epilepsy/albumin

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Neuronal uptake of serum albumin is associated with neuron damage during the development of epilepsy.

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It is well established that brain blood barrier dysfunction following the onset of seizures may lead to serum albumin extravasation into the brain. However, the effect of albumin extravasation on the development of epilepsy is yet to be fully elucidated. Previous studies have predominantly focused

Kainic acid-induced albumin leak across the blood-brain barrier facilitates epileptiform hyperexcitability in limbic regions.

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Systemic administration of kainic acid (KA) is a widely used procedure utilized to develop a model of temporal lobe epilepsy (TLE). Despite its ability to induce status epilepticus (SE) in vivo, KA applied to in vitro preparations induces only interictal-like activity and/or isolated ictal

Impact of Oxidative Stress and Newer Antiepileptic Drugs on the Albumin and Cortisol Value in Severe Motor and Intellectual Disabilities With Epilepsy.

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UNASSIGNED Epilepsy is a common complication in patients with severe motor and intellectual disabilities (SMID). There are no reports as yet of the effects of these medications in vivo other than their epileptic efficacy. The purpose of this study was to clarify the effects of the newer

Serum albumin-adjusted phenytoin levels: an approach for predicting drug efficacy in patients with epilepsy, suitable for developing countries.

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BACKGROUND The antiepileptic drug phenytoin has a high degree of plasma protein binding. Therefore, total phenytoin levels in plasma are misleading indicators of clinical efficacy. This study was designed to investigate whether serum albumin-adjusted phenytoin levels in Indian patients with epilepsy

Upregulation of D site of albumin promoter binding protein in the brain of patients with intractable epilepsy.

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The mechanisms that underlie the pathogenesis of intractable epilepsy (IE) remain to be elucidated. The present study aimed to investigate the expression of D site of albumin promoter binding protein (DBP) and mitogen‑activated protein kinases (MAPKs) in the temporal lobes of patients with IE, in

Albumin induces excitatory synaptogenesis through astrocytic TGF-β/ALK5 signaling in a model of acquired epilepsy following blood-brain barrier dysfunction.

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Post-injury epilepsy (PIE) is a common complication following brain insults, including ischemic, and traumatic brain injuries. At present, there are no means to identify the patients at risk to develop PIE or to prevent its development. Seizures can occur months or years after the insult, do not

Study on the interaction of the epilepsy drug, zonisamide with human serum albumin (HSA) by spectroscopic and molecular docking techniques.

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In the present investigation, an attempt has been made to study the interaction of zonisamide (ZNS) with the transport protein, human serum albumin (HSA) employing UV-Vis, fluorometric, circular dichroism (CD) and molecular docking techniques. The results indicated that binding of ZNS to HSA caused

Serum phenytoin, phenobarbital, carbamazepine, albumin; and plasma estradiol, progesterone concentrations during the menstrual cycle in women with epilepsy.

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Six menstrual cycles and three 1-month periods were studied in seven patients with epilepsy. The patients all had had anti-epileptic treatment for a long time. In each case, the dosages had been costant for at least 1 month prior to the start of the investigation. Blood samples were taken every

Immunohistochemical localization of extravasated serum albumin in the hippocampus of human subjects with partial and generalized epilepsies and epileptiform convulsions.

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Human serum albumin-like immunoreactivity was detected by the peroxidase-antiperoxidase method in histological sections of the hippocampus from epileptic and control brains obtained on routine autopsies. In the hippocampi of epileptic patients immunoreactive astrocytes were found, the number of

Neurological toxicity after phenytoin infusion in a pediatric patient with epilepsy: influence of CYP2C9, CYP2C19 and ABCB1 genetic polymorphisms.

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Pharmacogenetic studies have shown that genetic defects in drug-metabolizing enzymes encoded by CYP2C9, CYP2C19 genes and by the transporter ABCB1 gene can influence phenytoin (PTH) plasma levels and toxicity. The patient reported here is a 2-year-old girl with a medical history of cryptogenic

Elevated cerebrospinal fluid protein in POLG-related epilepsy: Diagnostic and prognostic implications.

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OBJECTIVE Epilepsy is common in individuals with mutations in POLG, the gene encoding the catalytic subunit of the mitochondrial DNA polymerase gamma. Early recognition and aggressive seizure management are crucial for patient survival. Disruption of the blood-brain barrier (BBB) is implicated in

Issues for mature women with epilepsy.

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Specific concerns regarding mature women with epilepsy (WWE), specifically epilepsy-associated issues during perimenopause, menopause, and postmenopause, have been emerging in the epilepsy community. This chapter presents evidence that for WWE, seizure frequency may increase during perimenopause and

No gender effect on binding characteristics of phenytoin to serum proteins in monotherapy for adult patients with epilepsy.

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The aim of the present study was to determine the gender-related binding characteristics of phenytoin (PHT) to serum proteins in adult patients with epilepsy. Serum samples examined in the study were obtained from 80 adult patients (40 men and 40 women) with epilepsy on PHT monotherapy. Their age

Reproductive endocrine considerations and hormonal therapy for men with epilepsy.

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Androgen deficiency is unusually common among men with epilepsy. It may contribute to reproductive and sexual dysfunction and possibly exacerbate seizure frequency. The most important androgen is testosterone. it exists in the serum in a free form or bound to albumin or sex hormone-binding globulin

Plasma magnesium and calcium levels in children with epilepsy in lagos.

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BACKGROUND Magnesium and calcium have been found to have increasing roles in the patho-physiology of epilepsy. Hypomagnesaemia and hypocalcaemia cause hyper-exitability of neurons and have been associated strongly with seizures in adults and children. OBJECTIVE To determine if hypomagnesaemia or

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