Manufacturing methods for machining spring ends parallel at loaded length

A first end surface of a coiled compression spring at its relaxed length is machined to a plane transverse to the spring axis. The spring is then placed in a press structure having first and second opposed planar support surfaces, with the machined spring end surface bearing against the first support surface, the unmachined spring end surface bearing against a planar first surface of a lateral force compensation member, and an opposite, generally spherically curved surface of the compensation member bearing against the second press structure support surface. The spring is then compressed generally to its loaded length, and a circumferentially spaced series of marks, lying in a plane parallel to the second press structure support surface, are formed on the spring coil on which the second spring end surface lies. The spring is then removed from the press structure, and the second spring end surface is machined to the mark plane. When the spring is subsequently compressed to its loaded length the precisely parallel relationship between the machined spring end surfaces substantially eliminates undesirable lateral deflection of the spring

Manufacturing methods for machining spring ends parallel at loaded length

A first end surface of a coiled compression spring at its relaxed length is machined to a plane transverse to the spring axis. The spring is then placed in a press structure having first and second opposed planar support surfaces, with the machined spring end surface bearing against the first support surface, the unmachined spring end surface bearing against a planar first surface of a lateral force compensation member, and an opposite, generally spherically curved surface of the compensation member bearing against the second press structure support surface. The spring is then compressed generally to its loaded length, and a circumferentially spaced series of marks, lying in a plane parallel to the second press structure support surface, are formed on the spring coil on which the second spring end surface lies. The spring is then removed from the press structure, and the second spring end surface is machined to the mark plane. When the spring is subsequently compressed to its loaded length the precisely parallel relationship between the machined spring end surfaces substantially eliminates undesirable lateral deflection of the spring

Intravascular ultrasound scanning improves long-term patency of iliac lesions treated with balloon angioplasty and primary stenting

AbstractPurpose: Underdeployment of an intravascular stent has been identified as a cause of restenosis or occlusion of a treated arterial lesion. Intravascular ultrasound (IVUS) has been shown to initially improve the anatomic and clinical stenting. The purpose of this study was to determine whether the use of IVUS increased long-term patency of this intervention. Methods: Between March 1992 and October 1995, 71 limbs (52 patients) with symptomatic aortoiliac occlusive disease underwent balloon angioplasty with primary stenting. IVUS and arteriography were used in 49 limbs (36 patients) to evaluate stent deployment. Arteriography alone was used in 22 limbs (16 patients) to evaluate stent deployment. Patients were captured prospectively in a vascular registry and retrospectively reviewed. Results: Mean age of patients treated with IVUS was 61.1 ± 9.0 years (range, 38-85) versus 70.0 ± 10.1 years (range, 57-87) in patients treated without IVUS (P <.01). There was no difference between the groups with respect to preoperative comorbidities, ankle-brachial indices, or number of stents per limb. Mean follow-up for IVUS patients was 62.1 ± 7.3 months (range, 15-81) and 57.9 ± 8.7 months (range, 8-80) for patients treated without IVUS (P = not significant). In 40% (20/49) of limbs, IVUS demonstrated inadequate stent deployment at the time of the original procedure. Kaplan-Meier 3- and 6-year primary patency estimates were 100% and 100% in the IVUS group and 82% and 69%, respectively, in limbs treated without IVUS (P <.001). There have been no secondary procedures performed in limbs treated with IVUS and a 23% (5/22) secondary intervention rate in the non-IVUS group (P <.05). Overall Kaplan-Meier survival estimates at 3 and 6 years for all patients were 84% and 67%, respectively. Conclusion: Balloon angioplasty and primary stenting of symptomatic aortoiliac occlusive lesions is a durable treatment option. Long-term follow-up of treated patients shows outcomes that are comparable with direct surgical intervention. IVUS significantly improved the long-term patency of iliac arterial lesions treated with balloon angioplasty and stenting by defining the appropriate angioplasty diameter endpoint and adequacy of stent deployment. (J Vasc Surg 2002;35:316-23.

Six Cycles of Doxorubicin and Cyclophosphamide or Paclitaxel Are Not Superior to Four Cycles As Adjuvant Chemotherapy for Breast Cancer in Women With Zero to Three Positive Axillary Nodes: Cancer and Leukemia Group B 40101

The ideal duration of adjuvant chemotherapy for patients with lower risk primary breast cancer is not known. Cancer and Leukemia Group B trial 40101 was conducted using a phase III factorial design to define whether six cycles of a chemotherapy regimen are superior to four cycles. We also sought to determine whether paclitaxel (T) is as efficacious as doxorubicin/cyclophosphamide (AC), but with reduced toxicity

Integrated Ugi-Based Assembly of Functionally, Skeletally, and Stereochemically Diverse 1,4-Benzodiazepin-2-ones

A practical, integrated and versatile U-4CR-based assembly of 1,4-benzodiazepin-2-ones exhibiting functionally, skeletally, and stereochemically diverse substitution patterns is described. By virtue of its convergence, atom economy, and bond-forming efficiency, the methodology documented herein exemplifies the reconciliation of structural complexity and experimental simplicity in the context of medicinal chemistry projects.This work was financially supported by the Galician Government (Spain), Projects: 09CSA016234PR and GPC-2014-PG037. J.A. thanks FUNDAYACUCHO (Venezuela) for a predoctoral grant and Deputación da Coruña (Spain) for a postdoctoral research grant. A.N.-V. thanks the Spanish government for a Ramón y Cajal research contract

Genetic Variants For Head Size Share Genes and Pathways With Cancer

The size of the human head is highly heritable, but genetic drivers of its variation within the general population remain unmapped. We perform a genome-wide association study on head size (N = 80,890) and identify 67 genetic loci, of which 50 are novel. Neuroimaging studies show that 17 variants affect specific brain areas, but most have widespread effects. Gene set enrichment is observed for various cancers and the p53, Wnt, and ErbB signaling pathways. Genes harboring lead variants are enriched for macrocephaly syndrome genes (37-fold) and high-fidelity cancer genes (9-fold), which is not seen for human height variants. Head size variants are also near genes preferentially expressed in intermediate progenitor cells, neural cells linked to evolutionary brain expansion. Our results indicate that genes regulating early brain and cranial growth incline to neoplasia later in life, irrespective of height. This warrants investigation of clinical implications of the link between head size and cancer

Inheritance of quantitative expression of erythrocyte glucose-6-phosphate dehydrogenase activity in the Negro—a twin study

Studies have been conducted on eight sets of monozygous and nine sets of dizygous female Negro twins, both members of whom were heterozygous for G-6-PD deficiency. Twins were studied both by assay of erythrocytic G-6-PD activity and by the methemoglobin elution test (MET). The MET is a procedure which identifies histochemically cells with appreciable G-6-PD activity and permits accurate determination of the percentage of such cells in heterozygotes. Monozygous twins showed significantly less “within-pair” variation than dizygous twins with both the MET and G-6-PD assay.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44115/1/10528_2004_Article_BF00487735.pd

Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects

Copy number variants (CNVs) have been strongly implicated in the genetic etiology of schizophrenia (SCZ). However, genome-wide investigation of the contribution of CNV to risk has been hampered by limited sample sizes. We sought to address this obstacle by applying a centralized analysis pipeline to a SCZ cohort of 21,094 cases and 20,227 controls. A global enrichment of CNV burden was observed in cases (OR=1.11, P=5.7×10−15), which persisted after excluding loci implicated in previous studies (OR=1.07, P=1.7 ×10−6). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 ×10−11) and neurobehavioral phenotypes in mouse (OR = 1.18, P= 7.3 ×10−5). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by non-allelic homologous recombination