A primary source in the sciences is usually a report on the results of an experiment by the person or group who performed it. They are usually published as scientific articles. Primary scientific articles contain high-level vocabulary and will usually present original data, often displayed in tables or charts.
The scientist reports the results of his or her own research. It is not a comment on someone else’s research, although the scientist may refer to someone else’s work in the body of the paper to illustrate the points he/she is trying to prove or disprove. Most scientific journals that are peer-reviewed are likely to contain primary literature. Peer-review means that a panel of experts will review all articles submitted for publication before they are accepted by the journal.
In a primary research article, you will typically see many or all of the following elements clearly presented:
The presence of these components indicate that the author is presenting new data and ideas.
Here is an example of a primary science article.
The journal title itself hints about the nature of the article: "clinical investigation." The abstract also provides clues (highlighted in italics below):
Author(s): Embury SH, Mohandas N, Paszty C, Cooper P, Cheung ATW
Source: JOURNAL OF CLINICAL INVESTIGATION 103 (6): 915-920 MAR 1999
Document Type: Article
Abstract: The accepted importance of circulatory impairment to sickle cell anemia remains to be verified by in vivo experimentation. Intravital microscopy studies of blood flow in patients are limited to circulations that can be viewed noninvasively and are restricted from deliberate perturbations of the circulation. Further knowledge of sickle blood flow abnormalities has awaited an animal model of human sickle cell disease. We compared blood flow in the mucosal-intestinal microvessels of normal mice with that in transgenic knockout sickle cell mice that have erythrocytes containing only human hemoglobin S and that exhibit a degree of hemolytic anemia and pathological complications similar to the human disease. In sickle cell mice, in addition to seeing blood flow abnormalities such as sludging in all microvessels, we detected decreased blood flow velocity in venules of all diameters. Flow responses to hyperoxia in both normal and sickle cell mice were dramatic, but opposite: Hyperoxia promptly slowed or halted flow in normal mice but markedly enhanced flow in sickle cell mice. Intravital microscopic studies of this murine model provide important insights into sickle cell blood flow abnormalities and suggest that this model can be used to evaluate the causes of abnormal flow and new approaches to therapy of sickle cell disease.