We evaluated the clinical effects of acupuncture/moxibustion therapy in 7 patients with vertigo that was uncontrollable with western medicine. The observation period was 6-15 months. The 7 patients consisted of 1 male and 6 females aged 29-73 years (mean, 44.7 years). More than 4 courses or more of acupuncture/moxibustion treatment (acupuncture + warm moxibustion) were performed in each patient, and the effects were evaluated based on the results of a daily living disability questionnaire before and after treatment. In practice, these effects were classified into 4 grades (cure, improvement, no change, aggravation). Cure was observed in1patient, improvement in 5 patients, and no change in1patient, indicating this therapy was effective in 85% of the patients. None of the patients showed aggravation of their condition. In addition, no adverse effects were observed.Our results suggest that acupuncture/moxibustion therapy has certain effects on intractable vertigo. Therefore, in patients with vertigo who do not respond to western medical care, such as the administration of anti-vertigo drugs, a beneficial effect of acupuncture/moxibustion as a complementary therapy can be expected.
Acupuncture ; Therapeutic procedure ; Vertigo ; Patients ; Effective

BACKGROUND/AIMS: The aim of this study was to determine the pharmacodynamics of cisplatin following three different treatment procedures for intrahepatic arterial infusion therapy for hepatocellular carcinoma (HCC). METHODS: We divided 13 HCC patients into the following three groups: group A, lone injection of cisplatin (n=3); group B, combined injection of cisplatin and lipiodol, with embolization using small gelatin cubes (GCs) (n=5); and group C, injection of suspended lipiodol with cisplatin powder, with embolization using small GCs (n=5). In each group, the free cisplatin concentration in the hepatic vein was measured at 0, 5, 10, and 30 minutes. RESULTS: The mean free cisplatin concentrations were as follows. For group A, the mean was 48.58 microg/mL at 0 minute, 7.31 microg/mL at 5 minutes, 5.70 microg/mL at 10 minutes, and 7.15 microg/mL at 30 minutes. For the same time points, for group B, the concentrations were 8.66, 4.23, 3.22, and 1.65 microg/mL, respectively, and for group C, the concentrations were 4.81, 2.61, 2.52, and 1.75 microg/mL, respectively. The mean area under the curve (AUC)0-infinity for the free cisplatin concentration was 7.80 in group A, 2.48 in group B, and 2.27 in group C. The AUC0-infinity for the free cisplatin concentration gradually decreased, from group A to group C. CONCLUSIONS: These results indicate that the combination of lipiodol and small GCs may be useful for delaying cisplatin drainage from the liver.
Carcinoma, Hepatocellular ; Cisplatin ; Drainage ; Drug Delivery Systems ; Ethiodized Oil ; Gelatin ; Hepatic Veins ; Humans ; Liver ; Pilot Projects

BACKGROUND/AIMS: It is important to determine the noninvasive parameters of histological features in nonalcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the value of genetic variations as surrogate markers of histological features. METHODS: The parameters that affected the histological features of NAFLD were investigated in 211 Japanese patients with biopsy-proven NAFLD. The relationships between genetic variations in PNPLA3 rs738409 or TM6SF2 rs58542926 and histological features were analyzed. Furthermore, the impact of genetic variations that affected the pathological criteria for the diagnosis of nonalcoholic steatohepatitis (NASH) (Matteoni classification and NAFLD activity score) was evaluated. RESULTS: The fibrosis stage of PNPLA3 GG was significantly more progressive than that of CG by multiple comparisons. Multivariate analysis identified PNPLA3 genotypes as predictors of fibrosis of stage 2 or more, but the impact tended to decrease at stage 3 or greater. There were no significant differences among the histological features of the three genotypes of TM6SF2. PNPLA3 genotypes partly affected the definition of NASH by the NAFLD activity score, but TM6SF2 genotypes did not affect the definition of NASH. CONCLUSIONS: In Japanese patients with biopsy-proven NAFLD, PNPLA3 genotypes may partly affect histological features, including stage of fibrosis, but the TM6SF2 genotype does not affect histological features.
Asian Continental Ancestry Group ; Biological Markers ; Classification ; Diagnosis ; Fatty Liver* ; Fibrosis ; Genetic Variation* ; Genotype ; Humans ; Japan* ; Multivariate Analysis

Miriplatin is a novel lipophilic platinum complex that was developed to treat hepatocellular carcinoma (HCC). Although HCC patients frequently have coexisting chronic renal failure, little prospective data are available regarding the clinical toxicity of chemotherapeutic agents used to treat HCC patients with chronic renal failure. In a phase II study, the plasma concentration of total platinum in patients who received miriplatin was very low, and no severe renal toxicity caused by miriplatin injection was reported. Here, we present three cases of HCC with stage 4 chronic renal failure who received transcatheter arterial chemotherapy with miriplatin. All cases were male, ages 72, 84, and 83 years, and had serum creatinine levels of 2.3, 1.6, and 1.9 mg/dL, respectively. Their estimated glomerular filtration rates were 21.9, 20.3, and 22.2 mL/min, respectively. All cases were treated for unresectable HCC with transcatheter arterial chemotherapy with miriplatin. No serious adverse events were observed, and serum creatinine levels did not elevate, even in the patient who experienced renal failure caused by cisplatin administration. These results might suggest that transcatheter arterial chemotherapy with miriplatin can be safely used in HCC patients with chronic renal failure.
Carcinoma, Hepatocellular ; Cisplatin ; Creatinine ; Glomerular Filtration Rate ; Humans ; Kidney Failure, Chronic ; Male ; Organoplatinum Compounds ; Plasma ; Platinum ; Renal Insufficiency

 Waon therapy uses a far infrared-ray dry sauna, which is evenly maintained at 60°C and differs from the traditional sauna. The patients were placed in a 60°C sauna system for 15 minutes, in which the deep-body temperature has increased by 1.0 to 1.2°C. Then, after leaving the sauna, they underwent bed rest with a blanket to keep them warm for an additional 30 minutes. All patients were weighed before and after the therapy, and they drank some water at the end of Waon therapy to compensate for weight lost due to perspiration and prevent the dehydration.  We have previously reported that Waon therapy improves the cardiac and vascular endothelial function in patients with chronic heart failure (CHF) and the limb ischemia and symptoms in patients with arteriosclerosis obliterans (ASO). As underlying molecular mechanisms, we demonstrated that Waon therapy upregulates nitric oxide (NO) and endothelial NO synthase (eNOS), which would improve vascular endothelial and cardiac function in TO-2 cardiomyopathic hamsters and augment ischemia-induced angiogenesis. In order to investigate the mechanism of Waon therapy, we examined the effect of Waon therapy on heat shock proteins (Hsp) in failed myocardium and ischemic limb. Hsp are stress response proteins that can be induced by stress signals, including thermal stimulation. Hsp function as chaperones to assist with protein folding in order to protect cells from protein denaturation or cell death under stress conditions.  In TO-2 cardiomyopathic hamsters, the cardiac expression of 4-hydroxy-2-nonenal (4HNE), a marker of oxidative stress, was decreased in the 4-week Waon therapy compared to untreated hamsters. Also, the cardiac expressions of Hsp 27, Hsp 32 and manganese superoxide dismutase (Mn-SOD), which reduce oxidative stress, were significantly upregulated by the 4-week Waon therapy compared to untreated hamsters. In addition, Waon therapy upregulated Hsp90, which contributes to the activation of the AkteNOSNO pathway, and induced angiogenesis in mice with hindlimb ischemia. However, Waon therapy did not increase the expression of Hsp70, Hsp60, Hsp32 and Hsp27 in the same model mice. The thermal stimulation with Waon therapy upregulated specific Hsp isoforms depending on different organs and diseases. The specific function of Hsp induced by Waon therapy is suggested to play an important role in improving cardiovascular diseases.

Introduction: Long-term cardiac hypertrophy causes heart failure. One of the mechanisms of this transition from hypertrophy to heart failure is collapse of hypoxic response and angiogenesis. Heat shock protein 27 (HSP27) was found to act as an anti-apoptotic protein and its phosphorylation is responsible for the protection of cells against heat stress. HSP27 has been reported to regulate p53 expression, which contributes to down-regulate angiogenic factors through hypoxia inducible factor-1α(HIF-1α). We have reported that thermal therapy, namely Waon therapy, improves cardiac and vascular function in patients with chronic heart failure. However, the effect of this therapy on cardiac hypertrophy due to pressure overload is unknown. The purpose of this study is to investigate the effects and mechanisms of thermal therapy (Waon therapy) on the transition from cardiac hypertrophy to heart failure after pressure overload. Methods: Cardiac hypertrophy was induced by transverse aortic constriction (TAC) in C57BL/6 mice. At 2 weeks after TAC, all mice were examined by echocardiography and showed left ventricular hypertrophy. Then, mice were randomly divided into thermal therapy or untreated group. Thermal therapy group received thermal therapy using an experimental far infrared ray dry sauna, which elevates the core temperature by 1 degree Celsius for 30 minutes, daily for 4 weeks. Sham operated mice were used as control. At 6 weeks after TAC, we measured body weight, heart rate and blood pressure before sacrifice, and eviscerated heart and leg muscle. Western blot analysis of p53, phosphorylated HSP27, HIF-1α and vascular endothelial growth factor (VEGF) was performed using extracted protein form heart. Results: At 6 weeks after TAC, body weight, heart rate and blood pressure did not differ in three groups. Echocardiography showed that left ventricular fractional shortening of thermal therapy group was significantly larger than that of untreated group (Sham vs. Untreated vs. Thermal; 50.0±1.7 vs. 36.7±1.3 vs. 46.2±0.5, P<0.01, n=6 each). Heart weight/tibia length ratio of thermal therapy group was significantly smaller than that of untreated group (6.7±0.1 vs. 9.7±0.5 vs. 7.9±0.2, P<0.01, n=9 each). Western blot showed that thermal therapy increased phosphorylation of HSP27 and reduced p53. Thermal therapy also increased HIF-1α and VEGF at 6 weeks after TAC. Capillary/myofiber ratio was larger in thermal therapy group than that in untreated group (1.71±0.05 vs. 2.04±0.04 vs. 2.41±0.10, P<0.01, n=4 each). Conclusion: Thermal therapy, namely Waon therapy, prevented the transition from cardiac hypertrophy to heart failure induced by pressure overload in mice. As the mechanism, thermal therapy amplified the phosphorylation of HSP27 and inhibited p53, increased HIF-1α and VEGF, and then increased angiogenesis.