The second edition of this acclaimed graduate text provides a unified treatment of two methods used in contemporary econometric research, cross section and data panel methods. By focusing on assumptions that can be given behavioral content, the book maintains an appropriate level of rigor while emphasizing intuitive thinking. The analysis covers both linear and nonlinear models, including models with dynamics and/or individual heterogeneity. In addition to general estimation frameworks (particular methods of moments and maximum likelihood), specific linear and nonlinear methods are covered in detail, including probit and logit models and their multivariate, Tobit models, models for count data, censored and missing data schemes, causal (or treatment) effects, and duration analysis. Econometric Analysis of Cross Section and Panel Data was the first graduate econometrics text to focus on microeconomic data structures, allowing assumptions to be separated into population and sampling assumptions. This second edition has been substantially updated and revised. Improvements include a broader class of models for missing data problems; more detailed treatment of cluster problems, an important topic for empirical researchers; expanded discussion of "generalized instrumental variables" (GIV) estimation; new coverage (based on the author's own recent research) of inverse probability weighting; a more complete framework for estimating treatment effects with panel data, and a firmly established link between econometric approaches to nonlinear panel data and the "generalized estimating equation" literature popular in statistics and other fields. New attention is given to explaining when particular econometric methods can be applied; the goal is not only to tell readers what does work, but why certain "obvious" procedures do not. The numerous included exercises, both theoretical and computer-based, allow the reader to extend methods covered in the text and discover new insights.

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Econometric Analysis of Cross Section and Panel Data

抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Preface.1. Introduction.1.1 Panel Data: Some Examples.1.2 Why Should We Use Panel Data? Their Benefits and Limitations.Note.2. The One-way Error Component Regression Model.2.1 Introduction.2.2 The Fixed Effects Model.2.3 The Random Effects Model.2.4 Maximum Likelihood Estimation.2.5 Prediction.2.6 Examples.2.7 Selected Applications.2.8 Computational Note.Notes.Problems.3. The Two-way Error Component Regression Model.3.1 Introduction.3.2 The Fixed Effects Model.3.3 The Random Effects Model.3.4 Maximum Likelihood Estimation.3.5 Prediction.3.6 Examples.3.7 Selected Applications.Notes.Problems.4. Test of Hypotheses with Panel Data.4.1 Tests for Poolability of the Data.4.2 Tests for Individual and Time Effects.4.3 Hausman's Specification Test.4.4 Further Reading.Notes.Problems.5. Heteroskedasticity and Serial Correlation in the Error Component Model.5.1 Heteroskedasticity.5.2 Serial Correlation.Notes.Problems.6. Seemingly Unrelated Regressions with Error Components.6.1 The One-way Model.6.2 The Two-way Model.6.3 Applications and Extensions.Problems.7. Simultaneous Equations with Error Components.7.1 Single Equation Estimation.7.2 Empirical Example: Crime in North Carolina.7.3 System Estimation.7.4 The Hausman and Taylor Estimator.7.5 Empirical Example: Earnings Equation Using PSID Data.7.6 Extensions.Notes.Problems.8. Dynamic Panel Data Models.8.1 Introduction.8.2 The Arellano and Bond Estimator.8.3 The Arellano and Bover Estimator.8.4 The Ahn and Schmidt Moment Conditions.8.5 The Blundell and Bond System GMM Estimator.8.6 The Keane and Runkle Estimator.8.7 Further Developments.8.8 Empirical Example: Dynamic Demand for Cigarettes.8.9 Further Reading.Notes.Problems.9. Unbalanced Panel Data Models.9.1 Introduction.9.2 The Unbalanced One-way Error Component Model.9.3 Empirical Example: Hedonic Housing.9.4 The Unbalanced Two-way Error Component Model.9.5 Testing for Individual and Time Effects Using Unbalanced Panel Data.9.6 The Unbalanced Nested Error Component Model.Notes.Problems.10. Special Topics.10.1 Measurement Error and Panel Data.10.2 Rotating Panels.10.3 Pseudo-panels.10.4 Alternative Methods of Pooling Time Series of Cross-section Data.10.5 Spatial Panels.10.6 Short-run vs Long-run Estimates in Pooled Models.10.7 Heterogeneous Panels.Notes.Problems.11. Limited Dependent Variables and Panel Data.11.1 Fixed and Random Logit and Probit Models.11.2 Simulation Estimation of Limited Dependent Variable Models with Panel Data.11.3 Dynamic Panel Data Limited Dependent Variable Models.11.4 Selection Bias in Panel Data.11.5 Censored and Truncated Panel Data Models.11.6 Empirical Applications.11.7 Empirical Example: Nurses' Labor Supply.11.8 Further Reading.Notes.Problems.12. Nonstationary Panels.12.1 Introduction.12.2 Panel Unit Roots Tests Assuming Cross-sectional Independence.12.3 Panel Unit Roots Tests Allowing for Cross-sectional Dependence.12.4 Spurious Regression in Panel Data.12.5 Panel Cointegration Tests.12.6 Estimation and Inference in Panel Cointegration Models.12.7 Empirical Example: Purchasing Power Parity.12.8 Further Reading.Notes.Problems.References.Index.

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Econometric Analysis of Panel Data

Co-Planar Stereotaxic Atlas of the Human Brain—3-Dimensional Proportional System: An Approach to Cerebral Imaging, J. Talairach, P. Tournoux. Georg Thieme Verlag, New York (1988), 122 pp., 130 figs. DM 268

Parkinson's disease: Mechanisms and models

Neurotoxicity of hydroxylated tryptamines: structure-activity relationships. 2. In vitro studies on monoamine uptake inhibition and uptake impairment.

Neural grafting has over the last decade emerged as a possible tool for the substitution of damaged neurons in the central nervous system and for the promotion of symptomatic recovery after brain damage. Transplantation studies in the 6-hydroxydopamine lesion rat model of Parkinson's disease were initiated in the late seventies. The first studies were based on the neuronal replacement paradigm, using developing dopamine brain cells obtained from the substantia nigra region of embryonic cadavers. When implanted into the striatum such grafts were found to reinnervate part of the previously denervated striatum and restore dopamine turnover and release to near-normal levels. In both rats and monkeys the nigral grafts have been shown to normalize some, but not all, Parkinson-like symptoms in the dopamine deficient recipients. Grafting of adrenal medullary tissue was introduced in the early eighties as an alternative to the use of embryonic cadaver tissue. The adrenal medullary grafts have, however, so far shown poor long-term survival in both rats and monkeys, and consistent with this no sustained dopamine release have been observed in the brain of long-term grafted animals. Likewise, no long-lasting effects of adrenal medullary grafts on spontaneous motor or sensori-motor behavior have so far been documented in either the rat or the monkey model. The results so far reported from trials using adrenal medullary grafts in patients with Parkinson's disease appear to conform to the available animal experimental data at least in two important respects: significant long-term graft survival has not been possible to document, and any clear-cut functional effects consistent with sustained graft-induced dopamine release have not been demonstrated. Initial results from ongoing trials using grafts of fetal nigral tissue are presented and discussed.

Transplantation strategies in the treatment of Parkinson's disease: experimental basis and clinical trials.

Serotonergic and dopaminergic mechanisms in graft-induced dyskinesia in a rat model of Parkinson's disease

I. The early stages of nervous system development: neurogenesis and neuronal migration (J. Altman). II. Development of central cholinergic neurons (K. Semba). III. Development of dopamine-containing systems in the CNS (A. Kalsbeek, P. Voorn and R.M. Buijs). IV. Immunocytochemical distribution of aromatic l-amino acid decarboxylase (AADC) in rat embryos (C.B. Jaeger and G. Teitelman). V. Phenylethanolamine n-methyltransferase - the adrenaline-synthesizing enzyme (G.A. Foster). VI. Ontogeny of histamine- immunoreactive neurons in the CNS (P. Panula, A. Kinnunen, M.S. Airaksinen, M. Ahonen, O. Happola and E. Castren). VII. Postnatal changes of glutaminase-like immunoreactivity in the olfactory bulb, thalamus, cerebral cortex and cerebellum of the rat (T. Kaneko and N. Mizuno). VIII. Development of neuronal elements with substance p-like immunoreactivity in the central nervous system (M. Sakanaka). IX. Ontogenetic and differential expression of the preproenkephalin and preprodynorphin genes in the rat brain (Y. Morita). X. Ontogeny of pro-opiomelanocortin (POMC)-derived peptides in the brain and pituitary (Y.-Q. Wang, J.-S. Li, H.-M. Li and M. Tohyama). XI. Ontogeny of calcitonin gene-related peptide (CGRP) (S. Inagaki). XII. Ontogeny of the central somatostatinergic system (S. Shiosaka). XIII. Ontogeny of neurotensin immunoreactivity and MRNA in the rat central nervous system (H. Kiyama, M. Sato and P.C. Emson). XIV. Ontogeny of cholecystokinin in the central nervous system (H.-J. Cho and K. Joo). XV. Vasoactive intestinal polypeptide and peptide histidine isoleucine (K. Hares and G.A. Foster). XVI. Development of corticotropin-releasing factor in rat brain (S. Daikoku and S. Hisano). XVII. Neuropeptide Y (G.A. Foster and P.L. Woodhams). XVIII. The development of vasopressin and oxytocin systems in the brain (R.M. Buijs). XIX. Ontogeny of gonadotropin releasing hormone containing neuronal systems in mammals (L. Jennes and M. Schwanzel-Fukuda). XX. Galanin (A.R. Sizer and G.A. Foster). XXI. The development of the serotonergic system in the rat and chick embryo (J.A. Wallace and J.M. Lauder). XXII. An overview of the ontogeny of neurotransmitters and neuromodulators in the central nervous system (M. Tohyama). Subject index.

Anders Björklund

Papers

Neurotoxicity of hydroxylated tryptamines: structure-activity relationships. 2. In vitro studies on monoamine uptake inhibition and uptake impairment.

Transplantation strategies in the treatment of Parkinson's disease: experimental basis and clinical trials.

Serotonergic and dopaminergic mechanisms in graft-induced dyskinesia in a rat model of Parkinson's disease

Ontogeny of transmitters and peptides in the CNS

Long-term recovery of serotonin concentrations in the rat CNS following 5,6-dihydroxytryptamine.