scholarly journals The Absence of Information about Hormones and Absence

2005 ◽  
Vol 5 (3) ◽  
pp. 101-103 ◽  
Author(s):  
Helen E. Scharfman
Keyword(s):  
Receptor Antagonist ◽  
Estrous Cycle ◽  
Hormonal Regulation ◽  
Time Course ◽  
Synthesis Inhibitor ◽  
Absence Seizures ◽  
Protein Levels ◽  
Time Course Study ◽  
Atypical Absence ◽  
Pharmacologic Study

Hormonal Regulation of Absence Seizures Persad V, Ting Wong CG, Cortez MA, Wang YT, Snead OC 3rd Ann Neurol 2004;44:353–361 A time course study that examined the effects of the female estrous cycle on the chronic slow spike-and-wave discharges (SSWDs), GABAB-receptor (GABABR) binding, and GABABR protein expression was conducted in Long-Evans hooded rats treated during development with a cholesterol synthesis inhibitor AY9944 (AY). In addition, a pharmacologic study using the hormones progesterone, 17 β-estradiol, mifepristone (intracellular progesterone-receptor antagonist), tamoxifen (intracellular estrogen-receptor antagonist), and allopregnanolone (progesterone metabolite) was performed to determine their effects on AY-induced seizures. The data indicate that a significant increase occurs in both the duration of SSWDs and GABABR binding in the AY model during the proestrus stage of the estrous cycle, the stage during which the levels of progesterone are at their highest. No changes in GABABR1a or R2 protein levels were observed. In addition, the administration of both progesterone and allopregnanolone exacerbated seizures in the AY model, whereas 17 β-estradiol attenuated the SSWD duration. Neither mifepristone nor tamoxifen blocked the effects of progesterone and 17 β-estradiol, respectively, on SSWD duration in the AY model, suggesting that these two sex hormones are working in a manner independent of their intracellular receptors. These data suggest an important role for steroid hormones in the regulation and maintenance of AY-induced atypical absence seizures.

scholarly journals Urine Annexin A1 as an Index for Glomerular Injury in Patients

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Shuk-Man Ka ◽  
Pei-Yi Tsai ◽  
Tai-Kuang Chao ◽  
Shun-Min Yang ◽  
Yi-Jen Hung ◽  
...  
Keyword(s):  
Time Course ◽  
Minimal Change Disease ◽  
Annexin A1 ◽  
Glomerular Injury ◽  
Protein Levels ◽  
Outcome Monitoring ◽  
Potential Biomarker ◽  
Time Course Study ◽  
Prognostic Prediction ◽  
Urine Levels

Background.We recently demonstrated high urine levels of annexin A1 (ANXA1) protein in a mouse Adriamycin-induced glomerulopathy (ADG) model.Objective.To establish ANXA1 as a potential biomarker for glomerular injury in patients.Methods.A time-course study in the mouse ADG model, followed by renal tissues and urine samples from patients with various types of glomerular disorders for ANXA1.Results.Urinary ANXA1 protein was (1) detectable in both the ADG model and in patients except those with minimal change disease (MCD); (2) positively correlated with renal lesions in patients; and (3) early detectable in diabetes patients with normoalbuminuria.Conclusions.ANXA1 is a universal biomarker that is helpful in the early diagnosis, prognostic prediction, and outcome monitoring of glomerular injury. Measurement of urinary ANXA1 protein levels can help in differentiating MCD from other types of glomerular disorders.

Hormonal regulation of atypical absence seizures

2004 ◽  
Vol 55 (3) ◽  
pp. 353-361 ◽  
Author(s):  
Vasan Persad ◽  
C. Guin Ting Wong ◽  
Miguel A. Cortez ◽  
Yu Tian Wang ◽  
O. Carter Snead
Keyword(s):  
Hormonal Regulation ◽  
Absence Seizures ◽  
Atypical Absence

Time course study of blood pressure in children over a three-year period. Bogalusa Heart Study

Hypertension ◽  
1980 ◽  
Vol 2 (4) ◽  
pp. 102-108 ◽  
Author(s):  
A. W. Voors ◽  
L. S. Webber ◽  
G. S. Berenson
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Bogalusa Heart Study ◽  
Heart Study ◽  
Time Course Study

scholarly journals 5-HT1A Serotonergic, α-Adrenergic and Opioidergic Receptors Mediate the Analgesic Efficacy of Vortioxetine in Mice

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3242
Author(s):  
Nazlı Turan Yücel ◽  
Ümmühan Kandemir ◽  
Ümide Demir Özkay ◽  
Özgür Devrim Can
Keyword(s):  
Analgesic Activity ◽  
Time Course ◽  
Motor Coordination ◽  
Antidepressant Drug ◽  
Area Under The Curve ◽  
Analgesic Efficacy ◽  
Synthesis Inhibitor ◽  
Tail Immersion ◽  
Adrenoceptor Blocker ◽  
The Central Nervous System

Vortioxetine is a multimodal antidepressant drug that affects several brain neurochemicals and has the potential to induce various pharmacological effects on the central nervous system. Therefore, we investigated the centrally mediated analgesic efficacy of this drug and the mechanisms underlying this effect. Analgesic activity of vortioxetine (5, 10 and 20 mg/kg, p.o.) was examined by tail-clip, tail-immersion and hot-plate tests. Motor performance of animals was evaluated using Rota-rod device. Time course measurements (30–180 min) showed that vortioxetine (10 and 20 mg/kg) administrations significantly increased the response latency, percent maximum possible effect and area under the curve values in all of the nociceptive tests. These data pointed out the analgesic effect of vortioxetine on central pathways carrying acute thermal and mechanical nociceptive stimuli. Vortioxetine did not alter the motor coordination of mice indicating that the analgesic activity of this drug was specific. In mechanistic studies, pre-treatments with p-chlorophenylalanine (serotonin-synthesis inhibitor), NAN-190 (serotonin 5-HT1A receptor antagonist), α-methyl-para-tyrosine (catecholamine-synthesis inhibitor), phentolamine (non-selective α-adrenoceptor blocker), and naloxone (non-selective opioid receptor blocker) antagonised the vortioxetine-induced analgesia. Obtained findings indicated that vortioxetine-induced analgesia is mediated by 5-HT1A serotonergic, α-adrenergic and opioidergic receptors, and contributions of central serotonergic and catecholaminergic neurotransmissions are critical for this effect.

scholarly journals Glutathione Deficiency during Early Postnatal Development Causes Schizophrenia-Like Symptoms and a Reduction in BDNF Levels in the Cortex and Hippocampus of Adult Sprague–Dawley Rats

2021 ◽  
Vol 22 (12) ◽  
pp. 6171
Author(s):  
Marta Anna Lech ◽  
Monika Leśkiewicz ◽  
Kinga Kamińska ◽  
Zofia Rogóż ◽  
Elżbieta Lorenc-Koci
Keyword(s):  
Postnatal Development ◽  
Time Course ◽  
Postnatal Life ◽  
Positive Symptoms ◽  
Gbr 12909 ◽  
Sprague Dawley ◽  
Bdnf Mrna ◽  
Synthesis Inhibitor ◽  
Early Postnatal Development ◽  
Middle Adolescence

Growing body of evidence points to dysregulation of redox status in the brain as an important factor in the pathogenesis of schizophrenia. The aim of our study was to evaluate the effects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and 1-[2-Bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl)piperazine dihydrochloride (GBR 12909), a dopamine reuptake inhibitor, given alone or in combination, to Sprague–Dawley pups during early postnatal development (p5–p16), on the time course of the onset of schizophrenia-like behaviors, and on the expression of brain-derived neurotrophic factor (BDNF) mRNA and its protein in the prefrontal cortex (PFC) and hippocampus (HIP) during adulthood. BSO administered alone decreased the levels of BDNF mRNA and its protein both in the PFC and HIP. Treatment with the combination of BSO + GBR 12909 also decreased BDNF mRNA and its protein in the PFC, but in the HIP, only the level of BDNF protein was decreased. Schizophrenia-like behaviors in rats were assessed at three time points of adolescence (p30, p42–p44, p60–p62) and in early adulthood (p90–p92) using the social interaction test, novel object recognition test, and open field test. Social and cognitive deficits first appeared in the middle adolescence stage and continued to occur into adulthood, both in rats treated with BSO alone or with the BSO + GBR 12909 combination. Behavior corresponding to positive symptoms in humans occurred in the middle adolescence period, only in rats treated with BSO + GBR 12909. Only in the latter group, amphetamine exacerbated the existing positive symptoms in adulthood. Our data show that rats receiving the BSO + GBR 12909 combination in the early postnatal life reproduced virtually all symptoms observed in patients with schizophrenia and, therefore, can be considered a valuable neurodevelopmental model of this disease.

scholarly journals Chronic Stress-Induced Changes in Pro-Inflammatory Cytokines and Spinal Glia Markers in the Rat: A Time Course Study

2012 ◽  
Vol 19 (6) ◽  
pp. 367-376 ◽  
Author(s):  
Viktoriya Golovatscka ◽  
Helena Ennes ◽  
Emeran A. Mayer ◽  
Sylvie Bradesi
Keyword(s):  
Chronic Stress ◽  
Inflammatory Cytokines ◽  
Time Course ◽  
Time Course Study ◽  
Induced Changes ◽  
Pro Inflammatory Cytokines

scholarly journals The hormonal regulation of enzymes in prenatal and postnatal rat liver. Effects of adenosine 3′,5′-(cyclic)-monophosphate

1969 ◽  
Vol 115 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Olga Greengard
Keyword(s):  
Growth Hormone ◽  
Hormonal Regulation ◽  
Time Course ◽  
Tyrosine Aminotransferase ◽  
Cyclic Monophosphate ◽  
Sequential Development ◽  
Foetal Liver ◽  
Old Rats ◽  
Postnatal Rats ◽  
Do So

1. The administration of glucagon, cAMP [adenosine 3′,5′-(cyclic)-monophosphate], BcAMP [6-N-2′-O-dibutyryladenosine 3′,5′-(cyclic)-monophosphate] or adrenaline to foetal rats during the last 2 days of gestation evoked the appearance of tyrosine aminotransferase and enhanced the accumulation of glucose 6-phosphatase in the liver. In foetuses 1–2 days younger only BcAMP was effective. After birth liver glucose 6-phosphatase no longer responds to glucagon or BcAMP. Tyrosine aminotransferase is still inducible by these agents in 2-day-old rats, but not in 50-day-old rats. After adrenalectomy of adults glucagon or BcAMP can enhance the induction of the enzyme by hydrocortisone. The results indicate that the ability to synthesize tyrosine aminotransferase and glucose 6-phosphatase when exposed to cAMP develops sooner than the ability to respond to glucagon with an increase in the concentration of cAMP; the responsiveness of enzymes to different hormones changes with age. A scheme illustrating the sequential development of competence in regulating the level of an enzyme is presented. 2. Actinomycin inhibited the effects of glucagon and BcAMP on liver tyrosine aminotransferase and glucose 6-phosphatase in foetal rats. Growth hormone, insulin and hydrocortisone did not enhance the formation of these enzymes. 3. The time-course of accumulation of glucose 6-phosphatase in the kidney is different from that in the liver. Hormones that increase the accumulation in foetal liver do not do so in the kidney of the same foetus or in the livers of postnatal rats.

Loss of Insulin Resistance after Roux-en-Y Gastric Bypass Surgery: a Time Course Study

2005 ◽  
Vol 15 (4) ◽  
pp. 474-481 ◽  
Author(s):  
Kusal Wickremesekera ◽  
Geoff Miller ◽  
Tissa DeSilva Naotunne ◽  
Graham Knowles ◽  
Richard S. Stubbs
Keyword(s):  
Insulin Resistance ◽  
Gastric Bypass ◽  
Time Course ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Time Course Study

scholarly journals Central Insulin Signaling Is Attenuated by Long-Term Insulin Exposure via Insulin Receptor Substrate-1 Serine Phosphorylation, Proteasomal Degradation, and Lysosomal Insulin Receptor Degradation

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 75-84 ◽  
Author(s):  
Christopher M. Mayer ◽  
Denise D. Belsham
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Insulin Signaling ◽  
Time Course ◽  
Proteasomal Degradation ◽  
Serine Phosphorylation ◽  
Neuronal Function ◽  
Protein Levels ◽  
Phosphorylated Akt

Abstract Central insulin signaling is critical for the prevention of insulin resistance. Hyperinsulinemia contributes to insulin resistance, but it is not yet clear whether neurons are subject to cellular insulin resistance. We used an immortalized, hypothalamic, clonal cell line, mHypoE-46, which exemplifies neuronal function and expresses the components of the insulin signaling pathway, to determine how hyperinsulinemia modifies neuronal function. Western blot analysis indicated that prolonged insulin treatment of mHypoE-46 cells attenuated insulin signaling through phospho-Akt. To understand the mechanisms involved, time-course analysis was performed. Insulin exposure for 4 and 8 h phosphorylated Akt and p70-S6 kinase (S6K1), whereas 8 and 24 h treatment decreased insulin receptor (IR) and IR substrate 1 (IRS-1) protein levels. Insulin phosphorylation of S6K1 correlated with IRS-1 ser1101 phosphorylation and the mTOR-S6K1 pathway inhibitor rapamycin prevented IRS-1 serine phosphorylation. The proteasomal inhibitor epoxomicin and the lysosomal pathway inhibitor 3-methyladenine prevented the degradation of IRS-1 and IR by insulin, respectively, and pretreatment with rapamycin, epoxomicin, or 3-methyladenine prevented attenuation of insulin signaling by long-term insulin exposure. Thus, a sustained elevation of insulin levels diminishes neuronal insulin signaling through mTOR-S6K1-mediated IRS-1 serine phosphorylation, proteasomal degradation of IRS-1 and lysosomal degradation of the IR.

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