid residual (223±46 µL vs. 44±22 µL, respectively; P=0.023), and increased contraction amplitudes (22.09±1.76 cm H2O vs. 43.84±6.87 cm H2O, respectively; P=0.012) and voiding efficiency (0.87±0.02 vs. 0.94±0.03, respectively; P=0.029). Conclusions Acotiamide showed effectiveness in the treatment of underactive bladder, possibly through activation of bladder afferent and detrusor activities.

Purpose: To investigate the effectiveness of acotiamide on lower urinary tract dysfunction by using a rat model of neurogenic underactive bladder induced through pelvic nerve crush (PNC) injury. Methods: Bilateral PNC injuries were performed on 8-week-old female Sprague-Dawley rats (PNC group); the sham surgery group was used as control (control group). Two weeks after surgery, awake cystometrography (CMG) was performed, and acotiamide (10 or 100 mg/kg) was subcutaneously administered to the control and PNC groups. Subsequently, CMG parameter values obtained before and after treatment were compared. Results: In baseline CMG, compared to control group, PNC group revealed statistically significant elevations in the intercontraction intervals (ICIs), number of nonvoiding contractions, baseline pressure, threshold pressure, bladder capacity, voided volumes, and postvoid residual. However, contraction amplitudes and voiding efficiency were significantly decreased. In the control group, compared with the baseline values, 10-mg/kg acotiamide resulted in statistically significant elevations in contraction amplitudes. Treatment with 100-mg/kg acotiamide led to statistically significant elevations in contraction amplitudes and decreases in ICI and bladder volume. In the PNC group, there were no statistically significant changes noted in CMG parameters after treatment with 10-mg/kg acotiamide (n=6). Compared with the baseline values, the administration of 100-mg/kg acotiamide significantly decreased ICI (1,025±186 seconds vs. 578±161 seconds; P=0.012), bladder capacity (1,841±323 µL vs. 871±174 µL, respectively; P=0.0059) and postvoid residual (223±46 µL vs. 44±22 µL, respectively; P=0.023), and increased contraction amplitudes (22.09±1.76 cm H2O vs. 43.84±6.87 cm H2O, respectively; P=0.012) and voiding efficiency (0.87±0.02 vs. 0.94±0.03, respectively; P=0.029). Conclusions Acotiamide showed effectiveness in the treatment of underactive bladder, possibly through activation of bladder afferent and detrusor activities.

Background/Aims: Intestinal fibrosis is a major complication of Crohn’s disease (CD). The profibrotic protein transforming growth factor-β (TGF-β) has been considered to be critical for the induction of the fibrotic program. TGF-β has the ability to induce not only the expression of extracellular matrix (ECM) including collagen, but also the production of plasminogen activator inhibitor-1 (PAI-1) that prevents enzymatic degradation of the ECM during the onset of fibrotic diseases. However, the significance of PAI-1 in the developing intestinal fibrosis has not been fully understood. In the present study, we examined the actual expression of PAI-1 in fibrotic legion of intestinal inflammation and its correlation with the abnormal ECM deposition. Methods: Chronic intestinal inflammation was induced in BALB/c mice using 8 repeated intrarectal injections of 2,4,6-trinitrobenzene sulfonic acid (TNBS). TM5275, a PAI-1 inhibitor, was orally administered as a carboxymethyl cellulose suspension each day for 2 weeks after the sixth TNBS injection. Results: Using a publicly available dataset (accession number, GSE75214) and TNBS-treated mice, we observed increases in PAI-1 transcripts at active fibrotic lesions in both patients with CD and mice with chronic intestinal inflammation. Oral administration of TM5275 immediately after the onset of intestinal fibrosis upregulated MMP-9 (matrix metalloproteinase 9) and decreased collagen accumulation, resulting in attenuation of the fibrogenesis in TNBS-treated mice. Conclusions PAI-1-mediated fibrinolytic system facilitates collagen degradation suppression. Hence, PAI-1 inhibitor could be applied as an anti-fibrotic drug in CD treatment.

　　In recent years, favorable therapeutic outcomes have been reported for arterial injection chemoradiotherapy for tongue cancer. The present case involves an 80-year-old woman in our palliative care department who had high-grade, advanced tongue cancer. Because there was a request for surgery to prevent airway occlusion due to growth of the tumor, she was referred to our department in April 2009. As a treatment policy for controlling tumor growth in high-grade, advanced tongue cancer, arterial injection chemoradiotherapy was carried out through the superficial temporal artery, with a tongue artery catheter in place on both sides. Therapeutic effect was obtained, and it was possible to avoid airway occlusion through tumor regression. Dysphagia and dysphemia were improved, which in turn improved quality of life. In this case, there was an opportunity to carry out multidisciplinary team medicine, including support from the oral care and palliative care teams as part of the process of cancer therapy. Here, we present our findings in this case.

　　Hematopoietic stem cell transplantation (HSCT) involves the administration of anticancer treatment at high doses that exceed the patient’s maximum required dose for total body irradiation, to eliminate malignancy and achieve myeloablation. Hematopoietic stem cells are then transfused to re-establish the lost hematopoietic function. The use of radiation, anticancer drugs, and immunosuppressive drugs can cause adverse events in the oral cavity such as mucositis, bleeding, opportunistic infections, and graft versus host disease. This collaborative report by the departments of hematology and oncology as well as dentistry and oral surgery at our institution discusses the perioperative oral functional management of patients undergoing HSCT. Subjects enrolled were 191 transplantation patients (52 autologous, 139 allogeneic) between 2008 and 2015. The subjects underwent professional tooth cleaning before commencing a transplant conditioning regimen. When the professional oral health care (POHC) treatment was completed, professional tooth cleaning (PTC), professional mechanical tooth cleaning (PMTC), and treatment with a dental drug delivery (3DS) system were provided. This perioperative oral functional management resulted in a decrease in the frequency of oropharyngeal candidiasis from 19.3% to 4.3%. We devised a standardized supportive oral care program from the preoperative period onward to minimize adverse oral events associated with HSCT. The program could effectively improve the quality of life of patients undergoing HSCT.

No abstract available.
Acanthosis Nigricans* ; Hyperandrogenism* ; Insulin Resistance* ; Insulin* ; Proliferating Cell Nuclear Antigen*

No abstract available.
Acanthosis Nigricans* ; Hyperandrogenism* ; Insulin Resistance* ; Insulin* ; Proliferating Cell Nuclear Antigen*

We investigated annual changes with respect to the period taken from the onset of illness to the prescription of lower extremity orthoses in hemiplegic patients after stroke, retrospectively from 1992 to 2007, in an acute phase hospital. We subdivided the initial period into three parts : the period of time from onset to the beginning of rehabilitation (T1), from the beginning of rehabilitation to the beginning of rehabilitation in the training room (T2), and from the beginning of rehabilitation in the training room to prescription (T3). Analysis was made with respect to the relationship between each of the aforementioned periods and the prescription time. Furthermore, we also analyzed the relationship between the length of stay of patients who had been prescribed orthoses, and the prescription time. The prescription time was found to have gradually shortened over time ; moreover, the period in question shortened in a rapid way in 2001, as compared with previous years (p <0.05). T3 showed the highest correlation coefficient (r =0.99), and the length of stay also exhibited a high correlation coefficient (r =0.97). We assume that the annual changes in prescription time might have been due to various underlying factors, namely, social factors, such as a shortening of the length of stay, caused by the differentiation of roles among hospitals, as well as medical factors such as the development of acute phase rehabilitation, or changes in perception of the ways in which orthoses may be used for stroke patients by rehabilitation staff.

The purpose of this study was to investigate heme oxygenase-1 (HO-1) mRNA expression and bilirubin concentration alteration in humans exposed to acute hypoxia. Fourteen healthy adult males were randomly assigned to a sea level group and a hypoxia group, and then exposed to normoxia (400 m, 20.0 %O₂) and hypoxia (3,000 m, 14.5 %O₂) respectively, in a hypoxic chamber for 3 hours. SpO₂ during hypoxia were significantly lower than those at sea level (P＜0.05). Indirect bilirubin levels after hypoxia were significantly higher than those at sea level (P＜0.05). However, HO-1 mRNA expression was unaltered by hypoxia. In conclusion, our data indicate that an acute exposure to hypoxia at resting state for 3 hours might lead to antioxidative cytoprotective response without any increase in HO-1 gene expression.