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No data available that match "Cells"
(1/1036) E-CELL: software environment for whole-cell simulation.
MOTIVATION: Genome sequencing projects and further systematic functional analyses of complete gene sets are producing an unprecedented mass of molecular information for a wide range of model organisms. This provides us with a detailed account of the cell with which we may begin to build models for simulating intracellular molecular processes to predict the dynamic behavior of living cells. Previous work in biochemical and genetic simulation has isolated well-characterized pathways for detailed analysis, but methods for building integrative models of the cell that incorporate gene regulation, metabolism and signaling have not been established. We, therefore, were motivated to develop a software environment for building such integrative models based on gene sets, and running simulations to conduct experiments in silico. RESULTS: E-CELL, a modeling and simulation environment for biochemical and genetic processes, has been developed. The E-CELL system allows a user to define functions of proteins, protein-protein interactions, protein-DNA interactions, regulation of gene expression and other features of cellular metabolism, as a set of reaction rules. E-CELL simulates cell behavior by numerically integrating the differential equations described implicitly in these reaction rules. The user can observe, through a computer display, dynamic changes in concentrations of proteins, protein complexes and other chemical compounds in the cell. Using this software, we constructed a model of a hypothetical cell with only 127 genes sufficient for transcription, translation, energy production and phospholipid synthesis. Most of the genes are taken from Mycoplasma genitalium, the organism having the smallest known chromosome, whose complete 580 kb genome sequence was determined at TIGR in 1995. We discuss future applications of the E-CELL system with special respect to genome engineering. AVAILABILITY: The E-CELL software is available upon request. SUPPLEMENTARY INFORMATION: The complete list of rules of the developed cell model with kinetic parameters can be obtained via our web site at: http://e-cell.org/. (+info)
(2/1036) Effector cells of both nonhemopoietic and hemopoietic origin are required for interferon (IFN)-gamma- and tumor necrosis factor (TNF)-alpha-dependent host resistance to the intracellular pathogen, Toxoplasma gondii.
Although interferon (IFN)-gamma-activated, mononuclear phagocytes are considered to be the major effectors of resistance to intracellular pathogens, it is unclear how they control the growth of microorganisms that reside in nonhemopoietic cells. Pathogens within such cells may be killed by metabolites secreted by activated macrophages or, alternatively, directly controlled by cytokine-induced microbicidal mechanisms triggered within infected nonphagocytic cells. To distinguish between these two basic mechanisms of cell-mediated immunity, reciprocal bone marrow chimeras were constructed between wild-type and IFN-gamma receptor-deficient mice and their survival assessed following infection with Toxoplasma gondii, a protozoan parasite that invades both hemopoietic and nonhemopoietic cell lineages. Resistance to acute and persistent infection was displayed only by animals in which IFN-gamma receptors were expressed in both cellular compartments. Parallel chimera experiments performed with tumor necrosis factor (TNF) receptor-deficient mice also indicated a codependence on hemopoietic and nonhemopoietic lineages for optimal control of the parasite. In contrast, in mice chimeric for inducible nitric oxide synthase (iNOS), an enzyme associated with IFN-gamma-induced macrophage microbicidal activity, expression by cells of hemopoietic origin was sufficient for host resistance. Together, these findings suggest that, in concert with bone marrow-derived effectors, nonhemopoietic cells can directly mediate, in the absence of endogenous iNOS, IFN-gamma- and TNF-alpha-dependent host resistance to intracellular infection. (+info)
(3/1036) Cellular microbiology: can we learn cell physiology from microorganisms?
Cellular microbiology is a new discipline that is emerging at the interface between cell biology and microbiology. The application of molecular techniques to the study of bacterial pathogenesis has made possible discoveries that are changing the way scientists view the bacterium-host interaction. Today, research on the molecular basis of the pathogenesis of infective diarrheal diseases of necessity transcends established boundaries between cell biology, bacteriology, intestinal pathophysiology, and immunology. The use of microbial pathogens to address questions in cell physiology is just now yielding promising applications and striking results. (+info)
(4/1036) Phase imaging by atomic force microscopy: analysis of living homoiothermic vertebrate cells.
Atomic force microscope-based phase imaging in air is capable of elucidating variations in material properties such as adhesion, friction, and viscoelasticity. However, the interpretation of phase images of specimens in a fluid environment requires clarification. In this report, we systematically analyzed atomic force microscope-derived phase images of mica, glass, and collagen under the same conditions as used for living cells at various tapping forces; the resulting data provide critical information for the interpretation of phase images of living cells. The peripheral regions of COS-1 cells consistently show a more negative phase shift than the glass substrate in phase images at set-point amplitude: free amplitude (Asp/A0) = 0.6-0.8. In addition, at all Asp/A0 values suitable for phase imaging, tapping frequency appears to be high enough to ensure that phase shifts are governed primarily by stiffness. Consequently, phase imaging is capable of high resolution studies of the cellular surface by detecting localized variations in stiffness. We demonstrate that phase imaging of a bifurcating fiber in COS-1 cell cytoplasm is readily capable of a lateral resolution of approximately 30 nm. (+info)
(5/1036) Single micro electrode dielectrophoretic tweezers for manipulation of suspended cells and particles.
Cells or particles in aqueous suspension close to a single capacitively coupled micro electrode (CCME) driven with high frequency electric fields experience dielectrophoretic forces. The effects near the CCME can be used for trapping and manipulation of single cells using externally metallised glass pipettes and might be used to develop a microscope based on force or capacitance measurements in conductive media. (+info)
(6/1036) Functional roles of S100 proteins, calcium-binding proteins of the EF-hand type.
A multigenic family of Ca2+-binding proteins of the EF-hand type known as S100 comprises 19 members that are differentially expressed in a large number of cell types. Members of this protein family have been implicated in the Ca2+-dependent (and, in some cases, Zn2+- or Cu2+-dependent) regulation of a variety of intracellular activities such as protein phosphorylation, enzyme activities, cell proliferation (including neoplastic transformation) and differentiation, the dynamics of cytoskeleton constituents, the structural organization of membranes, intracellular Ca2+ homeostasis, inflammation, and in protection from oxidative cell damage. Some S100 members are released or secreted into the extracellular space and exert trophic or toxic effects depending on their concentration, act as chemoattractants for leukocytes, modulate cell proliferation, or regulate macrophage activation. Structural data suggest that many S100 members exist within cells as dimers in which the two monomers are related by a two-fold axis of rotation and that Ca2+ binding induces in individual monomers the exposure of a binding surface with which S100 dimers are believed to interact with their target proteins. Thus, any S100 dimer is suggested to expose two binding surfaces on opposite sides, which renders homodimeric S100 proteins ideal for crossbridging two homologous or heterologous target proteins. Although in some cases different S100 proteins share their target proteins, in most cases a high degree of target specificity has been described, suggesting that individual S100 members might be implicated in the regulation of specific activities. On the other hand, the relatively large number of target proteins identified for a single S100 protein might depend on the specific role played by the individual regions that in an S100 molecule contribute to the formation of the binding surface. The pleiotropic roles played by S100 members, the identification of S100 target proteins, the analysis of functional correlates of S100-target protein interactions, and the elucidation of the three-dimensional structure of some S100 members have greatly increased the interest in S100 proteins and our knowledge of S100 protein biology in the last few years. S100 proteins probably are an example of calcium-modulated, regulatory proteins that intervene in the fine tuning of a relatively large number of specific intracellular and (in the case of some members) extracellular activities. Systems, including knock-out animal models, should be now used with the aim of defining the correspondence between the in vitro regulatory role(s) attributed to individual members of this protein family and the in vivo function(s) of each S100 protein. (+info)
(7/1036) The osmotic migration of cells in a solute gradient.
The effect of a nonuniform solute concentration on the osmotic transport of water through the boundaries of a simple model cell is investigated. A system of two ordinary differential equations is derived for the motion of a single cell in the limit of a fast solute diffusion, and an analytic solution is obtained for one special case. A two-dimensional finite element model has been developed to simulate the more general case (finite diffusion rates, solute gradient induced by a solidification front). It is shown that the cell moves to regions of lower solute concentration due to the uneven flux of water through the cell boundaries. This mechanism has apparently not been discussed previously. The magnitude of this effect is small for red blood cells, the case in which all of the relevant parameters are known. We show, however, that it increases with cell size and membrane permeability, so this effect could be important for larger cells. The finite element model presented should also have other applications in the study of the response of cells to an osmotic stress and for the interaction of cells and solidification fronts. Such investigations are of major relevance for the optimization of cryopreservation processes. (+info)
(8/1036) A polarization model overcoming the geometric restrictions of the laplace solution for spheroidal cells: obtaining new equations for field-induced forces and transmembrane potential.
We present a new model for a variety of electric polarization effects on oblate and prolate homogeneous and single-shell spheroids. For homogeneous spheroids the model is identical to the Laplace model. For single-shell spheres of cell-like geometry the calculated difference of the induced dipole moments is in the thousandths range. To solve Laplace's equation for nonspherical single-shell objects it is necessary to assume a confocal shell, which results in different cell membrane properties in the pole and equator regions, respectively. Our alternative model addresses this drawback. It assumes that the disturbance of the external field due to polarization may project into the medium to a characteristic distance, the influential radius. This parameter is related to the axis ratio of the spheroid over the depolarizing factors and allows us to determine the geometry for a finite resistor-capacitor model. From this model the potential at the spheroid's surface is obtained and, consequently, the local field inside a homogeneous spheroid is determined. In the single-shell case, this is the effective local field of an equivalent homogeneous spheroid. Finally, integration over the volume yields the frequency-dependent induced dipole moment. The resistor-capacitor approach allowed us to find simple equations for the critical and characteristic frequencies, force plateaus and peak heights of deformation, dielectrophoresis and electrorotation for homogeneous and single-shell spheroids, and a more generalized equation for the induced transmembrane potential of spheroidal cells. (+info)
What causes cells to become insulin resistant?
Is insulin resistance reversible? I am prediabetic ( in the form of impaired glucose tolerance) so I wanted to know if the cells in my body that have become insulin resistant will become normal again. I exercise regularly and eat small meals, I eat an average of about 120 or less carbs a day, I am in excellent shape (5'3' and 102lbs), and I am planning on taking supplements that lower blood sugar. So can my cells ever become non insulin resistant after doing all that?
Your body mass index is 18.1 kg/M2. If you are age 25 or older this would represent 'underweight' status. If you are younger than age 18 your will be above the 5th percentile which would be considered acceptable. There is a correlation between weight and insulin resistance but clearly that is not your case. This emphasizes the fact that diabetes is not simply a condition of the obese. Quite honestly we have no idea what the precise nature of insulin resistance is. If someone is over-weight - which you are not - reducing weight decreases insulin resistance. I doubt that your insulin resistance will be able to be reversed but I wonder where the diagnosis of insulin resistance came from. This requires rather sophisticated testing. Having 'glucose intolerance' or being a 'pre-diabetic' most definitely is not synonymous with having insulin resistance. I do not use terms such as glucose intolerance, pre-diabetic, or borderline diabetic as I believe that these terms miss the point entirely. There is an approximately 10 year lead-in time of pathophysiologic damage prior to the glucose becoming consistently elevated and being diagnosed with type 2 diabetes which I suspect is what is at issue here rather than type 1 diabetes where insulin resistance does not play a role. I do not have specific information but I must wonder from what you are saying if you are an 'early' diabetic. These individuals do not necessarily require pharmacologic intervention. The first step is typically a low glycemic index diet, weight loss (not an issue in your case), and exercise. It sounds as if you have all of these in order. I strongly believe that type 2 diabetes should be sub-divided into type 2A and type 2B. 2A would be type 2 diabetics with a 'lean' body mass index - which would be your case. 2B would be type 2 diabetics with a body mass index of greater than 30 kg/M2 - assuming that they are older than age 25. I start 2A diabetics - when pharmacologic intervention is required - on insulin. I start 2B diabetics - when pharmacologic intervention is required - on oral medications with the caveat that most type 2 diabetics will be on insulin within 10 years of diagnosis. I do not know of any so-called 'supplements' that lower blood glucose. Please do not be upset that I am suggesting that you might have early diabetes as I have far too little information to offer an informed opinion. Indeed one of the problems in answering questions in this forum is that people do not provide enough information. If you provide me with additional and more detailed information I will try to be of further assistance. I wish you the very best of health and in all things may God bless.
What are fat cells and how do they work depending on how much you eat?
I never understood but my dad told me your fat cells shrink but they can't go away when you get healthier. He said once you have them you have them forever. What do fat cells do anyway? and is it better to have bigger or smaller fat cells? why? I don 't really know anything about them and how they work. What are they bassically and how do they effect us? Pretty much.... What are fat cells?
Everyone has fat cells. They store fat (go figure). When you consume excess fat, the fat gets stored in these cells. This is a common misconseption. A 50lb man and a 500lb man have the same number of fat cells-they just shrink and swell. So to answer your question, smaller fat cells are healthier, because you have less fat. But don't try to get rid of your fat. although too much fat can cause health issues, fat is vital to life. Fat is what provides you with energy and stores vitamins when you're not using them. Hope that answers your question!
How do chemotherapy drugs interact chemically with cancer cells to get rid of the cancerous cells?
I have to give a chemistry project tomorrow in class and I need to have a basic understanding of what goes on chemically between chemotherapy drugs and the cancerous cells. Like what element interacts with what and how the chemo drugs stop the cancer cells from replicating. If anyone even has a most basic chemical explanation as to what occurs I would really appreciate it.
Chemotherapy works by destroying cancer cells; unfortunately, it cannot tell the difference between a cancer cell and some healthy cells. So chemotherapy eliminates not only the fast-growing cancer cells but also other fast-growing cells in your body, including, hair and blood cells.
Some cancer cells grow slowly while others grow rapidly. As a result, different types of chemotherapy drugs target the growth patterns of specific types of cancer cells. Each drug has a different way of working and is effective at a specific time in the life cycle of the cell it targets.
So, the chemicals are designed to go after specific cells that have a particular metabolic rate.
Chemotherapy has NOT been very effective and the 5 year survival rate is very poor. It is expensive; a cancer patient is worth about $300,000 to the medical community.
In 1972, according to the American Cancer Societies own figures, 33% of cancers had a five year survival rate. We should also point out that at that same time 33% of cancers went away on their own. Today, according to the ACS, the five year survival rate for cancer has risen to 40%. However, what they do not tell you is that:
1.The statistics are invalid because they combine data of both local and metastasized cancers; and that the comparisons are not randomized [Ulrich Abel, Advanced Epithelial Cancer", 1990 (no longer in print) ]
2.Cancers not factored into the original statistics are now factored in, such as skin cancers, many of which are not fatal and that the statistics are purposely inflated by including people with benign cancers.
3.Technology has helped us to find cancers earlier, thus the survival time from diagnosis to eventual death has lengthened.
4.They are now including in their stats non deadly skin cancers.
By shrinking tumors, chemotherapy encourages stronger cancer cells to grow and multiply and become chemo resistant. Then there are the new cancers caused by chemotherapy, or secondary cancers. This quaint side effect is often overlooked in the lists of side effects in a drug's accompanying literature, though you can find this information quite easily at the National Cancer Institute. We pride ourselves in America for being technologically advanced and that our technology is rooted in a foundation of good science.
When it comes to medicine, little at all is based upon science. Again we shall point to the Office of Technological Assessment’s paper: Assessing the Efficacy and Safety of Medical Technologies in which we are told that fewer than 20% of all medical procedures have been tested, and that of those tested, half were tested badly.
Medicine in America is not about healing.
Most telling, according to Ralph Moss in his book Questioning Chemotherapy, is that in a good number of surveys, chemotherapists have responded that they would neither recommend chemotherapy for their families nor would they use it themselves. In an unpublished cohort study in which it was revealed that only 9% of oncologists took chemotherapy for their cancers.
"Most cancer patients in this country die of chemotherapy.
Chemotherapy does not eliminate breast, colon, or lung cancers. This fact has been documented for over a decade, yet doctors still use chemotherapy for these tumors,” Allen Levin, MD UCSF The Healing of Cancer.
Additionally, Irwin Bross, a biostatistician for the National Cancer Institute, discovered that many cancers that are benign (though thought to be malignant) and will not metastasize until they are hit with chemotherapy. In other words, he's found that many people who've been diagnosed with metastatic cancer did not have metastatic cancer until they got their chemotherapy.
For many cancers, chemotherapy just does not improve your survival rate. Some of these are colorectal, gastric, pancreatic, bladder, breast, ovarian, cervical and corpus uteri, head and neck. Knowing this, oncologists still recommend a regimen of chemotherapy, why?
The answer you will get from oncologists that are honest is this: “We give it to patients so they won't give up hope and fall into the hands of quacks.” Quacks? Implicit in the definition of quackery is the sale of worthless or dangerous nostrums for profit. Who exactly are the quacks? Just because someone is wearing a white smock, has a title, and works in a nice air conditioned office, does NOT take away what he is. Con men don't look like crooks or they would never get anyone to buy into what they are selling. Looking credible does NOT mean they are.
Dr Ulrich Abel, who poured over thousands and thousands of cancer studies, published his shocking report in 1990 stating quite succinctly that chemotherapy has done nothing for 80% of all cancers; that 80% of chemotherapy administered was absolutely worthless.
To give a fair and accurate assessment of chemotherapy in your report, you should also tell people how it is NOT very effective and only a smal
How exactly does capsaicin induce apoptosis in cancer cells?
Could somebody explain in basic terms how capsaicin helps kill certain cancer cells? Also, has anyone figured out why it affects only particular cells?
This was an interesting question to research. Here's what I found:
This article - http://www.eurekalert.org/pub_releases/2006-03/aafc-pch031306.php - has done studies with capsaicin and prostate cancer. The researchers were able to demonstrate that the capsaicin interfered with NF-kappa Beta, which is one of the mechanisms that lead to apoptosis. It also prevents prostate cells from proliferating, thereby preventing prostate cancer growth. The article goes into more detail and is an interesting read if you want to learn more.
How are cancer cells different from ther cells? Why is cancer such a difficult condition to cure?
How are cancer cells different from other cells? Why is cancer such a dffiult condition to cure?
It is different because unlike normal cells cancer doesn't die. It also multiplies/spreads like crazy. The reason it is so difficult to treat or cure is because you have to kill off the good cells and your immune system as well. There is nothing that can get rid of it that won't affect your other cells.
Does anything happen to the brain cells if you smoke marijuana on a regular basis?
I know someone who smoke marijuana on a regular basis (everyday) and they tell me nothing can happen to your brain cells is that true? How does marijuana affect the brain and body as a whole. If anyone knows please let me know.
If regular pot smoking caused as much brain cell damage as some folks claim, I should be dead, or at least a blithering idiot by now. Actually, recent studies have shown that smokers show an increase in brain cell development that may prove to be of use in Alzheimer's disease since it seems to stimulate brain cell growth. Another study shows that THC may be a cancer inhibiting drug and may actually help prevent or reduce lung and other cancers. These kinds of study results are not what our government wants you to hear, but it seems that with each new study the benefits are beginning to outweigh the claimed harm. The illegal status of the drug has a long history based on racism and corporate greed, not on any real scientific study. Prohibition still doesn't work, but lines the pockets of law enforcement and rehab centers at the taxpayers expense. It forces law abiding citizens to deny themselves a true medicine and forces them to support big pharmaceuticals in the production of far more harmful, but legal, drugs.
What procedure is the best for removing pre-cancerous cells in the cervix?
I just recenly had an abnormal pap-smear. I was diginosed with CIN II pre-cancerous cells in my cervix. Has anyone had this and what procedure or steps were taken to rid of these dangerous cells?
The loop electrosurgical excision procedure (LEEP) is currently one of the most commonly used approaches to treating high grade cervical dysplasia discovered on colposcopic examination. It is also known as "large loop excision of the transformation zone" (LLETZ). The procedure has many advantages including low cost, high success rate, and ease of use. The procedure can be done in an office setting and usually only requires a local anesthetic, though sometimes a general anesthetic is used, especially if the patient is highly anxious about the procedure.
How do you get red blood cells back fast after losing blood?
I just got a blood transfusion and I have to run a 5mile marathon tomorrow. I didn't get to pick the day I got the blood transfusion, I had to do it today.
How can I get red blood cells back after losing blood?
Iron I believe helps build blood, but it's possible to overdose. Eat Spinach. Get some rest.