Defenses to Group Defamation Actions

The basic defenses applicable to ordinary individual defamation, of truth, privilege (including fair comment), and consent, also apply to group defamation. Most past group defamation cases have held that language including all members of a given group,or positively identifying the plaintiff, must be used. Tort actions have been upheld when small groups are defamed; tort claims are generally disallowed in the defamation of large groups unless the public readily recognizes the defamation as being directed at one individual. A number of group-hate statutes have been enacted by various states, making it a criminal offense to defame a class of citizens. Defenses based on truth are difficult to establish because of the statistical complications encountered in groups of large numbers. The best defense to these statutes appears to be based on fair comment and the constitutional guarantees of the First Amendment

Cytosolic calcium and protein kinase C reduce complement-mediated glomerular epithelial injury

Cytosolic calcium and protein kinase C reduce complement-mediated glomerular epithelial injury. In rat membranous nephropathy, proteinuria is due to formation of the C5b-9 membrane attack complex of complement (C), and is associated with morphological evidence of glomerular epithelial cell (GEC) injury. Analogous morphological changes are induced by C5b-9 in cultured GEC. In addition, in cultured GEC C5b-9 induces Ca2+ influx, as well as Ca2+ mobilization and increased 1,2-diacylglycerol due to the activation of phospholipase C. In this study we investigated how this GEC activation pattern might influence C-mecliated GEC injury. We demonstrate that the C5b-9-induced increase in cytosolic Ca2+ concentration ([Ca2+]i) did not impair ATP generation by mitochondria, suggesting that it does not contribute to cytotoxicity. Moreover, this increase in [Ca2+]i protected GEC from C-mediated cytolysis. However, a large increase in [Ca2+]i (produced by the Ca2+ ionophore A23187) impaired ATP generation and aggravated C-mediated cytotoxicity, suggesting that intact mitochondrial activity is necessary for GEC to withstand C attack. Activation of protein kinase C (PKC) by phorbol myristate acetate (PMA) also decreased C-mediated cytolysis. Conversely, C lysis was enhanced in GEC that had been pretreated for 18 hours with a high dose of PMA to deplete PKC, and following PKC inhibition with H-7. Therefore, PKC activation, possibly resulting from C5b-9-induced increase in 1,2-diacylglycerol, triggered mechanisms that protected GEC from C-mediated injury. Thus, as a consequence of C5b-9-induced phospholipase activation, the amount of C-induced GEC injury is diminished

Clinical Utility of Microarrays: Current Status, Existing Challenges and Future Outlook

Microarray-based clinical tests have become powerful tools in the diagnosis and treatment of diseases. In contrast to traditional DNA-based tests that largely focus on single genes associated with rare conditions, microarray-based tests are ideal for the study of diseases with underlying complex genetic causes. Several microarray based tests have been translated into clinical practice such as MammaPrint and AmpliChip CYP450. Additional cancer-related microarray-based tests are either in the process of FDA review or under active development, including Tissue of Tumor Origin and AmpliChip p53. All diagnostic microarray testing is ordered by physicians and tested by a Clinical Laboratories Improvement Amendment-certified (CLIA) reference laboratory. Recently, companies offering consumer based microarray testing have emerged. Individuals can order tests online and service providers deliver the results directly to the clients via a password-protected secure website. Navigenics, 23andMe and deCODE Genetics represent pioneering companies in this field. Although the progress of these microarray-based tests is extremely encouraging with the potential to revolutionize the recognition and treatment of common diseases, these tests are still in their infancy and face technical, clinical and marketing challenges. In this article, we review microarray-based tests which are currently approved or under review by the FDA, as well as the consumer-based testing. We also provide a summary of the challenges and strategic solutions in the development and clinical use of the microarray-based tests. Finally, we present a brief outlook for the future of microarray-based clinical applications

Spacings of Quarkonium Levels with the Same Principal Quantum Number

The spacings between bound-state levels of the Schr\"odinger equation with the same principal quantum number $N$ but orbital angular momenta $\ell$ differing by unity are found to be nearly equal for a wide range of power potentials $V = \lambda r^\nu$, with $E_{N \ell} \approx F(\nu, N) - G(\nu,N) \ell$. Semiclassical approximations are in accord with this behavior. The result is applied to estimates of masses for quarkonium levels which have not yet been observed, including the 2P $c \bar c$ states and the 1D $b \bar b$ states.Comment: 20 pages, latex, 3 uuencoded figures submitted separately (process using psfig.sty

Meson Mass Splittings in the Nonrelativistic Model

Mass splittings between isodoublet meson pairs and between $0^{-}$ and $1^{-}$ mesons of the same valence quark content are computed in a detailed nonrelativistic model. The field theoretic expressions for such splittings are shown to reduce to kinematic and Breit-Fermi terms in the nonrelativistic limit. Algebraic results thus obtained are applied to the specific case of the linear-plus-Coulomb potential, with resultant numbers compared to experiment.Comment: 29 pages with 2 tables and 4 figures, LBL-32872 and UCB-PTH-92/3

Importance of low-relief nursery habitat for reef fishes

Coastal restoration projects to mitigate environmental impacts have increased global demand for sand resources. Unfortunately, these resources are often extracted from sand/shell banks on the inner continental shelf, resulting in significant alteration or loss of low-relief reefs in coastal oceans. Experimental reefs (oyster shell, limestone rubble, composite) were deployed in the western Gulf of Mexico to assess their potential value as nurseries for newly settled reef fishes. Occurrence, abundance, and species richness of juvenile fishes were significantly higher on all three types of low-relief reefs compared with unconsolidated sediment. Moreover, reefs served as nursery habitat for a range of reef fish taxa (angelfishes, grunts, sea basses, snappers, and triggerfishes). Red snapper (Lutjanus campechanus) was the dominant species present on all experimental reefs (100% occurrence), and mean density of this species was markedly higher on each of the three low-relief reefs (\u3e40.0 individuals/reef) relative to comparable areas over unconsolidated sediment (0.2 individuals). Our results suggest creation or restoration of structurally complex habitat on the inner shelf has the potential to markedly increase early life survival and expedite the recovery of exploited reef fish populations, and therefore may represent a critical conservation tool for increasing recruitment and maintaining reef fish diversity

Hadrons with Charm and Beauty

By combining potential models and QCD spectral sum rules (QSSR), we discuss the spectroscopy of the $(b\bar c)$ mesons and of the $(bcq)$, $(ccq)$ and $(bbq)$ baryons (${q}\equiv {d}$ or $s$), the decay constant and the (semi)leptonic decay modes of the $B_c$ meson. For the masses, the best predictions come from potential models and read: $M_{B_c} = (6255 \pm 20)$~MeV, $M_{B^*_c} = (6330 \pm 20)$~MeV, $M_{\Lambda(bcu)} = (6.93\pm 0.05)$~GeV, $M_{\Omega(bcs)} = (7.00\pm 0.05)$~GeV, $M_{\Xi^*(ccu)} =(3.63\pm 0.05)$~GeV and $M_{\Xi^*(bbu)} = (10.21\pm 0.05)$~GeV. The decay constant $f_{B_c} = (2.94 \pm 0.21) f_\pi$ is well determined from QSSR and leads to: $\Gamma(B_c \rightarrow \nu_\tau \tau) = (3.0 \pm 0.4)( V_{cb}/0.037 )^2$ $\times 10^{10}$ s$^{-1}$.The uses of the vertex sum rules for the semileptonic decays of the $B_c$ show that the $t$-dependence of the form factors is much stronger than predicted by vector meson dominance. It also predicts the almost equal strength of about 0.30 $\times 10^{10}$ sec$^{-1}$ for the semileptonic rates $B_c$ into $B_s, B^*_s,\eta_c$ and J/$\psi$. Besides these phenomenological results, we also show explicitly how the Wilson coefficients of the $\langle\alpha_s G^2\rangle$ and $\langle G^3\rangle$ gluon condensates already contain the full heavy quark- ($\langle\bar QQ\rangle$) and mixed- ($\langle\bar QGQ\rangle$) condensate contributions in the OPE.}Comment: 32 pages, LaTeX, no changes in the 1994 paper, latex errors corrected in 201

Decay-accelerating factor expression in the rat kidney is restricted to the apical surface of podocytes

Decay-accelerating factor expression in the rat kidney is restricted to the apical surface of podocytes.BackgroundDecay-accelerating factor (DAF) has inhibitory activity toward complement C3 and C5 convertases. DAF is present in human glomeruli and on cultured human glomerular visceral epithelial cells (GEC). We studied the distribution and function of rat DAF.MethodsFunction-neutralizing antibodies (Abs) were raised against DAF. The distribution of DAF in vivo was determined by immunoelectron microscopy. Functional studies were performed in cultured GEC and following IV injection of anti-DAF Abs into rats.ResultsDAF was present exclusively on the apical surfaces of GEC, and was not present on the basal surfaces of GEC, nor other glomerular or kidney cells. DAF was functionally active on cultured GEC, and served to limit complement activation in concert with CD59, an inhibitor of C5b-9 formation. Upon injection into normal rats, anti-DAF F(ab′)2 Abs bound to GEC in vivo, yet there was no evidence for complement activation and animals did not develop abnormal albuminuria. Anti-megalin complement-activating IgG Abs were “planted” on GEC, which activated complement as evidenced by the presence of C3d on GEC. Attempts to inhibit DAF function with anti-DAF Abs did not affect the quantity of complement activation by these anti-megalin Abs, nor did it lead to development of abnormal albuminuria. In contrast, in the puromycin aminonucleoside model of GEC injury and proteinuria, anti-DAF Abs slowed the recovery from renal failure that occurs in this model.ConclusionIn cultured rat GEC, DAF is an effective complement regulator. In vivo, DAF is present on GEC apical surfaces. Yet, it appears that DAF is not essential to prevent complement activation from occurring under normal circumstances and in those cases in which complement-activating Abs are present on the basal surfaces of GEC in vivo. However, in proteinuric conditions, DAF appears to be protective to GEC