152 research outputs found

    Ethical Issues Arising When a Lawyer Leaves a Firm: Restrictions on Practice

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    Restriction on covenants not to compete have been a long-time feature of legal practice. Rules prohibiting law firms from restricting lawyers\u27 ability to practice or imposing penalties on lawyers that leave a firm attempt to balance the law firm\u27s interest in survival in a competitive market with the countervailing interests of attorney mobility, and protecting clients\u27 choice of counsel. Restrictions on covenants not to compete should be vigorously enforced, and the exception that allows for the forfeiture of retirement benefits by attorneys that choose to leave a firm should be narrowly applied to only those funds to which the departing attorney is not already entitled

    Ethical Issues Arising When a Lawyer Leaves a Firm: Restrictions on Practice

    Get PDF
    Restriction on covenants not to compete have been a long-time feature of legal practice. Rules prohibiting law firms from restricting lawyers\u27 ability to practice or imposing penalties on lawyers that leave a firm attempt to balance the law firm\u27s interest in survival in a competitive market with the countervailing interests of attorney mobility, and protecting clients\u27 choice of counsel. Restrictions on covenants not to compete should be vigorously enforced, and the exception that allows for the forfeiture of retirement benefits by attorneys that choose to leave a firm should be narrowly applied to only those funds to which the departing attorney is not already entitled

    Stranded Costs: Will They Torpedo Retail Choice in the Electric Industry?

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    Our speakers have come a long way and we will not allow them to leave without saying something. On our panel today we have Richard La Capra, Founder and Principal of La Capra Associates. He has been involved in major restructuring activity in all six New England states, other parts of the country, and overseas. His biography is contained in your materials. Our second speaker is Philip O\u27Connor. Dr. O\u27Connor is with Coopers & Lybrand Consulting and is a former chair of the Illinois Commerce Commission. He is a nationally recognized expert on the development and implementation of competitive strategies in regulated industries. His biography is also included in your package. We have an additional handout from Dr. O\u27Connor, located at the front of the room. Now, I\u27ll ask Richard to give us no more than a ten minute overview of his position on stranded costs and how that will impact retail competition. Then, we will have Dr. O\u27Connor speak and open up for questions

    Hsp72 is targeted to the mitotic spindle by Nek6 to promote K-fiber assembly and mitotic progression

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    Hsp70 proteins represent a family of chaperones that regulate cellular homeostasis and are required for cancer cell survival. However, their function and regulation in mitosis remain unknown. In this paper, we show that the major inducible cytoplasmic Hsp70 isoform, Hsp72, is required for assembly of a robust bipolar spindle capable of efficient chromosome congression. Mechanistically, Hsp72 associates with the K-fiber-stabilizing proteins, ch-TOG and TACC3, and promotes their interaction with each other and recruitment to spindle microtubules (MTs). Targeting of Hsp72 to the mitotic spindle is dependent on phosphorylation at Thr-66 within its nucleotide-binding domain by the Nek6 kinase. Phosphorylated Hsp72 concentrates on spindle poles and sites of MT-kinetochore attachment. A phosphomimetic Hsp72 mutant rescued defects in K-fiber assembly, ch-TOG/TACC3 recruitment and mitotic progression that also resulted from Nek6 depletion. We therefore propose that Nek6 facilitates association of Hsp72 with the mitotic spindle, where it promotes stable K-fiber assembly through recruitment of the ch-TOG-TACC3 complex

    Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

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    Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

    An astrocyte-dependent mechanism for neuronal rhythmogenesis

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    Communication between neurons rests on their capacity to change their firing pattern to encode different messages. For several vital functions, such as respiration and mastication, neurons need to generate a rhythmic firing pattern. Here we show in the rat trigeminal sensori-motor circuit for mastication that this ability depends on regulation of the extracellular Ca2+ concentration ([Ca2+]e) by astrocytes. In this circuit, astrocytes respond to sensory stimuli that induce neuronal rhythmic activity, and their blockade with a Ca2+ chelator prevents neurons from generating a rhythmic bursting pattern. This ability is restored by adding S100b, an astrocytic Ca2+-binding protein, to the extracellular space, while application of an anti-S100b antibody prevents generation of rhythmic activity. These results indicate that astrocytes regulate a fundamental neuronal property: the capacity to change firing pattern. These findings may have broad implications for many other neural networks whose functions depend on the generation of rhythmic activity
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