Preface to the Princeton Landmarks in Biology Edition vii Preface xi Symbols Used xiii 1. The Importance of Islands 3 2. Area and Number of Speicies 8 3. Further Explanations of the Area-Diversity Pattern 19 4. The Strategy of Colonization 68 5. Invasibility and the Variable Niche 94 6. Stepping Stones and Biotic Exchange 123 7. Evolutionary Changes Following Colonization 145 8. Prospect 181 Glossary 185 References 193 Index 201

The Theory of Island Biogeography

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(06)68175-0.pdf

Guillain-Barré syndrome

https://www.healio.com/psychiatry/journals/psycann/1976-12-6-12/{806b8887-c02e-40c8-a228-57f1cdb2bdba}/the-stress-of-life.pdf

The stress of life

Molecular profile of reactive astrocytes—Implications for their role in neurologic disease

Context A history of depression may increase risk for developing Alzheimer disease (AD) later in life. Clarifying this relation might improve understanding of risk factors for and disease mechanisms in AD. Objective To systematically review and complete a meta-analysis on the relation of depression and AD. Data sources We conducted electronic bibliographic searches of MEDLINE, PsychLit, EMBASE, and BIOSIS using search terms sensitive to studies of etiology combined with searches on terms related to depression and AD and reviewed reference lists of articles. Study selection Studies with data contrasting depressed vs nondepressed patients who did and did not later develop AD were included. Studies that related continuous measures of depression and cognitive status were excluded. Data extraction Numerical data were independently extracted by 3 reviewers. They also rated studies on a scale that assessed quality indicators for observational studies. Data on the interval between observation of depression and the diagnosis of AD were collected when available. Data synthesis Meta-analytic evaluation with random-effects models resulted in pooled odds ratios of 2.03 (95% confidence interval, 1.73-2.38) for case-control and of 1.90 (95% confidence interval, 1.55-2.33) for cohort studies. Findings of increased risk were robust to sensitivity analyses. Interval between diagnoses of depression and AD was positively related to increased risk of developing AD, suggesting that rather than a prodrome, depression may be a risk factor for AD. Conclusions A history of depression may confer an increased risk for later developing AD. This relation may reflect an independent risk factor for the disease.

https://jamanetwork.com/journals/jamapsychiatry/articlepdf/209578/yoa50281.pdf

Depression and Risk for Alzheimer Disease: Systematic Review, Meta-analysis, and Metaregression Analysis

Sixty patients with myasthenia gravis were examined prospectively by measuring serial titers of antibodies against human acetylcholine receptor, and these were correlated with a quantitative clinical score. Serial titers of antibodies detected by the standard immunoprecipitation assay (binding antibodies) correlated with the clinical score in most patients. Antibodies blocking the binding of alpha-bungarotoxin to receptors (blocking antibodies) were detected in 29 patients. Serial blocking antibody titers correlated with changes in muscle weakness less often than binding antibody titers. Titers of both classes of antibodies often followed a divergent course, suggesting that the autoimmune B-cell clones that formed these classes of antibodies may have been activated asynchronously.

Myasthenia gravis: Long‐term correlation of binding and bungarotoxin blocking antibodies against acetylcholine receptors with changes in disease severity

Myasthenia gravis is one of the best characterized human autoimmune disorders1–4. Circulating autoantibodies to the nicotinic acetylcholine receptor (AChR) at the neuromuscular junction play a prominent part in the effector phase of the disease5,6, but little is known about the induction phase, that is, the immunoregulation. Indirect evidence, such as thymic abnormalities7 and the association with certain histocompatibility antigens (for example HLA-B8,-DR38,9) suggests a defect of immunoregulation at the level of thymus-dependent (T) lymphocytes. We report here on the isolation of autoreactive T cells from six patients with myasthenia gravis. From one of these patients, who is homozygous for HLA-DR3, we established a long-term T-cell line. The line cells are specific for purified fish and human AChR, display the surface phenotype of inducer/helper T cells and are genetically restricted to HLA-DR3. AChR-induced proliferation could be inhibited with two monoclonal antibodies against monomorphic DR determinants and also with DR3-specific alloantiserum.

Autoimmune human T lymphocytes specific for acetylcholine receptor

Experimental allergic neuritis (EAN) can be prevented or ameliorated by global blockade of macrophages. How these cells damage peripheral nervous tissue in this autoimmune demyelinating polyneuropathy is not fully understood. Since macrophages exert a number of their inflammatory actions by the release of arachidonic acid-derived eicosanoids, we investigated the possible role of these mediators in the pathogenesis of EAN. Lewis rats with myelin-induced EAN were treated before and after onset of clinical signs. Administration of corticosteroids or of the cyclo-oxygenase inhibitors indomethacin and BW755c before the onset of neurological signs suppressed the disease, as judged by clinical assessment, serial electrophysiological testing and histological examination, while initiation of drug treatment on day 13 postimmunization still markedly attenuated the course of EAN. The selective lipoxygenase blocker nafazatrom had only a slight effect. Determination of the production by macrophages ex vivo of eicosanoids corroborated the predicted site of action of the pharmacological compounds applied. We infer that macrophage-derived proinflammatory arachidonic acid metabolites significantly contribute to functional and tissue damage in EAN. Our results may be relevant to future pharmacological treatment of the acute Guillain-Barre syndrome.

The role of macrophages and eicosanoids in the pathogenesis of experimental allergic neuritis. Serial clinical, electrophysiological, biochemical and morphological observations.

Guillain-Barre syndrome (GBS), chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), and multiple sclerosis (MS) are disorders with presumed immunopathogenesis. To obtain evidence for T cell activation, we determined serum concentrations of soluble interleukin-2 receptors (sIL-2 R) in 50 patients with GBS, 24 with CIDP, and 54 with MS. Both in GBS and clinically active MS sIL-2 R levels were markedly increased compared with those in patients with other neurologic diseases. Four of 24 CIDP patients had abnormally increased sIL-2 R concentrations. sIL-2 R concentrations decreased with clinical improvement in serial samples taken from GBS patients, but were not otherwise correlated with disease severity. These data establish that T cells are activated in GBS and some patients with CIDP, and corroborate earlier evidence that activated T cells are circulating in the blood of MS patients.

T cell activation in Guillain‐Barré syndrome and in MS: Elevated serum levels of soluble IL‐2 receptors

The role of interferon-gamma in the pathogenesis of experimental autoimmune disease of the peripheral nervous system was investigated. Administration of rat recombinant interferon-gamma markedly augmented both myelin-induced and T-cell line-mediated experimental autoimmune neuritis. Conversely, in vivo application of a monoclonal antibody to interferon-gamma suppressed the disease. Clinical and electrophysiological findings were corroborated by semiquantitative morphometric analysis. Mechanisms responsible for the enhancing effects of interferon-gamma include upregulation of major histocompatibility complex class II antigen expression in the nerve lesion, increased cellular influx of T cells and macrophages, and heightened macrophage activity with enhanced release of toxic oxygen species. These observations establish a pivotal role of the cytokine interferon-gamma in the pathogenesis of experimental autoimmune disease of the peripheral nervous system.

Kurt Heininger

Papers

Myasthenia gravis: Long‐term correlation of binding and bungarotoxin blocking antibodies against acetylcholine receptors with changes in disease severity

Autoimmune human T lymphocytes specific for acetylcholine receptor

The role of macrophages and eicosanoids in the pathogenesis of experimental allergic neuritis. Serial clinical, electrophysiological, biochemical and morphological observations.

T cell activation in Guillain‐Barré syndrome and in MS: Elevated serum levels of soluble IL‐2 receptors

The role of interferon-gamma in the pathogenesis of experimental autoimmune disease of the peripheral nervous system.