This class analyzes complex biological processes from the molecular, cellular, extracellular, and organ levels of hierarchy. Emphasis is placed on the basic biochemical and biophysical principles that govern these processes. Examples of processes to be studied include chemotaxis, the fixation of nitrogen into organic biological molecules, growth factor and hormone mediated signaling cascades, and signaling cascades leading to cell death in response to DNA damage. In each case, the availability of a resource, or the presence of a stimulus, results in some biochemical pathways being turned on while others are turned off. The course examines the dynamic aspects of these processes and details how biochemical mechanistic themes impinge on molecular/cellular/tissue/organ-level functions. Chemical and quantitative views of the interplay of multiple pathways as biological networks are emphasized. Student work culminates in the preparation of a unique grant application in an area of biological networks.

By the end of this section, you will be able to:Explain what a correlation coefficient tells us about the relationship between variablesRecognize that correlation does not indicate a cause-and-effect relationship between variablesDiscuss our tendency to look for relationships between variables that do not really existExplain random sampling and assignment of participants into experimental and control groupsDiscuss how experimenter or participant bias could affect the results of an experimentIdentify independent and dependent variables

Recent research in psychology has highlighted a number of replication problems in the discipline, with publication bias – the preference for publishing original and positive results, and a resistance to publishing negative results and replications- identified as one reason for replication failure. However, little empirical research exists to demonstrate that journals explicitly refuse to publish replications. We reviewed the instructions to authors and the published aims of 1151 psychology journals and examined whether they indicated that replications were permitted and accepted. We also examined whether journal practices differed across branches of the discipline, and whether editorial practices differed between low and high impact journals. Thirty three journals (3%) stated in their aims or instructions to authors that they accepted replications. There was no difference between high and low impact journals. The implications of these findings for psychology are discussed.

The goal of this course is to teach both the fundamentals of nuclear cell biology as well as the methodological and experimental approaches upon which they are based. Lectures and class discussions will cover the background and fundamental findings in a particular area of nuclear cell biology. The assigned readings will provide concrete examples of the experimental approaches and logic used to establish these findings. Some examples of topics include genome and systems biology, transcription, and gene expression.

Students will explore the steps in conducting scientific investigation in Agriculture and discuss safety precautions that should be followed in conducting agricultural research. Lesson plan from the New Mexico Animal, Plant, and Soil Science Lesson Plan Library.

Hank introduces us to that wondrous molecule deoxyribonucleic acid - also known as DNA - and explains how it replicates itself in our cells.

Chapters:
1) Nucleic Acids
2) DNA
-A) Polymers
-B) Three Ingredients
-C) Base Pairs
-D) Base Sequences
3) Pop Quiz
4) RNA
-A) Three Differences from DNA
5) Biolography
6) Replication
-A) Helicase and Unzipping
-B) Leading Strand
-C) DNA Polymerase
-D) RNA Primase
-E) Lagging Strand
-F) Okazaki Fragments
-F) DNA Ligase
Review

This activity will help students understand how the enzyme telomerase works to solve the "end replication problem."

This deep dive session on replications and large-scale collaborations introduces a glossary of relevant terms, the problems these initiatives address, and some tools to get started. Panelists start with content knowledge transfer but switch to more interactive conversation for Q&A and conversation.

This course discusses the principles of genetics with application to the study of biological function at the level of molecules, cells, and multicellular organisms, including humans. The topics include: structure and function of genes, chromosomes and genomes, biological variation resulting from recombination, mutation, and selection, population genetics, use of genetic methods to analyze protein function, gene regulation and inherited disease.

This webinar provides an overview of TOP Factor: its rationale, how it is being used, and how each of the TOP standards relate to individual scores. We also cover how to get involved with TOP Factor by inviting interested community members to suggest journals be added to the database and/or evaluate journal policies for submission.

Contemporary methods of computational cognitive modeling have recently been criticized by Addyman and French (2012) on the grounds that they have not kept up with developments in computer technology and human–computer interaction. They present a manifesto for change according to which, it is argued, modelers should devote more effort to making their models accessible, both to non-modelers (with an appropriate easy-to-use user interface) and modelers alike. We agree that models, like data, should be freely available according to the normal standards of science, but caution against confusing implementations with specifications. Models may embody theories, but they generally also include implementation assumptions. Cognitive modeling methodology needs to be sensitive to this. We argue that specification, replication and experimentation are methodological approaches that can address this issue.

The last ten years have witnessed increasing awareness of questionable research practices (QRPs) in the life sciences, including p-hacking, HARKing, lack of replication, publication bias, low statistical power and lack of data sharing (see Figure 1). Concerns about such behaviours have been raised repeatedly for over half a century but the incentive structure of academia has not changed to address them. Despite the complex motivations that drive academia, many QRPs stem from the simple fact that the incentives which offer success to individual scientists conflict with what is best for science. On the one hand are a set of gold standards that centuries of the scientific method have proven to be crucial for discovery: rigour, reproducibility, and transparency. On the other hand are a set of opposing principles born out of the academic career model: the drive to produce novel and striking results, the importance of confirming prior expectations, and the need to protect research interests from competitors. Within a culture that pressures scientists to produce rather than discover, the outcome is a biased and impoverished science in which most published results are either unconfirmed genuine discoveries or unchallenged fallacies. This observation implies no moral judgement of scientists, who are as much victims of this system as they are perpetrators.

Recently, many psychological effects have been surprisingly difficult to reproduce. This article asks why, and investigates whether conceptually replicating an effect in the original publication is related to the success of independent, direct replications. Two prominent accounts of low reproducibility make different predictions in this respect. One account suggests that psychological phenomena are dependent on unknown contexts that are not reproduced in independent replication attempts. By this account, internal replications indicate that a finding is more robust and, thus, that it is easier to independently replicate it. An alternative account suggests that researchers employ questionable research practices (QRPs), which increase false positive rates. By this account, the success of internal replications may just be the result of QRPs and, thus, internal replications are not predictive of independent replication success. The data of a large reproducibility project support the QRP account: replicating an effect in the original publication is not related to independent replication success. Additional analyses reveal that internally replicated and internally unreplicated effects are not very different in terms of variables associated with replication success. Moreover, social psychological effects in particular appear to lack any benefit from internal replications. Overall, these results indicate that, in this dataset at least, the influence of QRPs is at the heart of failures to replicate psychological findings, especially in social psychology. Variable, unknown contexts appear to play only a relatively minor role. I recommend practical solutions for how QRPs can be avoided.

The MIT Biology Department core courses, 7.012, 7.013, and 7.014, all cover the same core material, which includes the fundamental principles of biochemistry, genetics, molecular biology, and cell biology. Biological function at the molecular level is particularly emphasized and covers the structure and regulation of genes, as well as, the structure and synthesis of proteins, how these molecules are integrated into cells, and how these cells are integrated into multicellular systems and organisms. In addition, each version of the subject has its own distinctive material.
7.012 focuses on the exploration of current research in cell biology, immunology, neurobiology, genomics, and molecular medicine.
Acknowledgments
The study materials, problem sets, and quiz materials used during Fall 2004 for 7.012 include contributions from past instructors, teaching assistants, and other members of the MIT Biology Department affiliated with course #7.012. Since the following works have evolved over a period of many years, no single source can be attributed.

The MIT Biology Department core Introductory Biology courses, 7.012, 7.013, 7.014, 7.015, and 7.016 all cover the same core material, which includes the fundamental principles of biochemistry, genetics, molecular biology, and cell biology. The focus of 7.013 is on genomic approaches to human biology, including neuroscience, development, immunology, tissue repair and stem cells, tissue engineering, and infectious and inherited diseases, including cancer.

The MIT Biology Department core courses, 7.012, 7.013, and 7.014, all cover the same core material, which includes the fundamental principles of biochemistry, genetics, molecular biology, and cell biology. 7.013 focuses on the application of the fundamental principles toward an understanding of human biology. Topics include genetics, cell biology, molecular biology, disease (infectious agents, inherited diseases and cancer), developmental biology, neurobiology and evolution.
Biological function at the molecular level is particularly emphasized in all courses and covers the structure and regulation of genes, as well as, the structure and synthesis of proteins, how these molecules are integrated into cells, and how these cells are integrated into multicellular systems and organisms. In addition, each version of the subject has its own distinctive material.

The MIT Biology Department core courses, 7.012, 7.013, and 7.014, all cover the same core material, which includes the fundamental principles of biochemistry, genetics, molecular biology, and cell biology. Biological function at the molecular level is particularly emphasized and covers the structure and regulation of genes, as well as, the structure and synthesis of proteins, how these molecules are integrated into cells, and how these cells are integrated into multicellular systems and organisms. In addition, each version of the subject has its own distinctive material.
7.014 focuses on the application of these fundamental principles, toward an understanding of microorganisms as geochemical agents responsible for the evolution and renewal of the biosphere and of their role in human health and disease.
Acknowledgements
The study materials, problem sets, and quiz materials used during Spring 2005 for 7.014 include contributions from past instructors, teaching assistants, and other members of the MIT Biology Department affiliated with course 7.014. Since the following works have evolved over a period of many years, no single source can be attributed.

Effect sizes are the currency of psychological research. They quantify the results of a study to answer the research question and are used to calculate statistical power. The interpretation of effect sizes—when is an effect small, medium, or large?—has been guided by the recommendations Jacob Cohen gave in his pioneering writings starting in 1962: Either compare an effect with the effects found in past research or use certain conventional benchmarks. The present analysis shows that neither of these recommendations is currently applicable. From past publications without pre-registration, 900 effects were randomly drawn and compared with 93 effects from publications with pre-registration, revealing a large difference: Effects from the former (median r = .36) were much larger than effects from the latter (median r = .16). That is, certain biases, such as publication bias or questionable research practices, have caused a dramatic inflation in published effects, making it difficult to compare an actual effect with the real population effects (as these are unknown). In addition, there were very large differences in the mean effects between psychological sub-disciplines and between different study designs, making it impossible to apply any global benchmarks. Many more pre-registered studies are needed in the future to derive a reliable picture of real population effects.