Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Explain how the kidneys serve as the main osmoregulatory organs in mammalian systemsDescribe the structure of the kidneys and the functions of the parts of the kidneyDescribe how the nephron is the functional unit of the kidney and explain how it actively filters blood and generates urineDetail the three steps in the formation of urine: glomerular filtration, tubular reabsorption, and tubular secretion

The course covers basic concepts of biomedical engineering and their connection with the spectrum of human activity. It serves as an introduction to the fundamental science and engineering on which biomedical engineering is based. Case studies of drugs and medical products illustrate the product development-product testing cycle, patent protection, and FDA approval. It is designed for science and non-science majors.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"In diabetic nephropathy (DN), a common complication of diabetes, the structure and function of the kidneys deteriorate. One early sign of DN is proteinuria, or protein excretion in urine. Although the mechanism of DN-related proteinuria isn’t clear, rearrangement of the cellular skeleton, or cytoskeleton, might contribute. A recent study explored this theory by examining the role of the cytoskeletal protein MAP4 in DN proteinuria. In urine from patients with diabetes as well as kidney tissues from diabetic mice, the content of phosphate-modified (phosphorylated) MAP4 was elevated. In mice, inducing MAP4 phosphorylation promoted the development of DN-like proteinuria with aging and caused podocytes, specialized kidney cells that prevent proteins from entering urine, to lose their epithelial characteristics and die. In addition, mice with induced MAP4 phosphorylation were much more susceptible to diabetes than normal mice..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Mesangial proliferative glomerulonephritis (MsPGN) is a condition involving cell proliferation and tissue deposition in the kidney mesangium. MsPGN is a major cause of chronic kidney disease and kidney failure, but few treatment options are available. To explore new therapies, a recent study investigated the effects of extracellular vesicles from umbilical cord mesenchymal stem cells (ucMSC-EVs) on MsPGN in rats. The ucMSC-EVs reduced mesangial enlargement and fibrosis in rats in a dose-dependent manner, while suppressing mesangial cell proliferation. A mechanistic study revealed that the microRNA miR-378 was markedly upregulated by ucMSC-EV treatment, suggesting that the vesicles delivered miR-378 to the kidney tissues. Further analyses showed that miR-378 exerted beneficial anti-MsPGN effects by inhibiting the protein PSMD14, which in turn induced degradation of the protein TGFBR1, thereby suppressing the TGF-β1/Smad2/3 pathway..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.