The management of local and global power deposition in human subjects (Specific Absorption Rate, SAR) is a fundamental constraint to the application of parallel transmission (pTx) systems. Even though the pTx and single channel have to meet the same SAR requirements, the complex behavior of the spatial distribution of local SAR for transmission arrays poses problems that are not encountered in conventional single-channel systems and places additional requirements on pTx RF pulse design. We propose a pTx pulse design method which builds on recent work to capture the spatial distribution of local SAR in numerical tissue models in a compressed parameterization in order to incorporate local SAR constraints within computation times that accommodate pTx pulse design during an in vivo MRI scan. Additionally, the algorithm yields a Protocol-specific Ultimate Peak in Local SAR (PUPiL SAR), which is shown to bound the achievable peak local SAR for a given excitation profile fidelity. The performance of the approach was demonstrated using a numerical human head model and a 7T eight-channel transmit array. The method reduced peak local 10g SAR by 14–66% for slice-selective pTx excitations and 2D selective pTx excitations compared to a pTx pulse design constrained only by global SAR. The primary tradeoff incurred for reducing peak local SAR was an increase in global SAR, up to 34% for the evaluated examples, which is favorable in cases where local SAR constraints dominate the pulse applications.
This study shows that conductivity mapping of breast cancers is feasible using a noninvasive in vivo MREPT technique combined with a coil combination process. The method may provide a tool in the MR diagnosis of breast cancer.
Nasal-type NK/T cell lymphoma is an increasingly recognised disease entity of aggressive clinical behaviour. The objective of this study was to investigate clinical features and treatment outcomes in patients with nasal-type NK/T cell lymphoma. From January 1991 to December 2003, 26 patients diagnosed as nasal-type NK/T cell lymphoma were included in the analysis. One half of patients presented with poor performance status (ECOG X2); 46% of patients were categorised as high intermediate or high-risk group according to IPI; and 46% of patients were diagnosed at advanced stage. The median survival for 26 patients with nasal-type NK/T cell lymphoma was 7.4 months (95% CI, 0.1, 16.9). The treatment outcome of primary anthracycline-based chemotherapy was poor: 60% CR rate in localised disease and 0% CR rate in advanced disease. After a median follow-up of 24.4 months (range 3.1 -99.0) in patients with localised disease who had achieved a CR (range 29.6 -165.7), three patients (50.0%) developed disease recurrence at 6.1, 21.8, and 52.1 months, respectively, and all patients presented with locoregional failure. The predictive factors for poor survival were of age greater than 60, advanced stage and poor performance in multivariate analysis. In conclusion, Nasal-type NK/T cell lymphomas showed a poor response to the conventional anthracycline-based chemotherapy, and thus an investigation for an innovative therapy is urgently needed to improve survival in these patients.
Background:Docetaxel is widely used as a chemotherapeutic agent for gastric cancer treatment. A
combined regimen with sunitinib demonstrated a synergistic antitumour effect in a
preclinical model. The aim of this study was to evaluate the efficacy and safety of this
combination in patients with unresectable or metastatic advanced gastric cancer
following failure of treatment with a fluoropyrimidine and platinum combination.Methods:This open-label, phase II, randomised trial enrolled patients with unresectable or
metastatic gastric cancer. Patients were assigned to either a docetaxel monotherapy arm
(D only arm: 60 mg m−2, every 3 weeks) or a combination
arm (DS arm: docetaxel+sunitinib 37.5 mg every day). The primary end point
of the study was time to progression and the secondary end points were overall response
rate, disease control rate, overall survival, and toxicity profile. A pharmacokinetic
study was also performed.Results:A total of 107 patients were entered into the study. The TTP was not significantly
prolonged in the DS arm when compared with the D only arm (DS vs D only arm:
3.9 months (95% confidence interval (CI) 2.9–4.9) vs 2.6 months
(95% CI 1.8–3.5) (P=0.206). The hazard ratio for TTP was
0.77 (95% CI 0.52–1.16). However, the objective response rate was
significantly higher in the DS arm (41.1% vs 14.3%,
P=0.002). Patients in the DS arm experienced stomatitis, diarrhoea, and
hand–foot syndrome more frequently.Conclusion:The addition of sunitinib to docetaxel did not significantly prolong TTP, although it
significantly increased response.
Background:Statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, are commonly prescribed because of their therapeutic and preventive effects on cardiovascular diseases. Even though they have been occasionally reported to have antitumour activity, it is unknown whether statins have anti-angiogenic effect in human colorectal cancer (CRC).Methods:A total of 11 human CRC cell lines were used to test the effects of bevacizumab, statins, and bevacizumab plus statins on human umbilical vein endothelial cell (HUVEC) viability and invasion in vitro. To determine the molecular mechanism of statins as anti-angiogenic agents, we performed an angiogenesis antibody array and proteomics analysis and confirmed the results using immunoblot assay, HUVEC invasion rescue assay, and siRNA assay. The antitumoural effects of bevacizumab and statins were evaluated in xenograft models.Results:A conventional dose of statins (simvastatin 0.2 μM, lovastatin 0.4 μM, atorvastatin 0.1 μM, and pravastatin 0.4 μM) in combination with bevacizumab directly reduced the cell viability, migration, invasion, and tube formation of HUVECs. The culture media of the CRC cells treated with bevacizumab or statins were also found to inhibit HUVEC invasion by suppressing angiogenic mediators, such as angiopoietin2, binding immunoglobulin protein (BiP), and Hsp90α. The combined treatment with bevacizumab and simvastatin significantly reduced the growth and metastases of xenograft tumours compared with treatment with bevacizumab alone.Conclusions:The addition of simvastatin at a dose used in patients with cardiovascular diseases (40–80 mg once daily) may potentiate the anti-angiogenic effects of bevacizumab on CRC by suppressing angiopoietin2, BiP, and Hsp90α in cancer cells. A clinical trial of simvastatin in combination with bevacizumab in patients with CRC is needed.
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