Growth of quasi-1 dimensional (Bi1-xSbx)2S3nanowires on fluorine-doped tin oxide glass substrate by vapor transport.

(Bi1-xSbx)2S3solid solution nanowires (0≤x≤0.73) are grown on fluorine-doped tin oxide (FTO) glass via physical vapor transport. The compositions were controlled by varying the Sb2S3source temperature (300 °C-453 °C) by changing the upstream locations of the Sb2S3source in the furnace while keeping the Bi2S3source at the center of the furnace (497 °C). Defect-free nanowires with phase-pure orthorhombic and quasi-1 dimensional crystal structures were grown under a modified vapor-solid mechanism affected by FTO at initial growth stage. The aspect ratios of the nanowires reached the minimum at compositionx∼0.6.As the Sb2S3source approached the Bi2S3source,xincreased owing to the increase in the Sb2S3source temperature.x/(1-x), which is proportional to the evaporation flux of the Sb2S3source, could be well-fitted with a thermally activated equation with an apparent activation energy (105kJmol-1). However, at the distance between the Sb2S3and Bi2S3sources, with the Sb2S3source at temperatures higher than 410 °C, the compositions reduced despite the increased Sb2S3evaporation flux. Such retrograde behavior was confirmed by high-resolution transmission electron microscopy, x-ray diffraction, and micro-Raman studies. This retrograde behavior is ascribed to the loss due to the reaction of gaseous Sb species with the Bi2S3source.

Radiation therapy and immunotherapy-a potential combination in cancer treatment.

Background: Radiation therapy (rt) is a longstanding treatment modality for cancer. In addition, immune checkpoint blockade has been a significant development in the field of immunotherapy, modifying key immunosuppressive pathways of cancer cells. Methods: The aim of the present work was to review current concepts of rt and immunotherapy synergism, the abscopal effect, and the molecular effects of rt in the tumour microenvironment, its influence on immune stimulation, and potential clinical outcomes that might evolve from ongoing studies. We also discuss potential predictors of clinical response. Results: Up-to-date literature concerning the mechanisms, interactions, and latest knowledge about rt and immunotherapy was reviewed and summarized, and is presented here. Conclusions: The possibility of using hyperfractionated rt to combine an abscopal effect with the enhanced effect of immune treatment using checkpoint blockade is a very promising method for future tumour treatments.

Time dependent protection of amifostine from renal and hematopoietic cisplatin induced toxicity.

Efficacy of chemotherapy may be maximized and its toxicity can be minimized if drugs would be administered at specified daily times. The present study was aimed to examine if the protection of amifostine against cisplatin toxicity is time dependent. Amifostine is an organic thiophosphate that protects selectively normal tissues, but not tumors, against the cytotoxicity of DNA binding chemotherapeutic agents such as cisplatin. ICR male mice which were entrained to Light:Dark (L:D) 14:10 were injected (intrapritoneal bolus) for 5 consecutive days with either: cisplatin, cisplatin plus amifostine (administered 30 minutes prior to cisplatin). Injections were given at either 08:00, 13:00, 20:00 or 01:00. Five days later, on day 10, each set of mice was sacrificed (at the same hour corresponds to the injection hour), blood count, blood creatinine and blood urea nitrogen (BUN) were assayed. Cisplatin treated mice exhibited nephrotoxicity, as indicated by increased blood urea nitrogen values and by high blood urea nitrogen to creatinine ratios, as well as myelotoxicity that was indicated by low levels of hemoglobin and platelets. Co-administration of amifostine-cisplatin reversed both, the nephrotoxicity of cisplatin, and its myelosuppressive effects. For BUN, hemoglobin and platelets, maximal protections were observed at 08:00, (p <0.05, p <0.01 and p <0.01 respectively). For BUN/Cr ratio (p <0.05), maximal protections was observed at 13:00. These findings show that amifostine exhibits time dependent protection against cisplatin toxicity and thus it is recommended to use the protector when treatments are given during morning hours. The results also further validate the notion that chronochemotherapy is advantageous at least in reducing drug toxicity and thus should be integrated in the design of clinical protocols.

Choriocarcinoma arising in a squamous cell carcinoma of the esophagus.

Extragonadal germ cell tumors are rare neoplasms with histologic features comparable to those of gonadal origin. Squamous cell carcinoma of the esophagus was diagnosed in a 53-year-old male patient, and was palliated for a short period by cisplatin plus 5-fluorouracil. Clinical deterioration and development of gynecomastia led to diagnosis of hormone-secreting choriocarcinoma that originated within the squamous cell tumor of the esophagus. Salvage chemotherapy affected the markers but not the tumor. Extragonadal choriocarcinoma is a chemosensitive tumor, but when arising within squamous cell carcinoma of the esophagus it may be chemoresistant, and lead to a fatal outcome.

Factor C from rabbit liver. A new poly(dC) and poly[d(G-C)] template-selective stimulatory protein of DNA polymerases.

We have undertaken a search for mammalian DNA-binding proteins that enhance the activity of DNA polymerases in a template sequence-specific fashion. In this paper, we report the extensive purification and characterization of a new DNA-binding protein from rabbit liver that selectively stimulates DNA polymerases to copy synthetic poly[d(G-C)] and the poly(dC) strand of poly(dC).poly(dG) as well as single-stranded natural DNA that contains stretches of oligo(dC). The enhancing protein, a polypeptide of 65 kDa designated factor C, stimulates the copying of the two synthetic templates by Escherichia coli DNA polymerase I, Micrococcus luteus polymerase, and eukaryotic DNA polymerases alpha and beta, but not by avian myeloblastosis virus polymerase. Factor C, however, does not affect utilization by these polymerases of the poly(dG) strand of poly(dC).poly(dG), of poly(dC) primed by oligo(dG), or of poly(dA).poly(dT) and poly[d(A-T)]. With polymerase I, Michaelis constants (Km) of poly[d(G-C)] and of the poly(dC) strand of poly(dC).poly(dG) are decreased by factor C 37- and 4.7-fold, respectively, whereas maximum velocity (Vmax) remains unchanged. By contrast, neither the Km value of the poly(dG) strand of poly(dC).poly(dG) nor the Vmax value with this template is altered by factor C. Rates of copying of activated DNA, denatured DNA, or singly primed M13 DNA are not affected significantly by factor C. However, primer extension analysis of the copying of recombinant M13N4 DNA that contains runs of oligo(dC) within an inserted thymidine kinase gene shows that factor C increases processivity by specifically augmenting the efficiency at which polymerase I traverses the oligo(dC) stretches. Direct binding of factor C to denatured DNA is indicated by retention of the protein-DNA complex on columns of DEAE-cellulose. Binding of factor C to poly[d(G-C)] is demonstrated by the specific adsorption of the enhancing protein to columns of poly[d(G-C)]-Sepharose. We propose that by binding to poly[d(G-C)] and to poly(dC).poly(dG), factor C enables tighter binding of some DNA polymerases to these templates and facilitates enzymatic activity.

Monthly gemcitabine (days 1, 8 and 15) plus cisplatin (days 1-3) in advanced non-small cell lung cancer: a phase II study.

On the basis of the reported efficacy of gemcitabine plus cisplatin in patients with non-small cell lung cancer (NSCLC), this combination has been selected to be given as our firstline service regimen for advanced or metastatic disease. Patients recruitment was almost unlimited: no exclusion criteria were made, except for disease-related Karnofsky's performance status below 50%, the presence of central nervous system or spinal involvement by uncontrolled metastases, or creatinine clearance below 50 ml/min. Cisplatin 30 mg/m2/day on days 1-3 and gemcitabine 1250 mg/m2/day on days 1, 8 and 15 every 4 weeks were given on an outpatient schedule to consecutive patients with locally advanced or metastatic NSCLC. Forty-three successive NSCLC patients with histologically or cytologically proven disease were treated. Adenocarcinoma was diagnosed in 35% of cases, squamous cell carcinoma in 60% and broncho-alveolar type in 5%. Smoking was mentioned by 63% of the patients. Numerous medical problems were recorded in 75% of the patients. Stage IIIB was observed in 10 of 43 patients, while metastatic disease was found in the rest. All the patients, except for two, were symptomatic. Two patients achieved complete response (5%) and 16 achieved partial response (37%), yielding an overall objective response rate of 42%. Minimal response was observed in seven patients (16%) and disease stabilization in 7%. Adding the objective response rate to the minimal response and stabilization rates, the disease-control (progression-free) rate reaches 65%. The time to progression ranged from 0 to 69 weeks in all the patients. The overall survival of the group ranged from 4 to 98 weeks, with a median of 45 weeks. Clinical benefit response was observed mainly in patients who also achieved an objective response. We conclude that outpatient cisplatin plus gemcitabine combination is feasible, efficacious and justified in patients with advanced or metastatic NSCLC.