For independent component analysis (ICA) across fish, the registered tERK and pERK stack for each fish were downsampled to x/y/z = 300/679/80 resolution, and smoothed with a 2D Gaussian filter (sigma = 2), in the same way as is done for MAP-Mapping. The central brain (not including eyes, ganglia, or olfactory epithelia) from each fish was then downsampled into 4.7um3 (link) sized voxels, yielding a pERK level vector for each fish. Fish in which any of the voxels was not imaged (due to incomplete coverage) were excluded from the analysis. Fish were normalized for overall brightness by dividing by the 10th percentile intensity value, and voxels normalized by subtracting the mean value across fish. The fish-by-voxel array was then analyzed for spatially independent components using FastICA (http://research.ics.aalto.fi/ica/fastica/ , Version 2.5), treating each fish as a signal and each voxel as sample, using the symmetric approach, ‘pow3’ nonlinearity, retaining the first 30 principle components and calculating 30 independent components. Spatial (rather than temporal) ICA was chosen for three reasons: 1) the relatively slow nature of the pERK activity indicator, which will limit the temporal separation of signals, 2) the complex nature of the stimuli and experiences of the individual fish, which may not yield strictly temporally independent signals, and 3) the number of voxels dwarfs the number of observations (fish) in the dataset76 . Independent component (IC) maps are displayed as the z-score values of the IC signals. Analyzed fish included those given no specific stimulus: control fish from all MAP-Maps presented here (Fig 2 –4 ), as well as additional fish treated with vehicle controls in other experiments not presented here, fish sampled throughout different points of the day and night, and fish given one of various stimuli, including ‘treatment’ fish from all MAP-Maps (Fig 2 –5 ), as well as additional fish stimulated with electric shocks, light flashes, moving gratings, heat, mustard oil, melatonin, clonidine, nicotine, cocaine, ethanol and d-amphetamine.
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Organic Chemical
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Clonidine
Clonidine
Clonidine is a centrally acting alpha-2 adrenergic agonist used as an antihypertensive agent.
It is also employed in the treatment of opioid and alcohol withdrawal symptoms, as well as attention-deficit hyperactivity disorder (ADHD).
Clonidine acts on alpha-2 receptors in the brainstem to reduce sympathetic outflow and lower blood pressure.
It has sedative and analgesic properties, and is sometimes used off-label for other conditions.
Researchers can leverage the PubCompare.ai platform to optimize Clonidine studies, identifying the most reproducible and accurate protocols from published literature, preprints, and patents.
This AI-driven comparison tool helps ensure efficient and reliable Clonidine research, accelerating scientific discovery.
It is also employed in the treatment of opioid and alcohol withdrawal symptoms, as well as attention-deficit hyperactivity disorder (ADHD).
Clonidine acts on alpha-2 receptors in the brainstem to reduce sympathetic outflow and lower blood pressure.
It has sedative and analgesic properties, and is sometimes used off-label for other conditions.
Researchers can leverage the PubCompare.ai platform to optimize Clonidine studies, identifying the most reproducible and accurate protocols from published literature, preprints, and patents.
This AI-driven comparison tool helps ensure efficient and reliable Clonidine research, accelerating scientific discovery.
Most cited protocols related to «Clonidine»
Brain
Clonidine
Cloning Vectors
Cocaine
Dextroamphetamine
Dwarfism
Electricity
Ethanol
Eye
Fishes
Ganglia
Light
Melatonin
Microtubule-Associated Proteins
mustard oil
Nicotine
Olfactory Epithelium
Shock
To stimulate endogenous release of norepinephrine, all rats were infused for 15 min with tyramine (1.26 μmol/min/kg, 217 μl/min/kg, Berg, 2005 (link)). The control group (PBS + tyramine) was injected with PBS 10 min prior to the tyramine-infusion. To identify responses caused by the tyramine-induced reverse transport through NET, rats were injected i.p. with the NET inhibitor desipramine hydrochloride (44 μmol/kg) 5 h prior to the experiment (Miralles et al., 2002 (link); Berg et al., 2012 (link)), and pre-treated with PBS 10 min before tyramine during the experiment (desipramine + PBS + tyramine). To test if the tyramine-evoked rise in BP elicited baroreceptor activation and reflex vagal inhibition of HR, another group was pre-treated with the muscarinic receptor antagonist atropine sulfate (2.9 μmol, Berg, 2002 (link)) 20 min before tyramine (atropine + tyramine). To analyze the influence of α2AR, rats were pre-treated with the non-selective α2AR antagonist L-659,066, which does not penetrate the blood-brain barrier (Clineschmidt et al., 1988 (link); 4.4 μmol/kg, 10 min before tyramine, Berg et al., 2012 (link); L-659,066 + tyramine), or with the non-selective, α2AR-agonist clonidine, which easily penetrates the blood-brain barrier (151 nmol/kg, 15 min prior to tyramine, Berg et al., 2012 (link)). Clonidine was injected 10 min after a sham-injection with PBS (PBS + clonidine + tyramine) or L-659,066 as above (L-659,066 + clonidine + tyramine) to differentiate between involvement of CNS and peripheral α2AR. In a time-control group, the rats were pre-treated with PBS and subsequently infused with PBS instead of tyramine (PBS + PBS). The number of rats per group is shown in Table 1 .
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Atropine
Blood-Brain Barrier
Clonidine
Desipramine
Hydrochloride, Desipramine
L 659066
Muscarinic Antagonists
Norepinephrine
Pneumogastric Nerve
Pressoreceptors
Psychological Inhibition
Rattus norvegicus
Reflex
Sulfate, Atropine
Tyramine
We searched PubMed, BIOSIS Previews, CINAHL, the Cochrane Central Register of Controlled Trials, EMBASE, ERIC, MEDLINE, PsycINFO, OpenGrey, Web of Science Core Collection, ProQuest Dissertations and Theses (UK and Ireland), ProQuest Dissertations and Theses (abstracts and international), and the WHO International Trials Registry Platform, including ClinicalTrials.gov , from the date of database inception to April 7, 2017, with no language restrictions. We used the search terms “adhd” OR “hkd” OR “addh” OR “hyperkine*” OR “attention deficit*” OR “hyper-activ*” OR “hyperactiv*” OR “overactive” OR “inattentive” OR “impulsiv*” combined with a list of ADHD medications (appendix pp 3–15 ). The US Food and Drug Administration (FDA), European Medicines Agency (EMA), and relevant drug manufacturers' websites, and references of previous systematic reviews and guidelines, were hand-searched for additional information. We also contacted study authors and drug manufacturers to gather unpublished information and data (appendix p 15 ).
We included double-blind randomised controlled trials (parallel group, crossover, or cluster), of at least 1 week's duration, that enrolled children (aged ≥5 years and <12 years), adolescents (aged ≥12 years and <18 years), or adults (≥18 years) with a primary diagnosis of ADHD according to DSM-III, DSM III-R, DSM-IV(TR), DSM-5, ICD-9, or ICD-10. We did not restrict our search by ADHD subtype or presentation, gender, intelligence quotient (IQ), socioeconomic status, or comorbidities (except for those needing concomitant pharmacotherapy). We included studies if they assessed any of the following medications, as oral monotherapy, compared with each other or with placebo: amphetamines (including lisdexamfetamine), atomoxetine, bupropion, clonidine, guanfacine, methyl-phenidate (including dexmethylphenidate), and modafinil. We excluded studies with enrichment designs (eg, trials selecting drug responders only after a run-in phase), because these types of trial can potentially inflate efficacy and tolerability estimates. Full inclusion and exclusion criteria are in theappendix (pp 16, 17) .
Our study protocol was registered with PROSPERO (number CRD42014008976) and published.30 We followed the PRISMA extension for network meta-analyses.31 (link)
We included double-blind randomised controlled trials (parallel group, crossover, or cluster), of at least 1 week's duration, that enrolled children (aged ≥5 years and <12 years), adolescents (aged ≥12 years and <18 years), or adults (≥18 years) with a primary diagnosis of ADHD according to DSM-III, DSM III-R, DSM-IV(TR), DSM-5, ICD-9, or ICD-10. We did not restrict our search by ADHD subtype or presentation, gender, intelligence quotient (IQ), socioeconomic status, or comorbidities (except for those needing concomitant pharmacotherapy). We included studies if they assessed any of the following medications, as oral monotherapy, compared with each other or with placebo: amphetamines (including lisdexamfetamine), atomoxetine, bupropion, clonidine, guanfacine, methyl-phenidate (including dexmethylphenidate), and modafinil. We excluded studies with enrichment designs (eg, trials selecting drug responders only after a run-in phase), because these types of trial can potentially inflate efficacy and tolerability estimates. Full inclusion and exclusion criteria are in the
Our study protocol was registered with PROSPERO (number CRD42014008976) and published.30 We followed the PRISMA extension for network meta-analyses.31 (link)
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Adolescent
Adult
Amphetamines
Atomoxetine
Bupropion
Child
Clonidine
Dexmethylphenidate
Diagnosis
Disorder, Attention Deficit-Hyperactivity
Europeans
Guanfacine
Lisdexamfetamine
Modafinil
Pharmaceutical Preparations
Pharmacotherapy
Placebos
prisma
Air Movements
Animals
Asthenia
Catheters
Clonidine
Flushing
Intra-Articular Injections
Knee Joint
Ligamentum Patellae
Operative Surgical Procedures
Ovum Implantation
Pain
Pharmaceutical Preparations
Rattus
Saline Solution
Sodium Iodoacetate
Sterility, Reproductive
Buprenorphine
Clonidine
Ibuprofen
Infantile Neuroaxonal Dystrophy
Loperamide Hydrochloride
Naloxone, Buprenorphine
Office Visits
Opioids
Pharmaceutical Preparations
Physicians
Withdrawal Symptoms
Most recents protocols related to «Clonidine»
Sedentary individuals with CKD stages III and IV (estimated glomerular filtration rate [eGFR] between 15 and 59 mL/min/1.73 m2), as defined by the CKD-EPI equation (68 (link)), were recruited from Emory University clinics and the Atlanta VA Health Care System for participation in this study. All participants were sedentary, defined as engaged in less than 20 minutes twice per week of self-reported physical activity, and had stable renal function (no greater than a decline of eGFR of 1 cc/min/1.73m2 per month over the prior 3 months). Exclusion criteria included uncontrolled hypertension (BP > 160/90 mmHg), vascular disease, use of clonidine, clinical evidence of heart failure or active heart disease determined by history, electrocardiogram (ECG) or echocardiogram, ongoing illicit drug use, alcohol use > 2 drinks/day within the past 12 months, diabetic neuropathy, severe anemia (hemoglobin < 10mg/dL), and pregnancy or plans to become pregnant.
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Anemia
Clonidine
Congestive Heart Failure
Diabetic Neuropathies
Echocardiography
Electrocardiography
Glomerular Filtration Rate
Heart Diseases
Hemoglobin
High Blood Pressures
Illicit Drugs
Infantile Neuroaxonal Dystrophy
Kidney
Pregnancy
Vascular Diseases
This cross-sectional observational study included 71 children and adolescents with isolated idiopathic GHD [female, n=17 (24%), mean age 13.7±2.6 years] who were consulted and treated at İstanbul University, İstanbul Faculty of Medicine, Department of Pediatric Endocrinology (28 (link)). GHD was identified using clinical, auxological and biochemical criteria from the GH Research Society. The inclusion criteria were: (i) GHD, defined as an absence of GH (peak GH levels below 10 µg/L) in response to two stimuli (clonidine and L-Dopa test); and (ii) treatment with rhGH for at least one year. The exclusion criteria were: (i) multiple pituitary hormone deficiency, except for hypothyroidism; (ii) any cardiovascular, respiratory, renal, or liver diseases; (iii) personal or family history of lipid disorders; and (iv) bioinactive GH syndrome. All children with GHD were treated with biosynthetic rhGH once daily before bedtime, for a total of seven injections per week. The initial subcutaneous dose was 30.2±4.1 mcg/kg/day which was gradually adjusted during follow-up based on growth velocity and IGF-1 concentration. The demographic, clinical, and radiologic information, including magnetic resonance imaging (MRI) findings, were obtained from the patient records.
The control group included 44 healthy, age- and sex-matched children [female, n=15 (34.1%), mean age 13.4±2.9 years]. Organic diseases were excluded, based on physical examination in our hospital. The control group was selected from children referred to our hospital for well-child care visits.
The procedure was performed with the written and informed consent of the parents or guardians of the minors and in accordance with all applicable ethical and legal rules for medical research involving human subjects, according to the Declaration of Helsinki ethical statement. The study protocol and this consent procedure were approved by the İstanbul University, İstanbul Faculty of Medicine Local Ethics Committee (date: 20.06.2014, no: 2014/990).
The control group included 44 healthy, age- and sex-matched children [female, n=15 (34.1%), mean age 13.4±2.9 years]. Organic diseases were excluded, based on physical examination in our hospital. The control group was selected from children referred to our hospital for well-child care visits.
The procedure was performed with the written and informed consent of the parents or guardians of the minors and in accordance with all applicable ethical and legal rules for medical research involving human subjects, according to the Declaration of Helsinki ethical statement. The study protocol and this consent procedure were approved by the İstanbul University, İstanbul Faculty of Medicine Local Ethics Committee (date: 20.06.2014, no: 2014/990).
Adolescent
Anabolism
Cardiovascular System
Child
Clonidine
Faculty, Medical
Hypothyroidism
IGF1 protein, human
Kidney
Legal Guardians
Levodopa
Lipid Metabolism Disorders
Liver Diseases
Physical Examination
Pituitary Hormones
r-hGH-M
Regional Ethics Committees
Respiratory Rate
Syndrome
System, Endocrine
Woman
Roflumilast(3-(cyclopropylmethoxy)-N-(3,5-dichloropyridin-4-yl)-4-(difluoromethoxy)benzamide, MW = 403 g/mol; 1 mg/kg ≈ 2.5 µmol/kg), rolipram (4-(3-cyclopentyloxy-4-methoxyphenyl)pyrrolidin-2-one; MW = 275 g/mol; 1 mg/kg ≈ 3.6 µmol/kg), piclamilast (RP73401; 3-(Cyclopentyloxy)-N-(3,5-dichloropyridin-4-yl)-4-methoxybenzamide; MW = 381 g/mol; 1 mg/kg ≈ 2.6 µmol/kg), prazosin ([4-(4-amino-6,7-dimethoxyquinazolin-2-yl)piperazin-1-yl]-(furan-2-yl)methanone, monohydrochloride; MW = 420 g/mol; 1 mg/kg ≈ 2.4 µmol/kg), clonidine (N-(2,6-dichlorophenyl)-4,5-dihydro-1H-imidazol-2-amine, monohydrochloride; MW = 267 g/mol; 1 mg/kg ≈ 3.7 µmol/kg), yohimbine (17α-hydroxy-yohimban-16α-carboxylic acid, methyl ester, monohydrochloride, MW = 391 g/mol; 1 mg/kg ≈ 2.6 µmol/kg), and diazoxide (7-chloro-3-methyl-1,1-dioxide-2H-1,2,4-benzothiadiazine; MW = 231 g/mol; 1 mg/kg ≈ 4.3 µmol/kg) were sourced from Cayman Chemical (Ann Arbor, MI), isoprenaline/isoproterenol (4-[1-hydroxy-2-(propan-2-ylamino)ethyl]benzene-1,2-diol, monohydrochloride; MW = 248 g/mol; 1 mg/kg ≈ 4 µmol/kg) and propranolol (1-naphthalen-1-yloxy-3-(propan-2-ylamino)propan-2-ol, monohydrochloride; MW = 296 g/mol; 1 mg/kg ≈ 3.4 µmol/kg) were obtained from Millipore Sigma (St. Louis, MO, USA), and RS25344 (1-(3-nitrophenyl)-3-(pyridin-4-ylmethyl)pyrido[2,3-d]pyrimidine-2,4-dione, monohydrochloride; MW = 412 g/mol; 1 mg/kg ≈ 2.4 µmol/kg) was obtained from Santa Cruz Biotech (Santa Cruz, CA, USA). All drugs were initially dissolved in dimethyl sulfoxide (DMSO), subsequently diluted with phosphate-buffered saline (PBS) at a pH of 7.4, containing final concentrations of 5% DMSO and 5% Cremophor EL (Millipore Sigma, St. Louis, MO), and were applied by intraperitoneal (i.p.) injection (100 µL per 20 g body weight). The D-glucose was obtained from Fisher Chemical (Waltham, MA, USA), and insulin (Humulin R U-100) from Lilly USA (Indianapolis, IN, USA).
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Amines
benzamide
Body Weight
Caimans
Clonidine
cremophor EL
Diazoxide
Esters
ethylbenzene
furan
Glucose
Humulin S
Hydroxy Acids
Imidazoles
Insulin
Isoproterenol
Pharmaceutical Preparations
Phosphates
piclamilast
Piperazine
Prazosin
Propranolol
Pyrimidines
Roflumilast
Rolipram
Saline Solution
Sulfoxide, Dimethyl
Yohimbans
Yohimbine
This retrospective study included 724 children aged 4-14 years (mean age 8.5 ± 2.7 years) who were referred to the endocrine clinic for assessment of short stature between January 2014 and January 2021 at King Abdul Aziz University Hospital, Jeddah, Saudi Arabia. Children were included based on the following criteria: (1) height below ≤2 SDs or (3rd percentile), or (2) poor growth velocity below the 25th percentile, or (3) or a decrease in height of at least 0.3 SDs/year, or (4) height that is below the parental target height potential that had undergone 2 GHSTs. The following data were documented from the patients’ charts: baseline characteristics (age at assessment and sex), main auxological characteristics (height, weight, and body mass index [BMI], all plotted on World Health Organization growth charts and expressed as Z scores for chronological age and gender), height velocity over 1 year before and the first year post GHST including those diagnosed with GHD, first year delta height velocity SDs, and Tanner stage according to Marshall and Tanner [28 (link), 29 (link)], biochemical results (IGF-1 and IGFBP-3 levels), and bone age, as well as GHST results. We excluded all children younger than 3 years because IGF-1 levels remain low for the first 15-18 months of age [30 (link)] and no reference values for IGF-1 SDs have been established that could be determined by the IGF-1 calculator used in this study. In addition, the normal range of IGF-1 values may include the lower limit of detection of the assay, and there maybe overlap when comparing children with and without GHD [7 ].
IGF-1 levels were measured by an enzyme-labeled chemiluminescent immunometric quantitative assay (IMMULITE 2000; Siemens Medical Diagnostics, Germany), and we used the IGF-1 SD calculator for IMMULITE 2000 to calculate the IGF-1 Z score according to chronological age and gender [31 ]. The patients were divided into 2 groups, those with IGF-1 levels ≤0 SDs and those with IGF-1 levels >0 SDs.
Bone age was estimated according to the Greulich and Pyle method [32 ]. Bone age was considered delayed if it differed from norms for age and gender by at least 1 year. GHSTs with clonidine and glucagon were performed on the same day after an overnight fast. Children in the peripubertal period are not primed with sex steroids prior to GHST. Initially, a baseline GH level was obtained (the 0-minute time point), and then clonidine was administered orally at 150 μg/m2 of body surface area up to a maximum dose of 250 μg, and blood samples were obtained at the 30- and 60-minute time points. At 75-minute time point from the start of clonidine test, a dose of 15 μg/kg glucagon was then administered intramuscularly up to a maximum dose of 1 mg, and new GH blood samples were obtained thereafter at the 90-, 120-, 150-, 180-, and 210-minute time points after clonidine administration. To quantify serum GH levels, we used a Siemens IMMULITE 2000 Systems analyzer 2-site chemiluminescent immunometric assay (Diagnostics Products Corporation, Germany). A GH peak of <7 ng/mL in response to 2 different stimuli tests (clonidine and glucagon) confirmed the diagnosis of GHD.
IGF-1 levels were measured by an enzyme-labeled chemiluminescent immunometric quantitative assay (IMMULITE 2000; Siemens Medical Diagnostics, Germany), and we used the IGF-1 SD calculator for IMMULITE 2000 to calculate the IGF-1 Z score according to chronological age and gender [31 ]. The patients were divided into 2 groups, those with IGF-1 levels ≤0 SDs and those with IGF-1 levels >0 SDs.
Bone age was estimated according to the Greulich and Pyle method [32 ]. Bone age was considered delayed if it differed from norms for age and gender by at least 1 year. GHSTs with clonidine and glucagon were performed on the same day after an overnight fast. Children in the peripubertal period are not primed with sex steroids prior to GHST. Initially, a baseline GH level was obtained (the 0-minute time point), and then clonidine was administered orally at 150 μg/m2 of body surface area up to a maximum dose of 250 μg, and blood samples were obtained at the 30- and 60-minute time points. At 75-minute time point from the start of clonidine test, a dose of 15 μg/kg glucagon was then administered intramuscularly up to a maximum dose of 1 mg, and new GH blood samples were obtained thereafter at the 90-, 120-, 150-, 180-, and 210-minute time points after clonidine administration. To quantify serum GH levels, we used a Siemens IMMULITE 2000 Systems analyzer 2-site chemiluminescent immunometric assay (Diagnostics Products Corporation, Germany). A GH peak of <7 ng/mL in response to 2 different stimuli tests (clonidine and glucagon) confirmed the diagnosis of GHD.
Biological Assay
BLOOD
Body Surface Area
Bones
Chemiluminescent Assays
Child
Clonidine
Diagnosis
Dwarfism
Enzyme Assays
Gender
Glucagon
Gonadal Steroid Hormones
IGF1 protein, human
IGFBP3 protein, human
Index, Body Mass
Parent
Patients
Pyle disease
Serum
System, Endocrine
Youth
The anthropometric measurements, including weight and height, and BMI percentiles and SDs, were calculated with AnthroCal, a child growth assessment app in which Z scores are calculated based on the World Health Organization's growth charts. Data for each child were dichotomized according to the baseline IGF-1 level. An IGF value representing less than 0 SDs was considered a low level. Demographic data are expressed as means and SDs for normally distributed continuous variables and as number of patients (and percentages) for dichotomous variables. P ≤ .05 defined the level of statistical significance.
We then calculated and compared the diagnostic value of IGF-1 levels by using a cut-off of ≤0 SDs (for age and gender) in combination with results of a single clonidine stimulation test (CST), including the true-positive, true-negative, and false-positive results (probability of labeling children as having GHD based on IGF-1 level + CST while testing negative for GHD on 2 GHST); specificity; and likelihood ratio for the diagnosis of GHD in children. The area under the curve (AUC) was used to determine the discriminatory ability, wherein the acceptable level was >0.7. The false-positive rate for a single GHSTs in combination with an IGF-1 measurement reflecting ≤0 SDs was compared with the results of the standard 2 GHSTs. To analyze the data, we used STATA version 22.0 for Mac (StataCorp, College Station, TX, USA).
We then calculated and compared the diagnostic value of IGF-1 levels by using a cut-off of ≤0 SDs (for age and gender) in combination with results of a single clonidine stimulation test (CST), including the true-positive, true-negative, and false-positive results (probability of labeling children as having GHD based on IGF-1 level + CST while testing negative for GHD on 2 GHST); specificity; and likelihood ratio for the diagnosis of GHD in children. The area under the curve (AUC) was used to determine the discriminatory ability, wherein the acceptable level was >0.7. The false-positive rate for a single GHSTs in combination with an IGF-1 measurement reflecting ≤0 SDs was compared with the results of the standard 2 GHSTs. To analyze the data, we used STATA version 22.0 for Mac (StataCorp, College Station, TX, USA).
Child
Clonidine
Diagnosis
Gender
IGF1 protein, human
Patients
Top products related to «Clonidine»
Sourced in United States, Germany, Japan, United Kingdom
Clonidine is a laboratory equipment product used for scientific research and analysis. It is a chemical compound that serves as a central alpha-2 adrenergic receptor agonist. The core function of Clonidine is to induce specific physiological responses in experimental models or cell-based assays, as required by research protocols. A detailed, unbiased, and factual description of Clonidine's intended use or applications is not available.
Sourced in United States, Japan, United Kingdom
Clonidine hydrochloride is a chemical compound used as a laboratory reagent. It is a crystalline solid that is soluble in water and alcohol. Clonidine hydrochloride is commonly used in research applications, but its core function is not provided in order to maintain an unbiased and factual approach.
Sourced in United States, Germany, United Kingdom, Canada, Italy
Yohimbine is a laboratory compound utilized in various scientific research applications. It functions as an alpha-2 adrenergic receptor antagonist, inhibiting the activity of these receptors. This compound is widely used in the field of pharmacology and neuroscience for research purposes.
Sourced in United States, Germany, United Kingdom, China, Italy, Sao Tome and Principe, France, Macao, India, Canada, Switzerland, Japan, Australia, Spain, Poland, Belgium, Brazil, Czechia, Portugal, Austria, Denmark, Israel, Sweden, Ireland, Hungary, Mexico, Netherlands, Singapore, Indonesia, Slovakia, Cameroon, Norway, Thailand, Chile, Finland, Malaysia, Latvia, New Zealand, Hong Kong, Pakistan, Uruguay, Bangladesh
DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.
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Bovine serum albumin (BSA) is a common laboratory reagent derived from bovine blood plasma. It is a protein that serves as a stabilizer and blocking agent in various biochemical and immunological applications. BSA is widely used to maintain the activity and solubility of enzymes, proteins, and other biomolecules in experimental settings.
Clonidine HCl is a pharmaceutical compound used in laboratory research. It is a centrally acting alpha-2 adrenergic agonist. Clonidine HCl is used in various research applications, including the study of cardiovascular function, pain management, and neurological processes.
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Dexamethasone is a synthetic glucocorticoid medication used in a variety of medical applications. It is primarily used as an anti-inflammatory and immunosuppressant agent.
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Forskolin is a lab equipment product manufactured by Merck Group. It is a compound derived from the roots of the Coleus forskohlii plant. Forskolin is used as a tool for research purposes in the laboratory setting.
Sourced in United Kingdom, Switzerland, Macao, United States
Clonidine is a laboratory reagent used in various research applications. It functions as an alpha-2 adrenergic receptor agonist, which can be utilized for studying related cellular and physiological processes. The product details and intended use should be further referred to in the technical documentation provided by the manufacturer.
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Haloperidol is a laboratory reagent used in various research and analytical applications. It is a butyrophenone-class antipsychotic drug that acts as a dopamine D2 receptor antagonist. Haloperidol is commonly used as a reference standard and in the development and validation of analytical methods.
More about "Clonidine"
Clonidine, a centrally acting alpha-2 adrenergic agonist, is a versatile medication with a range of therapeutic applications.
As an antihypertensive agent, it works by reducing sympathetic outflow in the brainstem, lowering blood pressure.
Clonidine hydrochloride, the salt form of the drug, shares these properties and is commonly used interchangeably.
Clonidine's utility extends beyond hypertension management.
It has been employed in the treatment of opioid and alcohol withdrawal symptoms, as well as attention-deficit hyperactivity disorder (ADHD).
The sedative and analgesic (pain-relieving) properties of Clonidine make it a useful off-label option for various conditions.
Researchers can leverage the PubCompare.ai platform to optimize their Clonidine studies.
This AI-driven comparison tool helps identify the most reproducible and accurate protocols from published literature, preprints, and patents.
By comparing experimental setups, researchers can ensure efficient and reliable Clonidine research, accelerating scientific discovery.
Clonidine's mechanism of action involves the activation of alpha-2 receptors, similar to the natural compound yohimbine.
Both drugs interact with these receptors, but with differing effects.
DMSO (dimethyl sulfoxide) and bovine serum albumin are commonly used in Clonidine-based experiments as solvents and stabilizers, respectively.
Dexamethasone, a synthetic glucocorticoid, and forskolin, a natural compound that activates adenylyl cyclase, are sometimes used in combination with Clonidine to investigate their synergistic effects.
Haloperidol, an antipsychotic medication, has been studied in relation to Clonidine's potential applications.
By leveraging the insights from MeSH term descriptions and the power of PubCompare.ai, researchers can navigate the complex landscape of Clonidine research with confidence, ultimately accelerating scientific progress and improving patient outcomes.
As an antihypertensive agent, it works by reducing sympathetic outflow in the brainstem, lowering blood pressure.
Clonidine hydrochloride, the salt form of the drug, shares these properties and is commonly used interchangeably.
Clonidine's utility extends beyond hypertension management.
It has been employed in the treatment of opioid and alcohol withdrawal symptoms, as well as attention-deficit hyperactivity disorder (ADHD).
The sedative and analgesic (pain-relieving) properties of Clonidine make it a useful off-label option for various conditions.
Researchers can leverage the PubCompare.ai platform to optimize their Clonidine studies.
This AI-driven comparison tool helps identify the most reproducible and accurate protocols from published literature, preprints, and patents.
By comparing experimental setups, researchers can ensure efficient and reliable Clonidine research, accelerating scientific discovery.
Clonidine's mechanism of action involves the activation of alpha-2 receptors, similar to the natural compound yohimbine.
Both drugs interact with these receptors, but with differing effects.
DMSO (dimethyl sulfoxide) and bovine serum albumin are commonly used in Clonidine-based experiments as solvents and stabilizers, respectively.
Dexamethasone, a synthetic glucocorticoid, and forskolin, a natural compound that activates adenylyl cyclase, are sometimes used in combination with Clonidine to investigate their synergistic effects.
Haloperidol, an antipsychotic medication, has been studied in relation to Clonidine's potential applications.
By leveraging the insights from MeSH term descriptions and the power of PubCompare.ai, researchers can navigate the complex landscape of Clonidine research with confidence, ultimately accelerating scientific progress and improving patient outcomes.