bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of cell shape change on the function and differentiation of rabbit mammary cells in culture
Authors: Haeuptle M , Suard YLM , Bogenmann E , Reggio H , Racine L , Kraehenbuhl J 
Published: May 2004

We examined the role of cell shape, cytodifferentiation, and tissue topography on the induction and maintenance of functional differentiation in rabbit mammary cells grown as primary cultures on two-dimensional collagen surfaces or in three-dimensional collagen matrices. Mammary glands from mid-pregnant rabbits were dissociated into single cells, and epithelial cells were enriched by isopycnic centrifugation. Small spheroids of epithelial cells (approximately 50 cells) that formed on a rotary shaker were plated on or embedded in collagen gels. The cells were cultured for 1 d in serum-containing medium and then for up to 25 d in chemically defined medium. In some experiments, epithelial monolayers on gels were mechanically freed from the dishes on day 2 or 5. These gels retracted and formed floating collagen gels. On attached collagen gels, flat monolayers of a single cell type developed within a few days. The cells synthesized DNA until the achievement of confluence but did not accumulate milk proteins. No morphological changes were induced by prolactin (PRL). On floating gels, two cell types appeared in the absence of cell proliferation. The cells in direct contact with the medium became cuboidal and developed intracellular organelles typical of secretory cells. PRL-induced lipogenesis, resulting in large fat droplets filling the apical cytoplasm and accumulation of casein and α-lactalbumin in vesicles surrounding the fat droplets. We detected tranferrin in the presence or absence of PRL intracellularly in small vesicles but also in the collagen matrix in contact with the cell layer. The second cell type, rich in microfilaments and reminiscent of the myoepithelial cells, was situated between the secretory cell layer and the collagen matrix. In embedding gels, the cells formed hollow ductlike structures, which grew continuously in size. Secretory cells formed typical lumina distended by secretory products. We found few microfilament-rich cells in contact with the collagen gels. Storage and secretion of fat, caseins and alpha-lactalbumin required the presence of PRL, whereas the accumulation and vectorial discharge of transferrin was prolactin independent. There was no differentiation gradient between the tip and the cent of the outgrowth, since DNA synthesis and milk protein storage were random along the tubular structures.
These results indicate that establishment of functional polarity and induction of cytodifferentiation are influenced by the nature of the interaction of the cells with the collagen structure. The morphological differentiation in turn plays an important role in the synthesis, storage, and secretion of fat and milk proteins.
Gamma Knife Surgery in Mesial Temporal Lobe Epilepsy: A Prospective Multicenter Study
Authors: Régis Jean , Rey Marc , Bartolomei Fabrice , Vladyka Vilibald , Liscak Roman , Schröttner Oskar , Pendl Gerhard 
Published: May 2004

Summary:  Purpose: This article is the first prospective documentation of the efficacy and safety of gamma knife surgery (GKS) in the treatment of drug‐resistant epilepsies of mesial temporal lobe origin. Methods: From July 1996 to March 2000, three European centers selected 21 patients with mesial temporal lobe epilepsy (MTLE) for a temporal lobectomy. The preoperative investigations included video‐EEG with foramen ovale electrodes, magnetic resonance imaging, neuropsychological testing, and the ESI‐55 quality‐of‐life questionnaire. In place of a cortectomy, radiosurgical treatment was performed by using the Leksell Gamma Knife (LGK) at a dose of 24 ± 1 Gy at the margin. The target included the anterior parahippocampal cortex and the basal and lateral part of the amygdala and anterior hippocampus (head and body). One patient (a heavy smoker) died of a myocardial infarction. Twenty patients were available for prospective evaluation. A minimum 2‐year follow‐up period included clinical, neuropsychological, and radiologic evaluations. Results: At each 6‐month follow‐up evaluation, the frequency of seizures was significantly smaller than that at the previous visit. The median seizure frequency of 6.16 the month before treatment was reduced to 0.33 at 2 years after treatment. At 2 years, 65% of the patients (13 of 20) were seizure free. Five patients had transient side effects, including depression, headache, nausea, vomiting, and imbalance. There was no permanent neurological deficit reported except nine visual field deficits. No neuropsychological deterioration was observed 2 years after treatment. The quality of life was significantly better than that before surgery. Conclusions: The safety and efficacy of the radiosurgical treatment of MTLEs appears good in this group of patient over short‐to‐middle term. Delay of the seizure cessation was the major disadvantage of GKS. A longer follow‐up period is required for confirmation of these results.
Cognitive, Psychosocial, and Family Function One Year after Pediatric Epilepsy Surgery
Authors: Smith Mary Lou , Elliott Irene M. , Lach Lucyna 
Published: May 2004

Summary: Purpose:Assumptions regarding the benefits of seizure control after pediatric epilepsy surgery for cognitive, psychosocial, and family function were explored in a prospective study of 51 children with intractable epilepsy.Methods:Thirty children who underwent surgery were studied before and 1 year after surgery, and a comparison group of 21 children with medically refractory seizures was examined at comparable times.Results:One year after surgery, 57% of the surgical group was seizure free. Seizure status after surgery did not predict change over time in any of the areas measured. Cognitive and psychosocial status did not change over time in either group, and the strongest predictor of individual change in psychosocial status in the surgical group was baseline level of function. Within the surgical group, a trend toward an increase in independence promotion was noted in the family, but the children's satisfaction with the family declined.Conclusions:These findings challenge the assumption that elimination of seizures will result in improved cognitive, psychosocial, and family functioning, at least within the first year after surgery.
The Pathology of Rasmussen Syndrome: Stages of Cortical Involvement and Neuropathological Studies in 45 Hemispherectomies
Authors: Pardo Carlos A. , Vining Eileen P. G. , Guo Liping , Skolasky Richard L. , Carson Benjamin S. , Freeman John M. 
Published: May 2004

Summary:  Purpose: Rasmussen syndrome (RS) is a rare form of epilepsy characterized by progressive destruction of a single hemisphere. To characterize the profile of cortical involvement in RS, we studied the pathological changes in the cerebral cortex of 45 hemispherectomies performed at Johns Hopkins Hospital between 1985 and 2002. Methods: The patterns of pathologic changes and stages of cortical abnormalities were studied by histology and immunocy to chemistry methods. The burden of pathology (BP) was quantified in all brain regions of each of the 45 hemispheres. Results: Our study demonstrated significant heterogeneity in the stages of cortical pathology and the multifocal nature of the disease. These stages varied from early inflammation defined by infiltration of T lymphocytes and neuroglial reactions, to more severe stages with extensive neuronal cell death and cavitation of the cerebral cortex. A greater BP was significantly associated with an early age at onset (p = 0.01) and longer duration of disease (p ≤ 0.001). The BP was similar in all brain regions except the occipital lobe, where the BP was significantly lower (p = 0.032). Conclusions: The multifocal distribution of pathologic changes, as well as the heterogeneity in the stages of cortical damage in each patient, is consistent with an ongoing and progressive immune‐mediated process of neuronal damage that involves neuroglial and lymphocytic responses, resembling other autoimmune CNS disorders such as multiple sclerosis.
Genetic Architecture of Idiopathic Generalized Epilepsy: Clinical Genetic Analysis of 55 Multiplex Families
Authors: Marini Carla , Scheffer Ingrid E. , Crossland Kathryn M. , Grinton Bronwyn E. , Phillips Fiona L. , McMahon Jacinta M. , Turner Samantha J. , Dean Joanne T. , Kivity Sara , Mazarib Aziz , Neufeld Miriam Y. , Korczyn Amos D. , Harkin Louise A. , Dibbens Leanne M. , Wallace Robyn H. , Mulley John C. , Berkovic Samuel F. 
Published: May 2004

Summary:  Purpose: In families with idiopathic generalized epilepsy (IGE), multiple IGE subsyndromes may occur. We performed a genetic study of IGE families to clarify the genetic relation of the IGE subsyndromes and to improve understanding of the mode(s) of inheritance. Methods: Clinical and genealogic data were obtained on probands with IGE and family members with a history of seizures. Families were grouped according to the probands' IGE subsyndrome: childhood absence epilepsy (CAE), juvenile absence epilepsy (JAE), juvenile myoclonic epilepsy (JME), and IGE with tonic–clonic seizures only (IGE‐TCS). The subsyndromes in the relatives were analyzed. Mutations in genes encoding α1 and γ2 γ‐aminobutyric acid (GABA)‐receptor subunits, α1 and β1 sodium channel subunits, and the chloride channel CLC‐2 were sought. Results: Fifty‐five families were studied. 122 (13%) of 937 first‐ and second‐degree relatives had seizures. Phenotypic concordance within families of CAE and JME probands was 28 and 27%, respectively. JAE and IGE‐TCS families had a much lower concordance (10 and 13%), and in the JAE group, 31% of relatives had CAE. JME was rare among affected relatives of CAE and JAE probands and vice versa. Mothers were more frequently affected than fathers. No GABA‐receptor or sodium or chloride channel gene mutations were identified. Conclusions: The clinical genetic analysis of this set of families suggests that CAE and JAE share a close genetic relation, whereas JME is a more distinct entity. Febrile seizures and epilepsy with unclassified tonic–clonic seizures were frequent in affected relatives of all IGE individuals, perhaps representing a nonspecific susceptibility to seizures. A maternal effect also was seen. Our findings are consistent with an oligogenic model of inheritance.
The Relative Impact of Anxiety, Depression, and Clinical Seizure Features on Health‐related Quality of Life in Epilepsy
Authors: Johnson Erica K. , Jones Jana E. , Seidenberg Michael , Hermann Bruce P. 
Published: May 2004

Summary:  Purpose: To determine the independent effects of depression and anxiety on health‐related quality of life (HRQOL) in epilepsy as well as the relative explanatory power of psychiatric comorbidity compared with demographic and clinical epilepsy variables (e.g., seizure frequency, severity, and chronicity). Methods: Subjects (n = 87) with temporal lobe epilepsy completed self‐report measures of depression, anxiety, HRQOL, and seizure severity. Information was derived regarding subjects' seizure frequency, duration, and treatment. HRQOL status (QOLIE‐89) was examined in relation to self‐reported symptoms of anxiety and depression, clinical seizure features, and demographic characteristics. Results: Depression and anxiety were independently associated with reduced HRQOL. Psychiatric comorbidity explained more variance in HRQOL than did combined groups of clinical seizure or demographic variables. Although weaker in explanatory power than psychiatric comorbidity, several epilepsy factors were nonetheless significantly related to HRQOL, including seizure frequency, severity, and chronicity. Conclusions: Interictal anxiety and depression exert independent adverse effects on HRQOL. In addition, frequent, severe, and chronic seizures reduce HRQOL, but appear less powerful predictors of HRQOL than interictal psychiatric symptoms. Recognition and treatment of comorbid depression and anxiety is an important consideration in improving quality of life in epilepsy.
Intracranial EEG in Temporal Lobe Epilepsy: Location of Seizure Onset Relates to Degree of Hippocampal Pathology
Authors: Vossler David G. , Kraemer Diana L. , Haltiner Alan M. , Rostad Steven W. , Kjos Bent O. , Davis Bradley J. , Morgan John D. , Caylor Lisa M. 
Published: May 2004

Summary:  Purpose: To determine whether the specific location of electrographic seizure onset in the temporal lobe is related to hippocampal pathology in temporal lobe epilepsy (TLE). Methods: Consecutive presurgical patients with scalp EEG‐video evidence of TLE and no or mild hippocampal atrophy (HA) on magnetic resonance imaging (MRI) were prospectively studied by using depth and subdural strip electrode recordings to identify the site of the initial ictal discharge (IID). Thirty‐four patients had either no or mild HA (HA– group). Four additional patients with moderate or marked HA (HA+ group) who required depth and strip electrodes served as a comparison group. Hippocampal pathology was assessed by MRI volumetrics and histopathologic grade of sclerosis (HS). Results: Thirty‐eight patients were investigated. In the HA– group, 10 patients had lobar ictal EEG onsets in the hippocampus (HF), medial paleocortex (MPC), and lateral neocortex (LNC); eight cases had regional IIDs in both HF and MPC; 12 persons had IIDs completely outside the HF; three cases lacked depth electrodes, and only one case (3%) had an IID confined to the HF. By contrast, three (75%) of four HA+ cases had IIDs confined to the HF (p = 0.002). Similarly, in 12 patients with low‐grade HS, IIDs confined to the HF area were seen significantly less often than in six cases with high‐grade HS (p = 0.025). Conclusions: In this study of a large number of patients with no to mild and a smaller group with moderate to marked HA and HS, the location of seizure onset in the temporal lobe was related to the degree of hippocampal pathology. Absence of HA and low‐grade HS was each associated with IIDs in both the hippocampus and medial (with or without lateral) temporal cortex, or only the MPC or LNC. Marked HA and high‐grade HS both were associated with IIDs restricted to the HF.
Antimyoclonic Effect of Levetiracetam in 13 Patients with Unverricht–Lundborg Disease: Clinical Observations
Authors: Magaudda Adriana , Gelisse Philippe , Genton Pierre 
Published: May 2004

Summary: Purpose:Disabling myoclonus is the main symptom in long‐standing Unverricht–Lundborg disease (ULD), and levetiracetam (LEV) appears to be an effective anticonvulsant with promising short‐term antimyoclonic properties.Methods:LEV was prescribed to 13 patients with ULD. We retrospectively analyzed the efficacy of LEV on seizure frequency and on myoclonus, by using a simplified myoclonus rating score, and compared the patients' status before LEV and at the last follow‐up. They were two women and 11 men, aged 14 to 52 years (mean, 36.5 years), with a disease duration of 4 to 40 years (mean, 24.3 years). LEV was given at 2,000 to 4,000 mg/d for 0.5 to 26 months (mean, 13.8 months).Results:One patient stopped LEV within 2 weeks because of side effects and lack of efficacy. None of the other 12 patients reported side effects. The average myoclonus score significantly changed from 3.1 to 2.4 (p = 0.01), but only eight had a measurable improvement.Conclusions:The best effects were noted in the younger patients. In patients previously treated with high‐dose piracetam (PIR), discontinuation of PIR was not always well tolerated, and a combination of PIR at lower doses and LEV appeared to be a practical solution. LEV should probably be considered as a major treatment option early in the course of ULD.
Vasoconstriction as the Etiology of Hypercalcemia‐induced Seizures
Authors: Chen Tsung‐Hua , Huang Chih‐Cheng , Chang Yung‐Yee , Chen Ying‐Fa , Chen Wei‐Hsi , Lai Shung‐Lon 
Published: May 2004

Summary:  Purpose: Reversible cerebral vasoconstriction has been hypothesized to be the etiology of seizures due to hypercalcemia, but angiographic studies documenting vasoconstriction have not previously been available. Methods: We present a 43‐year‐old woman who had frequent seizures that later evolved to status epilepticus with marked hypercalcemia at the time of the seizures. Results: Magnetic resonance imaging (MRI) of the patient's brain revealed high signal changes in T2‐weighted imaging, fluorescence‐attenuated inversion recovery (FLAIR), and diffusion‐weighted imaging (DWI) over the bilateral occipital and thalamic areas. Cerebral angiography showed blood vessels narrowing, disappearing altogether over the right posterior cerebral artery (PCA) branch, which is compatible with vasoconstriction. Vasoconstriction caused the MRI high signal in the occipital area, which was associated with subsequent periodic lateralized epileptic discharges. The patient's clinical condition improved with management of seizures and hypercalcemia. A second brain MRI 2 weeks later revealed complete resolution of the high‐signal lesions. Follow‐up cerebral angiography study also showed total recovery of vasoconstriction. Conclusions: The sequence of events suggests the hypothesis that reversible cerebral vasoconstriction may play a role in hypercalcemia‐induced seizures.
Valproate Reduced Synaptic Activity Increase Induced by 4‐Aminopyridine at the Hippocampal CA3‐CA1 Synapse
Authors: Martín and Eduardo D. , Pozo Miguel A. 
Published: May 2004

Summary:  Purpose: We investigated the effects of valproate (VPA) on excitatory synaptic transmission changes induced by 4‐aminopyridine (4‐AP) to determine whether the antiepileptic effects shown by VPA can be ascribed to a modulation of spontaneous excitatory postsynaptic currents (sEPSCs) in the CA3‐CA1 synapse. Methods: Rat hippocampal slices were prepared and maintained in vitro with standard methods. Whole‐cell current and voltage‐clamp recordings were obtained from CA1 pyramidal neurons by using the “blind” patch‐clamp technique in an immersion recording chamber. Increase in the spontaneous excitatory synaptic activity was induced by addition of 4‐AP to the medium. Results: Perfusion with VPA significantly counteracted the increase of frequency and amplitude of the sEPSCs induced by application of 4‐AP and suppressed the epileptiform activity. Conclusions: We conclude that VPA decreases the 4‐AP–induced enhancement of excitatory synaptic activity at the CA3‐CA1 synapse, and that this reduction of excitation input to CA1 contributes to the anticonvulsant effects of VPA.
Does Glucocorticoid Administration Prevent Late Seizures after Head Injury?
Authors: Watson Nathaniel F. , Barber Jason K. , Doherty Michael J. , Miller John W. , Temkin Nancy R. 
Published: May 2004

Summary:  Purpose: Preventing posttraumatic epilepsy has been a difficult challenge. In this study we evaluated the association between glucocorticoid administration after traumatic brain injury (TBI) and posttraumatic seizures. Methods: We examined a seizure‐prevention trial database of 404 patients with severe TBI for exposure to glucocorticoids in the early (<1 week) posttraumatic period. After controlling for seizure risk, we compared the odds of developing first and second late posttraumatic seizures between those that received glucocorticoids and those that did not. Results: Patients dosed with glucocorticoids within 1 day of their TBI were more likely to develop first late seizures than were those without [p = 0.04; hazard ratio = 1.74; 95% confidence interval (CI), 1.01–2.98]; whereas those receiving glucocorticoids ≥2 days after their injury had no similar association (p = 0.66; hazard ratio = 0.77; 95% CI, 0.23–2.56; p = 0.10 among the three groups). Receiving glucocorticoids within 1 day, or ≥2 days after TBI was not associated with second late seizure development. Conclusions: Glucocorticoid treatment after TBI is not associated with decreased late posttraumatic seizures, and early treatment is associated with increased seizure activity.
Does Hyperventilation Elicit Epileptic Seizures?
Authors: Holmes Mark D. , Dewaraja Asanka S. , Vanhatalo Sampsa 
Published: May 2004

Summary:  Purpose: Voluntary hyperventilation has been advocated for many decades as an “activating” procedure to provoke clinical seizures and epileptiform discharges in subjects with suspected epilepsy who undergo standard EEG recordings. This study was undertaken to determine the effects of hyperventilation in patients with proven epilepsy. Methods: We examined the records of 433 consecutive patients with proven epilepsy, as documented by long‐term video‐EEG studies. The patients underwent 5 min of voluntary hyperventilation during standard EEG recordings. All EEGs were interpreted by board‐certified electroencephalographers. The patients ranged in age from 10 to 64 years; 384 (88.7%) had localization‐related and 48 (11.3%) generalized epilepsy syndromes. Results: Hyperventilation was associated with a clinical seizure in two (0.46%) of the subjects (partial seizures in both cases). Interictal epileptiform discharges were interpreted as showing in increase in frequency during hyperventilation in 19 (4.4%) patients, when compared with the baseline EEG. Conclusions: Voluntary hyperventilation in patients with unequivocal epilepsy is rarely associated with either clinical seizures or an increase in frequency of epileptiform discharges.
Prolonged Infusion of Tetrodotoxin Does Not Block Mossy Fiber Sprouting in Pilocarpine‐treated Rats
Authors: Buckmaster Paul S. 
Published: May 2004

Summary:  Purpose: Mossy fiber sprouting is a common abnormality found in patients and models of temporal lobe epilepsy. The role of mossy fiber sprouting in epileptogenesis is unclear, and its blockade would be useful experimentally and perhaps therapeutically. Results from previous attempts to block mossy fiber sprouting have been disappointing or controversial. In some brain regions, prolonged application of the sodium channel blocker tetrodotoxin prevents axon sprouting and posttrauma epileptogenesis. The present study tested the hypothesis that prolonged, focal infusion of tetrodotoxin would block mossy fiber sprouting after an epileptogenic treatment. Methods: Adult rats were treated with pilocarpine to induce status epilepticus. Several hours to 3 days after pilocarpine treatment, a pump with a cannula directed toward the dentate gyrus was implanted to deliver 10 μM tetrodotoxin or vehicle alone at 0.25 μl/h. This method blocks local EEG activity in the hippocampus (Galvan et al. J Neurosci 2000; 20:2904–16). After 28 days of continuous infusion, rats were perfused with fixative, and their hippocampi analyzed anatomically with stereologic techniques. Results: Tetrodotoxin infusion was verified immunocytochemically in tetrodotoxin‐treated but not vehicle‐treated hippocampi. Tetrodotoxin‐infused and vehicle‐infused hippocampi displayed similar levels of hilar neuron loss. The Timm stain revealed mossy fiber sprouting regardless of whether hippocampi were treated with tetrodotoxin infusion, vehicle infusion, or neither. Conclusions: Prolonged infusion of tetrodotoxin did not block mossy fiber sprouting. This finding suggests that sodium channel–mediated neuronal activity is not necessary for mossy fiber sprouting after an epileptogenic treatment.