Guidewire-catheter induced hydrodissection to assist radiofrequency ablation for subcapsular hepatocellular carcinoma with iodized oil retention in patients with failed artificial ascites due to perihepatic adhesion

PURPOSEWe aimed to evaluate the usefulness of guidewire-catheter induced hydrodissection (GIH) to assist radiofrequency ablation (RFA) for subcapsular hepatocellular carcinoma (HCC) with iodized oil retention in patients with failed artificial ascites due to perihepatic adhesion.METHODSThis retrospective study included 17 patients with small subcapsular HCC ineligible for ultrasonography-guided RFA who received RFA under guidance of fluoroscopy and cone-beam computed tomography immediately after iodized oil transarterial chemoembolization (TACE) between April 2011 and January 2016. In the study patients, creation of artificial ascites to protect the perihepatic structures failed due to perihepatic adhesion and GIH was attempted to separate the perihepatic structures from the ablation zone. The technical success rate of GIH, technique efficacy of RFA with GIH, local tumor progression (LTP), peritoneal seeding, and complications were evaluated.RESULTSThe technical success rate of GIH was 88.24% (15 of 17 patients). Technique efficacy was achieved in all 15 patients receiving RFA with GIH. During an average follow-up period of 48.1 months, LTP developed in three patients. Cumulative LTP rates at 1, 2, 3, and 5 years were 13.3%, 20.6%, 20.6%, and 20.6%, respectively. No patient had peritoneal seeding. Two of the 15 patients receiving RFA with GIH had a CIRSE grade 3 liver abscess, but none had complications associated with thermal injury to the diaphragm or abdominal wall near the ablation zone.CONCLUSIONGIH can be a useful method to assist RFA for subcapsular HCC with iodized oil retention in patients with failed artificial ascites due to perihepatic adhesion

Decreased Angiotensin II -Stimulated Aldosterone Production, but Normal Inositol Phosphate Response in Adrenal Glomerulosa Cells from Streptozotocin-Induced Diabetic Rats: Role of lnsulin

Streptozotocin(SlZ)-induced diabetic rats develop hyporeninemic hypoaldosteronism during the progression of diabetes mellitus. However,the nature and mechanism of aldosterone deficiency in diabetic rats still remain unclear and acute effects of insulin on aldosterone production in-vitro are not known. We evaluated the responses of aldosterone production to angiotensin 11 (AlI), potassium (K+), AClH and insulin in adrenal glomerulosa cells prepared from SlZ-induced diabetic rats with and without insulin treatment 2 weeks after diabetes induction. We also measured inositol phosphate<IP) levels in All-stimulated glomerulosa cells labeled with [3HI myoinositol using standardized anion exchange chromatography. Plasma renin activity and aldosterone level were not different among control rats,untreated and insulin-treated diabetic rats. Basal aldosterone production was similar in cells from the three groups. Cells from untreated diabetic rats showed a significant decrease in the maximal All (to-8M)-stimuiated aldosterone production and a tendency to be low in the maximal K+(8.7 mM)-stimulated aldosterone production, compared with control rats (3.2±2.2 \IS 7.7±2.4, P (0.05 and 4.8±1.8 \IS 8.0±3.2 ng/105 cells/hr, 0.05 (P (0.1, respectively). In contrast, there were no differences in All- and K+-stimulated aldosterone production between control and insulin-treated diabetic rats. AClH (to-8M), however, caused a similar effect on aldosterone production and insulin (I mU /ml for 1 hour) did not alter either basal or agonists-stimulated aldosterone production in cells from the three groups. All (to-8M)-induced IP formation among the three groups was similar and did not change with the addition of insulin u mU / ml), These results indicate that reduced response to All in the early phase of SlZ-induced diabetes in rats may be due to the zona glomerulosa dysfunction secondary to chronic lack of insulin and the main defect responsible for altered All effects may be located at some step(s) mediating All action downstream from IP formation

Recessive C10orf2 mutations in a family with infantile-onset spinocerebellar ataxia, sensorimotor polyneuropathy, and myopathy

Recessive mutations in chromosome 10 open reading frame 2 (C10orf2) are relevant in infantile-onset spinocerebellar ataxia (IOSCA). In this study, we investigated the causative mutation in a Korean family with combined phenotypes of IOSCA, sensorimotor polyneuropathy, and myopathy. We investigated recessive mutations in a Korean family with two individuals affected by IOSCA. Causative mutations were investigated using whole exome sequencing. Electrophysiological analyses and muscle and nerve biopsies were performed, along with magnetic resonance imaging (MRI) of the brain and lower extremities. Compound heterozygous mutations c.1460C>T and c.1485-1G>A in C10orf2 were identified as causative of IOSCA. Skeletal muscle showed mitochondrial DNA (mtDNA) deletions. Both patients showed a period of normal development until 12–15 months, followed by ataxia, athetosis, hearing loss, and intellectual disability. Electrophysiological findings indicated motor and sensory polyneuropathies. Muscle biopsy revealed variations in the size and shape of myofibers with scattered, small, and angulated degenerating myofibers containing abnormal mitochondria; these observations are consistent with myopathy and may be the result of mtDNA deletions. Sural nerve biopsy revealed an axonal neuropathy. High-signal-intensity lesions in the middle cerebellar peduncles were correlated with clinical severity, and MRI of the lower legs was compatible with the hypothesis of length-dependent axonal degeneration. We identified novel compound heterozygous mutations of the C10orf2 gene as the cause of IOSCA with sensorimotor polyneuropathy and myopathy. Signs of motor neuropathy and myopathy were discovered for the first time in IOSCA patients with C10orf2 mutations. These results suggest that the clinical spectrum of IOSCA caused by C10orf2 mutations may be more variable than previously reported. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10048-014-0405-1) contains supplementary material, which is available to authorized users

Extraarticular Subtalar Arthrodesis for Pes Planovalgus: An Interim Result of 50 Feet in Patients with Spastic Diplegia

BACKGROUND: There are no reports of the pressure changes across the foot after extraarticular subtalar arthrodesis for a planovalgus foot deformity in cerebral palsy. This paper reviews our results of extraarticular subtalar arthrodesis using a cannulated screw and cancellous bone graft. METHODS: Fifty planovalgus feet in 30 patients with spastic diplegia were included. The mean age at the time of surgery was 9 years, and the mean follow-up period was 3 years. The radiographic, gait, and dynamic foot pressure changes after surgery were investigated. RESULTS: All patients showed union and no recurrence of the deformity. Correction of the abduction of the forefoot, subluxation of the talonavicular joint, and the hindfoot valgus was confirmed radiographically. However, the calcaneal pitch was not improved significantly after surgery. Peak dorsiflexion of the ankle during the stance phase was increased after surgery, and the peak plantarflexion at push off was decreased. The peak ankle plantar flexion moment and power were also decreased. Postoperative elevation of the medial longitudinal arch was expressed as a decreased relative vertical impulse of the medial midfoot and an increased relative vertical impulse (RVI) of the lateral midfoot. However, the lower than normal RVI of the 1st and 2nd metatarsal head after surgery suggested uncorrected forefoot supination. The anteroposterior and lateral paths of the center of pressure were improved postoperatively. CONCLUSIONS: Our experience suggests that the index operation reliably corrects the hindfoot valgus in patients with spastic diplegia. Although the operation corrects the plantar flexion of the talus, it does not necessarily correct the plantarflexed calcaneus and forefoot supination. However, these findings are short-term and longer term observations will be needed.ope

Insulin Level, RBC Na+ Transport and Blood Pressure in Cushing's Syndrome

To test the hypothesis that hyperinsulinemia and / or abnormalities of RBC Na+ transport are concerned in the pathogenesis of hypertension in Cushing's syndrome, we 'investigated the relationship between insulin level, RBC Na + transport and blood pressure in patients with Cushing's syndrome which is frequently associated with hyperinsulinemia, abnormalities of RBC Na + transport and hypertension. Both systolic and diastolic pressure were significantly higher in Cushing's syndrome than in normal subjects. Fasting serum insulin level was higher and both serum glucose and insulin responses after a 75g glucose load were significantly increased in patients with Cushing's syndrome as compared with normal subjects. Both RBC Na+ concentration and passive Na + permeability were significantly lower but Vmax of Na +, K+-pump was significantly higher in patients with Cushing's syndrome than in normal subjects, while Vmaxs of Na+-K+ cotransport and Na+-Li + countertransport were similar in the two groups. In multiple stepwise regression analysis for patients with Cushing's syndrome, fasting serum insulin level was directly correlated with both systolic and diastolic pressures (r=O. 52, p=O. 01; r=O. 51, p=O. 02, respectively). On the other hand,RBC Na + transport parameters showed little correlation with either systolic or diastolic pressures. These results suggest that hyperinsulinemia may contribute to the hypertension in Cushing's syndrome, but that the abnormalities of RBC Na + transport seen in Cushing's syndrome are not causally related to hypertension

Cystatin C as an Early Biomarker of Nephropathy in Patients with Type 2 Diabetes

This study was done to evaluate clinical usefulness of cystatin C levels of serum and urine in predicting renal impairment in normoalbuminuric patients with type 2 diabetes and to evaluate the association between albuminuria and serum/urine cystatin C. Type 2 diabetic patients (n = 332) with normoalbuminuria (n = 210), microalbuminuria (n = 83) and macroalbuminuria (n = 42) were enrolled. Creatinine, urinary albumin levels, serum/urine cystatin C and estimated glomerular filtration rate (eGFR by MDRD [Modification of Diet in Renal Disease] and CKD-EPI [Chronic Kidney Disease Epidemiology Collaboration] equations) were determined. The cystatin C levels of serum and urine increased with increasing degree of albuminuria, reaching higher levels in macroalbuminuric patients (P < 0.001). In multiple regression analysis, serum cystatin C was affected by C-reactive protein (CRP), sex, albumin-creatinine ratio (ACR) and eGFR. Urine cystatin C was affected by triglyceride, age, eGFR and ACR. In multivariate logistic analysis, cystatin C levels of serum and urine were identified as independent factors associated with eGFR < 60 mL/min/1.73 m2 estimated by MDRD equation in patients with normoalbuminuria. On the other hand, eGFR < 60 mL/min/1.73 m2 estimated by CKD-EPI equation was independently associated with low level of high-density lipoprotein in normoalbuminuric patients. The cystatin C levels of serum and urine could be useful markers for renal dysfunction in type 2 diabetic patients with normoalbuminuria