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

Parental education gradients over the life cycle

In two recent postmortem studies, Jeffrey Kordower and colleagues report new findings that open up for an interesting discussion on the status of GDNF/NRTN signaling in patients with Parkinson's disease (PD), adding an interesting perspective on the, admittedly very limited, signs of restorative effects previously seen in GDNF/NRTN-treated patients. Their new findings show that the level of the GDNF signaling receptor Ret is overall reduced by about 65% relative to non-PD controls, and most severely, up to 80%, in nigral neurons containing α-synuclein inclusions, accompanied by impaired signaling downstream of the Ret receptor. Notably, however, the vast majority of the remaining nigral neurons retained a low level of Ret expression, and hence a threshold level of signaling. Further observations made in two patients who had received AAV-NRTN gene therapy 8-10 years earlier suggest the intriguing possibility that NRTN is able to restore Ret expression and upregulate its own signaling pathway. This "wind-up" mechanism, which is likely to depend on an interaction with dopaminergic transcription factor Nurr1, has therapeutic potential and should encourage renewed efforts to turn GDNF/NRTN therapy into success, once the recurring problem of under-dosing is resolved.

GDNF Therapy : Can We Make It Work?

Publisher Summary This chapter discusses the restoration of rhythmic slow activity (RSA) in the denervated hippocampus by brain transplants. It describes a study in which the experiments were carried out on adult rats with unilateral removal of the fimbria-fornix ans overlying neocortical tissue. The animals were trained to run in a wheel for water reward. EEG evoked field responses and cellular activity were recorded with fixed and movable microelectrodes. In animals without transplants, no recovery of RSA occurred up to 9 months after the lesion. Instead, large amplitude sharp waves and fast activity were present. In rats with solid grafts in the lesion cavity, RSA, theta, a characteristic EEG correlate of exploratory behavior in normal rats reappeared several months after transplantation. This normal EEG rhythm was present in all rats with septal grafts and in about one-third of the rats with hippocampal transplants. RSA showed a strict and constant covariation with behavior, that is, it was present during running in the wheel and absent while the animal was drinking or sitting still.

Restoration of RSA (theta) in the Denervated Hippocampus by Brain Transplants

Cholecystokinin content in the basal ganglia in huntingtons-disease - the expression of cholecystokinin immunoreactivity in striatal grafts to ibotenic acid-lesioned rat striatum

Functional neural transplantation has come a long way in the past four decades Pioneering studies during the1970s and early1980s established basic methods for achieving effective survival and integration of embryonic neuronal tissue grafts in the mammalian central nervous system so that, in the early 1980s, three major review volumes covering this new field appeared in close succession (Bjorklund and Stenevi, 1985; Sladek and Gash, 1984; Wallace and Das, 1983) Their focus was largely on the principles of defining the technical aspects of delivery, demonstrating neuronal survival, characterizing anatomical growth of connections between grafted cells and the host brain, and providing the first biochemical, physiological, and simple assessments of function From the outset, there was an interest in whether functional recovery in simple animal models might presage the way to eventual clinical applications of novel surgical strategies to treat hitherto untreatable neurological diseases By the early 1990s, the capacity of neural transplants to alleviate functional deficits in animal models of a range of neurodegenerative conditions was well established, and the feasibility of translation dramatically established by the first demonstration of unequivocal functional benefit in Parkinson’s disease, at least for some patients (Lindvall et al, 1990) This led us to coordinate the first major review volume, Functional Neural Transplantation, focusing explicitly on the range of animal models that were then being used to evaluate the functional efficacy of neural grafts, exploring the mechanisms and conditions for functional recovery, and summarizing the first clinical applications, most notably in Parkinson’s disease, but also looking forward to applications in a range of other conditions, including Huntington’s disease, aging, ischemia, spinal cord injury, and metabolic disease (Dunnett and Bjorklund, 1994) By the time of the second review volume, Functional Neural Transplantation II, 8 years later, alternative sources of cells were now being considered, including immortalized cell lines, cell encapsulation, and xenotransplantation (Dunnett and Bjorklund, 2000); although the first human embryonic stem cell lines were clearly appearing on the horizon, they had not yet translated to functional transplantation even in animal models Clinical studies had by now commenced in several other

Anders Björklund

Papers

Parental education gradients over the life cycle

GDNF Therapy : Can We Make It Work?

Restoration of RSA (theta) in the Denervated Hippocampus by Brain Transplants

Cholecystokinin content in the basal ganglia in huntingtons-disease - the expression of cholecystokinin immunoreactivity in striatal grafts to ibotenic acid-lesioned rat striatum

Introduction (Part I)