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Träfflista för sökning "WFRF:(Hassan S) srt2:(1995-1999)"

Sökning: WFRF:(Hassan S) > (1995-1999)

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  • Sohler, D, et al. (författare)
  • Spectroscopy of neutron deficient Ge-65
  • 1997
  • Ingår i: Zeitschrift für Physik A Hadrons and Nuclei. - : Springer Science and Business Media LLC. - 0939-7922 .- 1431-5831. ; 357:3, s. 239-240
  • Tidskriftsartikel (refereegranskat)abstract
    • Excited states of 65Ge were populated via the 12C + 58Ni (261 MeV) reaction using the NORDBALL detector array equipped with charged-particle and neutron detector systems for reaction channel separation. On the basis of γγ-coincidence relations and angular distribution ratios a significantly extended level scheme was constructed up to E x = 9 MeV and J π = (33/2−). The low-energy states of the nucleus are discussed in the framework of the interacting boson-fermion model.
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  • Hassan, M, et al. (författare)
  • A mechanism-based pharmacokinetic-enzyme model for cyclophosphamide autoinduction in breast cancer patients
  • 1999
  • Ingår i: British Journal of Clinical Pharmacology. - 0306-5251 .- 1365-2125. ; 48:5, s. 669-677
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims This study investigated the pharmacokinetics of cyclophosphamide (CP) and its main metabolite 4-hydroxycyclophosphamide (4-OH-CP) in patients with breast cancer undergoing high dose chemotherapy prior to autologous stem cell transplantation. An enzyme turn-over model was also developed to study the time course of cyclophosphamide induction. Methods Fourteen patients received a combination of CP (6 g m(-2)), thiotepum (500 mg m(-2)) and carboplatin (800 mg m(-2)) as a 96 h infusion. Plasma concentrations of CP and 4-OH-CP were determined with h.p.l.c. and a pharmacokinetic and enzyme turn-over model applied to data using NONMEM. Results CP plasma concentrations were described by a two-compartment model with a noninducible and an inducible pathway, the latter forming 4-OH-CP. In the final enzyme model, CP affects the amount of enzymes by increasing the enzyme production rate. CP concentrations decreased during the infusion with no subsequent change in 4-OH-CP concentrations. CP inducible and noninducible clearance were estimated to 1.76 1 h(-1) (90% C.I. 0.92-2.58) and 1.14 1 h(-1) (0.31-1.85), respectively. The induction resulted in an approximately doubled CP clearance through the inducible pathway at the end of treatment. The model predicted the enzyme turn-over half-life to be 24 h. Conclusions The presented mechanism-based enzyme induction model where the pharmacokinetics of the inducer and the enzyme pool counterbalance each other successfully described CP autoinduction. It is reasonable to believe that CP affects its own elimination by increasing the enzyme production rate and thereby increasing the amount of enzyme by which CP is eliminated.
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  • Imam, S. A. Hassan (författare)
  • Neuroendocrine tumors of the digestive system : Modulation of apoptosis and factors associated with growth regulation during biotherapies
  • 1998
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Neuroendocrine tumors of the gut have the potential to create life-threatening syndromes which become difficult to treat. Tumor mass reduction, by medical therapy, is one of the choices of treatments. Induction of apoptosis and modulation of factors related to apoptosis as well as different growth regulatory factors by treatment, alters tumor growth and improves symptoms.Interferon-α (IFN-α), somatostatin analogs and combination of both were used for medical treatment. Increased apoptosis was observed in 62% of patients who demonstrated a biochemical response to the treatment of high dose (12mg/day) of somatostatin analog, lanreotide. There was no significant change in apoptotic index with neither IFN-α, low dose somatostatin analog nor combination treatment. The xenographated tumors (BON-1 cell line) and in vitro test showed increased tumor growth inhibition with combination therapy of IFN-α and somatostatin analog even at a low dose (p=0.0011 & p<0.001 respectively). IFN-α did not increase apoptosis but induced the bcl-2 gene in patients responding to the treatment. This finding correlates with the inhibition of cell cycle progression, a described function of IFN-α. Carcinoid tumors, in patients with stable disease condition, expressed another apoptosis modulator bcl-xL, which is suitable as a prognostic marker. In endocrine pancreatic tumors, the adhesion molecule CD44 expression was analyzed. Variant isoforms of CD44, v6 and v9 expression were inversely correlated to malignant transformation (p=0.0352 and 0.0266 respectively) which are suitableas prognostic indicators.Interferon induced protein, MxA, expression was studied in 122 patients with neuroendocrine tumors. All of the patients were treated with IFN-α and showed MxA expression at the mRNA level with no correlation to the clinical outcome of the treatment and thus MxA is not suitable as a predictive marker for treatment response.
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