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Autore: Grafiati
Pubblicato: 25 luglio 2024

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Articoli di riviste sul tema "305.4/2/0973"

1

LoRusso, Patricia, Geoffrey Shapiro, Shuchi Sumant Pandya, Eunice Lee Kwak, Cheryl Jones, Marcia Belvin, Luna C. Musib et al. "A first-in-human phase Ib study to evaluate the MEK inhibitor GDC-0973, combined with the pan-PI3K inhibitor GDC-0941, in patients with advanced solid tumors." Journal of Clinical Oncology 30, n. 15_suppl (20 maggio 2012): 2566. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.2566.

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2566 Background: Both RAS/RAF/MEK and PI3K/Akt signaling pathways are deregulated in many tumor types. Targeting both pathways may be more efficacious than targeting either pathway alone. In preclinical models, concurrent administration of GDC‑0973, a potent, selective, MEK1/2 inhibitor and GDC-0941, a potent class I PI3K inhibitor, shows improved efficacy compared to either agent alone dosed continuously or intermittently. Methods: A phase Ib dose-escalation study with 3+3 design was initiated in patients (pts) with advanced solid tumors to evaluate the safety and pharmacokinetics (PK) of oral dosing of GDC-0973 and GDC-0941. Pts received: concurrent GDC-0973 + GDC-0941 once daily (qd) on a 21 day on/7 day off (21/7) schedule; intermittent GDC-0973 on Days 1, 4, 8, 11, 15, 18 of a 28 day cycle + GDC-0941 qd on a 21/7 schedule (MEK int); or GDC-0973 + GDC-0941 qd on a 7 day on /7 day off schedule (7/7). Starting doses were 20 mg GDC-0973 + 80 mg GDC-0941 (21/7), 100 mg GDC-0973 + 130 mg GDC-0941 (MEK int); 40 mg GDC-0973 + 130 mg GDC-0941 (7/7). Serial plasma PK samples, FDG-PET, and CT scans were obtained. Results: 78 pts have enrolled. DLTs were G3 lipase (n=1), G4 CPK elevation (n=1). Compared to the 21/7 MTD of 40 mg GDC-0973 + 100 mg GDC-0941, higher doses of GDC-0973 + GDC-0941 were tolerated on the MEK int schedule. Overall, adverse events related to the study drug combination in ≥ 20% pts were diarrhea, rash, nausea, fatigue, vomiting, decreased appetite, dysgeusia, and elevated CPK. Preliminary analysis indicated PK of GDC-0973 and GDC-0941 are not altered when dosed in combination. Of 46 evaluable pts, 26 had an FDG-PET partial metabolic response (≥ 20% decrease in mean SUVmax from baseline) at ≥1 time points. Partial responses were observed in 3 pts (mBRAF melanoma, mBRAF pancreatic ca, mKRAS endometrioid ca); 5 pts had stable disease ≥ 5 months. Conclusions: Combination dosing of GDC‑0973 and GDC-0941 is generally well tolerated, with toxicities similar to those observed in single agent GDC-0973 and GDC-0941 phase 1 trials. There are early signs of anti-tumor activity. Dose escalation on MEK int and 7/7 schedules continues and updated data will be presented.
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Padua, Rose Ann, Laure Sarda-Mantel, Mathieu Chiquet, Claire Kappel, Patricia Krief, Niclas Setterblad, Fortune Hontonnou et al. "BCL-2 Inhibitor Venetoclax (ABT-199) and MEK Inhibitor GDC-0973 Synergise to Target AML Progenitors and Overcome Drug Resistance with the Use of PET Scanning in a Mouse Model of HR-MDS to Monitor Response to Treatment". Blood 132, Supplement 1 (29 novembre 2018): 5497. http://dx.doi.org/10.1182/blood-2018-99-114212.

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Abstract Introduction: Targeted drugs are needed for HR-MDS/AML, particularly in elderly patients and Venetoclax, approved for some CLL, gives promising results in elderly AML. Assays to predict response to treatment may enable us to deliver personalized treatment. We sought to determine the most informative assay to predict response; viability assays can directly measure the effects of reagents on growth. Progenitor assays can potentially determine if the reagents can target diseased primitive cells. PET scanning can be used to follow response to treatment. Methods: Peripheral blood (PB) or bone marrow (BM) from 7 MDS/AML patients were incubated in a) no treatment, b) ABT-199 (1 µM) (Abbvie), c) GDC-0973 (1 µM) (Genentech) or d) ABT-199+GDC-0973 (1 µM of each) and assessed for viability using the MTT assay (n=2); cell death followed using the Incucyte® Zoom System (Essen Bioscience) (n=2) or methocult progenitor assays (Stem Cell Technologies) (n=4). Having shown that RAS:BCL-2 co-localization correlated with prognosis in MDS/AML patients (Leuk Res 37:312-9, 2013), immunofluorescence was undertaken. A micro PET device dedicated to mice was used to measure BM blast proliferation. After injection of 18F-FLT(a thymidine analogue) in mice untreated (n=7) or ABT-199 (75mg/kg)+GDC-0973(10mg/kg) treated (n=5) normal FVB/N, HR-MDS mice treated with vehicle (n=4), 2-month old HR-MDS before (n=5) and 3-month old before (n=4) and after ABT-199 (75mg/kg)+GDC-0973(10mg/kg) treatment (n=8), PET imaging was performed (Inveon Siemens Medical Systems), analyzed for signal and quantified. Results: Patient details and results are summarized on Table 1. Using the MTT assay 2 PB patient samples were found to be sensitive to ABT-199 treatment (Figure 1A, AS, p=0.00042 and YA, 0.00002) and more sensitive to the combination compared to untreated (AS, p=0.00007 and YA, 0.000003). With the incucyte the BM of one patient (AE) was found to be resistant to both ABT-199 and GDC-0973, but sensitive to the combination (Figure 1B). PB and BM from patient JA were assayed for apoptosis with the incucyte and were found to be sensitive to ABT-199 with increased apoptosis, resistant to GDC-0973 with decreased apoptosis and sensitive to the combination. Four bone marrow samples were tested in the 4 conditions using the progenitor assay (Figure 1C). Three patients were sensitive to GDC-0973, inhibiting any colony formation and the fourth had reduced colony numbers. In this assay patient JA appeared to be sensitive to GDC-0973 treatment whereas the incucyte assay scored this sample to be resistant to apoptosis; thus the cytotoxic effects of GDC-0973 may not be via apoptopsis. As the progenitor assay is likely to score the primitive disease population, this assay may prove more informative than the others without prior selection. One patient (DH) was clearly resistant to ABT-199, whereas the other three (JA, CB and FL) had reduced colony growth. All patients were sensitive to the combination treatment and inhibited colony growth. The RAS:BCL-2 co-localization in the PB revealed no complex in either the Mito or PM upon treatment with ABT-199 alone and some localization in the Mito with GDC-0973. With both ABT-199 and GDC-0973, there were hardly any cells confirming the cytotoxic effects of the combination. As we have previously shown that PM co-localization of the complex is associated with drug resistance (Blood 130:2613, 2017Suppl), we used the combination on our HR-MDS mouse model, where the complex co-localizes in the PM and followed the mice by PET scanning (Figure 1D). Weak signal was visualized in the femurs of untreated and ABT-199+GDC-0973 treated FVB/N mice (FBR 1.17+/-0.34 and 1.02+/-0.08 respectively). Mild PET signal was seen in the femurs of 2 month-old HR-MDS mice, (FBR 1.79+/-0.98). Intense PET signal was seen in the femurs and proximal humerus of HR-MDS mice treated with vehicle (3 month-old, FBR=2.35+/-1.32). Low PET signals were seen in the femurs of 5/8 HR-MDS mice treated with ABT-199+GDC-0973 (FBR=1.93+/-0.84). FBRs of the 3 groups of HR-MDS mice were significantly higher than those of FBV/N groups. Conclusion: Combined Venetoclax (ABT-199) and GDC-0973 targets MDS/AML progenitors and can potentially overcome drug resistance with the disruption of the RAS:BCL-2 complex. Bone marrow disease progression in HR-MDS mice can be monitored with 18F-FLT-PET imaging; PET data shows that the combination slows down disease progression. Disclosures Padua: Abbvie: Research Funding; Genentech: Research Funding. Giraudier:Novartis: Research Funding. Konopleva:Stemline Therapeutics: Research Funding. Andreeff:Oncoceutics: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; United Therapeutics: Patents & Royalties: GD2 inhibition in breast cancer ; Reata: Equity Ownership; Celgene: Consultancy; Jazz Pharma: Consultancy; Oncolyze: Equity Ownership; Amgen: Consultancy, Research Funding; Eutropics: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Aptose: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Daiichi-Sankyo: Consultancy, Patents & Royalties: MDM2 inhibitor activity patent, Research Funding; SentiBio: Equity Ownership; Astra Zeneca: Research Funding.
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Ali Khan, Mohd Wajid. "Optimization of methods for peripheral blood mononuclear cells isolation and expansion of human gamma delta T cells". Bioinformation 17, n. 3 (31 marzo 2021): 460–70. http://dx.doi.org/10.6026//97320630017460.

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Human Vγ9/Vδ2 T cells (γδ T cells) are immune surveillance cells both in innate and adaptive immunity and are a possible target for anticancer therapies, which can induce immune responses in a variety of cancers. Small non-peptide antigens such as zoledronate can do activation and expansion of T cells in vitro. It is evident that for adoptive cancer therapies, large numbers of functional cells are needed into cancer patients. Hence, optimization of methods needs to be carried out for the efficient expansion of these T cells. Standardization of peripheral blood mononuclear cells (PBMCs) isolation was devised. Cytokines (interleukin 2 (IL-2) and interleukin 15 (IL-15)) and zoledronate were also standardized for different concentrations. It was found that an increased number of PBMCs were recovered when washing was done at 1100 revolution per minute (rpm). Significantly high expansion fold was (2524 ± 787 expansion fold) achieved when stimulation of PBMCs was done with 1 μM of zoledronate and both cytokines IL-2 and IL-15 supported the expansion and survival of cells ISSN 0973-2063 (online) 0973-8894 (print) Bioinformation 17(3): 460-469 (2021) ©Biomedical Informatics (2021) 461 at the concentrations of 100 IU/ml and 10 ng/ml respectively. 14-day cultures showed highly pure (91.6 ± 5.1%) and live (96.5 ± 2.5%) expanded γδ T cells. This study aimed to standardize an easy to manipulate technique for the expansion of γδ T cells, giving a higher yield.
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Henao Castañeda, Isabel C., Jaime A. Pereañez e Lina M. Preciado. "Synthetic Inhibitors of Snake Venom Enzymes: Thioesters Derived from 2-Sulfenyl Ethylacetate". Pharmaceuticals 12, n. 2 (23 maggio 2019): 80. http://dx.doi.org/10.3390/ph12020080.

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Snakebite envenomings are a global public health issue. The therapy based on the administration of animal-derived antivenoms has limited efficacy against the venom-induced local tissue damage, which often leads to permanent disability. Therefore, there is a need to find inhibitors against toxins responsible for local damage. This work aimed to synthesize thioesters derived from 2-sulfenyl ethylacetate and to evaluate the inhibitory effects on two snake venom toxins. Ethyl 2-((4-chlorobenzoyl)thio)acetate (I), Ethyl 2-((3-nitrobenzoyl)thio)acetate (II) and Ethyl 2-((4-nitrobenzoyl)thio)acetate (III) were synthesized and spectroscopically characterized. Computational calculations were performed to support the study. The inhibitory capacity of compounds (I–III) was evaluated on a phospholipase A2 (Cdcum6) isolated from the venom of the Colombian rattlesnake Crotalus durissus cumanensis and the P-I type metalloproteinase Batx-I isolated from Bothrops atrox. I–III inhibited PLA2 with IC50 values of 193.2, 305.4 and 132.7 µM, respectively. Otherwise, compounds II and III inhibited the proteolytic activity of Batx-I with IC50 of 2774 and 1879 µM. Molecular docking studies show that inhibition of PLA2 may be due to interactions of the studied compounds with amino acids in the catalytic site and the cofactor Ca2+. Probably, a blockage of the hydrophobic channel and some amino acids of the interfacial binding surface of PLA2 may occur.
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Liu, Xiao Zhen, Jun Hua Yang, Gang Wang, Ling Ling Song e Ge Shi Zhuang. "Effect of Preparation Conditions on the Performance of Anodic Aluminum Oxide Films". Applied Mechanics and Materials 164 (aprile 2012): 223–26. http://dx.doi.org/10.4028/www.scientific.net/amm.164.223.

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Neodymium salt was used as additives in preparing anodic aluminum oxide (AAO) films to improve its performance. AAO films were prepared by anodization method from a 15 vol. % sulphuric acid solution containing neodymium salt. The effects of anodization voltage, anodization temperature and anodization time on microhardness and thickness of AAO films were researched, respectively. The thickness of AAO film increases with the increase of anodization voltage, the microhardness of AAO film decreases with the increase of anodization voltage in 19 V～23 V. The thickness of AAO film increases with the increase of anodization temperature, the microhardness of AAO film decreases with the increase of anodization temperature in 11 °C～19°C. The thickness of AAO film increases with the increase of anodization time, the microhardness of AAO film decreases with the increase of anodization time in 30 min～3 h. When the anodizing parameters: anodization voltage: 22 V, temperature: 15°C, anodization time: 2 h, the thickness and microhardness of AAO film is as high as 135μm and 305.4 HV.
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Žiak, Peter, Juraj Halička, Karolína Kapitánová e Peter Mojžíš. "The Effect of Botulinum TOxin Application if Neuro-Ophthalmological Indications on the Results of Schirmer’s Test and Tear Osmolarity". Czech and Slovak Ophthalmology 75, n. 2 (10 marzo 2019): 74–77. http://dx.doi.org/10.31348/2019/2/3.

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Botulinum toxin type A (BT-A) is used in the treatment of neuroophthalmologic disorders such as essential blepharospasm and facial hemispasm for more than 20 years. Although the long-term effect of repeated application of the BT-A was confirmed, the BT-A effect on tears production and retention is not clear. In our work we investigated whether applied BT-A in patients with blepharospasm and hemifacial spasm affect tears production. Tears quality was measured with Schirmer’s and tear osmolarity test during neuro-ophthalmologic diseases treatment, which was evaluated before and 14 days after application of BT-A (Botox inj, Allergan, Irvine, USA) into the orbicularis oculi muscle. BT-A doses of 16-18 U with unilateral and 32 to 36 U bilateral applications were used. The mean tear production in Schirmer’s test before BT-A application was 8.38 ± 0.63 mm, and 2 weeks after BT-A application was 7.12 ± 0,6 mm (n = 50). Tear osmolarity was 305.4 ± 9.2 mOsm before BT-A application, and 2 weeks after BT-A application it was 305.2 ± 8,6 mOsm (n = 13). We found significant difference between two groups in tear quantity (p < 0.012), but not quality (p > 0.05). Application of the BT-A reduced the amount of tears measured by Schirmer’s test. These results confirm rational basis of the empirical clinical experience where an artificial tears substitution is recommended for patients with neuro-ophthalmologic disorders treated by BT-A.
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Sumaryadi, Mas Yedi, Dadang Mulyadi Saleh, Aras Prasetiyo Nugroho, Nu'man Hidayat e Chomsiatun Nurul Hidayah. "Oxytocin Hormone Induction on Milk Production in Relation to Dairy Kid Performance". ANIMAL PRODUCTION 21, n. 3 (25 marzo 2020): 117. http://dx.doi.org/10.20884/1.jap.2019.21.3.747.

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The application of oxytocin induction to milk production in relation to the performance of kids in dairy goats had been carried out in the "PEGUMAS" dairy goat farmer group Gumelar District, Banyumas. This activity aimed to increase milk production and kid performance through the induction of the hormone oxytocin in dairy goats. The approach method was designed in two stages: the first stage carried out the socialization activities and demonstration of techniques for applying IPTEKS, and the second stage applied hormonal technology in the form of oxytocin hormone induction in dairy goats. The material used was dairy goat parity I aged 1.5 - 2 years allocated into 2 groups of 10 individuals each. Group I was dairy goat experiment not induced with the oxytocin hormone as the control. Group II was dairy goat experiment induced with the oxytocin hormone at a dose of 1 ml (10 IU) intramuscularly before milking. Milk production was measured morning and evening as daily milk production in milliliters (ml). Milk was given to the kid of each parent. The kid's performance was measured based on the daily weight gain of the kid during the study. Overall, the application of science and technology could be adopted by farmers, and oxytocin-induced dairy goat milk production (503.2 ml) was significantly higher (P<0.05) than control (305.4 ml) with an increase of 64.77%, with a positive level of correlation (r = 0.45) and contributed 19.83% to the kids daily body weight gain.
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Lieven, Elena V. M., Julian M. Pine e Helen Dresner Barnes. "Individual differences in early vocabulary development: redefining the referential-expressive distinction". Journal of Child Language 19, n. 2 (giugno 1992): 287–310. http://dx.doi.org/10.1017/s0305000900011429.

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ABSTRACTThe existence of stylistic variation between children in the early stages of language acquisition has been most frequently studied using Nelson's 0973) referential—expressive distinction. While the use of this distinction has generated a great deal of interesting research, there are a number of major problems associated with it. The present study presents a simple scheme, based on formal categories, for coding stylistic variation in the early lexicon. When applied to the first 50 and 100 words of 12 children collected between 0; 11 and 2; 3, the major dimensions of difference are found to be the relative proportion of common nouns and the relative proportion of frozen phrases. Moreover, the proportion of frozen phrases is also found to be significantly positively related to children's early productivity, suggesting that, rather than being a ‘deadend’ in early language development, the acquisition of frozen phrases may provide an alternative route into multiword speech.
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Izquierdo, César. "René VIRGOULAY (ed.), Le Christ de Maurice Blondel, Desclée, Paris 2003, 229 pp., 15 x 22, ISBN 2-7189-0973-0." Scripta Theologica 36, n. 1 (30 novembre 2017): 336. http://dx.doi.org/10.15581/006.36.13845.

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Han, Lina, Qi Zhang, Ce Shi, Joel Leverson, Monique Dail, Darren C. Phillips, Jun Chen et al. "Concomitantly Targeting BCL-2 with Venetoclax (ABT-199/GDC-0199) and MAPK Signaling with Cobimetinib (GDC-0973) in Acute Myeloid Leukemia Models". Blood 126, n. 23 (3 dicembre 2015): 2544. http://dx.doi.org/10.1182/blood.v126.23.2544.2544.

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Abstract Pro-survival molecules including BCL-2 play critical roles in leukemia transformation and chemoresistance. ABT-199/GDC-0199 (venetoclax) is an orally available BH3-mimetic that binds with high affinity to BCL-2, but lacks affinity for BCL-XL and MCL-1. We have recently demonstrated anti-leukemia potency of venetoclax in acute myeloid leukemia (AML) models (Pan et al. Cancer Discovery 2014). However, venetoclax poorly inhibits MCL-1, causing resistance in leukemia cells that rely on MCL-1 for survival. The RAF/MEK/ERK (MAPK) cascade is a major effector pathway in AML that is activated by upstream mutant proteins such as FLT3, KIT and RAS. Additionally, the MAPK pathway regulates BCL-2 family proteins by stabilizing anti-apoptotic MCL-1 and inactivating pro-apoptotic BIM. In this study, we evaluated the anti-tumor effects of concomitant BCL-2 and MAPK blockade by venetoclax in combination with MEK1/2 inhibitor GDC-0973 (cobimetinib).. We initially examined activity of these agents in a panel of myeloid leukemia cell lines with diverse genetic alterations (Fig. 1A). The IC50 values of cobimetinib ranged from < 0.01 µM to > 1 µM after 72 hours of drug treatment but did not correlate with the basal level of p-ERK1/2. In 7 out of 11 cell lines, combination of the agents elicited synergistic growth inhibition. Notably synergism of venetoclax with cobimetinib was observed in venetoclax-resistant cell lines (MOLM14, OCI-AML3, NB4 and THP1). Ongoing analysis of pharmacodynamic markers include transcriptome assessment by RNA sequencing, functional proteomics by reverse phase protein array (RPPA) and quantification of BCL-2:BIM and MCL-1:BIM complexes using the electrochemiluminescent ELISA assay (Meso Scale Discovery, MSD-ELISA). The preliminary MSD data revealed that BCL-2:BIM complex was disrupted in most cell lines and accumulated following cobimetinib treatment, which may be due to the disruption of MCL-1:BIM complex by inhibition of MEK (Fig. 1B). In a long-term culture of primary AML blasts in serum-free stem cell growth medium supplemented with cytokines and StemRegenin 1 (SR1) to main the immature state of leukemia cells, the combination of venetoclax and cobimetinib induced distinct apoptotic cell death, with AML #1 sensitive to venetoclax but resistant to cobimetinib. Alternatively, AML #2 and #3 samples were resistant to venetoclax but sensitive to cobimetinib and the combination of both drugs (Fig. 1C). We next investigated signaling patterns and BCL-2 family protein expression in AML stem/progenitor cells using a 34-antibody panel and time-of-flight mass cytometry (CyTOF). In AML#1, BCL-2 was expressed in leukemia blasts, with enrichment in a progenitor AML population phenotypically defined as CD45dim CD34+ CD38+ CD123+ CD33+ (Fig. 1D). The high expression level of BCL-2 and low expression of MCL-1 and BCL-XL may account for sensitivity to venetoclax in AML#1. Both basal and G-CSF- or SCF-stimulated p-ERK was efficiently down-regulated by cobimetinib; however, G-CSF-evoked p-STAT3/5 and SCF-induced p-AKT were only slightly reduced (Fig. 1E). Notably we observed increased phosphorylation of STAT5 pathway upon treatment with cobimetinib, suggesting that active MAPK signals inhibit phosphorylation of the JAK-STAT pathway, as previously reported (Krasilnikov et al. Oncogene, 2003 and Lee at al. Cancer Cell, 2014). To test the efficacy of both compounds in vivo, we injected NSG mice with genetically engineered OCI-AML3/Luc/GFP cells. Bioluminescent imaging (BLI) demonstrated significantly reduced leukemia burden in treated groups compared to controls, more prominently in the cobimetinib single agent and venetoclax plus cobimetinib co-treated mice (Fig. 1F). The efficacy study is ongoing and median survival for cobimetinib and venetoclax co-treated mice has yet to be determined (Fig. 1G). In summary, our data demonstrates that combinatorial blockade of MAPK and BCL-2 pathways is synergistic in the majority of AML cell lines tested and can overcome intrinsic resistance to venetoclax. Ongoing studies will evaluate efficacy of this combination therapy in primary human AML xenografts and elucidate mechanisms of synergy. Disclosures Leverson: AbbVie: Employment, Equity Ownership. Dail:Genentech: Employment, Equity Ownership. Phillips:AbbVie: Employment, Other: Shareholder, Patents & Royalties. Chen:Abbvie: Employment, Equity Ownership. Jin:Abbvie: Employment, Equity Ownership. Jabbour:Pfizer: Consultancy, Research Funding. Sampath:Genentech: Employment, Equity Ownership. Konopleva:Novartis: Research Funding; AbbVie: Research Funding; Stemline: Research Funding; Calithera: Research Funding; Threshold: Research Funding.
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Libri sul tema "305.4/2/0973"

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LaBrash, Betty Brehmer. The Brehmer/Fenske family history. Decorah, Iowa: Anundsen Pub. Co., 1990.

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Curry, Patricia B., Sesh Iyengar, Pamela A. Maloney e Marco Maroni, a cura di. Methods of Pesticide Exposure Assessment. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-0973-2.

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Capitoli di libri sul tema "305.4/2/0973"

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Hickey, Pierce, Mark Roantree, Alan Crilly e John Murphy. "Architectural Issues For Integrating Legacy Systems Using CORBA 2 in the LIOM Project". In OOIS’96, 135–51. London: Springer London, 1997. http://dx.doi.org/10.1007/978-1-4471-0973-0_10.

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Chakraborty, Tapash, e Pekka Pietiläinen. "Excitations in the Fractional Quantum Hall Effect at ν=1/2: Layered Electron Systems". In Recent Progress in Many-Body Theories, 113–18. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0973-4_11.

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"Front Matter". In Handbook of Immunological Investigations in Children, iii. Elsevier, 1990. http://dx.doi.org/10.1016/b978-0-7236-0973-5.50002-2.

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Watson, J. Graham, e A. Graham Bird. "Infections and immunizations". In Handbook of Immunological Investigations in Children, 137–70. Elsevier, 1990. http://dx.doi.org/10.1016/b978-0-7236-0973-5.50016-2.

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Sulemanji, Demet, Robert M. Kacmarek e Yandong Jiang. "Manual and Mechanical Ventilators". In The MGH Textbook of Anesthetic Equipment, 49–71. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4377-0973-5.10005-2.

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Chatburn, Jennifer A., e Warren S. Sandberg. "Patient Warming Devices". In The MGH Textbook of Anesthetic Equipment, 263–70. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4377-0973-5.10019-2.

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Lintner, Rebecca N., e Robert S. Holzman. "Pediatric Considerations". In The MGH Textbook of Anesthetic Equipment, 297–308. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4377-0973-5.10022-2.

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Sandberg, Warren S., Richard D. Urman e Jesse M. Ehrenfeld. "Preface". In The MGH Textbook of Anesthetic Equipment, ix. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4377-0973-5.10036-2.

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Jamil, George Leal. "Numbers Can Restrict Results?" In Handbook of Research on Information Management for Effective Logistics and Supply Chains, 1–22. IGI Global, 2017. http://dx.doi.org/10.4018/978-1-5225-0973-8.ch001.

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This chapter intends to evaluate how mixed researches are significant knowledge producers for business management. A discussion is conducted about the trade-off around the success and restrictions offered by the dominance of quantitative methods, especially when there is interest to study supply management and logistics. Quantitative methods are essential for any kind of management, but, as more dynamics in market competition produces more complex scenarios, qualitative answers are needed, along its approaches to formulate new questions that will help organizational decision-makers to apply knowledge for their planning activities. This chapter will explore three main points: 1) how the excessive concentration on quantitative methods can restrict managerial views; 2) how any organization can apply qualitative methods to enrich results observed from quantitative, resulting in better, more sustainable decisions; and 3) how qualitative and quantitative methods, associated, can implement this approach in real cases, with an overview of mixed scientific research methodologies.
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Atti di convegni sul tema "305.4/2/0973"

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Rosen, Lee, Patricia LoRusso, Wen Wee Ma, Johathan Goldman, Amy Weise, A. Dimitrios Colevas, Alex Adjei et al. "Abstract 4716: A first-in-human phase 1 study to evaluate the MEK1/2 inhibitor GDC-0973 administered daily in patients with advanced solid tumors". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4716.

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2

Bartley-Cho, Jonathan D., Tod Palm e Vipul Ranatunga. "Overview of Composite Airframe Life Extension Program Project 2: Tools For Assessing The Durability And Damage Tolerance Of Fastened Composite Joints". In 2018 AIAA/ASCE/AHS/ASC Structures, Structural Dynamics, and Materials Conference. Reston, Virginia: American Institute of Aeronautics and Astronautics, 2018. http://dx.doi.org/10.2514/6.2018-0973.

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3

Williams, Simon, Jill Fredrickson, Meghan Mckenzie, Cheryl Jones, Mary Gates, Klaus Hoeflich, Patricia LoRusso et al. "Abstract 1280: Preclinical and Clinical Evidence for MEK Pathway Inhibition by GDC-0973 using FDG-PET". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1280.

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4

Musib, Luna, Steve Eppler, Edna Choo, Alan Deng, Dale Miles, Bih Hsu, Lee Rosen et al. "Abstract 1304: Clinical pharmacokinetics of GDC-0973, an oral MEK inhibitor, in cancer patients: data from a Phase 1 study". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1304.

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5

Bendell, Johanna, Patricia LoRusso, Eunice Kwak, Susan Pandya, Luna Musib, Cheryl Jones, Alex De Crespigny et al. "Abstract LB-89: Clinical combination of the MEK inhibitor GDC-0973 and the PI3K inhibitor GDC-0941: A first-in-human phase Ib study in patients with advanced solid tumors". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-89.

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