ABSTRACT
AIM: To identify the relationship between contrast medium extravasation (CME) on dynamic contrast-enhanced computed tomography (DCT) and clinical information in intractable atonic postpartum haemorrhage (PPH) and its relevance to treatment with uterine artery embolisation (UAE). MATERIALS AND METHODS: Of 90 patients who underwent DCT to diagnose PPH, 60 diagnosed with intractable atonic PPH were investigated retrospectively. Maternal background and clinical indicators were analysed to compare the positive and negative factors of early phase CME. Regression analysis was used to investigate the factors associated with CME. The sensitivity, specificity, and positive and negative predictive values of early phase CME for predicting UAE were calculated. Clinical outcomes were compared between the two groups according to the timing of the decision to undergo UAE. RESULTS: Of the 60 patients with intractable atonic PPH, 21 underwent UAE, 20 of whom had early phase CME on DCT. Pre-DCT clinical parameters and clinical indices were not significantly different in presence of early phase CME. Early phase CME was associated with UAE performance, with a sensitivity of 95%, specificity of 87%, positive predictive value of 80%, and negative predictive value of 97%. In cases where UAE was performed after conservative management, there was a significant increase in blood loss and transfusion volume. CONCLUSION: Early phase CME is not indicated by background factors or clinical findings. UAE is not required when CME cannot be detected in the uterine cavity. If early phase CME is present, UAE should be considered immediately.
Subject(s)
Postpartum Hemorrhage , Uterine Artery Embolization , Female , Humans , Postpartum Hemorrhage/diagnostic imaging , Postpartum Hemorrhage/therapy , Retrospective Studies , Extravasation of Diagnostic and Therapeutic Materials/diagnostic imaging , Uterus , Uterine Artery Embolization/methods , Tomography, X-Ray ComputedABSTRACT
BACKGROUND: Atrial fibrillation is common after oesophageal surgery. The aim of this study was to evaluate whether landiolol hydrochloride was effective and safe in the prevention of atrial fibrillation after oesophagectomy, and to see whether a reduction in incidence of atrial fibrillation would reduce other postoperative complications. METHODS: This single-centre study enrolled patients scheduled for transthoracic oesophagectomy in a randomized, double-blind, placebo-controlled trial between March 2013 and January 2016. Enrolled patients were randomized with a 1 : 1 parallel allocation ratio to either landiolol prophylaxis or placebo. The primary endpoint was the occurrence of atrial fibrillation after oesophagectomy. Secondary endpoints were incidence of postoperative complications, and effects on haemodynamic and inflammatory indices. RESULTS: One hundred patients were enrolled, 50 in each group. Postoperative atrial fibrillation occurred in 15 patients (30 per cent) receiving placebo versus five (10 per cent) receiving landiolol (P = 0·012). The overall incidence of postoperative complications was significantly lower in the landiolol group (P = 0·046). In the landiolol group, postoperative heart rate was suppressed effectively, but the decrease in BP was not harmful. The interleukin 6 level was significantly lower on days 3 and 5 after surgery in the landiolol group (P = 0·001 and P = 0·002 respectively). CONCLUSION: Landiolol was effective and safe in preventing atrial fibrillation after oesophagectomy. Registration number: UMIN000010648 (http://www.umin.ac.jp/ctr/).
Subject(s)
Anti-Arrhythmia Agents/therapeutic use , Atrial Fibrillation/prevention & control , Esophagectomy/adverse effects , Morpholines/therapeutic use , Urea/analogs & derivatives , Adenocarcinoma/surgery , Aged , Aged, 80 and over , Carcinoma, Squamous Cell/surgery , Double-Blind Method , Esophageal Neoplasms/surgery , Female , Humans , Male , Middle Aged , Postoperative Complications/etiology , Treatment Outcome , Urea/therapeutic useABSTRACT
Squamous cell carcinoma of the esophagus (SCCE) has a poor prognosis compared with other gastrointestinal cancers. Many patients present with locoregional unresectable or metastatic disease at the time of diagnosis. For these patients with metastatic esophageal cancer, chemotherapy is generally indicated. The aim of this phase I/II study was to evaluate the efficacy and safety of the combined use of docetaxel, cisplatin (CDDP) and 5-fluorouracil (5-FU)(DCF) in patients with recurrent/metastatic SCCE. This study adopted divided doses of docetaxel and CDDP in order to reduce the toxicities of the treatment. The dose of docetaxel was escalated using the following protocol in the phase I stage: level 1, 30 mg/m2; level 2, 35 mg/m2 and level 3, 40 mg/m2, which was intravenously infused for 2 hours on days 1 and 8. CDDP was administered at a dose of 12 mg/m2 infused for 4 hours on days 1-5. The 5-FU was administered at a dose of 600 mg/m2 continuously infused from day 1 to 5. This regimen was repeated every 4 weeks. The study subjects were nine patients (phase I) and 48 patients (phase II). The recommended dose was determined as level 3 in phase I. In the phase II stage, the overall response rate was 62.5%, with a complete response rate of 12.5%. The median progression-free survival was 6 months, and the median overall survival was 13 months. Grade 3/4 toxicities of leukopenia, neutropenia and febrile neutropenia occurred in 64.6%, 68.8% and 14.6% of the patients, while grade 3/4 non-hematological toxicities were relatively rare. No treatment-related death was recorded. This modified DCF regimen with divided doses can be a tolerable and useful regimen of definitive chemotherapy for unresectable SCCE because of its high efficacy, although adequate care for severe neutropenia must be administered.
Subject(s)
Antineoplastic Combined Chemotherapy Protocols/administration & dosage , Carcinoma, Squamous Cell/drug therapy , Cisplatin/administration & dosage , Esophageal Neoplasms/drug therapy , Fluorouracil/administration & dosage , Taxoids/administration & dosage , Aged , Aged, 80 and over , Antineoplastic Combined Chemotherapy Protocols/adverse effects , Carcinoma, Squamous Cell/pathology , Cisplatin/adverse effects , Disease-Free Survival , Docetaxel , Drug Administration Schedule , Esophageal Neoplasms/pathology , Esophageal Squamous Cell Carcinoma , Esophagus/pathology , Fluorouracil/adverse effects , Humans , Male , Middle Aged , Neoplasm Recurrence, Local/drug therapy , Neoplasm Recurrence, Local/pathology , Neutropenia/chemically induced , Research Design , Taxoids/adverse effects , Treatment OutcomeABSTRACT
Atheoretical formulation of diffuse photon-density waves propagating in a waveguide structure, which consists of two regions with different wave speeds, is presented. In comparison with the usual optical waveguides for coherent radiation, unique features of the guided photon-density waves are found.
ABSTRACT
We show analytically that, at a critical point where the effective refractive index of a mode coincides with the bulk index of a substrate region, for certain graded-index planar waveguides there exists a family of bound modes with algebraic (power-law) tails in the evanescent field.
ABSTRACT
Corticotropin-releasing factor (CRF) increased intracellular Ca2+ concentration in single astrocytes. The effect in increasing intracellular Ca2+ was not observed in Ca2(+)-free solution. Furthermore, CRF at concentrations more than 10 nM stimulated 45Ca2+ uptake in cultured rat astrocytes. The action was blocked by alpha-helical CRF(9-41) in a competitive manner, but not by nifedipine and 3,4-dichlorobenzamil. On the other hand, CRF did not stimulate cAMP formation, cGMP formation and phosphoinositide hydrolysis in astrocytes. These results indicate that CRF increases Ca2+ influx via an activation of CRF receptors in a cAMP-independent mechanism in cultured astrocytes.
Subject(s)
Astrocytes/metabolism , Calcium/metabolism , Cerebral Cortex/metabolism , Corticotropin-Releasing Hormone/pharmacology , 1-Methyl-3-isobutylxanthine/pharmacology , Amiloride/pharmacology , Animals , Animals, Newborn , Astrocytes/drug effects , Cells, Cultured , Cyclic AMP/metabolism , Cyclic GMP/metabolism , Kinetics , Nifedipine/pharmacology , Phosphatidylinositols/metabolism , Rats , Rats, Sprague-Dawley , Time FactorsABSTRACT
We show numerically that, contrary to what has been believed so far, multidimensional optical solitons can propagate in cubic nonlinear media. To avoid a collapse along the propagation axis, we take advantage of the cross-phase modulations between fundamental- and harmonic-field components. A compact analytical expression for new solitonlike fields with an arbitrary transverse dimension is derived through a self-consistent-field approximation.
ABSTRACT
Effect of endothelin-3 (ET-3) on dibutyryl cAMP (DBcAMP)-induced stellation of rat cerebral cultured astrocytes was examined. Treatment with 1 mM DBcAMP, 10 microM forskolin, 100 microM isoproterenol and 500 nM phorbol 12-myristate 13-acetate changed protoplasmic cultured astrocytes into process-bearing ones. ET-3 (1 nM) completely prevented the astrocytic stellation induced by these agents. The effect of ET-3 showed a dose-dependence, where IC50 value and maximal effective dose were 49 pM and about 0.1 nM, respectively. ET-1 and sarafotoxin (SRTX) S6b prevented the DBcAMP-induced astrocytic stellation with potencies similar to that of ET-3. ET-3 (1 nM) did not affect the cAMP accumulation after DBcAMP treatment in cultured astrocytes. Stellate astrocytes were reversed to the protoplasmic type cells by addition of 1 nM ET-3 in the presence of DBcAMP. ET-1 and SRTX similarly reversed the astrocytic stellation. ET-3 reversed the astrocytic stellation in the absence of extracellular Ca2+. Pre-loading of BAPTA-AM, a permeable Ca2+ chelator, on stellate astrocytes had no effect on the reversal by ET-3. ET-3 did not increase intracellular free Ca2+ concentration ([Ca2+]i) of most astrocytes tested at 0.1 nM. A high concentration (100 nM) of ET-3 increased astrocytic [Ca2+]i which was negated by Ca(2+)-free and BAPTA-AM loading. These results suggest that ETs modulate morphological changes in astrocytes through cAMP- and Ca(2+)-independent mechanisms.