Pharmacoeconomic analysis of prostaglandin and prostamide therapy for patients with glaucoma or ocular hypertension

BACKGROUND: To determine monthly cost and cost effectiveness of bilateral prostaglandin/prostamide therapy for lowering intraocular pressure (IOP) in patients taking bimatoprost 0.03% (Lumigan(®), Allergan, Inc.), latanoprost 0.005% (Xalatan(®), Pfizer, Inc.), or travoprost 0.004% (Travatan(®), Alcon Laboratories, Inc.). METHODS: Drops in five new 2.5-mL bottles were counted and then averaged for each drug. Average retail price was determined by surveys of pharmacies. Drop count, average retail price, average wholesale price, and IOP reduction data were used to compute annual cost, and cost effectiveness (annual cost-per-mm Hg of IOP reduction) of the three drugs. RESULTS: Drops per 2.5-mL bottle averaged 113 for bimatoprost 0.03%, 84 for latanoprost 0.005%, and 83 for travoprost 0.004%. Average retail cost (2005) per bottle was $69.99 for bimatoprost 0.03$61.69 for latanoprost 0.005%, and $66.37 for travoprost 0.004$37.92 for bimatoprost 0.03%, $44.75 for latanoprost 0.005$49.25 for travoprost 0.004%. Cost effectiveness ranges were $57 to$65 per mm Hg reduction in IOP per year for bimatoprost, 0.03%, $67 to$90 per mm Hg for latanoprost 0.005%, and $74 to$84 per mm Hg for travoprost 0.004%. CONCLUSION: Bimatoprost 0.03% had the lowest monthly and annual costs and the greatest cost effectiveness for lowering IOP compared with latanoprost 0.005% and travoprost 0.004%

The Quantum Spectrum of the Conserved Charges in Affine Toda Theories

The exact eigenvalues of the infinite set of conserved charges on the multi-particle states in affine Toda theories are determined. This is done by constructing a free field realization of the Zamolodchikov-Faddeev algebra in which the conserved charges are realized as derivative operators. The resulting eigenvalues are renormalization group (RG) invariant, have the correct classical limit and pass checks in first order perturbation theory. For $n=1$ one recovers the (RG invariant form of the) quantum masses of Destri and DeVega.Comment: 38p, 1 fig. included, MPI-Ph/93-92, LATE

Effects of cellular iron deficiency on the formation of vascular endothelial growth factor and angiogenesis. Iron deficiency and angiogenesis

<p>Abstract</p> <p>Background</p> <p>Young women diagnosed with breast cancer are known to have a higher mortality rate from the disease than older patients. Specific risk factors leading to this poorer outcome have not been identified. In the present study, we hypothesized that iron deficiency, a common ailment in young women, contributes to the poor outcome by promoting the hypoxia inducible factor-1α (HIF-1α and vascular endothelial growth factor (VEGF) formation. This hypothesis was tested in an <it>in vitro </it>cell culture model system.</p> <p>Results</p> <p>Human breast cancer MDA-MB-231 cells were transfected with transferrin receptor-1 (TfR1) shRNA to constitutively impair iron uptake. Cellular iron status was determined by a set of iron proteins and angiogenesis was evaluated by levels of VEGF in cells as well as by a mouse xenograft model. Significant decreases in ferritin with concomitant increases in VEGF were observed in TfR1 knockdown MDA-MB-231 cells when compared to the parental cells. TfR1 shRNA transfectants also evoked a stronger angiogenic response after the cells were injected subcutaneously into nude mice. The molecular mechanism appears that cellular iron deficiency elevates VEGF formation by stabilizing HIF-1α. This mechanism is also true in human breast cancer MCF-7 and liver cancer HepG2 cells.</p> <p>Conclusions</p> <p>Cellular iron deficiency increased HIF-1α, VEGF, and angiogenesis, suggesting that systemic iron deficiency might play an important part in the tumor angiogenesis and recurrence in this young age group of breast cancer patients.</p

An Algebraic Approach to Form Factors

An associative $*$-algebra is introduced (containing a $TTR$-algebra as a subalgebra) that implements the form factor axioms, and hence indirectly the Wightman axioms, in the following sense: Each $T$-invariant linear functional over the algebra automatically satisfies all the form factor axioms. It is argued that this answers the question (posed in the functional Bethe ansatz) how to select the dynamically correct representations of the $TTR$-algebra. Applied to the case of integrable QFTs with diagonal factorized scattering theory a universal formula for the eigenvalues of the conserved charges emerges.Comment: A simplified form of the algebra is used that allows one to dispense with the extra generator C. To appear in Nucl. Phys.

Form Factors, Thermal States and Modular Structures

Form factor sequences of an integrable QFT can be defined axiomatically as solutions of a system of recursive functional equations, known as ``form factor equations''. We show that their solution can be replaced with the study of the representation theory of a novel algebra F(S). It is associated with a given two-particle S-matrix and has the following features: (i) It contains a double TTS algebra as a subalgebra. (ii) Form factors arise as thermal vector states over F(S) of temperature 1/2\pi. The thermal ground states are in correspondence to the local operators of the QFT. (iii) The underlying `finite temperature structure' is indirectly related to the ``Unruh effect'' in Rindler spacetime. In F(S) it is manifest through modular structures (j,\delta) in the sense of algebraic QFT, which can be implemented explicitly in terms of the TTS generators.Comment: 40 pages, Latex. Simplification of the algebra and updat

Aufzeichnungen ueber Frankfurter Persoenlichkeiten.

Report on Jewish life in Frankfurt in the 19th century. Pays special interest on Frankfurt rabbis.Brief summary in Max Kreutzberger: "Leo Baeck Institute New York, Bibliothek und Archiv; Katalog": C10

An oligogenic case of severe neonatal thrombocytopenia and a purportedly benign variant in GFI1B requiring reinterpretation

Although thrombocytopenia in neonatal intensive care patients is rarely due to inherited disorders, the number of genetic variants implicated in platelet defects has grown dramatically with increasing genome-wide sequencing. Here we describe a case of severe, oligogenic neonatal thrombocytopenia and reinterpret a reportedly benign mutation that is likely pathogenic. Despite this patient’s synonymous mutation (GFI1B 576 C>T, Phe192=) being annotated as benign, GFI1B is a well-known regulator of megakaryopoiesis, this variant alters splicing and megakaryocyte maturation, and our analysis of existing genome-wide associated studies demonstrates that it likely causes gray platelet syndrome. This variant has not been reported in a case of life-threatening thrombocytopenia. We propose that the severity of this patient’s phenotype is due to synergistic epistasis between the intrinsic platelet defect caused by this mutation and her concomitant inherited PMM2 congenital glycosylation disorder neither of which have been associated with such a severe phenotype. This case highlights the importance of whole-exome/genome sequencing for critically ill patients, reexamining variant interpretation when clinically indicated, and the need to study diverse genetic variation in hematopoiesis