Immunology: High fecundity rates following in- vitro fertilization and embryo transfer in antiphospholipid antibody seropositive women treated with heparin and aspirin

This study was undertaken to explore whether intervention withheparin and aspirin (H/A) in selected patients undergoing in-vitrofertilization (TVF) and embryo transfer could improve fecundityrates. Specifically, it explored the possibility that womendiagnosed with organic pelvic disease who demonstrated antiphospholipidantibodies (APA) could benefit from H/A administration in asimilar manner to that used in patients with recurrent pregnancyloss. We used an enzyme–linked immunosorbent assay forsix different phospholipids to identify patients who expressedAPA before they underwent IVF/embryo transfer. This study wasconfined to the first IVF/embryo transfer cycle that followedassessment of APA status and accordingly, the number of IVF/embryotransfer cycles corresponds with the number of patients treated.APA seropositive patients were treated with aspirin, 81 mg orallyq.d., and heparin 5000 IU s.c. b.i.d., beginning on day 1 ofcontrolled ovarian stimulation. The endpoint for success wasa live birth or an ultrasound confirming fetal cardiac activity(a viable pregnancy). The prevalence of APA in patients diagnosedwith organic pelvic disease (53%) was much higher than in thosewithout female pathology (14%). The administration of H/A toAPA seropositive patients significantly (P < 0.05) improvedthe viable pregnancy rate (49%) compared to the untreated APAseropositive group (16%). The viable pregnancy rate for APAseropositive women treated with H/A was also significantly (P< 0.001) higher than for untreated APA seronegative patients(27%). We conclude that all women undergoing IVF/embryo transfershould be tested for APA prior to initiating ovarian stimulation,and those with APA seropositivity should be treated with H/A.     

Neonatal repair of right interrupted aortic arch, aberrant left subclavian artery, ventricular septal defect and retroaortic innominate vein.

We report a rare case of neonatal biventricular repair of a right interrupted aortic arch (type B), with an aberrant left subclavian artery, ventricular septal defect and retroaortic innominate vein in a 4-week-old, 2.7 kg neonate with DiGeorge syndrome. The patient had an unremarkable postoperative recovery. We discuss the anatomy of this rare congenital anomaly, its surgical implications and issues surrounding the adequacy of the left ventricular outflow tract.     

Polyesters prepared by polycondensation in the presence of carbodiimides, 2. On the reaction of methyl α-(S)-malate with N,N′-dicyclohexylcarbodiimide under mild conditions

The reaction of methyl α-(S)-malate with N,N′-dicyclohexylcarbodiimide in the presence of amines under mild conditions was studied. It was established that in solvents with weak donor properties, N-acyl derivatives are preferentially formed instead of ester condensation products. An optically active polymer fraction was separated by precipitation in diethyl ether (yield up to 30%) with M?_n,GPC 1 000 to 4 000 and of low polydispersity M?_w/M?_n = 1,1–1,4. The method permits the preparation of optically active biodegradable condensation products with controlled molecular structure.     

Association analysis of a polymorphism in the G‐protein stimulatory α subunit in patients with major depression*

Growing evidence suggests that G‐proteins may be involved in pathogenesis and treatment of affective disorders. Several studies have reported altered levels and/or activities of stimulatory G‐proteins in depression. The aim of this study was to investigate whether a polymorphism in the stimulatory α subunit of G‐proteins (T/C point mutation in exon 5; ATT → ATC at codon 131) is associated with major depression or response to antidepressant treatment. Therefore, we performed a case‐control association study with 212 depressive patients and 137 healthy, unrelated controls. There was no evidence for an association between the investigated polymorphism in the Gα_s gene and major depression, as well as to treatment response. The results of our study are in concordance with recently published findings which do not support the hypothesis that the gene for the stimulatory α subunit of G‐proteins is a major susceptibility factor in the pathophysiology of major depression. © 2002 Wiley‐Liss, Inc.     

The influence of intermolecular interactions on the polymerization, 1·1H NMR investigation of solutions of naphthalene and methyl methacrylate,of 2-naphthyl methacrylate,and of 1-naphthyl methacrylate

The solutions of methyl methacrylate (MMA) and naphthalene (N), of 2-naphthyl methacrylate (2-NM) and of 1-naphthyl methacrylate (1-NM) in chloroform, acetone, acetonitrile and N,N-dimethylformamide are studied by ¹H NMR spectroscopy. In chloroform and in pure MMA, N causes a shift of the signal of the high field vinyl proton H_a of MMA to higher field, whereas in acetone and acetonitrile the signal of H_a has the τ-value for MMA in the absence of N. The H_a signals of 2-NM and 1-NM in acetone, acetonitrile and N,N-dimethylformamide shift downfield as compared with those in chloroform. The τ-value of the downfield vinyl proton H_b does not vary with a change of the solvent. The separation of the vinyl signals Δ=τ(H_a)—τ(H_b) becomes equal to that of pure MMA. The formation of 1:1 complexes between the electron donating naphthalene ring and the electron accepting methacrylic double bond is assumed. The stability constant of the MMA-N complex is 0,22 1.mol^?1. Some structures for the complexes are proposed on the basis of molecular models of the monomer molecules. The results confirm the known theories for the influence of the solvents in radical polymerization of MMA. They can explain the kinetic changes of polymerization of 2-NM and 1-NM.     

Multiple myeloma regression mediated by bruceantin.

PURPOSE: Bruceantin has been shown to induce cell differentiation in a number of leukemia and lymphoma cell lines. It also down-regulated c-MYC, suggesting a correlation of down-regulation with induction of cell differentiation or cell death. In the present study, we focused on multiple myeloma, using the RPMI 8226 cell line as a model. EXPERIMENTAL DESIGN: The effects of bruceantin on c-MYC levels and apoptosis were examined by immunoblotting, 4',6-diamidino-2-phenylindole staining, evaluation of caspase-like activity, and 3,3'-dihexyloxacarbocyanine iodide staining. The potential of bruceantin to inhibit primary tumor growth was assessed with RPMI 8226 xenografts in SCID mice, and apoptosis in the tumors was evaluated by the terminal deoxynucleotidyl transferase-mediated nick end labeling assay. RESULTS: c-MYC was strongly down-regulated in cultured RPMI 8226 cells by treatment with bruceantin for 24 h. With U266 and H929 cells, bruceantin did not regulate c-MYC in this manner. Apoptosis was induced in the three cell lines. In RPMI 8226 cells, apoptosis occurred through proteolytic processing of procaspases and degradation of poly(ADP-ribose) polymerase. The mitochondrial pathway was also involved. Because RPMI 8226 cells were the most sensitive, they were used in a xenograft model. Bruceantin treatment (2.5-5 mg/kg) resulted in a significant regression of tumors without overt toxicity. Apoptosis was significantly elevated in tumors derived from animals treated with bruceantin (37%) as compared with the control tumors (14%). CONCLUSIONS: Bruceantin interferes with the growth of RPMI 8226 cells in cell culture and xenograft models. These results suggest that bruceantin should be reinvestigated for clinical efficacy against multiple myeloma and other hematological malignancies.     

Prosthesis cost containment in total joint replacement: a physician-driven free-market approach

As an alternative to a limited vendor/volume discount approach, our hospital employed a physician-driven free market strategy aimed at reducing joint implant costs. Surgeons were provided with vendor pricing and peer profile comparisons of implant cost data and asked to select implants providing the best value based on patient need. Vendors were challenged to reduce prices where appropriate. Total savings based on the 1995-1997 volume-adjusted cost difference were $1,059,159, a 17.5% decrease. These results demonstrate the possibility of reducing joint implant costs using a strategy that does not limit vendors or cap prices.