Fracture mechanics is a branch of mechanics that studies the behavior of materials containing cracks or flaws. It aims to understand how and why materials fail when they are subjected to stress, and it helps in predicting the conditions under which a crack will grow, leading to the failure of a structure or component. The primary focus of fracture mechanics is on the propagation of cracks and the factors that influence that propagation.
Materials science journals are academic publications that focus on the study, development, and application of materials in various fields, including engineering, physics, chemistry, and biology. These journals publish research articles, reviews, and technical notes on topics such as: 1. **Material Properties**: Investigating mechanical, thermal, electrical, and optical properties of materials. 2. **Material Synthesis**: Methods for producing new materials, including nanomaterials, composites, and biomaterials.
Nanotechnology is the science and engineering of manipulating matter at the nanoscale, typically defined as involving structures ranging from 1 to 100 nanometers (nm) in size. To put this in perspective, a nanometer is one-billionth of a meter, which is about 100,000 times smaller than the diameter of a human hair. Nanotechnology involves the study, design, and application of materials and devices at this incredibly small scale, where unique physical and chemical properties often emerge.
Professorships in metallurgy and materials science refer to academic positions at universities or research institutions focused on teaching, research, and advancing knowledge in the fields of metallurgy— the study of metals and their properties—and materials science, which encompasses a broader range of materials, including ceramics, polymers, and composites.
CLCN3 is a gene that encodes a member of the chloride channel family, specifically a voltage-gated chloride channel. The protein produced by this gene is part of the CLC (chloride channel) family and plays a key role in maintaining ion homeostasis, regulating cell volume, and facilitating various physiological processes across different cell types. CLCN3 is located on chromosome 16 in humans and is expressed in various tissues, indicating its diverse functions.
Calcium release-activated channels (CRAC channels) are a type of ion channel that is primarily involved in the regulation of calcium ions (Ca²⁺) in cells. These channels play a crucial role in cellular signaling processes, particularly in response to various stimuli that lead to calcium release from internal stores, especially the endoplasmic reticulum (ER).
GABRD (Gamma-Aminobutyric Acid Receptor Delta) is a gene that encodes a subunit of the GABA receptor, which is a type of neurotransmitter receptor in the central nervous system. GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the brain, playing a crucial role in reducing neuronal excitability throughout the nervous system.
CatSper4 is a protein that is part of the CatSper (Cation channel of sperm) family of ion channels, which are critical for sperm motility and fertility in many animals, including humans. These channels primarily facilitate the influx of calcium ions (Ca²⁺) into sperm cells, which is essential for various physiological processes, including sperm activation, movement, and the ability to fertilize an egg.
Channelrhodopsin is a type of light-sensitive ion channel primarily derived from certain species of green algae. These proteins are important tools in the field of optogenetics, a technique that allows researchers to control neuronal activity using light. Channelrhodopsins function by changing conformation in response to light, typically blue or green wavelengths, which allows ions such as sodium or calcium to flow into the cell.
Cyclic nucleotide gated channel beta 3 (CNGB3) is a protein that is a part of the cyclic nucleotide-gated (CNG) channels, which are a type of ion channel that is activated by the binding of cyclic nucleotides, such as cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP).
Cys-loop receptors are a family of neurotransmitter receptors that are characterized by their structural signature known as the "Cys-loop." These receptors are integral membrane proteins that mediate fast synaptic transmission in the nervous system. They are named after a conserved cysteine (Cys) loop in their extracellular domain, which is pivotal for their function.
GLRA4, or Glycine Receptor Alpha-4, is a protein that is part of the glycine receptor family, which are neurotransmitter receptors primarily responsible for mediating inhibitory neurotransmission in the central nervous system. Glycine receptors are pentameric ligand-gated ion channels that allow for the passage of chloride ions (Cl^-) into the neuron when glycine, the endogenous ligand, binds to the receptor.
HCN4 refers to a specific type of hyperpolarization-activated cyclic nucleotide-gated ion channel, which plays a crucial role in generating and regulating electrical activity in the heart. Specifically, HCN4 is one of the four known members of the HCN channel family (HCN1, HCN2, HCN3, and HCN4).
The Ion Channel Hypothesis of Alzheimer's Disease (AD) suggests that dysfunction in ion channels, which are crucial for maintaining the balance of ions across cell membranes, plays a significant role in the pathogenesis of AD. This hypothesis posits that the dysregulation of calcium (Ca²⁺) homeostasis, due to altered function or expression of ion channels, contributes to the neuronal cell death and synaptic dysfunction observed in Alzheimer's patients.
KCND1 is a gene that encodes a protein known as potassium voltage-gated channel subfamily D member 1. This protein is part of the voltage-gated potassium channels, which are important for the regulation of electrical activity in neurons and other excitable cells. The KCND1 protein contributes to the repolarization phase of the action potential in nerve and muscle cells, allowing these cells to return to their resting potential after being activated.
KCNQ4 is a gene that encodes a potassium ion channel, which is part of the KCNQ (Kv7) family of voltage-gated potassium channels. These channels are important for the regulation of electrical activity in various tissues, particularly in the nervous system and the inner ear. KCNQ4 specifically plays a critical role in the auditory system, where it helps to control the membrane potential of hair cells in the cochlea.
Bi-isotropic materials are materials that exhibit isotropic properties in both mechanical and electromagnetic contexts. In simpler terms, these materials have the same mechanical and electromagnetic characteristics regardless of the direction in which they are measured. In mechanical terms, an isotropic material has uniform properties in all directions. This means that its mechanical response (like stress, strain, stiffness, etc.) is the same no matter the orientation of the applied forces.
KCNT2 (Potassium Channel, Subfamily T, Member 2) is a gene that encodes a protein contributing to the formation of ion channels in the cell membranes. These channels are regulated by potassium ions (K+), which are essential for a variety of physiological functions, including the regulation of cell excitability, electrical signaling in neurons, and muscle contraction.
KCNV2 is a gene that encodes a potassium voltage-gated channel subunit. Potassium channels are essential for various physiological processes, including the regulation of electrical activity in neurons and muscle cells. The KCNV2 protein is specifically involved in the formation of voltage-gated potassium channels that contribute to the repolarization phase of action potentials in excitable tissues.
Pinned article: Introduction to the OurBigBook Project
Welcome to the OurBigBook Project! Our goal is to create the perfect publishing platform for STEM subjects, and get university-level students to write the best free STEM tutorials ever.
Everyone is welcome to create an account and play with the site: ourbigbook.com/go/register. We belive that students themselves can write amazing tutorials, but teachers are welcome too. You can write about anything you want, it doesn't have to be STEM or even educational. Silly test content is very welcome and you won't be penalized in any way. Just keep it legal!
Intro to OurBigBook
. Source. We have two killer features:
- topics: topics group articles by different users with the same title, e.g. here is the topic for the "Fundamental Theorem of Calculus" ourbigbook.com/go/topic/fundamental-theorem-of-calculusArticles of different users are sorted by upvote within each article page. This feature is a bit like:
- a Wikipedia where each user can have their own version of each article
- a Q&A website like Stack Overflow, where multiple people can give their views on a given topic, and the best ones are sorted by upvote. Except you don't need to wait for someone to ask first, and any topic goes, no matter how narrow or broad
This feature makes it possible for readers to find better explanations of any topic created by other writers. And it allows writers to create an explanation in a place that readers might actually find it.Figure 1. Screenshot of the "Derivative" topic page. View it live at: ourbigbook.com/go/topic/derivativeVideo 2. OurBigBook Web topics demo. Source. - local editing: you can store all your personal knowledge base content locally in a plaintext markup format that can be edited locally and published either:This way you can be sure that even if OurBigBook.com were to go down one day (which we have no plans to do as it is quite cheap to host!), your content will still be perfectly readable as a static site.
- to OurBigBook.com to get awesome multi-user features like topics and likes
- as HTML files to a static website, which you can host yourself for free on many external providers like GitHub Pages, and remain in full control
Figure 3. Visual Studio Code extension installation.Figure 4. Visual Studio Code extension tree navigation.Figure 5. Web editor. You can also edit articles on the Web editor without installing anything locally.Video 3. Edit locally and publish demo. Source. This shows editing OurBigBook Markup and publishing it using the Visual Studio Code extension.Video 4. OurBigBook Visual Studio Code extension editing and navigation demo. Source. - Infinitely deep tables of contents:
All our software is open source and hosted at: github.com/ourbigbook/ourbigbook
Further documentation can be found at: docs.ourbigbook.com
Feel free to reach our to us for any help or suggestions: docs.ourbigbook.com/#contact





