Anti-Infective Agents, Local
Anti-Inflammatory Agents, Non-Steroidal
Characterization of the analgesic and anti-inflammatory activities of ketorolac and its enantiomers in the rat. (1/905)The marked analgesic efficacy of ketorolac in humans, relative to other nonsteroidal anti-inflammatory drugs (NSAIDs), has lead to speculation as to whether additional non-NSAID mechanism(s) contribute to its analgesic actions. To evaluate this possibility, we characterized (R,S)-ketorolac's pharmacological properties in vivo and in vitro using the nonselective cyclooxygenase (COX) inhibitors [indomethacin (INDO) and diclofenac sodium (DS)] as well as the selective COX-2 inhibitor, celecoxib, as references. The potency of racemic (R,S)-ketorolac was similar in tests of acetic acid-induced writhing, carrageenan-induced paw hyperalgesia, and carrageenan-induced edema formation in rats; ID50 values = 0.24, 0. 29, and 0.08 mg/kg, respectively. (R,S)-ketorolac's actions were stereospecific, with (S)-ketorolac possessing the biological activity of the racemate in the above tests. The analgesic potencies for (R,S)-, (S)-, and (R)-ketorolac, INDO, and DS were highly correlated with their anti-inflammatory potencies, suggesting a common mechanism. (R,S)-ketorolac was significantly more potent than INDO or DS in vivo. Neither difference in relative potency of COX inhibition for (R,S)-ketorolac over INDO and DS nor activity of (S)-ketorolac at a number of other enzymes, channels, or receptors could account for the differences in observed potency. The distribution coefficient for (R,S)-ketorolac was approximately 30-fold less than for DS or INDO, indicating that (R,S)-ketorolac is much less lipophilic than these NSAIDs. Therefore, the physicochemical and pharmacokinetics properties of (R,S)-ketorolac may optimize the concentrations of (S)-ketorolac at its biological target(s), resulting in greater efficacy and potency in vivo. (+info)
Cytokine-mediated inflammatory hyperalgesia limited by interleukin-4. (2/905)1. The effect of IL-4 on responses to intraplantar (i.pl.) carrageenin, bradykinin, TNFalpha, IL-1beta, IL-8 and PGE2 was investigated in a model of mechanical hyperalgesia in rats. Also, the cellular source of the IL-4 was investigated. 2. IL-4, 30 min before the stimulus, inhibited responses to carrageenin, bradykinin, and TNFalpha, but not responses to IL-1beta, IL-8 and PGE2. 3. IL-4, 2 h before the injection of IL-1beta, did not affect the response to IL-1beta, whereas IL-4, 12 or 12+2 h before the IL-1beta, inhibited the hyperalgesia (-30%, -74%, respectively). 4. In murine peritoneal macrophages, murine IL-4 for 2 h before stimulation with LPS, inhibited (-40%) the production of IL-1beta but not PGE2. Murine IL-4 (for 16 h before stimulation with LPS) inhibited LPS-stimulated PGE2 but not IL-1beta. 5. Anti-murine IL-4 antibodies potentiated responses to carrageenin, bradykinin and TNFalpha, but not IL-1beta and IL-8, as well as responses to bradykinin in athymic rats but not in rats depleted of mast cells with compound 40/80. 6. These data suggest that IL-4 released by mast cells limits inflammatory hyperalgesia. During the early phase of the inflammatory response the mode of action of the IL-4 appears to be inhibition of the production TNFalpha, IL-1beta and IL-8. In the later phase of the response, in addition to inhibiting the production of pro-inflammatory cytokines, IL-4 also may inhibit the release of PGs. (+info)
The effects of inflammation and inflammatory mediators on nociceptive behaviour induced by ATP analogues in the rat. (3/905)1. We have studied the behavioural effects of intraplantar injections of adenosine 5'-triphosphate (ATP) and related compounds in freely moving rats and investigated whether these nociceptive effects are augmented in the presence of inflammatory mediators. 2. We find that in normal animals ATP and analogues produce dose-dependent nocifensive behaviour (seen as bursts of elevation of the treated hindpaw), and localized thermal hyperalgesia. The rank order of potency was: alpha,beta-methyleneadenosine 5'-triphosphate (alpha,beta-methylene ATP) > 2-methylthioadenosine triphosphate (2-methylthio ATP) > ATP. After neonatal treatment with capsaicin, to destroy small calibre primary sensory neurones, nocifensive behaviour was largely absent. 3. The effects of ATP analogues were assessed in three models of peripheral sensitization: 2 h after dilute intraplantar carrageenan (0.25% w v(-1)); 24 h after irradiation of the hindpaw with ultraviolet (U.V.) B; immediately following prostaglandin E2 (PGE2) treatment. In all models the effect of alpha,beta-methylene ATP was greatly augmented. After carrageenan, significant hindpaw-lifting behaviour activity was induced by injection of only 0.05 nmol of alpha,beta-methylene ATP, some 100 times less than necessary in normal skin. 4. Our data suggest that it is much more likely that endogenous levels of ATP will reach levels capable of exciting nociceptors in inflamed versus normal skin. Our data also suggest the involvement of P2X3 receptor subunits in ATP-induced nociception. (+info)
Effect of sodium glycyrrhetinate on chemical peritonitis in rats. (4/905)AIM: To study the anti-inflammatory mechanisms of sodium glycyrrhetinate (SG). METHODS: Rat chemical peritonitis was used. The protein content and prostaglandin E2 (PGE2) content in exudate were measured by Folin-phenol assay and RIA, respectively. SOD activity in neutrophils (Neu) was determined by pyrogallol-NBT colorimetry. cAMP content in Neu was detected by competitive protein binding assay. RESULTS: In peritonitis caused by histamine, SG 10-20 mg.kg-1 i.m. reduced exudate volume and Neu counts, and 5-20 mg.kg-1 i.m. lowered the protein content in exudate. In peritonitis induced by carrageenan, SG 20 mg.kg-1 i.m. reduced exudate volume, Neu counts, protein content and PGE2 content in exudate, increased SOD activity in Neu, but did not affect beta-glucuronidase release from Neu. In peritonitis induced by arachidonic acid, SG 20 mg.kg-1 i.m. reduced Neu counts, protein content, and PGE2 content in exudate, and attenuated the reduction of cAMP level in Neu. CONCLUSION: SG exerts its anti-inflammatory action by lowering permeability of capillaries in inflammatory site, inhibiting Neu emigration and PGE2 biosynthesis, and scavenging oxygen free radicals. (+info)
Beneficial effects of raxofelast (IRFI 016), a new hydrophilic vitamin E-like antioxidant, in carrageenan-induced pleurisy. (5/905)1. Peroxynitrite is a strong oxidant that results from reaction between NO and superoxide. It has been recently proposed that peroxynitrite plays a pathogenetic role in inflammatory processes. Here we have investigated the therapeutic efficacy of raxofelast, a new hydrophilic vitamin E-like antioxidant agent, in rats subjected to carrageenan-induced pleurisy. 2. In vivo treatment with raxofelast (5, 10, 20 mg kg(-1) intraperitoneally 5 min before carrageenan) prevented in a dose dependent manner carrageenan-induced pleural exudation and polymorphonuclear migration in rats subjected to carrageenan-induced pleurisy. Lung myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels, as well as histological organ injury were significantly reduced by raxofelast. 3. Immunohistochemical analysis for nitrotyrosine, a footprint of peroxynitrite, revealed a positive staining in lungs from carrageenan-treated rats. No positive nitrotyrosine staining was found in the lungs of the carrageenan-treated rats, which received raxofelast (20 mg kg 1) treatment. 4. Furthermore, in vivo raxofelast (5, 10, 20 mg kg(-1)) treatment significantly reduced peroxynitrite formation as measured by the oxidation of the fluorescent dihydrorhodamine 123, prevented the appearance of DNA damage, the decrease in mitochondrial respiration and partially restored the cellular level of NAD+ in ex vivo macrophages harvested from the pleural cavity of rats subjected to carrageenan-induced pleurisy. 5. In conclusion, our study demonstrates that raxofelast, a new hydrophilic vitamin E-like antioxidant agent, exerts multiple protective effects in carrageenan-induced acute inflammation. (+info)
Bradykinin B1 and B2 receptors, tumour necrosis factor alpha and inflammatory hyperalgesia. (6/905)The effects of BK agonists and antagonists, and other hyperalgesic/antihyperalgesic drugs were measured (3 h after injection of hyperalgesic drugs) in a model of mechanical hyperalgesia (the end-point of which was indicated by a brief apnoea, the retraction of the head and forepaws, and muscular tremor). DALBK inhibited responses to carrageenin, bradykinin, DABK, and kallidin. Responses to kallidin and DABK were inhibited by indomethacin or atenolol and abolished by the combination of indomethacin + atenolol. DALBK or HOE 140, given 30 min before, but not 2 h after, carrageenin, BK, DABK and kallidin reduced hyperalgesic responses to these agents. A small dose of DABK+ a small dose of BK evoked a response similar to the response to a much larger dose of DABK or BK, given alone. Responses to BK were antagonized by HOE 140 whereas DALBK antagonized only responses to larger doses of BK. The combination of a small dose of DALBK with a small dose of HOE 140 abolished the response to BK. The hyperalgesic response to LPS (1 microg) was inhibited by DALBK or HOE 140 and abolished by DALBK + HOE 140. The hyperalgesic response to LPS (5 microg) was not antagonized by DALBK + HOE 140. These data suggest: (a) a predominant role for B2 receptors in mediating hyperalgesic responses to BK and to drugs that stimulate BK release, and (b) activation of the hyperalgesic cytokine cascade independently of both B1 and B2 receptors if the hyperalgesic stimulus is of sufficient magnitude. (+info)
Limited anti-inflammatory efficacy of cyclo-oxygenase-2 inhibition in carrageenan-airpouch inflammation. (7/905)1. Cyclo-oxygenase-2 (COX-2) is expressed at sites of inflammation and is believed to be the major source of inflammation-associated prostaglandin synthesis. Selective inhibition of COX-2 has been suggested to produce anti-inflammatory effects with reduced toxicity in the gastrointestinal tract. We examined the extent to which suppression of COX-2 led to inhibition of various components of inflammation in the carrageenan-airpouch model in the rat. 2. Indomethacin (> or =0.3 mg kg(-1)), nimesulide (> or =3 mg kg(-1)) and the selective COX-2 inhibitor, SC-58125 (> or =0.3 mg kg(-1)), significantly suppressed the production of prostaglandin E2 at the site of inflammation. At higher doses, indomethacin (> or =1 mg kg(-1)) and nimesulide (30 mg kg(-1)), but not SC-58125 (up to 10 mg kg(-1)), significantly inhibited COX-1 activity (as measured by whole blood thromboxane synthesis). 3. All three test drugs significantly reduced the volume of exudate in the airpouch, but only at doses greater than those required for substantial (>90%) suppression of COX-2 activity. Similarly, reduction of leukocyte infiltration was only observed with the doses of indomethacin and nimesulide that caused significant suppression of COX-1 activity. 4. SC-58125 did not significantly affect leukocyte infiltration into the airpouch at any dose tested (up to 10 mg kg(-1)). A second selective COX-2 inhibitor, Dup-697, was also found to suppress exudate PGE2 levels without significant effects on leukocyte infiltration. 5. These results indicate that selective inhibition of COX-2 results in profound suppression of PGE2 synthesis in the carrageenan-airpouch, but does not affect leukocyte infiltration. Exudate volume was only reduced with the highly selective COX-2 inhibitor when a dose far above that necessary for suppression of COX-2 activity was used. Inhibition of leukocyte infiltration was observed with indomethacin and nimesulide, but only at doses that inhibited both COX-1 and COX-2. (+info)
Spinal blockade of opioid receptors prevents the analgesia produced by TENS in arthritic rats. (8/905)Transcutaneous electrical nerve stimulation (TENS) is commonly used for relief of pain. The literature on the clinical application of TENS is extensive. However, surprisingly few reports have addressed the neurophysiological basis for the actions of TENS. The gate control theory of pain is typically used to explain the actions of high-frequency TENS, whereas, low-frequency TENS is typically explained by release of endogenous opioids. The current study investigated the role of mu, delta, and kappa opioid receptors in antihyperalgesia produced by low- and high-frequency TENS by using an animal model of inflammation. Antagonists to mu (naloxone), delta (naltrinodole), or kappa (nor-binaltorphimine) opioid receptors were delivered to the spinal cord by microdialysis. Joint inflammation was induced by injection of kaolin and carrageenan into the knee-joint cavity. Withdrawal latency to heat was assessed before inflammation, during inflammation, after drug (or artificial cerebral spinal fluid as a control) administration, and after drug (or artificial cerebral spinal fluid) administration + TENS. Either high- (100 Hz) or low- frequency (4 Hz) TENS produced approximately 100% inhibition of hyperalgesia. Low doses of naloxone, selective for mu opioid receptors, blocked the antihyperalgesia produced by low-frequency TENS. High doses of naloxone, which also block delta and kappa opioid receptors, prevented the antihyperalgesia produced by high-frequency TENS. Spinal blockade of delta opioid receptors dose-dependently prevented the antihyperalgesia produced by high-frequency TENS. In contrast, blockade of kappa opioid receptors had no effect on the antihyperalgesia produced by either low- or high-frequency TENS. Thus, low-frequency TENS produces antihyperalgesia through mu opioid receptors and high-frequency TENS produces antihyperalgesia through delta opioid receptors in the spinal cord. (+info)
There are several types of edema, including:
1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.
Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.
Hyperalgesia is often seen in people with chronic pain conditions, such as fibromyalgia, and it can also be a side effect of certain medications or medical procedures. Treatment options for hyperalgesia depend on the underlying cause of the condition, but may include pain management techniques, physical therapy, and medication adjustments.
In clinical settings, hyperalgesia is often assessed using a pinprick test or other pain tolerance tests to determine the patient's sensitivity to different types of stimuli. The goal of treatment is to reduce the patient's pain and improve their quality of life.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
3. Heart disease
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
There are several different types of pain, including:
1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.
The medical field uses a range of methods to assess and manage pain, including:
1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.
It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.
Types of Hyperesthesia:
1. Allodynia: This type of hyperesthesia is characterized by pain from light touch or contact that would normally not cause pain.
2. Hyperalgesia: This condition is marked by an increased sensitivity to pain, such as a severe response to mild stimuli.
3. Hyperpathia: It is characterized by an abnormal increase in sensitivity to tactile stimulation, such as feeling pain from gentle touch or clothing.
4. Thermal hyperalgesia: This condition is marked by an increased sensitivity to heat or cold temperatures.
Causes of Hyperesthesia:
1. Neurological disorders: Conditions such as migraines, multiple sclerosis, peripheral neuropathy, and stroke can cause hyperesthesia.
2. Injuries: Traumatic injuries, such as nerve damage or spinal cord injuries, can lead to hyperesthesia.
3. Infections: Certain infections, such as shingles or Lyme disease, can cause hyperesthesia.
4. Medications: Certain medications, such as antidepressants or chemotherapy drugs, can cause hyperesthesia as a side effect.
5. Other causes: Hyperesthesia can also be caused by other medical conditions, such as skin disorders or hormonal imbalances.
Symptoms of Hyperesthesia:
1. Pain or discomfort from light touch or contact
2. Increased sensitivity to temperature changes
3. Burning or stinging sensations
4. Itching or tingling sensations
5. Abnormal skin sensations, such as crawling or tingling
6. Sensitivity to sounds or lights
7. Difficulty with fine motor skills or hand-eye coordination
8. Mood changes, such as anxiety or depression
9. Fatigue or lethargy
10. Cognitive impairment or difficulty concentrating.
Diagnosis of Hyperesthesia:
To diagnose hyperesthesia, a healthcare provider will typically begin with a physical examination and medical history. They may also conduct tests to rule out other conditions that could be causing the symptoms. These tests may include:
1. Blood tests: To check for infections or hormonal imbalances
2. Imaging tests: Such as X-rays, CT scans, or MRI scans to look for nerve damage or other conditions
3. Nerve conduction studies: To test the function of nerves
4. Electromyography (EMG): To test muscle activity and nerve function.
5. Skin biopsy: To examine the skin tissue for signs of skin disorders.
Treatment of Hyperesthesia:
The treatment of hyperesthesia will depend on the underlying cause of the condition. In some cases, the symptoms may be managed with medication or lifestyle changes. Some possible treatments include:
1. Pain relief medications: Such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) to relieve pain and reduce inflammation.
2. Anti-seizure medications: To control seizures in cases of epilepsy.
3. Antidepressant medications: To manage depression or anxiety related to the condition.
4. Physical therapy: To improve mobility and strength, and to reduce stiffness and pain.
5. Occupational therapy: To help with daily activities and to improve fine motor skills.
6. Lifestyle changes: Such as avoiding triggers, taking regular breaks to rest, and practicing stress-reducing techniques such as meditation or deep breathing.
7. Alternative therapies: Such as acupuncture or massage therapy may also be helpful in managing symptoms.
It is important to note that the treatment of hyperesthesia is highly individualized and may take some trial and error to find the most effective combination of treatments. It is best to work with a healthcare provider to determine the best course of treatment for your specific case.
1. Strains and sprains: These are common injuries that occur when the muscles or ligaments in the foot are stretched or torn. They can be caused by overuse or sudden movement.
2. Fractures: A fracture is a break in a bone. In the foot, fractures can occur in any of the five long bones (metatarsals) or the heel bone (calcaneus).
3. Plantar fasciitis: This is a common condition that affects the plantar fascia, a band of tissue that runs along the bottom of the foot. It can cause pain and stiffness in the heel and bottom of the foot.
4. Achilles tendinitis: This is an inflammation of the Achilles tendon, which connects the calf muscles to the heel bone. It can cause pain and stiffness in the back of the ankle.
5. Bunions and hammertoes: These are deformities that can occur when the bones in the foot are not properly aligned. They can cause pain, swelling, and stiffness in the foot.
6. Infections: Foot injuries can increase the risk of developing an infection, especially if they become exposed to bacteria or other microorganisms. Signs of an infection may include redness, swelling, warmth, and pain.
7. Ulcers: These are open sores that can develop on the skin of the foot, often as a result of diabetes or poor circulation. They can be difficult to heal and can lead to further complications if left untreated.
Treatment for foot injuries will depend on the severity of the injury and may include rest, ice, compression, and elevation (RICE) as well as physical therapy exercises to improve strength and flexibility. In some cases, surgery may be necessary to repair damaged tissues or realign bones.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
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- Hundreds of years back, the Irish would make carrageenan in their kitchens by boiling salt, seaweed, and alcohol. (drstevebest.org)
- After the weight of kappa carrageenan plant is suitable enough, then it will be harvest to be used to make carrageenan substance that you question earlier. (kappacarrageenansuppliers.com)
- Carrageenan-induced mouse paw edema model was used for induction of inflammation. (ijp-online.com)
- The results showed that intraplantar injection of carrageenan led to time-dependent development of peripheral inflammation, which resulted in a significant increase in the levels of tumor necrosis factor α (TNF-α) and interleukin 1 (IL-1) β, nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) and also iNOS and COX-2 protein expression in inflamed paw. (ijp-online.com)
- To evaluate the antioxidant capacity of Chuquiraga spinosa extracts and prevention of carrageenan-induced inflammation in mice. (phcogj.com)
- However, it wasn't till World War II, when a comparable component called agar was no longer readily available, that carrageenan soared in appeal in the United States food supply. (drstevebest.org)
- Sales of carrageenan gum decline in 2020 due to the onset of the coronavirus outbreak. (marketresearchblog.org)
- In its latest report, FMI offers an unbiased analysis of the global carrageenan gum market, providing historical data for the period of 2016-2020 and forecast statistics for the period of 2021-2031. (marketresearchblog.org)
- Carrageenan is made from a kind of red seaweed referred to as Chondrus crispus. (drstevebest.org)
- Because tasty chocolate milk and nuttylicious almond milk, carrageenan is used as a stabilizer to keep the chocolate from separating or the ground nuts from settling to the bottom of the container. (drstevebest.org)
- Cystocarpic and non-fertile plants of Sarcopeltis (ex Gigartina ) skottsbergii produced kappa-carrageenans, while tetrasporophytes produced lambda-carrageenans, and yields were higher in cystocarpic and sterile specimens than in tetrasporophytes. (frontiersin.org)
- What is Kappa Carrageenan Usage and Production Process? (kappacarrageenansuppliers.com)
- There are some people that question about what is kappa carrageenan , as you might never hear about this substance before. (kappacarrageenansuppliers.com)
- If you want to know what is kappa carrageenan , then you should know that it is a kind of carrageenan that made using Kappaphycus alvarezii which is one species of red edible seaweed. (kappacarrageenansuppliers.com)
- Thus many products which made from diary is created using kappa carrageenan inside the mixture. (kappacarrageenansuppliers.com)
- The kappa carrageenan itself only has 1 sulphate set on each disaccharide. (kappacarrageenansuppliers.com)
- The kappa carrageenan itself is made using one species of red edible seaweed which actually is a plant, thus it is consider suitable for vegetarian and vegan product. (kappacarrageenansuppliers.com)
- Next question that needs to be answer is about what is kappa carrageenan production process. (kappacarrageenansuppliers.com)
- The farmer will use nylon line to control the kappa carrageenan growth, which usually hung in 2 meter depth. (kappacarrageenansuppliers.com)
- The harvested kappa carrageenan will be dried first since the water content need to be removed before being shipped into the factory location. (kappacarrageenansuppliers.com)
- Then we are ready to answer your question about what is kappa carrageenan production process inside the factory. (kappacarrageenansuppliers.com)
- First process that the factory will do is the grinding process to make the raw material which is the kappa carrageenan itself becomes easier to be processed. (kappacarrageenansuppliers.com)
- Then the heating process will be done to create the kappa carrageenan from the material, but there is also celluloses created during the making process. (kappacarrageenansuppliers.com)
- Those are all the information that you need to know when you have question about what is kappa carrageenan so you will be more informed. (kappacarrageenansuppliers.com)
- Then, they would blend those three ingredients to release natural carrageenan. (drstevebest.org)
- The enzyme was immobilized successfully on k- carrageenan - alginate gel carrier (CA) with 93 % immobilization yield. (bvsalud.org)
- In these experiments, we evaluated the antihyperalgesic activity of small-molecule inhibitors of FAAH and sEH, administered alone or in combination, in two pain models: carrageenan-induced hyperalgesia in mice and streptozocin-induced allodynia in rats. (nih.gov)
- Immobilization of halophilic Aspergillus awamori EM66 exochitinase on grafted k-carrageenan-alginate beads. (bvsalud.org)
- In this study, alpha-naphthyl acetate esterase (ANAE) extracted from Atta (wholemeal) wheat flour and grinded wheat grains was immobilized on k-carrageenan beads that were amino-functionalized using 2% polyethyleneimine (PEI). (iium.edu.my)
- The name Carrageenan is originated from a species of seaweed referred to as Carrageen Moss or Irish Moss in England, and Carraigin in Ireland. (drstevebest.org)
- Several studies reported that gametophytes and tetrasporophytes of Gigartinaceae produce different carrageenan types, as observed in Sarcopeltis species although they have isomorphic haploid and diploid phases. (frontiersin.org)
- What foods and beverages use carrageenan? (drstevebest.org)
- Increasing meat consumption in China will augment the carrageenan gum market growth. (marketresearchblog.org)
- Carrageenan is an inflammatory agent that is commonly used to test antiinflammatory drugs. (cdc.gov)
- A proprietary blend of natural moisturizers, including Carrageenan, Aloe Vera, and Vitamin E, creates a natural feeling moisturizer that emulates natural lubrication. (luckybloke.com)
- Increasing applications of carrageenan in the food & beverage industry, coupled with research and development for sustainable products will enable growth in the market during the assessment period," says the FMI analyst. (marketresearchblog.org)
- Being a plant-based emulsifying agent, carrageenan gum is finding applications in the cosmetic industry. (marketresearchblog.org)
- Why is carrageenan in our food? (drstevebest.org)
- Carrageenan is utilized as a food additive for several reasons. (drstevebest.org)
- Carrageenan: What's the Big Deal About this Food Additive? (ecosalon.com)
- This is the reason for the usage of carrageenan in creation of many kinds of product from personal care to food product. (kappacarrageenansuppliers.com)
- Unlike gelatin, which originates from animal items, carrageenan is appropriate for vegans and is naturally, grown in water. (drstevebest.org)
- Carlucci, Scolaro, Damonte, Herpes simplex virus type 1 variants arising after selection with an antiviral carrageenan: lack of correlation between drug susceptibility and syn phenotype, J. Med. (c19early.org)
- Furthermore this kind of carrageenan is only able to dissolve inside liquid in high temperature. (kappacarrageenansuppliers.com)
- What is the process of carrageenan? (drstevebest.org)
- Ever since, the process used to produce carrageenan is really similar and still, very minimal, implying it remains near the natural kind. (drstevebest.org)
- This study aims to evaluate the physical properties of encapsulated phycocyanin from Spirulina and the potential of maltodextrin in combination with κ-carrageenan in its microencapsulation process by spray drying. (undip.ac.id)
- Results indicated that microcapsules of phycocyanin with 9% of maltodetxrin and 1% of κ-carrageenan as coating material produced the highest bulk density, particle size, and encapsulation efficiency, which were 1,501.27 kg ∙ m-3, 1,152.33 nm, and 48.87%, respectively. (undip.ac.id)
- This kind of carrageenan is actually able to make strong as well as rigid gel if potassium ion is available inside the mixture. (kappacarrageenansuppliers.com)
- Carrageenan stimulated the reduction of NBT by PMNs, but did not stimulate membrane depolarization, oxygen consumption, hydrogen - peroxide production, or myeloperoxidase secretion. (cdc.gov)
- Home COVID-19 treatment studies for Iota-carrageenan COVID-19 treatment studies for Iota-carragee. (c19early.org)
- In the 19th century, the Irish believed carrageenan could treat sick calves in addition to human colds, flu and blockage. (drstevebest.org)
- Carrageenan stimulates reduction of nitroblue tetrazolium by human neutrophils without membrane depolarization, myeloperoxidase secretion, or increased oxygen consumption. (cdc.gov)
- The mode of action of carrageenan (9000071), a sulfated polyanionic polysaccharide, was investigated in human neutrophils (PMN), in a serum free medium. (cdc.gov)