Calcium Channel Blockers
Calcium Channels, L-Type
Calcium Channels, N-Type
Calcium Channels, T-Type
Calcium Channel Agonists
Ion Channel Gating
Potassium Channels, Inwardly Rectifying
Calcium Channels, P-Type
Calcium Channels, R-Type
Potassium Channel Blockers
Potassium Channels, Voltage-Gated
Potassium Channels, Calcium-Activated
Sodium Channel Blockers
TRPC Cation Channels
Shaker Superfamily of Potassium Channels
Large-Conductance Calcium-Activated Potassium Channels
Cyclic Nucleotide-Gated Cation Channels
Molecular Sequence Data
TRPV Cation Channels
Dose-Response Relationship, Drug
Amino Acid Sequence
Ryanodine Receptor Calcium Release Channel
TRPM Cation Channels
Acid Sensing Ion Channels
Epithelial Sodium Channels
Kv1.3 Potassium Channel
Ether-A-Go-Go Potassium Channels
Kv1.2 Potassium Channel
Kv1.1 Potassium Channel
Kv1.5 Potassium Channel
Small-Conductance Calcium-Activated Potassium Channels
Transient Receptor Potential Channels
KCNQ Potassium Channels
Shab Potassium Channels
Shaw Potassium Channels
Kv1.4 Potassium Channel
Protein Structure, Tertiary
G Protein-Coupled Inwardly-Rectifying Potassium Channels
Shal Potassium Channels
KCNQ2 Potassium Channel
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
NAV1.5 Voltage-Gated Sodium Channel
Intermediate-Conductance Calcium-Activated Potassium Channels
KCNQ3 Potassium Channel
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
Inositol 1,4,5-Trisphosphate Receptors
Delayed Rectifier Potassium Channels
NAV1.2 Voltage-Gated Sodium Channel
Voltage-Gated Sodium Channels
Cell Membrane Permeability
Protein Kinase C
Cyclic AMP-Dependent Protein Kinases
Sequence Homology, Amino Acid
NAV1.4 Voltage-Gated Sodium Channel
Voltage-Dependent Anion Channels
Differential distribution of three members of a gene family encoding low voltage-activated (T-type) calcium channels. (1/576)Low voltage-activated (T-type) calcium currents are observed in many central and peripheral neurons and display distinct physiological and functional properties. Using in situ hybridization, we have localized central and peripheral nervous system expression of three transcripts (alpha1G, alpha1H, and alpha1I) of the T-type calcium channel family (CaVT). Each mRNA demonstrated a unique distribution, and expression of the three genes was largely complementary. We found high levels of expression of these transcripts in regions associated with prominent T-type currents, including inferior olivary and thalamic relay neurons (which expressed alpha1G), sensory ganglia, pituitary, and dentate gyrus granule neurons (alpha1H), and thalamic reticular neurons (alpha1I and alpha1H). Other regions of high expression included the Purkinje cell layer of the cerebellum, the bed nucleus of the stria terminalis, the claustrum (alpha1G), the olfactory tubercles (alpha1H and alpha1I), and the subthalamic nucleus (alpha1I and alpha1G). Some neurons expressed high levels of all three genes, including hippocampal pyramidal neurons and olfactory granule cells. Many brain regions showed a predominance of labeling for alpha1G, including the amygdala, cerebral cortex, rostral hypothalamus, brainstem, and spinal cord. Exceptions included the basal ganglia, which showed more prominent labeling for alpha1H and alpha1I, and the olfactory bulb, the hippocampus, and the caudal hypothalamus, which showed more even levels of all three transcripts. Our results are consistent with the hypothesis that differential gene expression underlies pharmacological and physiological heterogeneity observed in neuronal T-type calcium currents, and they provide a molecular basis for the study of T-type channels in particular neurons. (+info)
Cloning and expression of a novel member of the low voltage-activated T-type calcium channel family. (2/576)Low voltage-activated Ca2+ channels play important roles in pacing neuronal firing and producing network oscillations, such as those that occur during sleep and epilepsy. Here we describe the cloning and expression of the third member of the T-type family, alpha1I or CavT.3, from rat brain. Northern analysis indicated that it is predominantly expressed in brain. Expression of the cloned channel in either Xenopus oocytes or stably transfected human embryonic kidney-293 cells revealed novel gating properties. We compared these electrophysiological properties to those of the cloned T-type channels alpha1G and alpha1H and to the high voltage-activated channels formed by alpha1Ebeta3. The alpha1I channels opened after small depolarizations of the membrane similar to alpha1G and alpha1H but at more depolarized potentials. The kinetics of activation and inactivation were dramatically slower, which allows the channel to act as a Ca2+ injector. In oocytes, the kinetics were even slower, suggesting that components of the expression system modulate its gating properties. Steady-state inactivation occurred at higher potentials than any of the other T channels, endowing the channel with a substantial window current. The alpha1I channel could still be classified as T-type by virtue of its criss-crossing kinetics, its slow deactivation (tail current), and its small (11 pS) conductance in 110 mM Ba2+ solutions. Based on its brain distribution and novel gating properties, we suggest that alpha1I plays important roles in determining the electroresponsiveness of neurons, and hence, may be a novel drug target. (+info)
L- and T-type voltage-gated Ca2+ currents in adrenal medulla endothelial cells. (3/576)We investigated voltage-dependent Ca2+ channels of bovine adrenal medulla endothelial cells with the whole cell version of the patch-clamp technique. Depolarization elicited an inward current that was carried by Ca2+ and was composed of a transient (T) current, present in all the cells tested, and a sustained (L) current, present in 65% of them. We separated these currents and measured their individual kinetic and gating properties. The activation threshold for T current was approximately -50 mV, and its maximum amplitude was -49.8 +/- 4.8 pA (means +/- SE, n = 19) at 0 mV. The time constant was 10.2 +/- 1.5 ms (n = 4) for activation and 18.4 +/- 2.8 ms (n = 4) for inactivation. The L current activated at -40 mV, and it reached a plateau at -20.1 +/- 2.3 pA (n = 6). Its activation time course was a single exponential with an activation time contant of 26.8 +/- 2.3 ms (n = 4). Current-voltage curves, kinetics, gating, response to BAY K 8644, nifedipine, amiloride, and different selectivity for Ba2+ and Ca2+ indicated that the underlying channels for the observed currents are only of the T- and L-types that resemble those of the endocrine secretory cells. (+info)
A role for T-type Ca2+ channels in the synergistic control of aldosterone production by ANG II and K+. (4/576)Independently, plasma K+ and ANG II stimulate aldosterone secretion from adrenal glomerulosa (AG) cells, but together they synergistically control production. We studied mechanisms to mediate this synergy using bovine AG cells studied under physiological conditions (in 1.25 mM Ca2+ at 37 degrees C). Increasing K+ from 2 to 5 mM caused a potentiation of ANG II-induced aldosterone secretion and a substantial membrane depolarization ( approximately 21 mV). ANG II inhibited a K+-selective conductance in both 2 and 5 mM K+ but caused only a slight depolarization because, under both conditions, membrane potential was close to the reversal potential of the ANG II-induced current. ANG II activated calcium/calmodulin-dependent protein kinase II (CaMKII) equivalently in 2 and 5 mM K+. However, CaMKII activation caused a hyperpolarizing shift in the activation of T-type Ca2+ channels, such that substantially more current was elicited at membrane potentials established by 5 mM K+. We propose that synergy in aldosterone secretion results from K+-induced depolarization and ANG II-induced modulation of T-type channel activation, such that together they promote enhanced steady-state Ca2+ flux. (+info)
Morphological transformation induced by activation of the mitogen-activated protein kinase pathway requires suppression of the T-type Ca2+ channel. (5/576)Transformation of fibroblasts by various oncogenes, including ras, mos, and src accompanies with characteristic morphological changes from flat to round (or spindle) shapes. Such morphological change is believed to play an important role in establishing malignant characteristics of cancer cells. Activation of the mitogen-activated protein kinase (MAPK) pathway is a converging downstream event of transforming activities of many oncogene products commonly found in human cancers. Intracellular calcium is known to regulate cellular morphology. In fibroblasts, Ca2+ influx is primarily controlled by two types of Ca2+ channels (T- and L-types). Here, we report that the T-type current was specifically inhibited in cells expressing oncogenically activated Ras as well as gain-of-function mutant MEK (MAPK/extracellular signal-regulated kinase (ERK) kinase, a direct activator of MAPK), whereas treatment of ras-transformed cells with a MEK-specific inhibitor restored T-type Ca2+ channel activity. Using a T-type Ca2+ channel antagonist, we further found that suppression of the T-type Ca2+ channel by the activated MAPK pathway is a prerequisite event for the induction and/or maintenance of transformation-associated morphological changes. (+info)
All thalamocortical neurones possess a T-type Ca2+ 'window' current that enables the expression of bistability-mediated activities. (6/576)1. The existence of a non-negligible steady-state ('window') component of the low threshold, T-type Ca2+current (IT) and an appropriately large ratio of IT to ILeak conductance (i.e. gT/gLeak) have been shown to underlie a novel form of intrinsic bistability that is present in about 15 % of thalamocortical (TC) neurones. 2. In the present experiments, the dynamic clamp technique was used to introduce into mammalian TC neurones in vitro either an artificial, i.e. computer-generated, IT in order to enhance endogenous IT, or an artificial inward ILeak to decrease endogenous ILeak. Using this method, we were able to investigate directly whether the majority of TC neurones appear non-bistable because their intrinsic ionic membrane properties are essentially different (i.e. presence of a negligible IT 'window' component), or simply because they possess a gT or gLeak conductance that is insufficiently large or small, respectively. 3. The validity of the dynamic clamp arrangement and the accuracy of artificial IT were confirmed by (i) recreating the low threshold calcium potential (LTCP) with artificial IT following its block by Ni2+ (0.5-1 mM), and (ii) blocking endogenous LTCPs with an artificial outward IT. 4. Augmentation of endogenous IT by an artificial analog or introduction of an artificial inward ILeak transformed all non-bistable TC neurones to bistable cells that expressed the full array of bistability-mediated behaviours, i.e. input signal amplification, slow oscillatory activity and membrane potential bistability. 5. These results demonstrate the existence of a non-negligible IT 'window' component in all TC neurones and suggest that rather than being a novel group of neurones, bistable cells are merely representative of an interesting region of dynamical modes in the (gT, gLeak) parameter space that may be expressed under certain physiological or pathological conditions by all TC neurones and other types of excitable cells that possess an IT 'window' component with similar biophysical properties. (+info)
Troglitazone inhibits voltage-dependent calcium currents in guinea pig cardiac myocytes. (7/576)BACKGROUND: It has been suggested that intracellular Ca2+ overload in cardiac myocytes leads to the development of diabetic cardiomyopathy. Troglitazone, an insulin-sensitizing agent, is a promising therapeutic agent for diabetes and has been shown to prevent diabetes-induced myocardial changes. To elucidate the underlying mechanism of troglitazone action on cardiac myocytes, the effects of troglitazone on voltage-dependent Ca2+ currents were examined and compared with classic Ca2+ antagonists (verapamil and nifedipine). METHODS AND RESULTS: Whole-cell voltage-clamp techniques were applied in single guinea pig atrial myocytes. Under control conditions with CsCl internal solution, the voltage-dependent Ca2+ currents consisted of both T-type (ICa,T) and L-type (ICa,L) Ca2+ currents. Troglitazone effectively reduced the amplitude of ICa,L in a concentration-dependent manner. Troglitazone also suppressed ICa,T, but the effect of troglitazone on ICa,T was less potent than that on ICa,L. The current-voltage relationships for ICa,L and the reversal potential for ICa,L were not altered by troglitazone. The half-maximal inhibitory concentration of troglitazone on ICa,L measured at a holding potential of -40 mV was 6.3 micromol/L, and 30 micromol/L troglitazone almost completely inhibited ICa,L. Troglitazone 10 micromol/L did not affect the time courses for inactivation of ICa,L and inhibited ICa,L mainly in a use-independent fashion, without shifting the voltage-dependency of inactivation. This effect was different from those of verapamil and nifedipine. Troglitazone also reduced isoproterenol- or cAMP-enhanced ICa,L. CONCLUSIONS: These results demonstrate that troglitazone inhibits voltage-dependent Ca2+ currents (T-type and L-type) and then antagonizes the effects of isoproterenol in cardiac myocytes, thus possibly playing a role in preventing diabetes-induced intracellular Ca2+ overload and subsequent myocardial changes. (+info)
The effects of verapamil and diltiazem on N-, P- and Q-type calcium channels mediating dopamine release in rat striatum. (8/576)1. The putative inhibitory effects of verapamil and diltiazem on neuronal non-L-type Ca2+ channels were studied by investigating their effects on either K+- or veratridine-evoked [3H]-dopamine ([3H]-DA) release in rat striatal slices. Involvement of N-, P- and Q-type channels was identified by sensitivity of [3H]-DA release to omega-conotoxin GVIA (omega-CTx-GVIA), omega-agatoxin IVA (omega-Aga-IVA) and omega-conotoxin MVIIC (omega-CTx-MVIIC), respectively. 2. KCl (50 mM)-evoked [3H]-DA release was abolished in the absence of Ca2+, and was insensitive to dihydropyridines (up to 30 microM). It was significantly blocked by omega-CTx-GVIA (1 microM), omega-Aga-IVA (30 nM) and was confirmed to be abolished by omega-CTx-MVIIC (3 microM), indicating involvement of N-, P- and Q-type channel subtypes. 3. Verapamil and diltiazem inhibited K+-evoked [3H]-DA release in a concentration-dependent manner. The inhibitory effects of verapamil or diltiazem (each 30 microM) were fully additive to the effect of omega-CTx-GVIA (1 microM), whereas co-application with omega-Aga-IVA (30 nM) produced similar effects to those of omega-Aga-IVA alone. 4. As shown previously, veratridine-evoked [3H]-DA release in Ca2+ containing medium exclusively involves Q-type Ca2+ channels. Here, diltiazem (30 microM) did not inhibit veratridine-evoked [3H]-DA release, whereas verapamil (30 microM) partially inhibited it, indicating possible involvement of Q-type channels in verapamil-induced inhibition. However, verapamil (30 microM) inhibited this release even in the absence of extracellular Ca2+, suggesting that Na+ rather than Q-type Ca2+ channels are involved. 5. Taken together, our results suggest that verapamil can block P- and at higher concentrations possibly N- and Q-type Ca2+ channels linked to [3H]-DA release, whereas diltiazem appears to block P-type Ca2+ channels only. (+info)
Some common types of streptococcal infections include:
1. Strep throat (pharyngitis): an infection of the throat and tonsils that can cause fever, sore throat, and swollen lymph nodes.
2. Sinusitis: an infection of the sinuses (air-filled cavities in the skull) that can cause headache, facial pain, and nasal congestion.
3. Pneumonia: an infection of the lungs that can cause cough, fever, chills, and shortness of breath.
4. Cellulitis: an infection of the skin and underlying tissue that can cause redness, swelling, and warmth over the affected area.
5. Endocarditis: an infection of the heart valves, which can cause fever, fatigue, and swelling in the legs and abdomen.
6. Meningitis: an infection of the membranes covering the brain and spinal cord that can cause fever, headache, stiff neck, and confusion.
7. Septicemia (blood poisoning): an infection of the bloodstream that can cause fever, chills, rapid heart rate, and low blood pressure.
Streptococcal infections are usually treated with antibiotics, which can help clear the infection and prevent complications. In some cases, hospitalization may be necessary to monitor and treat the infection.
Prevention measures for streptococcal infections include:
1. Good hygiene practices, such as washing hands frequently, especially after contact with someone who is sick.
2. Avoiding close contact with people who have streptococcal infections.
3. Keeping wounds and cuts clean and covered to prevent bacterial entry.
4. Practicing safe sex to prevent the spread of streptococcal infections through sexual contact.
5. Getting vaccinated against streptococcus pneumoniae, which can help prevent pneumonia and other infections caused by this bacterium.
It is important to seek medical attention if you suspect you or someone else may have a streptococcal infection, as early diagnosis and treatment can help prevent complications and improve outcomes.
There are several types of channelopathies, including:
1. Long QT syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
2. Short QT syndrome: This is a rare condition that has the opposite effect of long QT syndrome, causing the heart to beat too quickly.
3. Catecholaminergic polymorphic ventricular tachycardia (CPVT): This is a rare disorder that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
4. Brugada syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
5. Wolff-Parkinson-White (WPW) syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
6. Neuromuscular disorders: These are disorders that affect the nerve-muscle junction, leading to muscle weakness and wasting. Examples include muscular dystrophy and myasthenia gravis.
7. Dystrophinopathies: These are a group of disorders that affect the structure of muscle cells, leading to muscle weakness and wasting. Examples include Duchenne muscular dystrophy and Becker muscular dystrophy.
8. Myotonia: This is a condition that affects the muscles, causing them to become stiff and rigid.
9. Hyperkalemic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to abnormal potassium levels in the body.
10. Hypokalemic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to low potassium levels in the body.
11. Thyrotoxic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to an overactive thyroid gland.
12. Hyperthyroidism: This is a condition where the thyroid gland becomes overactive, leading to increased heart rate, weight loss, and muscle weakness.
13. Hypothyroidism: This is a condition where the thyroid gland becomes underactive, leading to fatigue, weight gain, and muscle weakness.
14. Pituitary tumors: These are tumors that affect the pituitary gland, which regulates hormone production in the body.
15. Adrenal tumors: These are tumors that affect the adrenal glands, which produce hormones such as cortisol and aldosterone.
16. Carcinoid syndrome: This is a condition where cancer cells in the digestive system produce hormones that can cause muscle weakness and wasting.
17. Multiple endocrine neoplasia (MEN): This is a genetic disorder that affects the endocrine system and can cause tumors to grow in the thyroid, adrenal, and parathyroid glands.
These are just some of the many potential causes of muscle weakness. It's important to see a healthcare professional for an accurate diagnosis and appropriate treatment.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Lack of exercise
* High sodium intake
* Low potassium intake
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
The symptoms of LEMS typically develop gradually over time and may include:
1. Muscle weakness that worsens with activity and improves with rest.
2. Weakness in the legs, hips, and shoulders.
3. Fatigue and muscle cramps.
4. Difficulty walking or standing upright.
5. Double vision or other eye problems.
6. Dry mouth and difficulty swallowing.
7. Increased heart rate and blood pressure.
8. Impaired reflexes.
9. Decreased sweating.
10. Weight loss.
The exact cause of LEMS is not known, but it is believed to be an autoimmune disorder in which the immune system mistakenly attacks the VGCCs in the neuromuscular junction. The condition is often associated with other autoimmune disorders such as thyroiditis, vitiligo, and adrenal insufficiency.
There is no cure for LEMS, but treatment options are available to manage the symptoms. These may include:
1. Immunosuppressive medications such as prednisone to reduce inflammation and suppress the immune system.
2. Intracranial pressure-lowering medications such as acetazolamide to reduce the pressure in the brain.
3. Muscle strengthening exercises to improve muscle function.
4. Physical therapy to maintain muscle strength and flexibility.
5. Orthostatic hypotension medications to manage orthostatic hypotension (a drop in blood pressure when standing).
6. Pain management medications to relieve muscle cramps, spasms, or pain.
7. Nutritional support to ensure adequate nutrition and prevent weight loss.
8. Respiratory support as needed to manage respiratory muscle weakness.
9. Speech therapy to improve communication skills.
10. Psychological support to cope with the emotional and social challenges of the condition.
It is important for individuals with LEMS to work closely with their healthcare team to manage their symptoms and prevent complications. With proper treatment, many people with LEMS can lead active and fulfilling lives.
The diagnosis of absence epilepsy is typically made based on a combination of clinical findings, including:
-A history of recurrent brief loss of awareness or staring spells
-Normal neurological examination between episodes
-Abnormal EEG activity during seizures (spikes or sharp waves)
Treatment for absence epilepsy usually involves medication, such as ethosuximide, valproic acid, or lamotrigine. In some cases, surgery may be considered if medications are ineffective or have significant side effects.
It is important to note that absence epilepsy can be a challenging condition to diagnose and treat, as the spells can be difficult to distinguish from other conditions such as daydreaming or attention deficit hyperactivity disorder (ADHD).
Some common types of calcium metabolism disorders include:
1. Hypocalcemia (low calcium levels): This can be caused by a deficiency in dietary calcium intake, malabsorption of calcium, or excessive urinary excretion of calcium. Symptoms can include muscle cramps, tremors, and tingling sensations in the fingers and toes.
2. Hypercalcemia (high calcium levels): This can be caused by an overactive parathyroid gland, cancer, or excessive intake of vitamin D. Symptoms can include fatigue, nausea, constipation, and kidney stones.
3. Osteoporosis: This is a condition characterized by weak and brittle bones that can lead to fractures. It is often associated with hormonal imbalances, vitamin D deficiency, or other factors that disrupt calcium metabolism.
4. Hyperparathyroidism (overactive parathyroid gland): This is a condition in which the parathyroid glands produce too much parathyroid hormone (PTH), leading to elevated calcium levels and potential complications such as kidney stones, bone loss, and cardiovascular disease.
5. Vitamin D-dependent rickets type 1: This is a rare genetic disorder that affects the body's ability to absorb vitamin D and maintain normal calcium levels. It can lead to softening of the bones and other skeletal deformities.
6. Familial hypophosphatemic rickets type 1: This is a rare genetic disorder that affects the body's ability to regulate phosphate levels, leading to softening of the bones and other skeletal deformities.
7. Tumor-induced osteomalacia: This is a condition in which cancerous tumors, typically found in the lung or breast, produce high levels of proteins that interfere with the body's ability to absorb vitamin D and maintain normal calcium levels. It can lead to softening of the bones and other skeletal deformities.
8. Chronic kidney disease: This is a condition in which the kidneys are not functioning properly, leading to elevated levels of phosphate and other waste products in the blood. It can lead to softening of the bones and other complications such as heart disease.
9. Paget's disease of bone: This is a condition that affects the way bones grow and repair themselves, leading to deformities and pain. It is often associated with inflammation and elevated levels of calcium in the blood.
10. Chronic alcoholism: Prolonged heavy drinking can lead to deficiencies in vitamin D and calcium, as well as other nutrients that are essential for bone health. It can increase the risk of osteoporosis and fractures.
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.
The QT interval is a measure of the time it takes for the ventricles to recover from each heartbeat and prepare for the next one. In people with LQTS, this recovery time is prolonged, which can disrupt the normal rhythm of the heart and increase the risk of arrhythmias.
LQTS is caused by mutations in genes that encode proteins involved in the cardiac ion channels, which regulate the flow of ions into and out of the heart muscle cells. These mutations can affect the normal functioning of the ion channels, leading to abnormalities in the electrical activity of the heart.
Symptoms of LQTS can include palpitations, fainting spells, and seizures. In some cases, LQTS can be diagnosed based on a family history of the condition or after a sudden death in an otherwise healthy individual. Other tests, such as an electrocardiogram (ECG), echocardiogram, and stress test, may also be used to confirm the diagnosis.
Treatment for LQTS typically involves medications that regulate the heart's rhythm and reduce the risk of arrhythmias. In some cases, an implantable cardioverter-defibrillator (ICD) may be recommended to monitor the heart's activity and deliver an electric shock if a potentially life-threatening arrhythmia is detected. Lifestyle modifications, such as avoiding stimuli that trigger symptoms and taking precautions during exercise and stress, may also be recommended.
In summary, Long QT syndrome is a rare inherited disorder that affects the electrical activity of the heart, leading to an abnormal prolongation of the QT interval and an increased risk of irregular and potentially life-threatening heart rhythms. It is important for individuals with LQTS to be closely monitored by a healthcare provider and to take precautions to manage their condition and reduce the risk of complications.
There are several types of kidney calculi, including:
1. Calcium oxalate calculi: These are the most common type of calculus and are often associated with conditions such as hyperparathyroidism or excessive intake of calcium supplements.
2. Uric acid calculi: These are more common in people with gout or a diet high in meat and sugar.
3. Cystine calculi: These are rare and usually associated with a genetic disorder called cystinuria.
4. Struvite calculi: These are often seen in women with urinary tract infections (UTIs).
Symptoms of kidney calculi may include:
1. Flank pain (pain in the side or back)
2. Pain while urinating
3. Blood in the urine
4. Cloudy or strong-smelling urine
5. Fever and chills
6. Nausea and vomiting
Kidney calculi are diagnosed through a combination of physical examination, medical history, and diagnostic tests such as X-rays, CT scans, or ultrasound. Treatment options for kidney calculi depend on the size and location of the calculus, as well as the severity of any underlying conditions. Small calculi may be treated with conservative measures such as fluid intake and medication to help flush out the crystals, while larger calculi may require surgical intervention to remove them.
Preventive measures for kidney calculi include staying hydrated to help flush out excess minerals in the urine, maintaining a balanced diet low in oxalate and animal protein, and avoiding certain medications that can increase the risk of calculus formation. Early detection and treatment of underlying conditions such as hyperparathyroidism or gout can also help prevent the development of kidney calculi.
Overall, kidney calculi are a common condition that can be managed with proper diagnosis and treatment. However, they can cause significant discomfort and potentially lead to complications if left untreated, so it is important to seek medical attention if symptoms persist or worsen over time.
The symptoms of hypokalemic periodic paralysis can vary in severity and may include:
* Muscle weakness or paralysis, typically affecting the legs but sometimes affecting the arms or face as well
* Muscle cramps and twitching
* Abnormal heart rhythms
* Weakness or paralysis of the respiratory muscles, which can lead to breathing difficulties
* Vision problems, such as blurred vision or double vision
* Dizziness and fainting
The exact cause of hypokalemic periodic paralysis is not known, but it is thought to be related to mutations in certain genes that affect the way potassium ions are regulated in the body. The disorder is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.
There is no cure for hypokalemic periodic paralysis, but treatment options may include:
* Potassium supplements to maintain normal potassium levels in the blood
* Medications to regulate heart rhythms and prevent abnormal heartbeats
* Physical therapy to improve muscle strength and function
* Avoiding triggers such as stress, certain medications, or changes in potassium levels
* In severe cases, a pacemaker may be implanted to regulate the heartbeat.
It is important to note that hypokalemic periodic paralysis can be a challenging disorder to manage and may have a significant impact on quality of life. However, with proper treatment and management, many individuals with this condition are able to lead active and fulfilling lives.
Some common causes of hypocalcemia include:
1. Vitamin D deficiency: Vitamin D is essential for the absorption of calcium from the diet. A lack of vitamin D can lead to low levels of calcium in the blood.
2. Parathyroid gland disorders: The parathyroid glands are located in the neck and regulate calcium levels in the blood. Disorders such as hypoparathyroidism (underactive parathyroid glands) or hyperparathyroidism (overactive parathyroid glands) can cause hypocalcemia.
3. Malabsorption: Certain conditions, such as celiac disease or Crohn's disease, can lead to malabsorption of nutrients, including calcium.
4. Kidney problems: Kidney failure can cause hypocalcemia by reducing the amount of calcium that is excreted in the urine.
5. Hypomagnesemia (low levels of magnesium): Magnesium is important for calcium metabolism, and low levels of magnesium can contribute to hypocalcemia.
Symptoms of hypocalcemia can include:
1. Muscle cramps
3. Twitching or tremors
5. Tingling or numbness in the fingers and toes
6. Difficulty swallowing
Treatment for hypocalcemia usually involves addressing the underlying cause of the condition. For example, if the condition is caused by a vitamin D deficiency, supplements may be prescribed. If the condition is caused by a parathyroid gland disorder, surgery may be necessary to remove the affected gland or glands. In some cases, calcium supplements may be prescribed to help restore normal calcium levels.
It's important to note that hypocalcemia can be a sign of an underlying condition, and it should be treated promptly to prevent complications. If you suspect you or someone you know may have hypocalcemia, it is important to seek medical attention as soon as possible. A healthcare professional can diagnose the condition and recommend appropriate treatment.
* Genetic mutations or deletions
* Infections such as meningitis or encephalitis
* Stroke or bleeding in the brain
* Traumatic head injury
* Multiple sclerosis or other demyelinating diseases
* Brain tumors
* Cerebellar degeneration due to aging
* Coordination difficulties, such as stumbling or poor balance
* Tremors or shaky movements
* Slurred speech and difficulty with fine motor skills
* Nystagmus (involuntary eye movements)
* Difficulty with gait and walking
* Fatigue, weakness, and muscle wasting
* Physical examination and medical history
* Neurological examination to test coordination, balance, and reflexes
* Imaging studies such as MRI or CT scans to rule out other conditions
* Genetic testing to identify inherited forms of cerebellar ataxia
* Electromyography (EMG) to test muscle activity and nerve function
* Physical therapy to improve balance, coordination, and gait
* Occupational therapy to help with daily activities and fine motor skills
* Speech therapy to address slurred speech and communication difficulties
* Medications to manage symptoms such as tremors or spasticity
* Assistive devices such as canes or walkers to improve mobility
* The prognosis for cerebellar ataxia varies depending on the underlying cause. In some cases, the condition may be slowly progressive and lead to significant disability over time. In other cases, the condition may remain stable or even improve with treatment.
Living with cerebellar ataxia can be challenging, but there are many resources available to help individuals with the condition manage their symptoms and maintain their quality of life. These resources may include:
* Physical therapy to improve balance and coordination
* Occupational therapy to assist with daily activities
* Speech therapy to address communication difficulties
* Assistive devices such as canes or walkers to improve mobility
* Medications to manage symptoms such as tremors or spasticity
* Support groups for individuals with cerebellar ataxia and their families
Overall, the key to managing cerebellar ataxia is early diagnosis and aggressive treatment. With proper management, individuals with this condition can lead active and fulfilling lives despite the challenges they face.
There are many different types of cardiac arrhythmias, including:
1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.
Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.
The symptoms of hypercalcemia may include:
* Nausea and vomiting
* Abdominal pain
* Kidney stones
* Bone pain or fractures
If left untreated, hypercalcemia can lead to complications such as kidney damage, heart problems, and an increased risk of osteoporosis. Treatment options may include medications to reduce calcium levels, surgery to remove a tumor or overactive parathyroid gland, or dialysis if the patient has kidney failure.
Early diagnosis and treatment are important to prevent long-term complications and improve the patient's quality of life.
Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.
There are several different types of neuroblastoma, including:
1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.
Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:
* Abdominal pain
* Loss of appetite
* Weight loss
* Bone pain
* Swelling in the abdomen or neck
* Increased heart rate
Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.
Neuralgia is often difficult to diagnose and treat, as the underlying cause can be challenging to identify. However, various medications and therapies can help manage the pain and other symptoms associated with this condition. These may include pain relievers, anticonvulsants, antidepressants, and muscle relaxants, as well as alternative therapies such as acupuncture or physical therapy.
Some common forms of neuralgia include:
1. Trigeminal neuralgia: This is a condition that affects the trigeminal nerve, which carries sensation from the face to the brain. It is characterized by sudden, intense pain in the face, typically on one side.
2. Postherpetic neuralgia (PHN): This is a condition that occurs after a shingles infection, and is characterized by persistent pain in the affected area.
3. Occipital neuralgia: This is a condition that affects the nerves in the back of the head and neck, and can cause pain in the back of the head, neck, and face.
4. Geniculate neuralgia: This is a rare condition that affects the nerves in the jaw and ear, and can cause pain in the jaw, face, and ear.
Overall, neuralgia is a complex and debilitating condition that can significantly impact an individual's quality of life. It is important for individuals experiencing symptoms of neuralgia to seek medical attention to determine the underlying cause and develop an appropriate treatment plan.
There are several types of ataxia, each with different symptoms and causes. Some common forms of ataxia include:
1. Spinocerebellar ataxia (SCA): This is the most common form of ataxia and is caused by a degeneration of the cerebellum and spinal cord. It can cause progressive weakness, loss of coordination, and difficulty with speaking and swallowing.
2. Friedreich's ataxia: This is the second most common form of ataxia and is caused by a deficiency of vitamin E in the body. It can cause weakness in the legs, difficulty walking, and problems with speech and language.
3. Ataxia-telangiectasia (AT): This is a rare form of ataxia that is caused by a gene mutation. It can cause progressive weakness, loss of coordination, and an increased risk of developing cancer.
4. Acute cerebellar ataxia: This is a sudden and temporary form of ataxia that can be caused by a variety of factors such as infections, injuries, or certain medications.
5. Drug-induced ataxia: Certain medications can cause ataxia as a side effect.
6. Vitamin deficiency ataxia: Deficiencies in vitamins such as vitamin B12 or folate can cause ataxia.
7. Metabolic disorders: Certain metabolic disorders such as hypothyroidism, hyperthyroidism, and hypoglycemia can cause ataxia.
8. Stroke or brain injury: Ataxia can be a result of a stroke or brain injury.
9. Multiple system atrophy (MSA): This is a rare progressive neurodegenerative disorder that can cause ataxia, parkinsonism, and autonomic dysfunction.
10. Spinocerebellar ataxia (SCA): This is a group of rare genetic disorders that can cause progressive cerebellar ataxia, muscle wasting, and other signs and symptoms.
It's important to note that this is not an exhaustive list and there may be other causes of ataxia not mentioned here. If you suspect you or someone you know may have ataxia, it is important to consult a healthcare professional for proper diagnosis and treatment.
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.
There are several different types of calcinosis, each with its own unique causes and symptoms. Some common forms of calcinosis include:
1. Dystrophic calcinosis: This type of calcinosis occurs in people with muscular dystrophy, a group of genetic disorders that affect muscle strength and function. Dystrophic calcinosis can cause calcium deposits to form in the muscles, leading to muscle weakness and wasting.
2. Metastatic calcinosis: This type of calcinosis occurs when cancer cells spread to other parts of the body and cause calcium deposits to form. Metastatic calcinosis can occur in people with a variety of different types of cancer, including breast, lung, and prostate cancer.
3. Idiopathic calcinosis: This type of calcinosis occurs for no apparent reason, and the exact cause is not known. Idiopathic calcinosis can affect people of all ages and can cause calcium deposits to form in a variety of different tissues.
4. Secondary calcinosis: This type of calcidosis occurs as a result of an underlying medical condition or injury. For example, secondary calcinosis can occur in people with kidney disease, hyperparathyroidism (a condition in which the parathyroid glands produce too much parathyroid hormone), or traumatic injuries.
Treatment for calcinosis depends on the underlying cause and the severity of the condition. In some cases, treatment may involve managing the underlying disease or condition that is causing the calcium deposits to form. Other treatments may include medications to reduce inflammation and pain, physical therapy to improve mobility and strength, and surgery to remove the calcium deposits.
Causes: There are several causes of night blindness, including:
1. Vitamin A deficiency: Vitamin A is essential for the health of the retina, and a deficiency can lead to night blindness.
2. Retinitis pigmentosa: This is a group of inherited conditions that can cause progressive damage to the retina and result in night blindness.
3. Cataracts: A cataract can cause a person to become night blind by blocking the light that enters the eye.
4. Glaucoma: This is a group of eye conditions that can damage the optic nerve and lead to vision loss, including night blindness.
5. Other medical conditions: Certain medical conditions such as diabetes, multiple sclerosis, and stroke can cause night blindness.
Symptoms: The symptoms of night blindness can vary depending on the underlying cause, but common symptoms include:
1. Difficulty seeing in low light environments
2. Blind spots or missing areas of vision
3. Sensitivity to light
4. Glare or halos around lights
5. Difficulty adjusting to changes in light levels
Diagnosis: Night blindness is typically diagnosed through a comprehensive eye exam, which may include a visual acuity test, refraction test, and retinal examination. Imaging tests such as an OCT scan or retinal photography may also be used to evaluate the retina and optic nerve.
Treatment: The treatment of night blindness depends on the underlying cause. For example, vitamin A supplements may be prescribed for a vitamin A deficiency, while cataract surgery may be recommended for cataracts. In some cases, no treatment may be necessary, and the condition may resolve on its own over time.
Prevention: While some cases of night blindness are unavoidable, there are steps you can take to reduce your risk of developing the condition. These include:
1. Maintaining a healthy diet that includes foods rich in vitamin A and other essential nutrients for eye health.
2. Wearing sunglasses with UV protection to protect your eyes from excessive sunlight.
3. Avoiding smoking and excessive alcohol consumption, which can damage the optic nerve and retina.
4. Getting regular eye exams to detect any underlying eye problems early on.
5. Wearing protective eyewear when engaging in activities that could potentially harm your eyes, such as sports or working with hazardous materials.
Migraine with aura is considered to be a more severe form of migraine than migraine without aura, which does not have the same neurological symptoms before the headache. Migraine with aura is also associated with a higher risk of other health problems, such as stroke and dementia.
There are several treatments available for migraine with aura, including medications that can help to reduce the frequency and severity of the headaches, as well as lifestyle changes such as avoiding triggers and getting regular exercise. It is important for people who experience migraine with aura to work closely with their healthcare provider to develop an effective treatment plan.
* Type 1: Hypokalemic Periodic Paralysis (Hyperkalemia-induced muscle weakness)
* Type 2: Hyperkalemic Periodic Paralysis (K+ channels dysfunction, leading to muscle weakness)
* Type 3: Peripheral nerve damage causing FPPA
* Type 4: Central nervous system damage causing FPPA
Slide 3: Causes of Familial Periodic Paralysis (FPPA)
* Genetic mutations in SCN4A, KCNA1, and other genes involved in ion channel function
* Abnormalities in the expression and function of ion channels
* Autosomal dominant or recessive inheritance pattern
Slide 4: Symptoms of Familial Periodic Paralysis (FPPA)
* Muscle weakness or paralysis, often triggered by changes in diet, physical activity, or other environmental factors
* Weakness of the lower extremities more pronounced than the upper extremities
* Muscle cramps and twitching
* Abdominal pain
* Nausea and vomiting
Slide 5: Diagnosis of Familial Periodal Paralysis (FPPA)
* Clinical evaluation, including patient history and physical examination
* Electromyography (EMG) to assess muscle activity and diagnose FPPA
* Genetic testing to identify genetic mutations associated with FPPA
* Blood tests to measure potassium levels and rule out other conditions
Slide 6: Treatment of Familial Periodic Paralysis (FPPA)
* Potassium supplements to maintain normal potassium levels
* Avoiding triggers such as stress, cold temperature, and certain medications
* Physical therapy to improve muscle strength and function
* Pain management with analgesics and other medications as needed
Slide 7: Prognosis of Familial Periodic Paralysis (FPPA)
* FPPA is a chronic condition with no cure, but with proper management, patients can lead relatively normal lives
* The prognosis varies depending on the severity and frequency of attacks, as well as the presence of any complications
* Early diagnosis and treatment can improve the quality of life for patients with FPPA
Slide 8: Current Research in Familial Periodic Paralysis (FPPA)
* Genetic research to better understand the underlying causes of FPPA and develop new treatments
* Studies on the effectiveness of new medications and therapies for FPPA
* Investigation into the potential use of stem cells for treating FPPA
Slide 9: Current Challenges in Familial Periodic Paralysis (FPPA)
* Limited awareness and understanding of FPPA among healthcare professionals and the general public
* Lack of effective treatments for severe cases of FPPA
* Limited availability of specialized care and support for patients with FPPA
Slide 10: Conclusion
* Familial periodic paralysis (FPPA) is a rare and complex condition that affects both children and adults
* Early diagnosis and proper management are critical to improving the quality of life for patients with FPPA
* Ongoing research offers hope for new treatments and therapies, but more work needs to be done to increase awareness and understanding of this condition.
Insulinoma is a rare type of pancreatic tumor that produces excess insulin, leading to low blood sugar levels. These tumors are typically benign and can be treated with surgery or medication.
Insulinomas account for only about 5% of all pancreatic neuroendocrine tumors. They usually occur in the head of the pancreas and can cause a variety of symptoms, including:
1. Hypoglycemia (low blood sugar): The excess insulin produced by the tumor can cause blood sugar levels to drop too low, leading to symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Hyperinsulinism (elevated insulin levels): In addition to hypoglycemia, insulinomas can also cause elevated insulin levels in the blood.
3. Abdominal pain: Insulinomas can cause abdominal pain and discomfort.
4. Weight loss: Patients with insulinomas may experience unexplained weight loss.
5. Nausea and vomiting: Some patients may experience nausea and vomiting due to the hypoglycemia or other symptoms caused by the tumor.
Insulinomas are usually diagnosed through a combination of imaging tests such as CT scans, MRI scans, and PET scans, and by measuring insulin and C-peptide levels in the blood. Treatment options for insulinomas include surgery to remove the tumor, medications to control hypoglycemia and hyperinsulinism, and somatostatin analogs to reduce hormone secretion.
Insulinoma is a rare and complex condition that requires careful management by a multidisciplinary team of healthcare professionals, including endocrinologists, surgeons, and radiologists. With appropriate treatment, most patients with insulinomas can experience long-term remission and improved quality of life.
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 different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
There are two main types of myotonia:
1. Thomsen's disease: This is an inherited form of myotonia that affects the muscles of the face, neck, and limbs. It is caused by mutations in the CLCN1 gene and can be severe, causing difficulty with speaking, swallowing, and breathing.
2. Becker's muscular dystrophy: This is a form of muscular dystrophy that affects both the skeletal and cardiac muscles. It is caused by mutations in the DMPK gene and can cause myotonia, muscle weakness, and heart problems.
The symptoms of myotonia can vary depending on the severity of the condition and may include:
* Muscle stiffness and rigidity
* Spasms or twitches
* Difficulty with movement and mobility
* Fatigue and weakness
* Muscle wasting
Myotonia can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electromyography (EMG) and muscle biopsy. There is no cure for myotonia, but treatment options may include:
* Physical therapy to improve movement and mobility
* Medications to relax muscles and reduce spasms
* Lifestyle modifications such as avoiding triggers and taking regular breaks to rest
* Surgery in severe cases to release or lengthen affected muscles.
It is important to note that myotonia can be a symptom of other underlying conditions, so proper diagnosis and management by a healthcare professional is essential to determine the best course of treatment.
There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:
1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.
Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.
The exact cause of malignant hyperthermia is not fully understood, but it is believed to be related to a genetic predisposition and exposure to certain anesthetic agents. The condition can be triggered by a variety of factors, including the use of certain anesthetics, stimulation of the sympathetic nervous system, and changes in blood sugar levels.
Symptoms of malignant hyperthermia can include:
* Elevated body temperature (usually above 104°F/40°C)
* Muscle rigidity and stiffness
* Heart arrhythmias and palpitations
* Shivering or tremors
* Confusion, agitation, or other neurological symptoms
* Shortness of breath or respiratory failure
If left untreated, malignant hyperthermia can lead to serious complications such as seizures, brain damage, and even death. Treatment typically involves the immediate discontinuation of any triggering anesthetic agents, cooling measures such as ice packs or cold compresses, and medications to help regulate body temperature and reduce muscle rigidity. In severe cases, mechanical ventilation may be necessary to support breathing.
Overall, malignant hyperthermia is a rare but potentially life-threatening condition that requires prompt recognition and treatment to prevent serious complications and improve outcomes.
The condition is characterized by the excessive growth of gum tissue, which can lead to:
1. Redness and swelling of the gums
2. Bleeding while brushing or flossing
3. Bad breath (halitosis)
4. Pocket formation between the teeth and gums
5. Gum recession
6. Tooth loss
Gingival hyperplasia can be treated by addressing the underlying cause, improving oral hygiene, and undergoing scaling and root planing procedures to remove plaque and tartar. In severe cases, surgical intervention may be necessary to remove excess gum tissue and restore the natural contours of the mouth.
It is important for individuals to practice good oral hygiene, including brushing at least twice a day with fluoride toothpaste, flossing daily, and receiving regular dental cleanings to prevent gingival hyperplasia and other gum diseases. Early detection and treatment can help prevent the progression of the condition and restore the health of the teeth and gums.
Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.
There are several types of myocardial ischemia, including:
1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.
Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.
There are several types of acidosis, including:
1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.
The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching
If left untreated, acidosis can lead to complications such as:
1. Kidney damage
4. Heart arrhythmias
5. Respiratory failure
Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:
1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.
In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.
There are many different types of epilepsy, each with its own unique set of symptoms and characteristics. Some common forms of epilepsy include:
1. Generalized Epilepsy: This type of epilepsy affects both sides of the brain and can cause a range of seizure types, including absence seizures, tonic-clonic seizures, and atypical absence seizures.
2. Focal Epilepsy: This type of epilepsy affects only one part of the brain and can cause seizures that are localized to that area. There are several subtypes of focal epilepsy, including partial seizures with complex symptoms and simple partial seizures.
3. Tonic-Clonic Epilepsy: This type of epilepsy is also known as grand mal seizures and can cause a loss of consciousness, convulsions, and muscle stiffness.
4. Lennox-Gastaut Syndrome: This is a rare and severe form of epilepsy that typically develops in early childhood and can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
5. Dravet Syndrome: This is a rare genetic form of epilepsy that typically develops in infancy and can cause severe, frequent seizures.
6. Rubinstein-Taybi Syndrome: This is a rare genetic disorder that can cause intellectual disability, developmental delays, and various types of seizures.
7. Other forms of epilepsy include Absence Epilepsy, Myoclonic Epilepsy, and Atonic Epilepsy.
The symptoms of epilepsy can vary widely depending on the type of seizure disorder and the individual affected. Some common symptoms of epilepsy include:
1. Seizures: This is the most obvious symptom of epilepsy and can range from mild to severe.
2. Loss of consciousness: Some people with epilepsy may experience a loss of consciousness during a seizure, while others may remain aware of their surroundings.
3. Confusion and disorientation: After a seizure, some people with epilepsy may feel confused and disoriented.
4. Memory loss: Seizures can cause short-term or long-term memory loss.
5. Fatigue: Epilepsy can cause extreme fatigue, both during and after a seizure.
6. Emotional changes: Some people with epilepsy may experience emotional changes, such as anxiety, depression, or mood swings.
7. Cognitive changes: Epilepsy can affect cognitive function, including attention, memory, and learning.
8. Sleep disturbances: Some people with epilepsy may experience sleep disturbances, such as insomnia or sleepiness.
9. Physical symptoms: Depending on the type of seizure, people with epilepsy may experience physical symptoms such as muscle weakness, numbness or tingling, and sensory changes.
10. Social isolation: Epilepsy can cause social isolation due to fear of having a seizure in public or stigma associated with the condition.
It's important to note that not everyone with epilepsy will experience all of these symptoms, and some people may have different symptoms depending on the type of seizure they experience. Additionally, some people with epilepsy may experience additional symptoms not listed here.
Symptoms of pheochromocytoma can include:
* Rapid heartbeat
* High blood pressure
* Weight loss
* Nausea and vomiting
If left untreated, pheochromocytoma can lead to complications such as heart failure, stroke, and even death. Therefore, it is important that individuals who experience any of the above symptoms seek medical attention as soon as possible.
Treatment options for pheochromocytoma may include surgery to remove the tumor, medication to manage symptoms, and in some cases, radiation therapy. In rare cases, the tumor may recur after treatment, so regular monitoring is necessary to ensure that any new symptoms are detected early on.
Overall, while pheochromocytoma is a rare and potentially life-threatening condition, prompt medical attention and appropriate treatment can help manage symptoms and prevent complications.
R-type calcium channel
T-type calcium channel
N-type calcium channel
L-type calcium channel
Q-type calcium channel
P-type calcium channel
Calcium channel, voltage-dependent, T type, alpha 1H subunit
Calcium channel blocker
Voltage-gated calcium channel
Calcium-dependent chloride channel
Calcium-activated potassium channel
Calcium channel opener
Calcium-induced calcium release
Childhood absence epilepsy
Dihydropyridine calcium channel blockers
Voltage-gated ion channel
Environmental effects of shipping
Hyperosmolar hyperglycemic state
Olfactory receptor neuron
Histamine H3 receptor
Novel Therapeutic Targets for Antiarrhythmic Drugs
Yale School of Medicine
Metabotropic glutamate receptor
Benign paroxysmal positional vertigo
Defender (association football)
Effects of cannabis
Index of biochemistry articles
Altitude Illness - Pulmonary Syndromes Medication: Calcium channel blockers, Phosphodiesterase (type 5) enzyme inhibitor,...
JCI Insight - SNAP23 depletion enables more SNAP25/calcium channel excitosome formation to increase insulin exocytosis in type...
How do T-type calcium channels control low-threshold exocytosis? - Inserm - Institut national de la santé et de la recherche...
T-type calcium channels trigger a hyperpolarization induced afterdepolarization in vulnerable subpopulation of substantia nigra...
Calcium- and voltage-activated potassium channels in adrenocortical cell membranes
April 15, 1998 | AAFP
Calcium channel blocker nisoldipine in chronic renal failure - PubMed
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- Patients with a stable progression of chronic renal failure with a creatinine clearance of 15-45 mL/min were randomly assigned to two groups of antihypertensive therapy: 1--nisoldipine as the only antihypertensive agent and 2--antihypertensive drugs without calcium channel blockers and a placebo tablet instead of nisoldipine. (nih.gov)
- The patients were already on a low-protein diet and some form of antihypertensive therapy but without calcium channel blockers. (nih.gov)
- Furthermore, punch biopsies of the skin showed a markedly different calcium content in the two groups, which was significantly less in the nisoldipine-treated patients as compared with the patients not receiving calcium blockers. (nih.gov)
- Questioning the renoprotective role of L-type calcium channel blockers in chronic kidney disease using physiological modeling. (nih.gov)
- Calcium-channel blockers are a type of medicine used to treat high blood pressure and heart rhythm disturbances. (medlineplus.gov)
- Other medicines may also contain calcium-channel blockers. (medlineplus.gov)
- Calcium channel blockers, such as diltiazem , are a type of medicine usually used to treat high blood pressure (hypertension). (www.nhs.uk)
- However, topical calcium channel blockers that are applied directly to the anus have also proved useful in treating some people with anal fissures. (www.nhs.uk)
- Topical calcium channel blockers work by relaxing the sphincter muscle and increasing blood supply to the fissure. (www.nhs.uk)
- Topical calcium channel blockers are thought to be about as effective as GTN ointment for treating anal fissures, and may be recommended if other medicines have not helped. (www.nhs.uk)
- The mouse FST for mental depression to investigate the effect of model has been widely used in screening the calcium channel blockers, nifedipine and antidepressants because it is simple and has been verapamil, on the antidepressant action of reported to be reliable across laboratories. (who.int)
- Although studies have suggested that calcium channel blocker (CCB) therapy mitigates the decline in renal function in humans with essential HTN, there are few long-term clinical studies that have determined the impact of CCBs in patients with hypertensive CKD. (nih.gov)
- This is a dose-escalation study that will assess the safety and determine the maximum tolerated dose (MTD) of mibefradil dihydrochloride, a partially selective T-type calcium channel blocker, combined with hypofractionated radiation therapy (RT) in subjects with recurrent glioblastoma multiforme (GBM). (clinicaltrials.gov)
- Calcium-channel blocker overdose occurs when someone takes more than the normal or recommended amount of this medicine. (medlineplus.gov)
- The specific ingredients in each type of calcium-channel blocker vary. (medlineplus.gov)
- Taking too much of a calcium-channel blocker can be very dangerous. (medlineplus.gov)
- Verapamil (a type of calcium channel blocker) overdose is associated with the highest mortality risk. (medlineplus.gov)
- four groups each received a single dose of the calcium channel blocker followed by a single dose of the antidepressant (with same doses used for either in the previous four groups). (who.int)
- Isradipine (Sandoz PN 200-110), a new dihydropyridine calcium channel antagonist, was evaluated in a randomized, double-blind, placebo-controlled trial for antihypertensive efficacy in 24 patients with essential hypertension. (nih.gov)
- However, the main ingredient is called a calcium-channel antagonist. (medlineplus.gov)
- It is transmission of dopamine or NA decrease a highly specific antagonist of the L-type channel immobility, whereas agents having the opposite blocks . (who.int)
- This may be due to the fact that nifedipine on its own might act as an antidepressant but blocks one imipramine mechanism that depends on L-type calcium channel activation. (who.int)
- Description: A competitive ELISA for quantitative measurement of Mouse Voltage dependent L type calcium channel subunit Alpha 1S(CACNA1S) in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (operatiebrp.nl)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Mouse Calcium Channel, Voltage Dependent, L-Type, Alpha 1S Subunit (CACNa1S) in Tissue homogenates and other biological fluids. (operatiebrp.nl)
- Open-channel blockade is less effective on GluN3B than GluN3A subunit-containing NMDA receptors European Journal of Pharmacology. (nottingham.ac.uk)
- 1. Dubel SJ, Starr TV, Hell J, Ahlijanian MK, Enyeart JJ, Catterall WA, and Snutch TP (1992) Molecular cloning of the α 1 subunit of an ω-conotoxin-sensitive calcium channel. (aspetjournals.org)
- Interacts with the α2δ subunit of L-type voltage gated Ca 2+ channels. (abcam.com)
- Because these channels can cause large calcium transients they may contribute to the vulnerability of specific SNc dopamine neurons in Parkinson's Disease. (nih.gov)
- Recently, their activity has been related to the block of N-type voltage-gated Ca2+ channels (Cav2.2) in dorsal root ganglia ( DRG ) neurons . (bvsalud.org)
- A Chay-Keizer-like model with bursting driven by calcium-activated potassium channels but ionic currents based more closely on measurements in beta cells rather than neurons. (nih.gov)
- It inhibits calcium ions from entering the slow channels or select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization, producing a relaxation of coronary vascular smooth muscle and coronary vasodilation. (medscape.com)
- There are previous reports suggesting a role for calcium ions in the secretory response of adrenocortical cells to ACTH. (nih.gov)
- Dihydropyridine (DHP) or L-type CCBs preferentially vasodilate the afferent arteriole and have been associated with glomerular HTN and increases in proteinuria in animal models with low renal function. (nih.gov)
- Therefore, it is possible that, as in other endocrine cells, these K channels modulate Ca influx across the plasma membrane and thus contribute to regulate steroid biosynthesis and release. (nih.gov)
- Familial periodic paralyses are a group of inherited neurological disorders caused by mutations in genes that regulate sodium and calcium channels in nerve cells. (nih.gov)
- The mathematical models and papers on this page trace out four decades of work from our lab and other labs building up progressively through iteration of experiment and theory a picture of how pancreatic beta cells generate the oscillations of electrical activity and calcium that regulate insulin secretion. (nih.gov)
- Bursting was achieved by appending a calcium-activated potassium channel to voltage-dependent squid axon channels. (nih.gov)
- 2. Stea A, Dubel SJ, and Snutch TP (1999) α 1B N-type calcium channel isoforms with distinct biophysical properties. (aspetjournals.org)
- How do T-type calcium channels control low-threshold exocytosis? (inserm.fr)
- However, the underlying molecular mechanisms linking T-type calcium channels to vesicular exocytosis have remained enigmatic. (inserm.fr)
- This interaction that relies on specific Ca(v)3.2 molecular determinants, not only modulates T-type channel activity, but was also found essential to support low-threshold exocytosis upon Ca(v)3.2 channel expression in MPC 9/3L-AH chromaffin cells. (inserm.fr)
- Overall, we have indentified an unrecognized regulation pathway of T-type calcium channels by SNARE proteins, and proposed the first molecular mechanism by which T-type channels could mediate low-threshold exocytosis. (inserm.fr)
- Several reports have uncovered an unrecognized feature of T-type channels in the control of vesicular neurotransmitter and hormone release, a process so far thought to be mediated exclusively by high-voltage-activated calcium channels. (inserm.fr)
- Tadalafil is a phosphodiesterase type 5 (PDE5) selective inhibitor. (medscape.com)
- However, we have recently found that under hyperpolarized conditions, the T-type calcium channel can trigger a large after-depolarization and a corresponding influx of calcium into dopamine neuron dendrites. (nih.gov)
- Around one-third of people with diabetes ( Type 1 or Type 2 ) develop gastroparesis. (clevelandclinic.org)
- Diabetes-related gastroparesis is a type of diabetes-related neuropathy . (clevelandclinic.org)
- 29. Understanding the glucoregulatory mechanisms of metformin in type 2 diabetes mellitus. (nih.gov)
- As an example of specific treatment, sodium-glucose co-transporter 2 (SGLT2) inhibitors (eg, canagliflozin, empagliflozin) have gained wide use in the management of type 2 diabetes mellitus and have effects beyond glucose lowering that include reducing the risk of development or worsening of albuminuria. (medscape.com)
- Specifically we have used computational modeling, electrophysiology, and two-photon calcium imaging in mouse midbrain slices to show that this hyperpolarization-induced afterdepolarization (HI-ADP) depends on T-type, but not L-type calcium channels. (nih.gov)
- Survival depends on how much and what type of this medicine the person took and how quickly they receive treatment. (medlineplus.gov)
- This paper explores calcium-dependent inactivation of L-type calcium channels in beta cells, proposing that inactivation depends on calcium in the micro- or nano-domain near open calcium channels rather than bulk calcium. (nih.gov)
- Acute visceral pain relief mediated by A3AR agonists in rats: involvement of N-type voltage-gated calcium channels. (bvsalud.org)
- Both impaired tubuloglomerular feedback and low baseline renal function exacerbated glomerular pressure, glomerulosclerosis, and the decline in renal function during L-type CCB treatment. (nih.gov)
- However, simulating CCB therapy that inhibited both L- and T-type calcium channels increased efferent arteriolar vasodilation and alleviated glomerular damage. (nih.gov)
- These simulations support the evidence that DHP (L-type) CCBs potentiate glomerular HTN during CKD and suggest that T/L-type CCBs are valuable in proteinuric renal disease treatment. (nih.gov)
- Low-voltage-activated T-type calcium channels act as a major pathway for calcium entry near the resting membrane potential in a wide range of neuronal cell types. (inserm.fr)
- The rest of neuroscience is moving towards more systematic technologies, large scale recording, thorough descriptions of cell types throughout the brain. (nih.gov)
- This should apply to L-type calcium channels in other cell types. (nih.gov)
- In this study, the effects of calcium channel antagonists on the antidepressant action of alprazolam and imipramine were investigated. (who.int)
- With larger Ca concentrations, channel open probability increases and its voltage dependence is greater. (nih.gov)
- 25. Multicenter, Prospective, Phase II and Biomarker Study of High-Dose Bevacizumab as Induction Therapy in Patients With Neurofibromatosis Type 2 and Progressive Vestibular Schwannoma. (nih.gov)
- Most work on this calcium toxicity hypothesis implicates the L-type calcium channel. (nih.gov)
- Laxatives are a type of medicine that can help you poo more easily. (www.nhs.uk)
- By default, all articles on GreenMedInfo.com are sorted based on the content type which best reflects the data which most users are searching for. (greenmedinfo.com)
- What is the most common type of gastroparesis? (clevelandclinic.org)
- All types of volunteers are needed- those who are healthy or may have an illness or disease- of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them. (nih.gov)
- When internal Ca concentration is close to 0.01 microM, channels are usually closed even at large depolarizing voltages. (nih.gov)
- In intact cells, single-channel current amplitude and the time a channel stays in the open state increase with membrane depolarization. (nih.gov)
- In excised patches bathed in symmetrical 130 mM K solutions, single-channel conductance is 170 pS. (nih.gov)
- This model introduced the concept of phantom bursting, i.e., that the process that drives bursting may not be a single channel but a composite of two or more channels. (nih.gov)
- Channel open probability is heavily influenced by the concentration of ionic Ca at the inner surface of the membrane in the range between 0.01 and 10 microM. (nih.gov)
- Current flowing through single Ca- and voltage-activated K channels has been recorded from cell-attached and inside-out excised membrane patches of cultured Y-1 adrenocortical cells. (nih.gov)