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Thyrotropin

Thyrotropin, also known as thyroid-stimulating hormone (TSH), is a glycoprotein hormone produced by the anterior pituitary gland.
It plays a central role in regulating the function of the thyroid gland, which is responsible for the production of thyroid hormones essential for metabolism, growth, and development.
Thyrotropin stimulates the thyroid gland to secrete thyroid hormones, thyroxine (T4) and triiodothyronine (T3), and is a key regulator of thyroid function.
Disturbances in thyrotropin levels can lead to thyroid disorders, such as hypothyroidismm and hyperthyroidism.
Understanding the mechanisms and regulation of thyrotropin is crucial for the diagnosis and management of thyroid-related conditions.

Most cited protocols related to «Thyrotropin»

KEEPS was designed as a randomized, placebo-controlled, double-blinded, prospective trial (KEEPS; NCT000154180) to evaluate effects of MHT on progression of atherosclerosis as defined by carotid intima–media thickness (CIMT) [44 (link)] and coronary arterial calcification (CAC) [8 (link), 73 (link)] in women who more closely match the age of initiation of MHT reported by prior observational studies. Women meeting inclusion criteria subsequently were randomized to daily placebo, oral CEE, or transdermal 17β-estradiol with placebo or pulsed progesterone for 12 days/month. The detailed inclusion and exclusion criteria for KEEPS have been published elsewhere [36 (link)]. In brief, women between the ages of 42 and 58 years of age who were at least 6 months and no more than 36 months from their last menses with plasma follicle-stimulating hormone (FSH) level ≥35 ng/mL and/or E2 levels <40 pg/mL were eligible. A history of clinical CVD including myocardial infarction, angina, congestive heart failure, or thromboembolic disease excluded women from KEEPS. Other major cardiovascular risk factors excluding participation were current heavy smoking (more than ten cigarettes/day by self-report), morbid obesity [body mass index (BMI) >35 mm2/kg], dyslipidemia (LDL cholesterol >190 mg/dL), hypertriglyceridemia (triglycerides >400 mg/dL), and uncontrolled hypertension (systolic blood pressure >150 mm Hg and/or diastolic blood pressure >95 mm Hg) and glucose >126 mg/dL. Complete blood count and chemistry panel, estradiol, and FSH were performed at the clinical laboratories at each recruiting center. Lipid profiles and thyroid-stimulating hormone (TSH) were performed at the Kronos Science Laboratories (Phoenix, AZ, USA). At screening, women were asked to rank their menopausal symptoms (hotflashes, night sweats, vaginal dryness, dyspareunia, palpitations, insomnia, depression, mood swings, and irritability) as either none, mild, moderate, or severe. Finally, all subjects were screened for CAC and women with Agatston score ≥50 U, indicating significant subclinical coronary artery disease, were excluded. All women meeting inclusion criteria underwent baseline measurements of CIMT by B-mode ultrasound [44 (link)]. All imaging results are read centrally by individuals blinded to participant demographics (CAC at the Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA, USA under the direction of Dr. M. Budoff and CIMT at the Atherosclerosis Research Unit Core Imaging and Reading Center, University of Southern California, Los Angeles, CA, USA under the direction of Dr. H. Hodis).
Analysis of variance was used to determine statistical significance except where an alternative test is specified. Statistical significance was accepted at P < 0.05.
Publication 2009
Angina Pectoris Artery, Coronary Atherosclerosis Calcinosis Carotid Intima-Media Thickness Cholesterol, beta-Lipoprotein Clinical Laboratory Services Complete Blood Count Comprehensive Metabolic Panel Congestive Heart Failure Coronary Arteriosclerosis Desiccation Disease Progression Dyslipidemias Estradiol Glucose High Blood Pressures Human Follicle Stimulating Hormone Hypertriglyceridemia Index, Body Mass Lipids Menopause Menstruation Mood Myocardial Infarction Obesity, Morbid Placebos Plasma Pressure, Diastolic Progesterone Sleeplessness Sweat Systolic Pressure Thromboembolism Thyrotropin Triglycerides Ultrasonography Vagina Woman
A total of 2470 participants were recruited, including 1151 cognitively normal controls (NC), 898 patients with amnestic mild cognitive impairment (aMCI), and 421 patients with mild Alzheimer disease (AD).
We recruited the controls using cluster sampling in Jingansi Community Shanghai, China. The inclusion criteria for NC were: age between 50 and 90; no memory complaints verified by an informant; cognitively normal, based on the absence of significant impairment in cognitive functions or activities of daily living (ADL); Clinical Dementia Rating (CDR)  =  0; and Hamilton depression rating scale (HAMD) scored ≤ 12 on the 17-item scale in past 2 weeks. They had adequate visual and auditory acuity to allow cognitive testing. Participants with any significant neurologic disease and psychiatric disorders/psychotic features were excluded.
All the patients with aMCI and AD were recruited from the Memory Clinic, Huashan Hospital, from Jun 2004 to Oct 2011.They finished the laboratory tests and cranial CT/MRI scan, and had no clinically significant abnormalities in vitamin B12, folic acid, thyroid function (free triiodothyronine-FT3, free tetraiodothyronine-FT4, thyroid stimulating hormone-TSH), rapid plasma regain (RPR), or treponema pallidum particle agglutination (TPPA).
The aMCI patients were diagnosed according to the following criteria19]: (1) cognitive complaints verified by an informant; (2) cognitive impairment lasting more than 3 months; (3) Mini-mental state examination-Chinese version (C-MMSE)[25] (link) ≥ cut-off score for adjusted education; (4) Abnormal objective memory impairment documented by scoring below the age and education adjusted cutoff on an episodic memory test (Auditory Verbal Learning Test); (5) preserved basic ADL/minimal impairment in complex instrumental functions; (6) etiology unknown; (7) normal sense of hearing and sight; (8) has not met diagnostic criteria of dementia based on the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA).
The AD patients (n = 421) met the following criteria: (1) diagnosed as probable AD according to the NINCDS-ADRDA; (2) no obvious medical, neurological or psychiatric diseases or psychological dysfunction including anxiety and depression within the previous one month; (3) no visual or auditory deficit.
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Publication 2013
Agglutination Alzheimer's Disease Anxiety Auditory Perception Chinese Cognition Cognitive Impairments, Mild Congenital Abnormality Cranium Dementia Disorders, Cognitive Folic Acid Hearing Tests Liothyronine Memory Memory, Episodic Memory Deficits Mental Disorders Mini Mental State Examination Nervous System Disorder Patients Plasma Thyroid Gland Thyrotropin Treponema pallidum Vision Vitamin B12 X-Ray Computed Tomography
First, a standard FI (FI-CSHA) was constructed from data obtained during the clinical evaluation as described in detail in previous studies by our group (for example, [11 (link),16 (link),17 (link)]). The FI was composed of up to 38 variables used in the initial CSHA clinical examination [see Additional file 1: Table S1]. Each self-reported medical condition, disease history, symptom, and health rating variable satisfied the criteria for being a deficit as described previously [11 (link)]. An FI score was calculated where more than 60% of the variables were available for a given individual. Although clinical data were available for 1,375 individuals, 362 were excluded from analysis due to missing data to yield a total sample size of 1,013.
Next, we developed an FI (the FI-LAB) of up to 23 variables based on 21 routine blood tests plus measured systolic and diastolic blood pressure (Table 1). This latter, novel FI was called the ‘laboratory FI’ or ‘FI-LAB’. The FI-LAB was constructed by first coding each variable as either 0 or 1, where ‘0’ indicates that values are within the normal cut-offs and ‘1’ indicates that values are either above or below the normal cut off values illustrated in Table 1. An FI-LAB score was calculated only if more than 70% of the lab variables were available for a given individual. Each person’s FI-LAB score was calculated as the number of deficits present divided by the total number of deficits measured. For example, an individual with no deficits would have an FI-LAB score of 0, whereas one in whom all possible deficits were present would have the theoretical maximal FI-LAB score of 1. In a separate analysis, we added the deficit scores in the FI-LAB and the deficit scores in the FI-CSHA and divided by the new total to produce a ‘combined’ FI score.

Clinical and laboratory data used to construct the FI-LAB

VariableaLow cut-offHigh cut-off
Albumin (g/L)3245
AST (SGOT; IU/L)833
BP, supine systolic (mmHg)90140
BP, supine diastolic (mmHg)6090
Calcium (mM)2.32.7
Creatinine (μM)53106
Folate (nM)1157
Folate, RBC (nM)3761450
Glucose, fasting (mM)3.96.1
Hemoglobin (g/L)b135180
Mean corpuscular volume (fL)8096
Phosphatase, alkaline (IU/L)20130
Phosphorus, inorganic (mM)0.741.52
Potassium (mM)3.85
Protein, total (g/L)6078
Sodium (mM)136142
TSH (μIU/L)0.55
Thyroxine (T4; nM)71161
T4, Free (pM)1230
Urea (mM)2.98.2
VDRL00
Vitamin B12 (pg/L)118701
White blood cells (number/L)1.8 × 1097.8 × 109

aNormal reference values for blood work were from Henry [18 ]. Reference values for normal blood pressure were from Jones et al. [19 ] and Pickering et al. [20 (link)]. bNote that normal references values for hemoglobin differed between the sexes so for women, the low cut-off was 120 g/L and the high cut-off was 160 g/L. AST, aspartate aminotransferase; BP, blood pressure; FI-LAB, Laboratory frailty indes; RBC, red blood cells; TSH, thyroid-stimulating hormone; VDRL, Venereal Disease Research Laboratory.

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Publication 2014
BLOOD Blood Cells Blood Pressure Diastole Erythrocytes Gender Hematologic Tests Hemoglobin Physical Examination Pressure, Diastolic Sexually Transmitted Diseases Systole Thyrotropin Transaminase, Serum Glutamic-Oxaloacetic Woman
Other covariates or potential confounders measured in JECS include socioeconomic status (e.g. education, employment, house-hold income, social capital, and community support), lifestyle factors (stress levels, diet, smoking and alcohol habits, physical exercise activities, sleep, infections, and medications), and physical environment (heat, ionizing radiation, housing condition, and neighborhood). Biochemical tests (e.g. immunoglobulin E, glycated hemoglobin, and cholesterol) are performed on maternal, partners’, and cord blood samples. Thyroid-stimulating hormone is analyzed for in dried blood spots from new born babies.
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Publication 2014
BLOOD Cholesterol Diet Ethanol Exanthema Hemoglobin, Glycosylated Households Immunoglobulin E Infant, Newborn Infection Mothers Pharmaceutical Preparations Physical Examination Radiation, Ionizing Sleep Thyrotropin Umbilical Cord Blood
The UK ADC longitudinal research program follows 500 subjects with normal cognition who undergo annual medical, neurological and neuropsychological examination (table 1) [16 (link)]. All subjects presented here were required to have undergone a previous examination, with a consensus diagnosis of ‘normal’. All subjects transitioning from normal cognition to MCI in the period from July 1, 2005, to December 31, 2006 (n = 48) were included in the analysis. The diagnosis of MCI in this study was based on the examining physician’s review of each case, including all available current and longitudinal data.
Subjects given the diagnosis of MCI were contacted by a study physician who conveyed this diagnosis to each participant using a standardized protocol. This communication included disclosure of the diagnosis, as well as a systematic explanation of its prognostic value for predicting future cognitive decline and the possible development of a degenerative dementia. All subjects were invited and encouraged to undergo a medical workup for reversible causes of cognitive decline according to the American Academy of Neurology practice parameter on the initial diagnosis and workup of dementia [17 (link)].
Demographic variables recorded included: age, education, gender, duration of MCI (<1 year in all cases) and willingness to undergo diagnostic medical workup for reversible causes of memory decline. Clinical variables included: laboratory testing (complete blood count; comprehensive metabolic panel including electrolytes, glucose, liver and renal functions; rapid plasma reagent; sensitive thyroid-stimulating hormone; vitamin B12, andfolate), MRI or CT scan of the brain (including semiquantitative estimates of hippocampal and cortical atrophy [18 (link), 19 (link)]), cognitive domain involvement (memory, attention, language, executive and visuospatial), Folstein Mini-Mental State Examination (MMSE) [20 (link), 21 (link)], and Clinical Dementia Rating scale (CDR) global and sum-of-boxes (CDR-SOB) scores [22 (link)].
Publication 2008
Atrophy Attention Brain Cobalamins Cognition Complete Blood Count Comprehensive Metabolic Panel Cortex, Cerebral Diagnosis Disorders, Cognitive Electrolytes Gender Glucose Kidney Liver Memory Mini Mental State Examination Neuropsychological Tests Physicians Plasma Presenile Dementia Thyrotropin X-Ray Computed Tomography

Most recents protocols related to «Thyrotropin»

Example 4

An overview of the immunization strategies for lectin-binding proteins, such as galectin-3, is shown in Table 18.

BALB/c mice were immunized with 2 mg/kg mRNA, complexed with LNPs, or 20 μg recombinant protein as indicated in Table 18. Plasma anti-galectin-3 IgG titers were assayed 7 days after the final boost, which was delivered at day 55.

FIG. 3 shows that the use of galectin-3 mRNA as a final boosting agent resulted in a significantly higher target-specific IgG titer than when purified recombinant protein (a traditional immunogen) was used. This effect was observed regardless of whether the antigens were delivered subcutaneously or intravenously.

Hybridomas producing galectin-3-specific antibodies were generated, and high affinity monoclonal anti-galectin-3 antibodies were obtained from further screens.

TABLE 18
Priming ImmunizationBoostFinal Boost
(Day 0)(Day 7)(Day 55)
mRNA (I.V.)mRNA (I.V.)mRNA (I.V.)
mRNA (I.V.)mRNA (I.V.)Recombinant protein
(I.V.)
mRNA (S.C.)mRNA (S.C.)mRNA (S.C.)
mRNA (S.C.)mRNA (S.C.)Recombinant protein
(S.C.)
Summary of the Hit Rates Attainable by mRNA-Mediated Immunization

Table 19 provides a target protein-specific summary of the total number of hybridoma wells (generally about one third (⅓) of these wells contain hybridomas) screened and the number of confirmed target-specific antibodies obtained from those hybridomas wells following the use of lipid-encapsulated mRNA as an immunogen.

Table 20 provides a comparison of mRNA-LNP immunization methods with other conventional methods of immunization by number of hybridomas producing target-specific antibodies. In general, these data suggest that mRNA-LNP immunization is an effective method for inducing an immune response to a target protein antigen and for obtaining a higher number/rate of target protein-specific antibodies. In particular, these results confirm that mRNA-LNP immunization is surprisingly more effective than conventional immunization methods for obtaining antibodies specific for transmembrane proteins, e.g., multi-pass transmembrane proteins, such as GPCRs, which are difficult to raise antibodies against, and for poorly immunogenic proteins (e.g., proteins which produce low or no detectable target-specific IgGs in plasma of animals immunized with traditional antigen).

TABLE 19
Number of
Number ofhybridomas
hybridomaproducing
Proteinwellstarget-specific
targetType of proteinscreenedantibodies
RXFP1Multi-pass Transmembrane20240207
protein/GPCR
SLC52A2Multi-pass Transmembrane12880228
protein
ANGPTL8Soluble protein22816542
TSHRTransmembraneTBD130
protein/GPCR
APJTransmembrane22080230
protein/GPCR
GP130Single-pass Transmembrane23920614
protein

TABLE 20
Method of immunization and number of hybridomas producing
target-specific antibodies
Whole Virus-likeProtein/
ProteinType ofmRNA-cellsparticlesCDNApeptide
targetproteinLNP1onlyonlyonlyonly
RXFP1GPCR/20766NDNDND
multi-pass
SLC52A2multi-228NSTNSTNDNST
pass
TSHRGPCR/130NDND42413
multi-pass
APJGPCR/230 94621 ND
multi-pass
1Immunization with mRNA-LNP alone or in combination with another antigen format (e.g., protein/peptide).
2Sanders et al. 2002 Thyroid stimulating monoclonal antibodies Thyroid 12(12): 1043-1050.
3Oda et al. 2000. Epitope analysis of the human thyrotropin (TSH) receptor using monoclonal antibodies. Thyroid 10(12): 1051-1059.
ND—Not determined; antigen format not tested
NST—No specific titers detected. Because no target-specific IgG titers were detectable in plasma, hybridoma generation was not initiated on these groups.

In general, successful generation of hybridomas producing antigen-specific antibodies have been achieved for at least 15 different targets utilizing mRNA-LNP immunization methods as exemplified herein. These results show that the mRNA immunization methods described herein are capable of eliciting an immune response against a wide range of antigens (e.g., transmembrane proteins, for example multi-pass transmembrane proteins, such as GPCRs) in host animals, and are effective methods for producing high affinity monoclonal antibodies, which can serve as parentals for generation of chimeric variants, humanized variants, and affinity matured variants.

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Patent 2024
Animals anti-IgG Antibodies Antigens Binding Proteins Cells Chimera DNA, Complementary Epitopes Galectin 3 Histocompatibility Antigens Class II Homo sapiens Hybridomas Integral Membrane Proteins Lectin Lipids Mice, Inbred BALB C Monoclonal Antibodies Parent Peptides Plasma Proteins Protein Targeting, Cellular Recombinant Proteins Response, Immune RNA, Messenger Soluble Glycoprotein 130 Thyroid Gland Thyrotropin Thyrotropin Receptor Vaccination Viral Proteins
The Jazan Research Ethics Committee of the General Directorate of Health Affairs (Jazan), Ministry of Health, Saudi Arabia, approved the current study, which complies with the Declaration of Helsinki. All participants provided written informed consent. A total of 158 age-matched (30–60 years) male and female subjects were recruited for the current case–control study from King Fahad Central Hospital, the outpatient clinic (control), and the Endocrine and Diabetes Center (hypothyroid patients) in the Jazan area of southwest Saudi Arabia. These subjects were chosen at random from a population of Saudis primarily from the Jazan region. Samples were collected during the period from November 2018 to March 2019. At the time of diagnosis, AHT patients had high levels of thyroid-stimulating hormone and low levels of free thyroxine, as well as anti-thyroid peroxidase and/or anti-thyroglobulin autoantibodies. The healthy control group included subjects who had no history of thyroid or other autoimmune diseases, severe illness, or a chronic inflammatory condition.
Publication 2023
anti-thyroglobulin antibody Autoimmune Diseases Diabetes Mellitus Diagnosis Disease, Chronic Ethics Committees, Research Healthy Volunteers Hypothyroidism Inflammation Iodide Peroxidase Males Patients System, Endocrine Thyroid Gland Thyrotropin Thyroxine Woman
Blood samples were collected in the morning after an overnight fast before participants received any medical treatment. Serum levels of free triiodothyronine (FT3), free thyroxine (FT4), thyroid stimulating hormone (TSH), antithyroglobulin (TgAb), thyroid peroxidase antibody (TPOAb), TC, TG, high-density lipoprotein (HDL-C), low-density lipoprotein (LDL-C), and glucose were assessed. Lipid markers (TC, TG, HDL-C, LDL-C) and glucose were measured on a Cobas E610 (Roche, Basel, Switzerland). Thyroid hormones were assayed on a Roche C6000 Electrochemiluminescence Immunoassay Analyzer (Roche Diagnostics, Indianapolis, IN, USA). Measurements were conducted in the laboratory of the First Hospital, Shanxi Medical University. The nurses measured the patients’ weight, height, and blood pressure. We calculated body mass index (BMI) according to the following formula: BMI = Weight (kg)/Height (m) 2.
According to previous studies in the Chinese population (38 (link), 39 (link)), metabolic disturbances and thyroid dysfunction were defined as follows: (1) overweight or obesity: BMI≥24; (2) hyperglycemia: glucose≥6.1mmol/L; (3) hypertension: SBP≥140 mmHg and/or DBP≥90mmHg; (4) hypertriglyceridemia: TG≥2.3 mmol/L; (5) low HDL: HDL-C ≤ 1.0 mmol/L; (6) hypercholesterolemia: TC≥6.2 mmol/L or LDL-C≥4.1 mmol/L; (7)abnormal TgAb: TgAb≥115 IU/L; (8) abnormal TPOAb: TPOAb ≥34 IU/L; (9) subclinical hypothyroidism (SCH): TSH >4.2 mIU/L with normal fT4 concentration (10–23 pmol/L); (10) hyperthyroidism: TSH<0.27 mIU/L and FT4 >23 pmol/L, and (11) hypothyroidism: TSH >4.2 mIU/L with low FT4 concentration (<10 pmol/L).
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Publication 2023
anti-thyroglobulin antibody BLOOD Blood Pressure Chinese Diagnosis Glucose High Blood Pressures high density lipoprotein-1 High Density Lipoproteins Hypercholesterolemia Hyperglycemia Hyperthyroidism Hypertriglyceridemia Hypothyroidism Immunoassay Index, Body Mass LDL-1 Liothyronine Lipids Low-Density Lipoproteins Nurses Obesity Patients Serum Thyroid Gland Thyroid Hormones thyroid microsomal antibodies Thyrotropin Thyroxine
The participant timeline is summarized in Table 3. Candidates who consent to participate will be checked for eligibility based on the inclusion/exclusion criteria, and enrollment will be completed after confirmation of participant eligibility. Physical examination, Eastern Cooperative Oncology Group performance status (PS), body weight, body height, complete blood count (CBC), serum biochemistry, activated partial prothrombin time, prothrombin time-international normalized ratio, thyroid stimulating hormone, free T4, and urine analyses are performed within 14 days before registration. Echocardiography, electrocardiography, contrast-enhanced computed tomography (CT) of the chest, abdomen, and pelvis, and additional CT/magnetic resonance imaging (MRI) of the lesions will be performed within 28 days before registration. Plain CT is acceptable when contrast agents cannot be administered due to allergies, asthma, etc.

The study schedule

#Echocardiography is performed in Arm C if any cardiac-related symptoms are observed.§ECG will be performed on Day 28 of Arm C and every 8
weeks thereafter.*Enhanced CT of chest-abdomen-pelvis, and additional CT/MRI of the lesions to determine efficacy will be performed every 4 weeks on the first four occasions after initiation of protocol treatment, and every 6 weeks thereafter

Participants will commence the treatment protocol within 14 days of registration. The treatment protocol is continued until one of the following termination criteria are met: (1) exacerbation of disease (judged as ineffective treatment); (2) the treatment protocol cannot be continued due to adverse events including grade 4 non-hematologic toxicity and delay of 56 days before the start of the next course; (3) the patient requests termination of treatment for reasons related to adverse events; (4) the patient requests termination of treatment for reasons unrelated to adverse events; (5) death during treatment; and (6) post-enrollment exacerbation prior to the initiation of treatment (inability to start the treatment protocol due to rapid progression), discovery of protocol violation, change of treatment due to a change in the pathological diagnosis after enrollment, or other reasons that make the patient ineligible for treatment.
Treatment efficacy will be determined by performing contrast-enhanced chest-abdomen-pelvis CT and additional CT/MRI of the lesions every 4 weeks on the first four occasions after initiation of the treatment protocol, and every 6 weeks thereafter. After termination of the treatment protocol, physical examination, PS, body weight, CBC, serum biochemistry, and adverse events will be assessed every 6 months. If treatment is terminated for reasons other than progression of the disease, 6-weekly CT examination will be continued until disease progression.
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Publication 2023
Abdomen Asthma Body Height Body Weight Chest Diagnosis Disease Progression Echocardiography Eligibility Determination Heart Hypersensitivity International Normalized Ratio Neoplasms Patients Pelvis Physical Examination Serum Thyrotropin TimeLine Times, Prothrombin Treatment Protocols Urinalysis X-Ray Computed Tomography
Adverse events were assessed according to the Common Terminology Criteria for Adverse Events, version 5.0. All patients were evaluated prior to inclusion with a medical examination by the treating physician. This included spleen palpation (no ultasonography nor computed tomography was performed), blood sample analyses (Hemoglobin, leukocyte differentiation count, platelets, IgG, IgA, IgM, Hematocrit, Bilirubin, Potassium, Sodium, Creatinine, albumin, uric acid, lactate dehydrogenase, Alkaline Phosphatase, Alanine transaminase, amylase, bilirubin, D-dimer, ionized calcium, C-Reactive Protein, Thyrotropin, thyroxin, Luteinizing Hormone, Adrenocorticotropic Hormone, Cortisol, Hepatitis B, hepatitis C (IgG), HIV, HTLV-1(IgG), IgG and IgM for Cytomegalovirus (CMV), Epstein-Barr Virus (EBV) and toxoplasmosis) and an electrocardiogram. According to the treatment plan, patients were evaluated at inclusion, during treatment pause, and at the end of the trial (EOT). At every vaccine treatment, an investigator recorded the patient’s symptoms, and when necessary, conducted a medical examination and evaluation. Bone marrow biopsies were acquired from patients before trial entry and at end of the trial. Histopathological evaluation of nonblinded biopsies was performed by a trained hematopathologist.
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Publication 2023
Alanine Transaminase Albumins Alkaline Phosphatase Amylase Bilirubin Biopsy Blood Platelets Bone Marrow Calcium Corticotropin C Reactive Protein Creatinine Cytomegalovirus Electrocardiography Epstein-Barr Virus fibrin fragment D Hematologic Tests Hemoglobin Hepatitis B Hepatitis C virus Human T-lymphotropic virus 1 Hydrocortisone Lactate Dehydrogenase Leukocyte Count Luteinizing hormone Palpation Patients Physicians Potassium Sodium Spleen Thyrotropin Thyroxine Toxoplasmosis Uric Acid Vaccines Volumes, Packed Erythrocyte X-Ray Computed Tomography

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More about "Thyrotropin"

Thyrotropin, also known as thyroid-stimulating hormone (TSH), is a vital glycoprotein hormone produced by the anterior pituitary gland.
It plays a central role in regulating the function of the thyroid gland, which is responsible for the production of essential thyroid hormones like thyroxine (T4) and triiodothyronine (T3) that are crucial for metabolism, growth, and development.
Thyrotropin stimulates the thyroid gland to secrete these hormones, making it a key regulator of thyroid function.
Disturbances in thyrotropin levels can lead to various thyroid disorders, such as hypothyroidism and hyperthyroidism.
Understanding the mechanisms and regulation of thyrotropin is crucial for the accurate diagnosis and effective management of thyroid-related conditions.
Several analytical platforms, including Cobas e601, ADVIA Centaur XP, Immulite 2000, Cobas 8000, UniCel DxI 800, Cobas 6000, Elecsys 2010, and ARCHITECT i2000, are commonly used to measure thyrotropin levels.
These advanced systems, combined with the latest research insights, enable healthcare professionals to optimize the assessment and treatment of thyroid disorders.
Additinally, the interplay between thyrotropin and other hormones, such as insulin, can also impact thyroid function and overall health.
By leveraging the latest advancements in thyrotropin research and diagnostic technologies, healthcare providers can enhance their ability to identify, monitor, and manage thyroid-related conditions effectively.