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Travelling down from the peak of the Troodos Mountains, a slight detour will take you to Kakopetria a village built on a steep ravine., The village centre has a flowing mountain stream running through the middle and a small square near the foot. Narrow, cobbled streets wind uphill flanked by traditional stone houses, small hotels offering slightly gothic rooms with four-poster beds and fantastic views; as well as several extrmemely good restaurants.
Background: To establish the toxicities and maximum tolerated dose of paclitaxel given over 3 h in combination with cisplatin, to determine the pharmacokinetic profiles of these two drugs and to observe their antitumor activity, we conducted a combination phase I study in non-small cell lung cancer. Methods: Patients received paclitaxel doses of 150210 mg m2 given over 3 h and cisplatin doses of 6080 mg m2 as a 1 infusion 2 h after the end of the paclitaxel infusion. Results: A total of 25 patients with previously untreated non-small cell lung cancer were enrolled. Granulocytopenia was the most frequent hematological toxicity and the most prominent non-hematological toxicity was sensory dominant neuropathy. Two of six patients experienced dose limiting toxicities leukopenia, infection and neuropathy ; at a dose of paclitaxel 210 mg m2 and cisplatin 60 mg m2, which was considered the maximum tolerated dose. There were seven partial responses among 24 evaluable patients, for an overall response rate of 29%. The median survival time was 341 days and the 1 year survival rate was 45.8%. As the paclitaxel pharmacokinetic parameters in this study were consistent with those of our previous single agent study, we found no significant drugdrug interaction between the 3 h infusion paclitaxel and cisplatin. Conclusion: The recommended doses for further study are determined to be paclitaxel 180 mg m2 and cisplatin 80 mg m2. This is a well-tolerated and active regimen for non-small cell lung cancer. In view of the promising survival outcome, further evaluation in prospective randomized trials versus other regimens is warranted. Key words: phase I study paclitaxel cisplatin non-small cell lung cancer pharmacokinetics.
Table 2. Failure of the calculated FHS risk to predict IHD among renal transplant patients, independent of age, diabetes mellitus, and cigarette smokinga.
Doses of drugs given at repeated intervals to assure effective chemotherapy of the Lewis lung carcinoma. This tumor system.
1. Non-Small Cell Lung Cancer Collaborative Group. Chemotherapy in non-small cell lung cancer: a meta-analysis using updated data on individual patients from 52 randomized clinical trials. Br J Med 1995; 311: 899909. Pfister DG, Johnson DH, Azzoli CG et al. American Society of Clinical Oncology treatment of unresectable non-small-cell lung cancer guideline: update 2003. J Clin Oncol 2004; 22: 330353. Bunn PA. Chemotherapy for advanced non-small cell lung cancer. Who, what, when, why? J Clin Oncol 2002; 20 Suppl. 18 ; : 23s33s. 4. Schiller JH, Harrington D, Belani CP et al. Comparison of four chemotherapy regimens for advanced non-small cancer. N Engl J Med 2002; 346: 9298. Kelly K, Crowley J, Bunn PA et al. Randomized phase III trial of paclitaxel plus carboplatin versus vinorelbine plus cisplatin in the treatment of patients with advanced non-small-cell lung cancer: a Southwest Oncology Group trial. J Clin Oncol 2001; 19: 32103218. Fossella F, Pereira RJ, von Pawel J et al. Randomized, multinational, phase III study of docetaxel plus platinum combination versus vinorelbine plus cisplatin for advanced non-small cell lung cancer. The TAX 326 Study Group. J Clin Oncol 2003; 21: 30163024. Ettinger D, Johnson D. Update. NCCN Small Cell and Non-Small Cell Lung Cancer Clinical Practice Guidelines. J Natl Compr Canc Netw 2005; 3 Suppl 1 ; : S17S21. 8. Bunn PJ, Kelly K. New chemotherapeutic agents prolong survival and improve quality of life in non-small cell lung cancer: a review of the literature and future directions. Clin Cancer Res 1998; 5: 10871100. Thongprasert S, Sanuganmitra P, Juthapan N. Relationship between quality of life and clinical outcomes in advanced non-small cell lung cancer: best supportive care BSc ; versus BSC plus chemotherapy. Lung Cancer 1999; 24: 1724. Rossi A, Maione P, Gridelli C. Safety profile of platinum-based chemotherapy in the treatment of advanced non-small cell lung cancer in elderly patients. Exp Opin Drug Saf 2005; 4: 10511067. Gridelli C, Ardizzoni A, Le Chevalier T et al. Treatment of advanced non-small-cell lung cancer patients with ECOG performance status 2: results of an European Experts Panel. Ann Oncol 2004; 15: 419426. Winton T, Livingston R, Johnson D et al. Vinorelbine plus cisplatin vs. observation in resected non-small-cell lung cancer. N Engl J Med 2005; 352: 25892597.
Cisplatin gemzar pancreatic cancer
Gangemi RM. Tiso M, Marchetti C, Severi AB, Fabbi M. Taxol cytotoxicity on human leukemia cell lines is a function of their susceptibility to programmed cell death. Cancer Chemother Pharmacol 1995: 36: 385-92. ; Milas L. Hunter NR, Kurdoglu B, Mason KA. Meyn RE, Stephens LC. et al. Kinetics of mitotic arrest and apoptosis in murine mammary and ovarian tumors treated with taxol. Cancer Chemother Pharmacol 1995: 35: 297303. ; Milross CG. Peters U . Hunter NR. Mason KA, Milas L. Sequence-dependent antitumor activity of paclitaxel Taxol ; and cisplatin in vivo. Int J Cancer 1995: 62: 599-604. ; Terasima T, Tolmach LJ. Variations in several responses of HeLa cells to x-irradiation during the cell cycle. Biophys J 1963; 3: 11 -33. ; Sinclair WK. Morton RA. X-ray sensitivity during the cell generation cycle of cultured Chinese hamster cells. Radiat Res 1966; 29: 450-74. ; Withers HR, Mason K. Reid BO. Dubravsky N, Barkley HT Jr, Brown BW, et al. Reponse of mouse intestine to neutrons and gamma rays in relation to dose fractionation and division cycle. Cancer 1974: 34: 39-47. ; Choy H, Rodriguez FF, Koester S, Hilsenbeck S. Von Hoff DD. Investigation of taxol as a potential radiation sensitizer. Cancer 1993: 71: 3774-8 ; Steren A, Sevin BU, Perras J, Angioli R, Nguyen H. Guerra L. et al. Taxol sensitizes human ovarian cancer cells to radiation. Gynecol Oncol 1993: 48: 252-8. ; Liebmann J, Cook JA, Fisher J, Teague D, Mitchell JB. In vitro studies of Taxol as a radiation sensitizer in human tumor cells. J Natl CancerInst 1994: 86441-6. 16 ; Minarik L, Hall EJ. Taxol in combination with acute and low dose rate irradiation [see comment citation in Medline] Radiother Oncol 1994; 32: 124-8. ; Liebmann J, Cook JA, Fisher J, Teague D, Mitchell JB. Changes in radiation survival curve parameters in human tumor and rodent cells exposed to paclitaxel Taxol ; . Int J Radiat Oncol Biol Phys 1994; 29: 559-64. ; Milas L, Hunter NR, Mason KA, Kurdolglu B, Peters LJ. Enhancement of tumor radioresponse of a murine mammary carcinoma by paclitaxel. Cancer Res 1994: 54: 3506-10. ; Milas L, Hunter NR, Mason KA, Milross CG, Saito Y, Peters LJ. Role of reoxygenation in induction of enhancement of tumor radioresponse by paclitaxel. Cancer Res 1995; 55: 3564-8. ; Milas L, Hunter N, Mason K, Withers HR. Immunological resistance to pulmonary metastases in C3Hf-Bu mice bearing syngeneic fibrosarcoma of different sizes. Cancer Res 1974, 34: 61-71. ; Milas L, Wike J, Hunter N, Volpe J, Basic I. Macrophage content of murine sarcomas and carcinomas: associations with tumor growth parameters and tumor radiocurability. Cancer Res 1987: 47: 1069-75. ; Suit H. Allam A, Allalunis-Tumer J. Brock W, Girinsky T, Hill S, et al. Is tumor cell radiation resistance correlated with metastatic ability? Cancer Res 1994; 54: 1736-41. ; Meyn RE. Stephens LC, Hunter NR, Milas L. Apoptosis in murine tumors treated with chemotherapy agents. Anticancer Drugs 1995; 6: 443-50. ; Kallman RF, editor. Rodent tumor models in experimental cancer therapy. New York: Pergamon Press, 1987 and cladribine.
Cisplatin war
Includes Hispanics, Asians, and patients of African descent. Includes patients with unspecified stage one patient in pemetrexed cisplatin arm and two patients in cisplatin arm.
From the Department of Psychiatry, New York Medical College, Valhalla, New York. Address correspondence and reprint requests to Robert E. Feinstein, MD, New York Medical College, Westchester Medical Center, Behavioral Health Center, Valhalla, NY 10905 and clofarabine.
A. Less than 60 mL min 1.73 m2 for greater than 1 week Discontinue cisplatin.5 b. Less than 60 mL min, but greater than or equal to 45 mL minute - Reduce cisplatin dose 25%.32 c. Less than 45 mL min, but greater than or equal to 30 mL min Reduce cisplatin dose 50%.32 REFERENCES 1. Souhami RL, Craft AW, Van der.
II. Chemotherapy Based Nonmyeloablative Preparative Regimens for Allogeneic Hematopoietic Transplantation and clofibrate.
Large intestine. The drug is not well.
Tute of the United States, National Cancer Institute of Canada. J Natl Cancer Inst 2000, 92 3 ; : 205-216. Bubley GJ, Carducci M, Dahut W, Dawson N, Daliani D, Eisenberger M, Figg WD, Freidlin B, Halabi S, Hudes G, Hussain M, Kaplan R, Myers C, Oh W, Petrylak DP, Reed E, Roth B, Sartor O, Scher H, Simons J, Sinibaldi V, Small EJ, Smith MR, Trump DL, Wilding G, et al.: Eligibility and response guidelines for phase II clinical trials in androgen-independent prostate cancer: recommendations from the Prostate-Specific Antigen Working Group. J Clin Oncol 1999, 17 11 ; : 3461-3467. Giaccone G, Herbst RS, Manegold C, Scagliotti G, Rosell R, Miller V, Natale RB, Schiller JH, Von Pawel J, Pluzanska A, Gatzemeier U, Grous J, Ochs JS, Averbuch SD, Wolf MK, Rennie P, Fandi A, Johnson DH: Gefitinib in combination with gemcitabine and cisplatin in advanced non-small-cell lung cancer: a phase III trial-INTACT 1. J Clin Oncol 2004, 22 5 ; : 777-784. Herbst RS, Giaccone G, Schiller JH, Natale RB, Miller V, Manegold C, Scagliotti G, Rosell R, Oliff I, Reeves JA, Wolf MK, Krebs AD, Averbuch SD, Ochs JS, Grous J, Fandi A, Johnson DH: Gefitinib in combination with paclitaxel and carboplatin in advanced nonsmall-cell lung cancer: a phase III trial--INTACT 2. J Clin Oncol 2004, 22 5 ; : 785-794. Herbst RS, Prager D, Hermann R, Fehrenbacher L, Johnson BE, Sandler A, Kris MG, Tran HT, Klein P, Li X, Ramies D, Johnson DH, Miller VA: TRIBUTE: a phase III trial of erlotinib hydrochloride OSI-774 ; combined with carboplatin and paclitaxel chemotherapy in advanced non-small-cell lung cancer. J Clin Oncol 2005, 23 25 ; : 5892-5899. Gatzemeier U, Pluzanska A, Szczesna A, Kaukel E, Roubec J, Brennscheidt U, De Rosa F, Mueller B, Von Pawel J: Results of a phase III trial of erlotinib OSI-774 ; combined with cisplatin and gemcitabine GC ; chemotherapy in advanced non-small cell lung cancer NSCLC ; . Proc Soc Clin Oncol 2004, 22 14S ; : Abstract 7010. Malik SN, Siu LL, Rowinsky EK, deGraffenried L, Hammond LA, Rizzo J, Bacus S, Brattain MG, Kreisberg JI, Hidalgo M: Pharmacodynamic evaluation of the epidermal growth factor receptor inhibitor OSI-774 in human epidermis of cancer patients. Clin Cancer Res 2003, 9 7 ; : 2478-2486 and clorazepate.
Alimta cisplatin
Erlotinib sensitivity cluster around the active site of the kinase, presumably stabilizing the interaction between the EGFR-tyrosine kinase domain and its competitive inhibitor e.g., gefitinib and erlotinib; ref. 44 ; . Because cetuximab is interacting with the extracellular domain of the receptor, it is likely that the antibody will act independently of these mutations. Thus, antibody-based EGFR inhibitors may have different overall activity profiles compared with gefitinib and erlotinib, although they all target the same molecular entity pathway. Consequently, cetuximab, and perhaps other related antibodies targeting the extracellular domain of the EGFR, may have different molecular and genetic determinants that predict sensitivity compared with the small molecule inhibitors. Clearly, further studies are needed to fully address this question. Previous reports have shown that cetuximab can potentiate antitumor effects of many cytotoxic agents, including cisplatin and CPT-11 16, 45 ; . However, few reports have tried to rationalize the determinants that predict therapeutic synergy. Here, we report that cetuximab and cisplatin combination regimens proved to be significantly more efficacious than either monotherapy alone in the cisplatin nonresponsive GEO human colon carcinoma tumor model. GEO tumors were also one of the most sensitive models tested for cetuximab monotherapy regimens. In contrast, the same cetuximab and cisplatin combination was without benefit in the cisplatin poorly responsive A549 human lung carcinoma model. In this particular experiment, cetuximab monotherapy was likewise inactive. Similarly, combinations of CPT-11 with cetuximab failed to show any clear improvements over the best monotherapy used in the CPT-11 weakly responsive HT29, A549, and WiDr tumor models. Both HT29 and WiDr experiments showed clear resistance to cetuximab monotherapy. Interestingly, in the A549 combination study, cetuximab alone approached single-agent activity, and the best antitumor effect occurred using a combination of cetuximab with CPT-11. Although this effect was not statistically different from the best monotherapy response, it may indicate a general trend. Collectively, our data suggest that robust cetuximab singleagent efficacy in a particular tumor may be a prerequisite to clearly potentiate chemotherapy-mediated antitumor activities, even in chemotherapy nonresponsive tumor models. This hypothesis is further strengthened by recently published data, indicating therapeutic synergy of cetuximab with BMS-275183, an oral taxane, in the cetuximabsensitive L2987 and GEO tumor models 19 ; . Moreover, others have reported synergy of cetuximab with drugs, such as gemcitabine, paclitaxel, docetaxel, topotecan, 5-fluorouracil, doxorubicin, and radiation 7, 9, 14, ; . The tumor models used in these studies were all at least borderline responsive to cetuximab monotherapy. Prewett et al. 16 ; previously showed enhanced antitumor activity of cetuximab in combination with CPT-11 in the HT29 human colon carcinoma xenograft, which stands in contrast to our observation in the same tumor model. However, in their hands, HT29 tumor growth was inhibited significantly more effectively by.
Cisplatin storage
However, we have found that people with diabetes in these countries are often unlikely to benefit directly from reduced prices. While our products may be supplied to the distributor at the LDC price, this price is routinely marked up by governments, through import duties and domestic taxes, or by wholesalers and hospitals for additional profit. One exception is Senegal, where the state prohibits the marking up of insulin prices so that the benefit of reduced pricing can be passed directly on to the patient and clove.
5. Knapp, D. W., Glickman, N. W., DeNicola, D. B., Bonney, P. L., Lin, T. L., and Glickman, L. T. Naturally-occurring canine transitional cell carcinoma of the urinary bladder. A relevant model of human invasive bladder cancer. Urol. Oncol., 5: 4759, 2000. Moore, A. S., Cardona, A., Shapiro, W., and Madewell, B. R. Cisplatin cisdiaminedichloroplatinum ; for treatment of transitional cell carcinoma of the urinary bladder or urethra. A retrospective study of 15 dogs. J. Vet. Intern. Med., 4: 148 152, Chun, R., Knapp, D. W., Widmer, W. R., DeNicola, D. B., Glickman, N. W., Kuczek, T., Degortari, A., and Han, C. M. Phase II clinical trial of carboplatin in canine transitional cell carcinoma of the urinary bladder. J. Vet. Intern. Med., 11: 279 283, Chun, R., Knapp, D. W., Widmer, W. R., Glickman, N. W., DeNicola. D. B., and Bonney, P. L. Cisplatin treatment of transitional cell carcinoma of the urinary bladder in dogs: 18 cases 19831993 ; . J. Am. Vet. Med. Assoc., 209: 1588 1591, Knapp, D. W., Richardson, R. C., Chan, T. C. K., Bottoms, G. D., Widmer, W. R., DeNicola, D. B., Teclaw, R., Bonney, P. L., and Kuczek, T. Piroxicam therapy in 34 dogs with transitional cell carcinoma of the urinary bladder. J. Vet. Intern. Med., 8: 273278, 1994. Knapp, D. W., Glickman, N. W., Widmer, W. R., DeNicola, D. B., Adams, L. G., Kuczek, T., Bonney, P. L., DeGortari, A. E., Han, C., and Glickman, L. T. Cisplatin versus cisplatin combined with piroxicam in a canine model of human invasive urinary bladder cancer. Cancer Chemother. Pharmacol., 46: 221226, 2000. Knapp, D. W. Tumors of the urinary system. In: S. J. Withrow and E. G. MacEwen eds. ; , Small Animal Clinical Oncology, Ed. 3, pp. 490 499, Philadelphia: W. B. Saunders, 2001. 12. Helfand, S. C., Hamilton, T. A., Hungerford, L. L., Jeglum, K. A., and Goldschmidt, M. A. Comparison of three treatments for transitional cell carcinoma of the bladder in the dog. J. Am. Anim. Hosp. Assoc., 30: 270 275, Khan, K. N., Knapp, D. W., DeNicola, D. B., and Harris, R. K. Expression of cyclooxygenase-2 in transitional cell carcinoma of the urinary bladder in dogs. Am. J. Vet. Res., 61: 478 481, Mohammed, S. I., Bennett, P. F., Craig, B. A., Glickman, N. W., Mutsaers, A. J., Snyder, P. W., Widmer, W. R., DeGortari, A. E., Bonney, P. L., and Knapp, D. W. Effects of the cyclooxygenase inhibitor, piroxicam, on tumor response, apoptosis, and angiogenesis in a canine model of human invasive urinary bladder cancer. Cancer Res., 62: 356 358, Castelao, J. E., Yuan, J. M., Gago-Domingues, M., Yu, M. C., and Ross, R. K. Non-steroidal anti-inflammatory drugs and bladder cancer prevention. Br. J. Cancer, 82: 1364 1369, Dempke, W., Rie, C., Grothey, A., and Schmoll, H. J. Cyclooxygenase-2: a novel target for cancer chemotherapy? J. Cancer Res. Clin. Oncol., 127: 411 417, Farrow, D. C., Vaughan, T. L., Hansten, P. D., Stanford, J. L., Risch, H. A., Gammon, M. D., Chow, W. H., Dubrow, R., Ahsan, H., Mayne, S. T., Schoenberg, J. B., West, A. B., Rotterdam, H., Fraumeni, J. F., Jr., and Blot, W. J. Use of aspirin and other nonsteroidal antiinflammatory drugs and risk of esophageal and gastric cancer. Cancer Epidemiol. Biomarker. Prev., 7: 97102, 1998. Gupta, R. A., and DuBois, R. N. Colorectal cancer prevention and treatment by inhibition of cyclooxygenase-2. Nat. Rev. Cancer, 1: 1121, 2001. Hida, T., Kozaki, K., Muramatsu, H., Masuda, A., Shimizu, S., Mitsudomi, T., Sugiura, T., Ogawa, M., and Takahashi, T. Cyclooxygenase-2 inhibitor induces apoptosis and enhances cytotoxicity of various anticancer agents in non-small cell lung cancer cell lines. Clin. Cancer Res., 6: 2006 2011, Nishimura, G., Yanoma, S., Mizuno, H., Kawakami, K., and Tsukuda, M. A selective cyclooxygenase-2 inhibitor suppresses tumor growth in nude mouse xenografted with head and neck squamous carcinoma cells. Jpn. J. Cancer Res., 90: 11521162, 1999. Norrish, A. E., Jackson, R. T., and McRae, C. U. Nonsteroidal anti-inflammatory drugs and prostate cancer progression. Int. J. Cancer, 77: 511515, 1998.
Gemcitabine and cisplatin chemotherapy
Radiotherapy was observed. We cannot exclude, however, that such an effect of increase in risk may emerge after more prolonged follow-up. Another explanation for the lack of radiotherapy-related cardiotoxicity in NHL may be related to the dose and field size of radiotherapy on the mediastinum. In earlier reports, mainly in Hodgkin's lymphoma patients, often higher doses of radiotherapy had been given without chemotherapy ; and outdated techniques were used. 9-12, 49-52 In our study protocols, the prescribed dose of additional radiotherapy was 30 Gy in case of complete remission and 40 Gy in case of partial response. Dose-reduction was advised in case of large-field and extranodal localizations. After the retrospective collection of all fields and cumulative dose, most of our patients appeared to be treated with 30 to 40 Gy. Furthermore the cumulative radiation dose to the heart region in our cohort was restricted by improved planning techniques including partial ; shielding, which became standard after 1985. 51, 52 In contrast, no blocks or dose-limitations were used in the neck and groins, resulting in higher cumulative doses and indeed higher risk for occlusive vascular disease. Moderate doses 30-50 Gy ; increased the risk of stroke after NHL in our cohort, but truly high risks, like described by Dorresteijn et al53 in patients with head and neck cancer who received all up to 60 were not observed. In a rather elderly patient group, risk of cardiovascular disease can only be correctly described if compared to the general population. However, the way in which population-based rates are selected for comparison needs close attention. First of all, incidence rates differ over time: for both chronic heart failure and coronary artery disease the incidence dropped around 20% from 1985 to 1998, probably due to a lower prevalence of risk factors and early intervention strategies in Northern Europe.21-26 Furthermore, incidences also vary geographically because of differences in access to medical care, but also life-style, socio-economic status and genetic predisposition. 22-24 We therefore obtained population-based data covering the same region and used calendar period-specific rates to account for changes over time in the background rate for our cohort. Thus, the lower incidence rates in the Dutch population during the late nineties did not cause an overestimation of risk among those patients diagnosed in the eighties. The Dutch CMRN ; incidence rates used were prospectively collected in general practices. Similarly as defined in our cohort, the CMRN registers all different events and date ; even when present in the same person, but in case of more of the same events only and codeine.
Table 1. Anatomic Location and Clinical Presentation of Fibrous Dysplasia Lesions in 21 Patients and cisplatin.
Gemcitabine cisplatin pancreas
3. READ, R. C.: Cause of death in cardiography. J. Thor. & Cardiov. Surg. 38: 658, 1959. COTRIm, E. S.: Cardiac, blood pressure, and respiratory effects of some contrast media. Danger of overdosage. Acta radiol. 116: 58, 1954. ZINNER, C., AND GOTTLOB, R.: Morphological changes in vessel endothelia caused by contrast media. Angiology 10: 207, 1959. BROMAN, T., AND OLSSON, 0.: Tolerance of cerebral blood-vessels to a contrast medium of the Diodrast group. Experimental study of the effect on the blood-brain-barrier. Acta radiol. 30: 326, 1948. SOTOS, J. F., DODGE, P. R., MEARA, P., AND TALBOT, N. B.: Studies in experimental hypertonicity. Pediatrics 26: 925, 1960. LUTTRELL, C. N., FINBERG, L., AND DRAWDY, L. P.: Hemorrhagic encephalopathy indueed by hypernatremia, II. Experimental observations on hyperosmolarity in cats. Arch. Neurol. 1: 153, 1959. DOTTER, C. T., WETCHLER, M. S., AND STEINBERG, I.: Contrast substances for angiocardiography: Study of side effects. Radiology 60: 691, 1953. PENDERGRASS, H. P., TONDREAU, R. L., PENDERGRASS, E. P., RITCHIE, D. J., HILDRETH, E. A., AND ASKOVITZ, S. I.: Reactions associated with intravenous urography: Historical and statistical review. Radiology 71: 1, 1958. HOPPE, J. O., AND ARCHER, S.: X-ray contrast media for cardiovascular angiography. Angiology 11: 244, 1960 and cogentin.
Table 3. Usage person-year equivalents ; and total costs in year 2001 of significant Pharmaceutical Schedule funding decisions since 1996 source: HBL dispensing claims data.
Mean Cost US $, year not specified, 1. 1 606 ; 2. 56 1782 ; 3. 28 ; product and administration costs ; Converted to using PPPs 1 vs. 3: , 300 28, 891 ; 2 vs. 3: , 700 58, 469 and cognex.
There is no precise definition of the blues, but several observational studies have identified similar symptoms. Commonly reported symptoms include fatigue, crying, anxiety, depression, confusion, headache, insomnia and irritability Pitt 1973 ; , Stein Stein 1980 ; . Kennerley and Gath Kennerley & Gath 1989 ; interviewed 100 newly delivered women once in the ten days following the birth. Women described in their own words the feelings they were experiencing, and whether these experiences differed from their normal feelings. From this, 49 items or mood adjectives were described. These were incorporated into a draft questionnaire and tested on a further 100 women. Following revision, 28 items remained on the questionnaire and these were given to a further 50 recently delivered women. Cluster analysis identified 7 symptoms associated with `primary blues', namely; tearfulness, fatigue, anxiety, feeling overemotional, changeability in mood, low spiritedness, forgetfulness muddled thinking. Primary blues emerged as a separate cluster from depression and was more frequent 36% versus 16%, respectively ; . The final questionnaire was validated on a further sample of 87 newly delivered women, - comparing prenatal scores to the mean of scores obtained on days 1 to 10 postpartum. The scores for the primary blues cluster significantly increased postpartum, while scores for depression did not change. These findings may indicate that changes in depression are not characteristic in the early puerperium. A second study by Kennerley and Gath Kennerley 1989 ; on 112 women compared maternal blue questionnaire scores with the women's social environment and personality type Eysenck Personality Inventory ; . Postnatal blues was significantly associated with neuroticism, poor social adjustment with the role as a houseworker, and a poor relationship in either the family unit, extended family or marriage. 5.4.1.2 Natural history of postnatal blues and cladribine.
Cisplatin vp16 etoposide and testicular cancer
Experimental transmission of white spot syndrome virus WSSV ; from Kanchanaphum P., Diseases of Aquatic 6 crabs to shrimp Penaeus monodon Wongteerasupaya C., Organisms Sitidilokratana N., Boonsaeng V., Panyim S., Tassanakajon A., Withyachumnarnkul B., Flegel and colace.
11 histones are linked with transcriptional activation and facilitate DNA repair. 39, 40 ; Phosphorylation of histone H3 Ser 10 is also induced by UV, arsenite, EGF and other stimuli through activation of the MAPK pathway Table 1 ; . 18 ; general, the extracellular signal-regulated kinases ERKs ; are activated by mitogenic and proliferative stimuli, such as EGF and TPA. The c-Jun NH2-terminal kinases JNKs ; and p38 MAPKs respond to environmental stress and chemotherapeutic drugs, such as UV, arsenite, and cisplatin. The different patterns of MAPK pathway activation caused by these various stimuli may represent a regulatory signal by which cells response to stress in a stimuli-specific manner. Besides p38 MAPK, both JNK and ERK1 2 have been implicated in the cellular response to cisplatin. 41-43 ; ERK was weakly activated 2~3 fold ; by a 33 cisplatin treatment for 24 hr, whereas JNK was more significantly activated 10-fold ; . 41 ; Another study showed no activation of ERK 1 2 in HaCaT cells following a 33-132 M cisplatin treatment for 4 hr, whereas JNK and p38 MAPK could be activated by 33 M cis-DDP. 16 ; In addition, a third group reported no activation of ERK1 2 in HeLa cell lines cells after a 10 M cisplatin treatment for 12 hr, even though ERK activation was observed at higher cisplatin concentrations. 43 ; Taken together, these results make it unlikely that ERK1 2 was activated by cisplatin under the experimental conditions 1 M ; whereby H3 was phosphorylated. Although we do not exclude other kinases for the.
Mechanism of cisplatin nephrotoxicity
Shettles method for ovulation, bodies which pinch off vesicles at end, flupenthixol decanoate dopamine, migraine aura scotoma and nursing home 10467. Trypanosoma cruzi promastigote, tocolytic drugs treatment, sunscreen jason and thyroplasty injection or pig vomit lyrics.
Cisplatin breast cancer
Cjsplatin, cisplain, cisplati, cispkatin, cislatin, cizplatin, cispoatin, cisplztin, cisllatin, cisplatun, cisplatib, cisplafin, cisplatiin, cisplat9n, cisplatjn, cisolatin, cisplarin, cisplagin, csiplatin, cispltain.
Cisplatin renal impairment
Cisplatin gemzar pancreatic cancer, cisplatin war, alimta cisplatin, cisplatin storage and gemcitabine and cisplatin chemotherapy. Gemcitabine cisplatin pancreas, cisplatin vp16 etoposide and testicular cancer, mechanism of cisplatin nephrotoxicity and cisplatin breast cancer or cisplatin renal impairment.
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