Gotowe bibliografie tematyczne / 305.5/69/0973

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Gotowa bibliografia na temat „305.5/69/0973”

Autor: Grafiati
Data publikacji: 29 lipca 2024
Data aktualizacji: 31 lipca 2024

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Artykuły w czasopismach na temat "305.5/69/0973"

1

Robbins, Brian L., Edmund V. Capparelli, Ellen G. Chadwick, Ram Yogev, Leslie Serchuck, Carol Worrell, Mary Elizabeth Smith i in. "Pharmacokinetics of High-Dose Lopinavir-Ritonavir with and without Saquinavir or Nonnucleoside Reverse Transcriptase Inhibitors in Human Immunodeficiency Virus-Infected Pediatric and Adolescent Patients Previously Treated with Protease Inhibitors". Antimicrobial Agents and Chemotherapy 52, nr 9 (wrzesień 2008): 3276–83. http://dx.doi.org/10.1128/aac.00224-08.

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ABSTRACT Human immunodeficiency virus (HIV)-infected children and adolescents who are failing antiretrovirals may have a better virologic response when drug exposures are increased, using higher protease inhibitor doses or ritonavir boosting. We studied the pharmacokinetics and safety of high-dose lopinavir-ritonavir (LPV/r) in treatment-experienced patients, using an LPV/r dose of 400/100 mg/m2 orally every 12 h (p.o. q12h) (without nonnucleoside reverse transcriptase inhibitor [NNRTI]), or 480/120 mg/m2 p.o. q12h (with NNRTI). We calculated the LPV inhibitory quotient (IQ), and when the IQ was <15, saquinavir (SQV) 750 mg/m2 p.o. q12h was added to the regimen. We studied 26 HIV-infected patients. The median age was 15 years (range, 7 to 17), with 11.5 prior antiretroviral medications, 197 CD4 cells/ml, viral load of 75,577 copies/ml, and a 133-fold change in LPV resistance. By treatment week 2, 14 patients had a viral-load decrease of >0.75 log10, with a median maximal decrease in viral load of −1.57 log10 copies/ml at week 8. At week 2, 19 subjects showed a median LPV area under the concentration-time curve (AUC) of 157.2 (range, 62.8 to 305.5) μg·h/ml and median LPV trough concentration (C trough) of 10.8 (range, 4.1 to 25.3) μg/ml. In 16 subjects with SQV added, the SQV median AUC was 33.7 (range, 4.4 to 76.5) μg·h/ml and the median SQV C trough was 2.1 (range, 0.2 to 4.1) μg/ml. At week 24, 18 of 26 (69%) subjects remained in the study. Between weeks 24 and 48, one subject withdrew for nonadherence and nine withdrew for persistently high virus load. In antiretroviral-experienced children and adolescents with HIV, high doses of LPV/r with or without SQV offer safe options for salvage therapy, but the modest virologic response and the challenge of adherence to a regimen with a high pill burden may limit the usefulness of this approach.
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Bridoux, Frank, Bertrand Arnulf, Lionel Karlin, Nicolas Blin, Nolwenn Rabot, Margaret Macro, Vincent Audard i in. "Randomized Trial Comparing Double Versus Triple Bortezomib-Based Regimen in Patients With Multiple Myeloma and Acute Kidney Injury Due to Cast Nephropathy". Journal of Clinical Oncology 38, nr 23 (10.08.2020): 2647–57. http://dx.doi.org/10.1200/jco.20.00298.

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PURPOSE We report a multicenter controlled trial comparing renal recovery and tolerance profile of doublet versus triplet bortezomib-based regimens in patients with initial myeloma cast nephropathy (CN) and acute kidney injury (AKI) without need for dialysis. METHODS After symptomatic measures and high-dose dexamethasone, patients were randomly assigned to receive bortezomib plus dexamethasone (BD), or BD plus cyclophosphamide (C-BD). In patients with < 50% reduction of serum free light chains (sFLCs) after 3 cycles, chemotherapy was reinforced with either cyclophosphamide (BD group) or thalidomide (C-BD group). RESULTS Ninety-two patients were enrolled in each group. At random assignment, characteristics of the 2 groups were similar, including median age (68 years) and serum creatinine level (305.5 and 273.5 µmol/L in BD and C-BD group, respectively). At 3 months, renal response rate (primary end point) was not different (41 v 47 responders in the BD and C-BD groups, respectively; relative risk [RR], 0.87; P = .46). Very good partial response (free light chain reduction ≥ 90%) or more was achieved in 36 and 47 patients, respectively (RR, 0.76; P = .10). After 1 cycle of chemotherapy, 69 in the BD group and 67 patients in the C-BD group had achieved sFLC level ≤ 500 mg/L. Serious adverse events were recorded in 30 and 40 patients, respectively. At 12 months, 19 patients had died (9 in the BD group v 10 in the C-BD group), including 10 (6 in the BD group and 4 in the C-BD group) from myeloma progression and 3 (0 in the BD group and 3 in the C-BD group) from infection. Within median follow-up of 27 months, 43 and 42 patients switched to new therapy, respectively. Overall, 50 patients (24 in the BD group and 26 in the C-BD group) had died. CONCLUSION This randomized study did not show any benefit of C-BD compared with BD on renal recovery of patients with initial CN not requiring dialysis. Adding cyclophosphamide did not sufficiently improve the efficacy-toxicity balance. Patients with myeloma with AKI are fragile, and indication for doublet or triplet regimen should be adapted to frailty.
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Beggs, Simon A. S., Awatif Al-Nafussi, C. Michael Lambert, Daniel Porter i J. T. Patton. "A chronic thigh mass in a 69-year-old man". Skeletal Radiology 39, nr 12 (22.06.2010): 1259–61. http://dx.doi.org/10.1007/s00256-010-0973-6.

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Krychtiuk, KA, M. Lenz, P. Hohensinner, K. Distelmaier, L. Schrutka, SP Kastl, K. Huber, C. Hengstenberg, J. Wojta i WS Speidl. "Circulating levels of proprotein convertase subtilisin/kexin type 9 (PCSK9) are associated with monocyte subsets in patients with stable coronary artery disease". European Journal of Preventive Cardiology 28, Supplement_1 (1.05.2021). http://dx.doi.org/10.1093/eurjpc/zwab061.278.

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Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): FWF Background and aims Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis and can be divided into three subsets. The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets. Methods We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14 + CD16++; NCM). Results Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n = 55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p = 0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R = 0.29; p = 0.04), while NCM showed an inverse correlation with PCSK9 levels (R=-0.33; p = 0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK-9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p = 0.05). Conversely, PCSK9 levels &gt;median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 &lt;median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p = 0.02). In contrast, IM showed no association with PCSK-9 levels. Conclusions We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.
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Krychtiuk, Konstantin, Max Lenz, Philipp Hohensinner, Klaus Distelmaier, Lore Schrutka, Stefan Kastl, Stefan Pfaffenberger i in. "Abstract 15930: Circulating Levels of Proprotein Convertase Subtilisin/kexin Type 9 (pcsk9) are Associated With Monocyte Subsets in Patients With Stable Coronary Artery Disease". Circulation 142, Suppl_3 (17.11.2020). http://dx.doi.org/10.1161/circ.142.suppl_3.15930.

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Introduction: Proprotein convertase subtilisin/kexin type-9 (PCSK9) is an enzyme promoting the degradation of low-density lipoprotein receptors (LDL-R) in hepatocytes. Inhibition of PCSK9 has emerged as a novel target for lipid-lowering therapy. Monocytes are crucially involved in the pathogenesis of atherosclerosis. Circulating monocytes can be divided into three subsets. The aim of this study was to examine whether circulating levels of PCSK9 are associated with monocyte subsets. Methods: We included 69 patients with stable coronary artery disease. PCSK9 levels were measured and monocyte subsets were assessed by flow cytometry and divided into classical monocytes (CD14++CD16-; CM), intermediate monocytes (CD14++CD16+; IM) and non-classical monocytes (CD14+CD16++; NCM). Results: Mean age was 64 years and 80% of patients were male. Patients on statin treatment (n=55) showed higher PCSK9-levels (245.4 (206.0-305.5) ng/mL) as opposed to those without statin treatment (186.1 (162.3-275.4) ng/mL; p=0.05). In patients on statin treatment, CM correlated with circulating PCSK9 levels (R=0.29; p=0.04), while NCM showed an inverse correlation with PCSK9 levels (R=-0.33; p=0.02). Patients with PCSK9 levels above the median showed a significantly higher proportion of CM as compared to patients with PCSK-9 below the median (83.5 IQR 79.2-86.7 vs. 80.4, IQR 76.5-85.2%; p=0.05). Conversely, patients with PCSK9 levels >median were associated with a significantly lower proportion of NCM as compared to those with PCSK9 <median (10.2, IQR 7.3-14.6 vs. 14.3, IQR 10.9-18.7%; p=0.02). In contrast, IM showed no association with PCSK-9 levels. Conclusions: We hereby provide a novel link between PCSK9 regulation, innate immunity and atherosclerotic disease in statin-treated patients.
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Wallett, Alice M., Naroa Etxebarria, Nicole A. Beard, Philo U. Saunders, Marijke Welvaert, Julien D. Périard, Andrew J. McKune i David B. Pyne. "Running at Increasing Intensities in the Heat Induces Transient Gut Perturbations". International Journal of Sports Physiology and Performance, 2020, 1–7. http://dx.doi.org/10.1123/ijspp.2019-0973.

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Purpose: The risk of exercise-induced endotoxemia is increased in the heat and is primarily attributable to changes in gut permeability resulting in the translocation of lipopolysaccharides (LPS) into the circulation. The purpose of this study was to quantify the acute changes in gut permeability and LPS translocation during submaximal continuous and high-intensity interval exercise under heat stress. Methods: A total of 12 well-trained male runners (age 37 [7] y, maximal oxygen uptake [VO2max] 61.0 [6.8] mL·min−1·kg−1) undertook 2 treadmill runs of 2 × 15-minutes at 60% and 75% VO2max and up to 8 × 1-minutes at 95% VO2max in HOT (34°C, 68% relative humidity) and COOL (18°C, 57% relative humidity) conditions. Venous blood samples were collected at the baseline, following each running intensity, and 1 hour postexercise. Blood samples were analyzed for markers of intestinal permeability (LPS, LPS binding protein, and intestinal fatty acid–binding protein). Results: The increase in LPS binding protein following each exercise intensity in the HOT condition was 4% (5.3 μg·mL−1, 2.4–8.4; mean, 95% confidence interval, P < .001), 32% (4.6 μg·mL−1, 1.8–7.4; P = .002), and 30% (3.0 μg·mL−1, 0.03–5.9; P = .047) greater than in the COOL condition. LPS was 69% higher than baseline following running at 75% VO2max in the HOT condition (0.2 endotoxin units·mL−1, 0.1–0.4; P = .011). Intestinal fatty acid–binding protein increased 43% (2.1 ng·mL−1, 0.1–4.2; P = .04) 1 hour postexercise in HOT compared with the COOL condition. Conclusions: Small increases in LPS concentration during exercise in the heat and subsequent increases in intestinal fatty acid–binding protein and LPS binding protein indicate a capacity to tolerate acute, transient intestinal disturbance in well-trained endurance runners.
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Książki na temat "305.5/69/0973"

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Alan, Walker, Walker Carol i Child Poverty Action Group (Great Britain), red. The Growing divide: A social audit, 1979-1987. London: Child Poverty Action Group, 1987.

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1949-, Henderson John, i Wall Richard 1944-, red. Poor women and children in the European past. London: Routledge, 1994.

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Domhoff, G. William. Who rules America?: Challenges to corporate and class dominance. Wyd. 6. Boston: McGraw Hill Higher Education, 2010.

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Domhoff, G. William. Who rules America?: Challenges to corporate and class dominance. Wyd. 6. Boston: McGraw Hill Higher Education, 2010.

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Domhoff, G. William. Who rules America?: Power and politics in the year 2000. Wyd. 3. Mountain View, Calif: Mayfield Pub. Co., 1998.

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Domhoff, G. William. Who rules America?: Power and politics. Wyd. 4. Boston: McGraw Hill, 2002.

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Domhoff, G. William. Who rules America?: Power, politics, and social change. Wyd. 6. Boston: McGraw-Hill Higher Education, 2009.

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Domhoff, G. William. Who rules America?: Challenges to corporate and class dominance. Wyd. 6. Boston: McGraw Hill Higher Education, 2010.

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Domhoff, G. William. Who rules America?: Power, politics, and social change. Wyd. 5. Boston: McGraw-Hill, 2006.

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Domhoff, G. William. Who rules America?: Power and politics, and social change. Wyd. 5. Boston, MA: McGraw-Hill, 2006.

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