8,822 research outputs found

    The Plaintiff\u27s Burden in Sex-Based Wage Discrimination Claims—\u3ci\u3eInternational Union, United Automobile, Aerospace & Agricultural Implement Workers of America v. State of Michigan\u3c/i\u3e, 886 F.2d 766 (6th Cir. 1989)

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    International Union, United Automobile, Aerospace & Agricultural Implement Workers of America v. State of Michigan (UAW) is the most recent interpretation of a plaintiff\u27s evidentiary burden under a Title VII claim of sex-based wage discrimination. UAW held that job evaluation studies showing pay differentials between female and male dominated jobs of equal worth are insufficient to prove intentional discrimination. The court\u27s holding was not required by previous case law and serves to make sex-based wage discrimination claims more difficult to prove than other Title VII claims. A plaintiff bringing a sex-based wage discrimination claim can no longer create an inference of intent; the plaintiff must prove intent. This Note examines those arguments addressing the issue of intent and analyzes the effect of the court\u27s holding. First, the Note introduces the UAW case, its facts, and the arguments related to intent that the court relied on. Second, this Note analyzes the court\u27s justifications for holding job evaluations insufficient to prove discrimination. The Note focuses on the court\u27s erroneous interpretation of previous discrimination cases involving statistical evidence, the court\u27s unprecedented and unwise decision that employers should be able to rely on the market to set wages, and the court\u27s failure to consider traditional considerations in allocating the burden of proof. The Note then addresses the court\u27s illogical concerns about imposing a wage scale on employers. The Note concludes that the UAW decision effectively denies employees their Title VII claims by disproportionately increasing the plaintiff\u27s burden in these cases. Finally, the Note suggests that shifting the burden of proof to the employer would permit employees to bring claims and still protect the employer\u27s interests. A model for this allocation is presented along with a discussion as to how this shift would address valid concerns raised by the court in UAW, including the employer\u27s disincentive to conduct job evaluation studies if the studies could be used to create an irrebuttable presumption of discrimination

    Effects of Career Plateauing on Turnover: A Test of a Model

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    The structure of most organizations dictates that only 1% of the employees will retire before they reach a career plateau. It is estimated that the number of people perceiving they are career plateaued will only increase in the future since more unusually well-qualified candidates will be competing for a diminishing number of positions. Given that an estimated 80% of the work conducted in organizations is performed by employees who are career plateaued, it would be beneficial to better understand if these plateaued individuals are likely to remain with the organization despite being plateaued. Therefore adding career plateauing to an existing turnover model could be beneficial in furthering our understanding of the turnover process. As such the primary purpose of this research was the introduction of the concept of career plateauing into an existing turnover model to investigate potential effects on turnover. Results from this study showed that perceptions of begin career plateaued did account for variance in turnover and the degree to which one believed himself to be plateaued was positively associated with one\u27s intent to leave an organization

    Anti-tumor necrosis factor-alpha therapy during murine Klebsiella pneumoniae bacteremia: increased mortality in the absence of liver injury.

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    Klebsiella pneumoniae is a leading cause of gram-negative bacterial pneumonia, often resulting in bacteremia concurrent with the localized pulmonary infection. The beneficial role of tumor necrosis factor (TNF)-alpha during pulmonary infection has been well documented; however, consequences of TNF-alpha production during systemic bacterial infection are controversial. A murine model of K. pneumoniae was developed to address this important issue. Liver-associated TNF-alpha mRNA was induced within 30 min after intravenous bacterial inoculation and remained elevated through 6 h before returning to near-baseline at 24 h postinfection. Intravenous K. pneumoniae infection induced liver cellular injury that was completely ablated when mice were pretreated with a neutralizing anti-TNF-alpha antibody. Interestingly, this reduction in liver injury failed to translate into improved survival. Mice receiving anti-TNF-alpha continued to succumb to the infection even out to day 10 postinfection. Bacterial clearance after TNF-alpha neutralization was significantly impaired at later time points during infection. Correlating with impaired bacterial clearance was diminished production of liver-associated MIP-2, MIP-1alpha, MCP-1, and interferon-gamma. Further evidence of diminished antibacterial immune responses was noted when the activational status of splenic natural killer cells in anti-TNF-alpha-treated mice was examined 24 h postinfection. Natural killer cells displayed decreased CD69 expression. Combined, these data indicate that the beneficial effects of TNF-alpha during systemic K. pneumoniae infection outweigh the detrimental effects of TNF-alpha-mediated hepatocyte cellular injury. Anti-TNF-alpha therapy, although preventing liver injury during blood-borne bacterial infection, results in a dampened anti-bacterial host response, resulting in decreased bacterial clearance and overall survival

    Individual heat map assessments demonstrate vestronidase alfa treatment response in a highly heterogeneous mucopolysaccharidosis VII study population.

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    Mucopolysaccharidosis (MPS) VII is an ultra-rare, progressively debilitating, life-threatening lysosomal disease caused by deficiency of the enzyme, β-glucuronidase. Vestronidase alfa is an approved enzyme replacement therapy for MPS VII. UX003-CL301 was a phase 3, randomized, placebo-controlled, blind-start study examining the efficacy and safety of vestronidase alfa 4 mg/kg intravenously administered every 2 weeks to 12 patients with MPS VII. Due to the rarity of disease, broad eligibility criteria resulted in a highly heterogeneous population with variable symptoms. For an integrated view of the diverse data, the changes from baseline (or randomization for the placebo period) in clinical endpoints were grouped into three functional domains (mobility, fatigue, and fine motor + self-care) and analyzed post-hoc as subject-level heat maps. Mobility assessments included the 6-minute walk test, 3-minute stair climb test, Bruininks-Oseretsky test (BOT-2) gross motor function subtests, and patient-reported outcome assessments (PROs) related to movement, pain, and ambulation. Fatigue assessments included the Pediatric Quality of Life Multidimensional Fatigue Scale and other fatigue-related PROs. Fine motor + self-care assessments included BOT-2 fine motor function subtests and PROs for eating, dressing, hygiene, and caregiver assistance. Most subjects showed improvement in at least one domain. Two subjects improved in two or more domains and two subjects did not show clear improvement in any domain. Both severely and mildly affected subjects improved with vestronidase alfa in clinical assessments, PRO results, or both. Heat map analysis demonstrates how subjects responded to treatment across multiple domains, providing a useful visual tool for studying rare diseases with variable symptoms

    Poly(2-cyclopropyl-2-oxazoline): from rate acceleration by Cyclopropyl to Thermoresponsive properties

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    The synthesis and microwave-assisted living cationic ring-opening polymerization of 2-cyclopropyl-2-oxazoline is reported revealing the fastest polymerization for an aliphatic substituted 2-oxazoline to date, which is ascribed to the electron withdrawing effect of the cyclopropyl group. The poly(2-cyclopropyl-2-oxazoline) (pCPropOx) represents an alternative thermo-responsive poly(2-oxazoline) with a reversible critical temperature close to body temperature. The cloud point (CP) of the obtained pCPropOx in aqueous solution was evaluated in detail by turbidimetry, dynamic light scattering (DLS) and viscosity measurements. pCPropOx is amorphous with a significantly higher glass transition temperature (T(g) similar to 80 degrees C) compared to the amorphous poly(2-n-propyl-2-oxazoline) (pnPropOx) (T(g) similar to 40 degrees C), while poly(2-isopropyl-2-oxazoline) piPropOx is semicrystalline. In addition, a pCPropOx comb polymer was prepared by methacrylic acid end-capping of the living cationic species followed by RAFT polymerization of the macromonomer. The polymer architecture does not influence the concentration dependence of the CP, however, both the CP and T(g) of the comb polymer are lower due to the increased number of hydrophobic end groups

    The Drosophila Caspase DRONC Cleaves following Glutamate or Aspartate and Is Regulated by DIAP1, HID, and GRIM

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    The caspase family of cysteine proteases plays important roles in bringing about apoptotic cell death. All caspases studied to date cleave substrates COOH-terminal to an aspartate. Here we show that the Drosophila caspase DRONC cleaves COOH-terminal to glutamate as well as aspartate. DRONC autoprocesses itself following a glutamate residue, but processes a second caspase, drICE, following an aspartate. DRONC prefers tetrapeptide substrates in which aliphatic amino acids are present at the P2 position, and the P1 residue can be either aspartate or glutamate. Expression of a dominant negative form of DRONC blocks cell death induced by the Drosophila cell death activators reaper, hid, and grim, and DRONC overexpression in flies promotes cell death. Furthermore, the Drosophila cell death inhibitor DIAP1 inhibits DRONC activity in yeast, and DIAP1's ability to inhibit DRONC-dependent yeast cell death is suppressed by HID and GRIM. These observations suggest that DRONC acts to promote cell death. However, DRONC activity is not suppressed by the caspase inhibitor and cell death suppressor baculovirus p35. We discuss possible models for DRONC function as a cell death inhibitor

    Tooley Brooks No Exceptions—Equity Dilution Is Direct

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    Today\u27s corporate pie versus the classical view of equity dilution as a derivative claim
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