Introduction to Cancer Biology (Part 1): Abnormal Signal Transduction Mechanisms in Medicine 2012-10-26 | This animation is the first part of the series "An Introduction to Cancer Biology", and explains the mechanism of abnormal signal transduction resulting in uncontrolled cell proliferation. This animation also provides an overview of the potential targets of anticancer therapies.REFERENCES:1. Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000 Jan 7;100(1):57-70.2. Herbst RS. Review of epidermal growth factor receptor biology. Int J Radiat Oncol Biol Phys. 2004;59(2 Suppl):21-6.3. Gerharz CD, Ramp U, Reinecke P, et al. Analysis of growth factor-dependent signalling in human epithelioid sarcoma cell lines. Clues to the role of autocrine, juxtacrine and paracrine interactions in epithelioid sarcoma. Eur J Cancer. 2000 Jun;36(9):1171-9.4. Potapova O, Fakhrai H, Mercola D. Growth factor PDGF-B/v-sis confers a tumorigenic phenotype to human tumor cells bearing PDGF receptors but not to cells devoid of receptors: evidence for an autocrine, but not a paracrine, mechanism. Int J Cancer. 1996 May 29;66(5):669-77.5. Andl CD, Mizushima T, Nakagawa H, et al. Epidermal growth factor receptor mediates increased cell proliferation, migration, and aggregation in esophageal keratinocytes in vitro and in vivo. J Biol Chem. 2003 Jan 17;278(3):1824-30.6. Di Fiore PP, Pierce JH, Kraus MH, Segatto O, King CR, Aaronson SA. erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells. Science. 1987 Jul 10;237(4811):178-82. 7. Batra SK, Castelino-Prabhu S, Wikstrand CJ, et al. Epidermal growth factor ligand-independent, unregulated, cell-transforming potential of a naturally occurring human mutant EGFRvIII gene. Cell Growth Differ. 1995 Oct;6(10):1251-9.8. Egeblad M, Mortensen OH, Jaattela M. Truncated ErbB2 receptor enhances ErbB1 signaling and induces reversible, ERK-independent loss of epithelial morphology. Int J Cancer. 2001 Oct 15;94(2):185-91.9. Lage A, Crombet T, González G. Targeting epidermal growth factor receptor signaling: early results and future trends in oncology. Ann Med. 2003; 35(5):327-36.10. Adjei AA, Hidalgo M. Intracellular signal transduction pathway proteins as targets for cancer therapy. J Clin Oncol. 2005 Aug 10;23(23):5386-403. 11. Beeram M, Patnaik A, Rowinsky EK. Raf: a strategic target for therapeutic development against cancer. J Clin Oncol. 2005 Sep 20;23(27):6771-90.12. Schmelzle T, Hall MN. TOR, a central controller of cell growth. Cell. 2000 Oct 13;103(2):253-62.13. Yarden Y, Sliwkowski MX. Untangling the ErbB signalling network. Nat Rev Mol Cell Biol. 2001 Feb;2(2):127-37.14. Igney FH, Krammer PH. Death and anti-death: tumour resistance to apoptosis. Nat Rev Cancer. 2002 Apr; 2(4):277-88.15. Delhalle S, Duvoix A, Schnekenburger M, Morceau F, Dicato M, Diederich M. An introduction to the molecular mechanisms of apoptosis. Ann N Y Acad Sci. 2003 Dec;1010:1-8. 16. Veiby OP, Read MA. Chemoresistance: impact of nuclear factor (NF)-kappaB inhibition by small interfering RNA. Clin Cancer Res. 2004 May 15;10(10):3333-41. 17. Foo P. Metastasis: The journey of mobile cancer cells. Harvard Science Review. Spring 2002;30-2.18. Hicklin DJ, Ellis LM. Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis. J Clin Oncol. 2005 Feb 10;23(5):1011-27.19. Ellis LM. Epidermal growth factor receptor in tumor angiogenesis. Hematol Oncol Clin North Am. 2004 Oct; 18(5):1007-21. 20. Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus Irinotecan, Fluorouracil, and Leucovorin for Metastatic Colorectal Cancer. N Engl J Med. 2004 Jun 3;350(23):2335-42.21. Motzer RJ, Michaelson MD, Redman BG, et al. Activity of SU11248, a multitargeted inhibitor of vascular endothelial growth factor receptor and platelet-derived growth factor receptor, in patients with metastatic renal cell carcinoma. J Clin Oncol. 2006 Jan 1;24(1):16-24.
The Role of Insulin in the Human Body Mechanisms in Medicine 2023-12-12 | Animation Description: This patient-friendly animation describes the main role of insulin in the human body.When food is ingested, it travels along the digestive tract where it is broken down into its component nutrients in order to be absorbed into the bloodstream. One such nutrient is glucose, a simple sugar.Glucose gets absorbed by intestines and then enters the bloodstream. It travels through the circulation to all body cells.Once absorbed into the bloodstream, glucose circulates causing the blood sugar level to rise. An increased level of blood sugar sends a signal to the pancreatic beta cells, which respond by secreting the hormone insulin into the circulation.Insulin is necessary for glucose to reach and be used by several important target tissues throughout the body. These include the liver, muscle, and adipose tissue. Insulin is necessary to keep blood glucose levels stable in the body.Circulating insulin binds to specific insulin receptors located on the cell membrane of tissue cells throughout the body.Upon binding, intracellular signals send transport glucose channels to the cell surface. These channels allow glucose to enter the cell.Glucose enters the cell through a process called facilitated diffusion.
Genetic Predispositions for Multiple Myeloma Mechanisms in Medicine 2023-12-11 | Some of the most important prognostic factors in multiple myeloma are determined by cytogenetics.These factors are typically assessed in two ways: by karyotype analysis and by fluorescence in situ hybridization (FISH).Karyotyping can be performed to reveal the ploidy status of myeloma cells and whether there have been any substantial chromosomal gains or losses.More than half of all myeloma patients have hyperdiploid karyotypes with chromosome numbers ranging between 48 and 74. These patients tend to have a favorable prognosis, although there are some exceptions. Patients with losses of chromosome 13, for example, typically have a worse prognosis. By comparison, FISH is used to detect specific chromosomal translocations.Most non-hyperdiploid patients have translocations between the strong immunoglobulin enhancer of the IgH locus and one of several common oncogenes, resulting in their overexpression.Specifically, non-random early-onset translocations of the IgH enhancer are frequently observed to be juxtaposed with c-MAF, cyclin D1, cyclin D3, FGFR3 and MMSET, and MAFB.The prognostic outcome of a patient depends then on the specific translocation present.Ultimately, those patients who are identified as belonging to a poor prognostic subpopulation are typically administered more aggressive treatment.
Waldenström’s Macroglobulinemia Mechanisms in Medicine 2023-12-10 | Waldenström’s macroglobulinemia is a rare, slow-growing non-Hodgkin lymphoma in which malignant lymphoplasmacytic B-cells multiply out of control, infiltrate the bone marrow and produce large amounts of IgM-derived M-protein. This in turn results in the symptoms of Waldenström’s macroglobulinemia, which include anemia, hyperviscosity, and cryoglobulinemia. When serum levels of the M-protein are high, haemoglobin and platelet counts are low, and the patient presents with substantial symptoms, treatment is usually initiated.Current treatment options are not curative and traditionally consist of nucleoside analogues and alkylators. However, molecular-targeted agents have been explored.One prominent example is rituximab, a monoclonal antibody that targets CD20 cell-surface proteins. Once bound to CD20 receptors, rituximab recruits and activates natural killer cells, which release cytotoxic molecules and trigger apoptosis of drug-bound malignant B-cells.In order to increase its efficacy, rituximab has also been combined with a variety of other agents in several clinical trials.
Novel Anti-Cancer Agents for Multiple Myeloma Mechanisms in Medicine 2023-12-09 | For many years, dexamethasone has been at the forefront of multiple myeloma therapy. Belonging to a class of drugs called corticosteroids, it exhibits anti-inflammatory, immunosuppressive, and anti-tumor effects. As a long-standing standard of care in the management of myeloma, many newer agents are typically used in combination with dexamethasone.Three of the most important novel agents for the treatment of multiple myeloma patients are bortezomib, thalidomide and lenalidomide.Bortezomib inhibits enzymatic complexes, known as proteasomes, which mediate the degradation of many proteins in the cell.Myeloma cells depend upon proteasomal degradation of a specific subset of proteins in order to regulate and promote their own survival. One such protein is IκB, which serves to inhibit the transcription factor, NF-κB.When the degradation of IκB is blocked by bortezomib, it accumulates in the cell and actively inhibits the NF-κB pathway, an important process for myeloma cell survival.By comparison, while the mechanisms of action of thalidomide and lenalidomide are not yet fully understood, they appear to work through multiple means.First, these agents are immunomodulatory through their global effects on cytokine activity and enhancement of anti-tumor immunity.Second, they are anti-angiogenic through the blockage of VEGF and bFGF signaling pathways.Third, they are pro-apoptotic by inhibiting the growth and survival of both stromal and myeloma cells.Bortezomib, thalidomide, and lenalidomide as novel anti-multiple myeloma agents has changed the management of disease.
Amyloidosis Mechanisms in Medicine 2023-12-08 | Amyloidosis is a condition involving the deposition of insoluble proteins within various tissues and organs of the body.When certain protein monomers unravel into characteristic beta-pleated ribbon structures, partially denatured monomers are formed. These aberrantly folded proteins can act as seeds for recruiting additional monomers and triggering oligomerization. The resulting prefibrilar oligomers continue to elongate, eventually forming mature amyloid fibrils.These amyloid fibrils are insoluble and can accumulate throughout the body, affecting one or more organs. As a result, the symptoms of amyloidosis depend upon which organs are involved and can be quite variable. In fact, the diagnosis of amyloidosis often starts with the detection of high protein levels in the urine. For proper diagnosis, however, an abdominal fat pad biopsy must be analyzed.Amyloid proteins in the fat pad biopsy stained with Congo Red dye produce apple-green birefringence under polarized light, allowing for a confirmation of amyloidosis.In the case of primary, or acute light-chain (AL) amyloidosis, the amyloid protein is derived from kappa or lambda immunoglobulin light chain molecules.This can be positively identified by serum or urine protein electrophoresis to detect the presence of an M-spike. To further characterize the nature of the aberrant immunoglobulin, immunofixation is generally used to demonstrate whether the monoclonal gammopathy is derived from kappa or lambda light chains.
Monoclonal Gammopathy of Undetermined Significance, Smoldering Multiple Myeloma and Multiple Myeloma Mechanisms in Medicine 2023-12-07 | Multiple myeloma is a disease characterized by the clonal expansion of malignant plasma cells.While the cause of myeloma is unknown, it is presumed that multiple mutations induce the transformation of plasma cells. Such mutations may permit the cell to expand into a small clonal population, resulting in a condition called monoclonal gammopathy of undetermined significance (or MGUS).If this clonal population becomes larger while retaining a low proliferative capacity, it results in smoldering multiple myeloma.As both MGUS and smoldering myeloma feature an absence of symptoms and end-organ damage, the levels of M-protein and bone marrow plasma cells are used to distinguish between the two.If the M-protein is lower than 3g/dL and the bone marrow contains fewer than 10% plasma cells, then a diagnosis of MGUS is conferred.In contrast, if either the M-protein is higher than 3g/dL or if more than 10% of the bone marrow population includes plasma cells, then smoldering myeloma is diagnosed.Although patients with MGUS or smoldering myeloma are asymptomatic, it is thought that additional mutations drive the clonal plasma cell populations to evolve towards a more aggressive state that leads to end-organ damage and then becomes symptomatic, active multiple myeloma.Active disease is diagnosed if end-organ damage is detected with the development of symptoms and high levels of both the M-protein and plasma cells within the bone marrow. Clinical diagnosis of active myeloma is based on at least three objective laboratory tests, as well as the presence of bone destruction, anemia, renal and nervous system dysfunction, and/or multiple severe infections. These symptoms vary and may exist in various combinations in newly diagnosed multiple myeloma patients.
Transperineal Prostate Biopsies Under Local Anesthesia Mechanisms in Medicine 2021-07-29 | This animation describes the Transperineal Prostate Biopsies (TPBx) procedures with particular focus on Local Anesthetic Transperineal Prostate Biopsy (LATP). LATP is a better and cost-effective alternative to Transrectal Ultrasound Guided Biopsy (TRUSBx) to detect prostate cancer. It is safer for patients due to the low risk of complications, particularly urosepsis, and it is well tolerated.References1. Stefanova V, Buckley R, Flax S, et al. Transperineal prostate biopsies using local anesthesia: Experience with 1287 patients. Prostate cancer detection rate, complications and patient tolerability. Journal of Urology 2019;201:1121-1126. doi: 10.1097/JU.0000000000000156.2. Liss MA, Ehdaie B, Loeb S, et al. An update of the American Urological Association white paper on the prevention and treatment of the more common complications related to prostate biopsy. J Urol 2017;198:329-334. doi: 10.1016/j.juro.2017.01.103.3. Grummet, J., Gorin, M.A., Popert, R. et al. “TREXIT 2020”: why the time to abandon transrectal prostate biopsy starts now. Prostate Cancer Prostatic Dis 23, 62–65 (2020). Available at doi.org/10.1038/s41391-020-0204-8. Accessed May 7, 2020.
Understanding Adoptive Cell Therapy for Sarcoma Mechanisms in Medicine 2021-05-27 | This animation provides an overview of Understanding Adoptive Cell Therapy for Sarcoma. Adoptive cell therapy is a type of cancer treatment that uses your own immune system to treat your cancer. It may be an option for patients with some types of sarcoma. Adoptive cell therapy may also be called by other names (cellular immunotherapy, adoptive immunotherapy, immune cell therapy). Most types of adoptive cell therapy use a type of immune cell called a T cell. T cells are a type of white blood cell. This animation explains how adoptive cell therapy works, the steps involved, why it sometimes doesn’t work, potential side effects, and who is eligible. Adoptive cell therapy for sarcoma is being tested in clinical trials. To learn more about adoptive cell therapy for sarcoma, talk with your doctor or ask for a referral to a sarcoma specialist.0:00 Introduction0:08 What is adoptive cell therapy?0:34 Your immune system and cancer1:00 How adoptive cell therapy works2:20 Why adoptive cell therapy sometimes doesn't work2:54 Side effects of adoptive cell therapy4:16 Who is eligible for adoptive cell therapy for sarcoma?
What are the symptoms of Non-Small Cell Lung Cancer? Mechanisms in Medicine 2021-03-05 | Learn more about lung cancer at http://www.YouAndLungCancer.comThe symptoms of non-small cell lung cancer (NSCLC) are not specific.Possible symptoms are:A cough that doesn’t go away or gets worseCoughing up bloodRust-colored spitHoarse voiceUnexpected weight loss and loss of appetiteShortness of breathFeeling tired or weakA lung infection (bronchitis or pneumonia) that won’t go awayWheezing with no known cause (like asthma)
Vaccins et réponse immunitaire : Quel est le mode d’action des vaccins? (en français) Mechanisms in Medicine 2020-04-15 | En regardant cette animation, les utilisateurs auront une meilleure idée du mode d’action des vaccins en réponse au système immunitaire de l’hôte.English version: youtu.be/Atrx1P2EkiQ
Inhibiteurs de la neuraminidase : Mode d’action (en français) Mechanisms in Medicine 2020-04-15 | En regardant cette animation, les utilisateurs comprendront mieux les mécanismes d’action des inhibiteurs de la neuraminidase.English version: youtu.be/caMne7nQUL8
Cassure antigénique et le virusde la grippe A H1N1 (en français) Mechanisms in Medicine 2020-04-15 | En regardant cette animation, les utilisateurs comprendront mieux la cassure antigénique découlant du réarrangement des génomes entre différentes souches.English version: youtu.be/4H9PV65PUmQ
Antigenic Shift and the H1N1 Influenza A Virus Mechanisms in Medicine 2020-01-30 | Antigenic Shift and the H1N1 Influenza A Virus This animation provides an overview of the principles of antigenic shift and the H1N1 influenza A virus. One way influenza viruses change is called “antigenic shift” (the other is “antigenic drift”.) Antigenic shift is an abrupt, major change in an influenza A virus, resulting in new HA and/or new HA and NA proteins in influenza viruses that infect humans. Shift can result in a new influenza A subtype in humans. One way shift can happen is when an influenza virus from an animal population gains the ability to infect humans. Such animal-origin viruses can contain an HA or HA/NA combination that is so different from the same subtype in humans that most people do not have immunity to the new (e.g., novel) virus. Such a “shift” occurred in the spring of 2009, when an H1N1 virus with genes from North American Swine, Eurasian Swine, humans and birds emerged to infect people and quickly spread, causing a pandemic. When shift happens, most people have little or no immunity against the new virus.
Neuraminidase Inhibitors: Mechanism of Action Mechanisms in Medicine 2020-01-30 | Neuraminidase Inhibitors: Mechanism of Action This animation provides an overview of the mechanism of action of neuraminidase inhibitors. Neuraminidase inhibitors disrupt the release of influenza virus from the host cell. These neuraminidase inhibitors mimic neuraminidase’s sialic acid binding site. When introduced, they bind neuraminidase on the budding viruses, blocking its enzymatic activity.
Vaccines and the Immune Response: How Vaccines Work Mechanisms in Medicine 2020-01-30 | Vaccines and the Immune Response: How Vaccines WorkThis animation provides an overview of vaccines and the immune response, and how influenza vaccines work. Influenza vaccines are able to trigger an immune response by mimicking viral infection. They are usually manufactured using inactivated or killed virus particles taken from various circulating influenza strains.
Understanding Genetics in Gynecologic Cancers Mechanisms in Medicine 2019-01-15 | Developed by the Society of Gynecologic Oncology, the Foundation for Women’s Cancer and Mechanisms in Medicine Inc.http://www.sgo.orghttp://www.foundationforwomenscancer.orghttp://www.mechanismsinmedicine.comGynecologic cancers are cancers that affect the organs of a woman’s reproductive system. They include ovarian and endometrial cancer, among others.“Ovarian cancer” is an umbrella term used to discuss cancers of the ovaries, Fallopian tubes, and peritoneum, because all these cancers behave similarly. Endometrial cancer affects the endometrium, the lining of the uterus.Genetic testing helps you as well as your family.Today, doctors use knowledge of genetic mutations to choose the most effective cancer treatments. So genetic testing can help your doctor select the best treatment for you. PARP inhibitors, immunotherapy, and chemotherapy are some of the treatment options available.Better understanding of inherited cancer syndromes has led to improved treatments for ovarian and endometrial cancer. Now, identifying genetic mutations will move doctors closer to finding cures for those with cancer and preventing it altogether in their family members. It is important to talk to a genetics expert about genetic testing.
What is Lung Cancer? Mechanisms in Medicine 2018-02-02 | This animation is from our new program http://www.YouandLungCancer.com and explains how healthy lungs function and how lung cancer can occur. Non-small cell lung cancer and small cell lung cancer are the two major types of lung cancer. Physicians use noninvasive tests and invasive tests to diagnose lung cancer. Noninvasive tests include Chest x-rays, and CT scans and PET scans. Invasive tests include Bronchoscopy; Endobronchial ultrasound; Thoracentesis; Biomarker testing; and Biopsies, such as Fine needle aspiration (or FNA), Core needle biopsy, and surgical lung biopsy. Physicians need lung cancer staging information to plan treatment. Lung cancer is classified into numerous stages - the higher the stage the more advanced the spread of the cancer and typically the more aggressive the treatment. In Stage 0 cancer it is only the top layers of cells in the lining of air passages in the lungs. This is the easiest stage to treat with highest survivorship. Stage IV lung cancer is the most difficult to treat, having spread to the other lung, the lymph nodes outside the lungs, and other parts of the body.
Mechanism of Action of Cell-based Therapies Mechanisms in Medicine 2017-06-06 | This animation discusses the mechanism of action of Cell-based Therapies. To learn more, visit the CME activity “New Frontiers: The Management of IBD: The Future is Bright” at http://bit.ly/2s1FB4bDeveloped and produced by http://www.MechanismsinMedicine.com
Mechanism of Action of SMAD7 Inhibitors Mechanisms in Medicine 2017-06-06 | This animation discusses the mechanism of action of SMAD7 Inhibitors. To learn more, visit the CME activity “New Frontiers: The Management of IBD: The Future is Bright” at http://bit.ly/2s1FB4bDeveloped and produced by http://www.MechanismsinMedicine.com
Mechanism of Action of JAK Inhibitors Mechanisms in Medicine 2017-06-06 | This animation discusses the mechanism of action of JAK inhibitors. To learn more, visit the CME activity “New Frontiers: The Management of IBD: The Future is Bright” at http://bit.ly/2s1FB4bDeveloped and produced by http://www.MechanismsinMedicine.com
Etiology of IBD Mechanisms in Medicine 2017-06-06 | This animation discusses the etiology of inflammatory bowel disease (IBD). To learn more, visit the CME activity “New Frontiers: The Management of IBD: The Future is Bright” at http://bit.ly/2s1FB4bDeveloped and produced by http://www.MechanismsinMedicine.com
Pathogenesis and Treatment of Myeloma Bone Disease Mechanisms in Medicine 2016-03-21 | Animation Description:Osteolytic bone lesions are commonly observed in patients with active multiple myeloma. For example, osteolytic bone is characterized by sparse trabeculae and is often associated with brittle bones.These bone lesions result from an imbalance which favors bone resorption and osteoclast activity over that of the osteoblasts.This imbalance is maintained through the activation or repression of multiple signaling pathways that are mediated by a variety of physical interactions between multiple myeloma plasma cells and bone marrow stromal cells.For example, RANK ligand-mediated activation of osteoclasts is enhanced due to increased expression and secretion of RANK ligand from bone marrow stromal cells.Additionally, the secretion of osteoprotegerin by osteoblasts and bone marrow stromal cells is decreased, thereby decreasing suppression of RANK-ligand signaling.Many other cytokines are also released to stimulate osteoclasts and/or inhibit osteoblasts.The identification of patients who may benefit from bone-directed therapy is often based on assessing the levels of some of these cytokines.The class of drugs known as bisphosphonates has been developed to target and inhibit osteoclast activity.Once administered to the patient, bisphosphonates are resorbed by the bone and then taken up by the osteoclasts.Following drug uptake, osteoclast activity is inhibited, usually resulting in apoptosis.
The Coagulation Cascade Mechanisms in Medicine 2015-01-27 | Animation description: The Coagulation CascadeThis animation provides an in-depth review of the coagulation cascade.To learn more, go to http://www.MechanismsInHematology.com -- a freely available, educational resource that combines the clinical expertise of hematologists, oncologists, and related researchers with instructive visuals and animations. Essential concepts pertaining to the science and biology of clinical hematology are presented.
3D Animation Demo Reel - Mechanisms in Medicine Mechanisms in Medicine 2014-11-27 | This 3D animation reel is a selection of our recent work. Visit us at http://www.MechanismsinMedicine.com to learn more about our 3D medical animations and educational programs. Mechanisms In Medicine Inc. is a digital healthcare company dedicated to the development of visually compelling, animated educational materials designed to ease the understanding of complex medical concepts.
Fatty Acids and Disease in Type 2 Diabetes Mechanisms in Medicine 2013-07-17 | This animation helps the learner to understand the lipid abnormalities commonly seen in patients with type 2 diabetes. The animation focuses on the major role that elevated plasma free fatty acids (FFAs) play in the development of type 2 diabetes.
How Lipoproteins Affect Metabolism in Diabetes Mechanisms in Medicine 2013-07-16 | There is a strong connection between type 2 diabetes and dyslipidemia. This animation describes the lipid abnormalities commonly seen in patients with type 2 diabetes: elevated levels of triglycerides, raised small dense LDL levels, increased glycation and oxidation of LDLs and reduction of HDLs. These factors increase the risk of cardiovascular disease.
HIV: Basic Function of Immune System Mechanisms in Medicine 2013-07-11 | This animation describes the various types of white blood cells and how they contribute to your body's immunity and defence against infection. Special attention is paid to CD4 cells, the primary target of HIV. Narrated by Dr. Mark Wainberg, Professor of Medicine and of Microbiology at McGill University, Montreal, Quebec, a Canadian AIDS researcher and activist.For more information please visit http://www.AnimatedHIVScience.com
HIV: Mechanisms of Action of NRTIs Mechanisms in Medicine 2013-07-11 | This animation describes how NRTI drugs work by incorporating themselves into viral DNA as it is being transcribed, and thus, blocking further extension of the viral DNA chain. Narrated by Dr. Mark Wainberg, Professor of Medicine and of Microbiology at McGill University, Montreal, Quebec, a Canadian AIDS researcher and activist.For more information please visit http://www.AnimatedHIVScience.com
HIV: Mechanisms of Action of NNRTIs Mechanisms in Medicine 2013-07-11 | This animation describes how Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs) work by blocking the ability of the viral reverse transcriptase enzyme to convert viral RNA into viral DNA. Narrated by Dr. Mark Wainberg, Professor of Medicine and of Microbiology at McGill University, Montreal, Quebec, a Canadian AIDS researcher and activist.For more information please visit http://www.AnimatedHIVScience.com
HIV: Mechanisms of NRTI Resistance (Nucleoside Analogue Discrimination) Mechanisms in Medicine 2013-07-11 | This animation explains the first mechanism of resistance of reverse transcriptase enzyme to some of NRTI drugs, known as nucleoside analogue discrimination. Narrated by Dr. Mark Wainberg, Professor of Medicine and of Microbiology at McGill University, Montreal, Quebec, a Canadian AIDS researcher and activist.For more information please visit http://www.AnimatedHIVScience.com
HIV: Mechanisms of Action of Protease Inhibitors (PIs) Mechanisms in Medicine 2013-07-11 | This animation describes how PI drugs work by directly binding viral proteases. Narrated by Dr. Mark Wainberg, Professor of Medicine and of Microbiology at McGill University, Montreal, Quebec, a Canadian AIDS researcher and activist.For more information please visit http://www.AnimatedHIVScience.com
HIV: Mechanisms of NNRTI Resistance Mechanisms in Medicine 2013-07-11 | This animation describes how mutations acquired by the HIV reverse transcriptase enzyme can effectively prevent NNRTI medicines from being able to bind to it. Narrated by Dr. Mark Wainberg, Professor of Medicine and of Microbiology at McGill University, Montreal, Quebec, a Canadian AIDS researcher and activist.For more information please visit http://www.AnimatedHIVScience.com
HIV: Mechanisms of NRTI Resistance (Primer Nucleoside Unblocking) Mechanisms in Medicine 2013-07-11 | This animation describes the second mechanism of resistance of reverse transcriptase enzyme to some of NRTI drugs, called primer nucleoside unblocking. Narrated by Dr. Mark Wainberg, Professor of Medicine and of Microbiology at McGill University, Montreal, Quebec, a Canadian AIDS researcher and activist.For more information please visit http://www.AnimatedHIVScience.com
HIV: Mechanisms of PI Resistance Mechanisms in Medicine 2013-07-11 | This animation describes how mutations in viral proteases can lead to resistance to PI drugs. Narrated by Dr. Mark Wainberg, Professor of Medicine and of Microbiology at McGill University, Montreal, Quebec, a Canadian AIDS researcher and activist.For more information please visit http://www.AnimatedHIVScience.com
Candiduria: Risk Factors, Symptoms and Treatment Mechanisms in Medicine 2013-01-02 | Developed and produced for http://www.MechanismsinMedicine.comAnimation Description:Candiduria refers to the presence of candida organisms in the urine in quantities of at least 10^5/mL or 100 x 10^6/L. Candiduria can affect different sites of the urinary tract and can be associated with many risk factors. Watch this animation for more information.
Candidemia/Invasive Candidiasis Treatment Algorithm Mechanisms in Medicine 2013-01-02 | Developed and produced for http://www.MechanismsinMedicine.comAnimation Description:The Infectious Diseases Society of America has developed guidelines for the initial treatment of candidemia and invasive candidiasis. Simple steps for treatment are outlined in this clinical practice algorithm. Successful treatment depends on the ability to differentiate between clinically stable and unstable patients. Watch this animation for more information.
Zygomycosis: In the Immunocompromised Patient Mechanisms in Medicine 2013-01-02 | Developed and produced for http://www.MechanismsinMedicine.comAnimation Description:Another common form of zygomycosis is characterized by contamination of traumatic or surgical wounds with spores, resulting in local infection and occasional dissemination in immunocompromised hosts (such as critically ill patients). Watch this animation for more information.
Zygomycosis Overview – Type of Fungal Infection Mechanisms in Medicine 2013-01-02 | Developed and produced by http://www.MechanismsinMedicine.comAnimation Description:Zygomycetes have a wide geographical distribution, and are often found in decaying organic matter. Sporangiospores are released into the environment that if inhaled, can lead to a life-threatening disease. Watch this animation for more information.
Extrapulmonary Aspergillosis – Type of Fungal Infection Mechanisms in Medicine 2012-12-28 | Developed and produced by http://www.MechanismsinMedicine.comAnimation Description:One of the most lethal complications of invasive aspergillosis is dissemination to the brain. The diagnosis is difficult and it has been associated with near 100% mortality, however aggressive antifungal therapy can improve outcomes. Watch this animation for more information.
Aspergillosis – Type of Fungal Infection Mechanisms in Medicine 2012-12-28 | Developed and produced by http://www.MechanismsinMedicine.comAnimation Description:Aspergillosis is a fungal infection caused by Aspergillus, a type of mold (fungus). Aspergillus species have a wide geographical distribution and are often found in decaying organic matter. The conidia (spores) can be inhaled into the lung air spaces and cause invasive pulmonary aspergillosis. Watch this animation for more information.
Renin Angiotensin Aldosterone System Mechanisms in Medicine 2012-11-05 | This animation focuses on the renin angiotensin aldosterone system (RAAS), a classic endocrine system that helps to regulate long-term blood pressure and extracellular volume in the body. Many aspects of cardiovascular disease progression can be directly linked to the RAAS system. Mechanisms such as vascular inflammation, generation of reactive oxygen species and alterations of endothelial function are all known to play a role in atherosclerosis.
The Role of Angiotensin II in the Process of Atherosclerosis Mechanisms in Medicine 2012-11-02 | This animation reviews the physiological effects of Angiotensin II in the cardiovascular system that contribute to the development of atherosclerosis.
Introduction to Cancer Biology (Part 4): Angiogenesis Mechanisms in Medicine 2012-10-29 | As the tumor grows, it eventually reaches a size where it requires additional vasculature in order to sustain continued growth. To achieve this, tumor cells excrete certain proteins that stimulate blood vessel growth into and around the tumor - a process called angiogenesis. This animation is the fourth and final part of the series "An Introduction to Cancer Biology".REFERENCES:1. Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000 Jan 7;100(1):57-70.2. Herbst RS. Review of epidermal growth factor receptor biology. Int J Radiat Oncol Biol Phys. 2004;59(2 Suppl):21-6.3. Gerharz CD, Ramp U, Reinecke P, et al. Analysis of growth factor-dependent signalling in human epithelioid sarcoma cell lines. Clues to the role of autocrine, juxtacrine and paracrine interactions in epithelioid sarcoma. Eur J Cancer. 2000 Jun;36(9):1171-9.4. Potapova O, Fakhrai H, Mercola D. Growth factor PDGF-B/v-sis confers a tumorigenic phenotype to human tumor cells bearing PDGF receptors but not to cells devoid of receptors: evidence for an autocrine, but not a paracrine, mechanism. Int J Cancer. 1996 May 29;66(5):669-77.5. Andl CD, Mizushima T, Nakagawa H, et al. Epidermal growth factor receptor mediates increased cell proliferation, migration, and aggregation in esophageal keratinocytes in vitro and in vivo. J Biol Chem. 2003 Jan 17;278(3):1824-30.6. Di Fiore PP, Pierce JH, Kraus MH, Segatto O, King CR, Aaronson SA. erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells. Science. 1987 Jul 10;237(4811):178-82. 7. Batra SK, Castelino-Prabhu S, Wikstrand CJ, et al. Epidermal growth factor ligand-independent, unregulated, cell-transforming potential of a naturally occurring human mutant EGFRvIII gene. Cell Growth Differ. 1995 Oct;6(10):1251-9.8. Egeblad M, Mortensen OH, Jaattela M. Truncated ErbB2 receptor enhances ErbB1 signaling and induces reversible, ERK-independent loss of epithelial morphology. Int J Cancer. 2001 Oct 15;94(2):185-91.9. Lage A, Crombet T, González G. Targeting epidermal growth factor receptor signaling: early results and future trends in oncology. Ann Med. 2003; 35(5):327-36.10. Adjei AA, Hidalgo M. Intracellular signal transduction pathway proteins as targets for cancer therapy. J Clin Oncol. 2005 Aug 10;23(23):5386-403. 11. Beeram M, Patnaik A, Rowinsky EK. Raf: a strategic target for therapeutic development against cancer. J Clin Oncol. 2005 Sep 20;23(27):6771-90.12. Schmelzle T, Hall MN. TOR, a central controller of cell growth. Cell. 2000 Oct 13;103(2):253-62.13. Yarden Y, Sliwkowski MX. Untangling the ErbB signalling network. Nat Rev Mol Cell Biol. 2001 Feb;2(2):127-37.14. Igney FH, Krammer PH. Death and anti-death: tumour resistance to apoptosis. Nat Rev Cancer. 2002 Apr; 2(4):277-88.15. Delhalle S, Duvoix A, Schnekenburger M, Morceau F, Dicato M, Diederich M. An introduction to the molecular mechanisms of apoptosis. Ann N Y Acad Sci. 2003 Dec;1010:1-8. 16. Veiby OP, Read MA. Chemoresistance: impact of nuclear factor (NF)-kappaB inhibition by small interfering RNA. Clin Cancer Res. 2004 May 15;10(10):3333-41. 17. Foo P. Metastasis: The journey of mobile cancer cells. Harvard Science Review. Spring 2002;30-2.18. Hicklin DJ, Ellis LM. Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis. J Clin Oncol. 2005 Feb 10;23(5):1011-27.19. Ellis LM. Epidermal growth factor receptor in tumor angiogenesis. Hematol Oncol Clin North Am. 2004 Oct; 18(5):1007-21. 20. Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus Irinotecan, Fluorouracil, and Leucovorin for Metastatic Colorectal Cancer. N Engl J Med. 2004 Jun 3;350(23):2335-42.21. Motzer RJ, Michaelson MD, Redman BG, et al. Activity of SU11248, a multitargeted inhibitor of vascular endothelial growth factor receptor and platelet-derived growth factor receptor, in patients with metastatic renal cell carcinoma. J Clin Oncol. 2006 Jan 1;24(1):16-24.
Introduction to Cancer Biology (Part 3): Tissue Invasion and Metastasis Mechanisms in Medicine 2012-10-27 | Another common mechanism of cancer biology is the ability of malignant cells to migrate from their original site to organs throughout the body. This animation provides a closer look at how the EGFR pathway activates and modulates this process of metastasis. This animation is the third part of the series "An Introduction to Cancer Biology".REFERENCES:1. Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000 Jan 7;100(1):57-70.2. Herbst RS. Review of epidermal growth factor receptor biology. Int J Radiat Oncol Biol Phys. 2004;59(2 Suppl):21-6.3. Gerharz CD, Ramp U, Reinecke P, et al. Analysis of growth factor-dependent signalling in human epithelioid sarcoma cell lines. Clues to the role of autocrine, juxtacrine and paracrine interactions in epithelioid sarcoma. Eur J Cancer. 2000 Jun;36(9):1171-9.4. Potapova O, Fakhrai H, Mercola D. Growth factor PDGF-B/v-sis confers a tumorigenic phenotype to human tumor cells bearing PDGF receptors but not to cells devoid of receptors: evidence for an autocrine, but not a paracrine, mechanism. Int J Cancer. 1996 May 29;66(5):669-77.5. Andl CD, Mizushima T, Nakagawa H, et al. Epidermal growth factor receptor mediates increased cell proliferation, migration, and aggregation in esophageal keratinocytes in vitro and in vivo. J Biol Chem. 2003 Jan 17;278(3):1824-30.6. Di Fiore PP, Pierce JH, Kraus MH, Segatto O, King CR, Aaronson SA. erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells. Science. 1987 Jul 10;237(4811):178-82. 7. Batra SK, Castelino-Prabhu S, Wikstrand CJ, et al. Epidermal growth factor ligand-independent, unregulated, cell-transforming potential of a naturally occurring human mutant EGFRvIII gene. Cell Growth Differ. 1995 Oct;6(10):1251-9.8. Egeblad M, Mortensen OH, Jaattela M. Truncated ErbB2 receptor enhances ErbB1 signaling and induces reversible, ERK-independent loss of epithelial morphology. Int J Cancer. 2001 Oct 15;94(2):185-91.9. Lage A, Crombet T, González G. Targeting epidermal growth factor receptor signaling: early results and future trends in oncology. Ann Med. 2003; 35(5):327-36.10. Adjei AA, Hidalgo M. Intracellular signal transduction pathway proteins as targets for cancer therapy. J Clin Oncol. 2005 Aug 10;23(23):5386-403. 11. Beeram M, Patnaik A, Rowinsky EK. Raf: a strategic target for therapeutic development against cancer. J Clin Oncol. 2005 Sep 20;23(27):6771-90.12. Schmelzle T, Hall MN. TOR, a central controller of cell growth. Cell. 2000 Oct 13;103(2):253-62.13. Yarden Y, Sliwkowski MX. Untangling the ErbB signalling network. Nat Rev Mol Cell Biol. 2001 Feb;2(2):127-37.14. Igney FH, Krammer PH. Death and anti-death: tumour resistance to apoptosis. Nat Rev Cancer. 2002 Apr; 2(4):277-88.15. Delhalle S, Duvoix A, Schnekenburger M, Morceau F, Dicato M, Diederich M. An introduction to the molecular mechanisms of apoptosis. Ann N Y Acad Sci. 2003 Dec;1010:1-8. 16. Veiby OP, Read MA. Chemoresistance: impact of nuclear factor (NF)-kappaB inhibition by small interfering RNA. Clin Cancer Res. 2004 May 15;10(10):3333-41. 17. Foo P. Metastasis: The journey of mobile cancer cells. Harvard Science Review. Spring 2002;30-2.18. Hicklin DJ, Ellis LM. Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis. J Clin Oncol. 2005 Feb 10;23(5):1011-27.19. Ellis LM. Epidermal growth factor receptor in tumor angiogenesis. Hematol Oncol Clin North Am. 2004 Oct; 18(5):1007-21. 20. Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus Irinotecan, Fluorouracil, and Leucovorin for Metastatic Colorectal Cancer. N Engl J Med. 2004 Jun 3;350(23):2335-42.21. Motzer RJ, Michaelson MD, Redman BG, et al. Activity of SU11248, a multitargeted inhibitor of vascular endothelial growth factor receptor and platelet-derived growth factor receptor, in patients with metastatic renal cell carcinoma. J Clin Oncol. 2006 Jan 1;24(1):16-24.
Introduction to Cancer Biology (Part 2): Loss of Apoptosis Mechanisms in Medicine 2012-10-26 | Apoptosis or "programmed cell death" is a mechanism by which organisms limit the growth and replication of cells. Loss of apoptosis is one of the key mechanisms behind cancer.This animation is the second part of the series "An Introduction to Cancer Biology", and reveals the faulty apoptotic pathways that tumor cells often have.REFERENCES:1. Hanahan D, Weinberg RA. The hallmarks of cancer. Cell. 2000 Jan 7;100(1):57-70.2. Herbst RS. Review of epidermal growth factor receptor biology. Int J Radiat Oncol Biol Phys. 2004;59(2 Suppl):21-6.3. Gerharz CD, Ramp U, Reinecke P, et al. Analysis of growth factor-dependent signalling in human epithelioid sarcoma cell lines. Clues to the role of autocrine, juxtacrine and paracrine interactions in epithelioid sarcoma. Eur J Cancer. 2000 Jun;36(9):1171-9.4. Potapova O, Fakhrai H, Mercola D. Growth factor PDGF-B/v-sis confers a tumorigenic phenotype to human tumor cells bearing PDGF receptors but not to cells devoid of receptors: evidence for an autocrine, but not a paracrine, mechanism. Int J Cancer. 1996 May 29;66(5):669-77.5. Andl CD, Mizushima T, Nakagawa H, et al. Epidermal growth factor receptor mediates increased cell proliferation, migration, and aggregation in esophageal keratinocytes in vitro and in vivo. J Biol Chem. 2003 Jan 17;278(3):1824-30.6. Di Fiore PP, Pierce JH, Kraus MH, Segatto O, King CR, Aaronson SA. erbB-2 is a potent oncogene when overexpressed in NIH/3T3 cells. Science. 1987 Jul 10;237(4811):178-82. 7. Batra SK, Castelino-Prabhu S, Wikstrand CJ, et al. Epidermal growth factor ligand-independent, unregulated, cell-transforming potential of a naturally occurring human mutant EGFRvIII gene. Cell Growth Differ. 1995 Oct;6(10):1251-9.8. Egeblad M, Mortensen OH, Jaattela M. Truncated ErbB2 receptor enhances ErbB1 signaling and induces reversible, ERK-independent loss of epithelial morphology. Int J Cancer. 2001 Oct 15;94(2):185-91.9. Lage A, Crombet T, González G. Targeting epidermal growth factor receptor signaling: early results and future trends in oncology. Ann Med. 2003; 35(5):327-36.10. Adjei AA, Hidalgo M. Intracellular signal transduction pathway proteins as targets for cancer therapy. J Clin Oncol. 2005 Aug 10;23(23):5386-403. 11. Beeram M, Patnaik A, Rowinsky EK. Raf: a strategic target for therapeutic development against cancer. J Clin Oncol. 2005 Sep 20;23(27):6771-90.12. Schmelzle T, Hall MN. TOR, a central controller of cell growth. Cell. 2000 Oct 13;103(2):253-62.13. Yarden Y, Sliwkowski MX. Untangling the ErbB signalling network. Nat Rev Mol Cell Biol. 2001 Feb;2(2):127-37.14. Igney FH, Krammer PH. Death and anti-death: tumour resistance to apoptosis. Nat Rev Cancer. 2002 Apr; 2(4):277-88.15. Delhalle S, Duvoix A, Schnekenburger M, Morceau F, Dicato M, Diederich M. An introduction to the molecular mechanisms of apoptosis. Ann N Y Acad Sci. 2003 Dec;1010:1-8. 16. Veiby OP, Read MA. Chemoresistance: impact of nuclear factor (NF)-kappaB inhibition by small interfering RNA. Clin Cancer Res. 2004 May 15;10(10):3333-41. 17. Foo P. Metastasis: The journey of mobile cancer cells. Harvard Science Review. Spring 2002;30-2.18. Hicklin DJ, Ellis LM. Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis. J Clin Oncol. 2005 Feb 10;23(5):1011-27.19. Ellis LM. Epidermal growth factor receptor in tumor angiogenesis. Hematol Oncol Clin North Am. 2004 Oct; 18(5):1007-21. 20. Hurwitz H, Fehrenbacher L, Novotny W, et al. Bevacizumab plus Irinotecan, Fluorouracil, and Leucovorin for Metastatic Colorectal Cancer. N Engl J Med. 2004 Jun 3;350(23):2335-42.21. Motzer RJ, Michaelson MD, Redman BG, et al. Activity of SU11248, a multitargeted inhibitor of vascular endothelial growth factor receptor and platelet-derived growth factor receptor, in patients with metastatic renal cell carcinoma. J Clin Oncol. 2006 Jan 1;24(1):16-24.
The Effects of Hyperglycemia on the Immune System Mechanisms in Medicine 2012-10-23 | Developed and produced for http://www.MDPracticeGuide.com, a CME resource for physicians and healthcare providers.Animation Description: Under normal circumstances, bacterial infection results in the release of chemokines that attract circulating neutrophils to the endothelium. This process is known as chemotaxis.A variety of molecules are expressed on the endothelial cell surface that allow the neutrophil to be captured, then roll along the endothelium, then adhere.Following adherence, the neutrophil migrates into the subendothelial tissue to reach the site of infection.The neutrophil engulfs the bacteria and eliminates them via breakdown within the phagosomes — a process known as phagocytosis. In states of hyperglycemia, chemotaxis is reduced. Adherence is also adversely affected.Phagocytosis is also impaired by hyperglycemia.Hyperglycemia also adversely affects the macrophage system. Under normal circumstances, circulating monocytes are attracted to sites of infection, roll, adhere, and then migrate into the subendothelial space. The monocyte then transforms into a macrophage.which is then activated by cytokines released by the bacteria. The activated macrophage then engulfs the bacteria.However, hyperglycemia results in decreased activation of macrophages, thereby arresting the process of macrophage phagocytosis of bacteria.In addition to affecting neutrophil and macrophage function, hyperglycemia also affects the complement cascade. Under situations of normal glycemia, bacteria can activate the complement cascade.Activation of the complement cascade results in the formation of transmembrane protein channels known as membrane attack complex (MAC) in bacterial membrane.Membrane attack complexes make the bacterial membrane porous and the rapid influx of fluid results in the bacterial cell death.Hyperglycemia inhibits the proper activation of the complement cascade, thereby reducing another pathway of the immune system.
Stroke Prevention & Transient Ischemic Attack (TIA) Mechanisms in Medicine 2012-10-22 | Developed and produced for http://www.MDPracticeGuide.com, a CME resource for physicians and healthcare providers.Animation Description: Primary prevention of stroke requires the management of Atherosclerotic Risk Factors, such as hypertension, diabetes, smoking, and dyslipidemia. As the risk increases, secondary stroke prevention factors include identifying whether or not the patient has suffered from: prior transient ischemic attack (TIA) / Stroke; coronary artery disease (CAD) / peripheral vascular disease (PVD); asymptomatic carotid stenosis; or atrial fibrillation. All patients with ischemic stroke or transient ischemic attack should be on antiplatelet therapy (ASA) for secondary prevention of recurrent stroke unless there is an indication for anticoagulation or a contraindication to ASA.Anticoagulation long term with warfarin is the superior antithrombotic if atrial fibrillation or other definite cardiac source of embolism is identified as the cause of stroke/TIA.Surgical intervention is very effective in the prevention of stroke in symptomatic severe internal carotid artery stenosis. Earlier intervention yields greatest benefit.
COPD: Pathophysiology and Diagnosis Mechanisms in Medicine 2012-10-22 | Developed and produced for http://www.MDPracticeGuide.com, a CME resource for physicians and healthcare providers.Animation Description: Cigarette smoking is by far the most common primary risk factor of COPD worldwide. According to global statistics, approximately 210 million people have COPD.By 2030, COPD is predicted to be the fourth leading cause of death worldwide.Epithelial cells lining the airways will respond to smoke inhalation by undergoing cellular changes due to long-term exposure.Over time, chronic irritation and inflammation of the air passages causes small airways disease and parenchymal destruction.Irritation and inflammation of the air passages causes constriction in the bronchi and bronchioles of the lung.In a healthy individual, standing at rest at the foot of a staircase while breathing normally, lung volume is well balanced in terms of:- IRV (Inspirational Reserve Volume);- VT (Tidal Volume); - FRC (Functional Residual Capacity).In the severe COPD patient, lung function is extremely imbalanced with only a tiny capacity for IRV. A patient with severe COPD has a very difficult time managing everyday tasks such as stair climbing. (Spirometry test) The patient is asked to inhale and then forcefully exhale until the lungs are completely emptied via a tube attached to a recording device.The most important values from the spirometry readings are FEV1 and FVC. If the ratio of these values is less than 0.7 then COPD is suspected. More detailed results from spirometry can reveal the stage of COPD in the patient.
Sources of Candida Organisms Mechanisms in Medicine 2012-10-19 | Developed and produced by http://www.MechanismsinMedicine.comAnimation Description: Candida species are normal comensals of the gastrointestinal tract, skin, genitourinary tract and occasionally respiratory tract. Watch this animation for more information on where these organisms can readily be found and why.
