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Biomedical subjects

Y Shapira

Publications and source records attributed to Y Shapira.

At least 127 records · Page 7Linked to original sources
PubMed1995

Simultaneous formation of inv dup(15) and dup(15q) in a girl with developmental delay: origin of the abnormal chromosomes.

Two de novo abnormal derivatives of chromosome 15, inv dup(15) and dup(15q) were found in a girl with developmental delay and mild dysmorphological signs. Fluorescence in situ hybridization, using DNA probes of the Prader-Willi/Angelman syndromes (PWS/AS) critical region and chromosome-15-specific alpha-satellite, combined with molecular analysis using dinucleotide repeat polymorphisms within the PWS/AS region and the parent-of-origin specific methylation sites at the locus D15S63, shed light on how the abnormal karyotype was formed. We suggest that a translocation between the two homologues of maternal chromosomes 15 resulted in the formation of dup(15q) and two reciprocal products: an acentric fragment of 15q that was lost and a centric fragment that underwent U-type reunion to form inv dup(15).

Angelman Syndrome↗
PubMed1995

A model for global symmetry detection in dense images.

In this paper, a model is proposed for bilateral symmetry detection in images consisting of dense arrangements of local features. The model is elaborated on the basis of a psychophysical experiment showing that grouping precedes and facilitates symmetry detection. The proposed computational model consists of three stages: a grouping stage, a symmetry-detection stage, and a symmetry-subsumption stage. Reliance upon a preliminary grouping stage enables a significant reduction of the computational load for detecting symmetry. An implementation of the model is described, and results are presented, showing a good agreement of the model performance with human symmetry perception.

Computer Simulation↗
PubMed1995

A case report. Bilateral transmigration of impacted mandibular canines.

Case reports have described displacement and migration of teeth in the upper and lower dental arches, but migration of a tooth across the mandibular midline is rare. The authors describe an extremely rare case of bilateral transmigration of impacted permanent canines across the midline of the mandible.

Adolescent↗
PubMed1995

Brain edema and neurological status with rapid infusion of lactated Ringer's or 5% dextrose solution following head trauma.

Rapid infusion of 0.25 ml/g of 0.9% saline over 30 minutes has been shown to have no effect on electrolyte balance, neurological severity score (NSS), or brain edema, following closed head trauma (CHT). Rapid infusion of the same volume of 5% dextrose solution decreased blood sodium concentration, increased edema, and decreased NSS following CHT. In the present study the authors examined the effect of rapid infusion (30 minutes) of smaller volumes of 5% dextrose (0.08 ml/g and 0.16 ml/g) and of 0.25 ml/g lactated Ringer's solution on blood electrolyte concentrations, plasma osmolality, brain edema, and NSS. The purposes of this study were to determine whether rapid infusion of a large volume of lactated Ringer's solution could be given after CHT without increasing mortality or brain edema or producing electrolyte disturbances, and whether small volumes of 5% dextrose could be infused with few or none of the deleterious effects expected from large volumes of 5% dextrose. One hundred eighteen rats, which survived halothane anesthesia and CHT, were randomly assigned to one of 15 experimental groups. Fluids were administered beginning 1 hour after scalp incision or CHT. The NSS, extent of edema, blood electrolyte concentrations, and plasma osmolality in the groups treated with lactated Ringer's solution were not significantly different from those values in the nontreated groups. In addition, the mortality rate after CHT was not increased by administration of lactated Ringer's solution. The groups treated with 5% dextrose solution showed a significantly higher mortality rate, but the NSSs of the surviving rats were not different from controls. None of the groups treated with 0.16 ml/g 5% dextrose solution survived 24 hours. Although blood glucose concentration increased to 1126 +/- 102 g% (mean +/- standard deviation) and 1568 +/- 283 g% and blood sodium concentration decreased to 110.4 +/- 4.6 mEq/L and 92.0 +/- 5.2 mEq/L in the groups treated with 0.08 ml/g and 0.16 ml/g of 5% dextrose solution, respectively, plasma osmolality was normal and no significant difference could be found between the brain tissue specific gravity of animals in the nontreated and 5% dextrose treatment groups. It is concluded that in the CHT model used in this study, the large volume of lactated Ringer's solution did not affect blood electrolyte concentration, neurological outcome, or formation of brain edema, whereas smaller volumes of 5% dextrose solution increased blood glucose and decreased blood sodium concentrations, did not affect plasma osmolality, and had a deleterious effect on neurological outcome.

Animals↗
PubMed1995

MELAS syndrome: peripheral neuropathy and cytochrome C-oxidase deficiency: a case report and review of the literature.

A 4-year-old boy presented with developmental delay, aggressive behavior, and incoordination. His EEG showed a diffuse encephalopathy. At age 10 he developed convulsions and severe migraine-like headaches. Muscle wasting, arreflexia, and lactic acidemia following exercise were noted. Electromyography was myopathic and nerve conduction studies revealed a peripheral neuropathy. Muscle biopsy demonstrated variation in fiber size and an excess of lipid droplets. He than had several stroke-like episodes and periods of unconsciousness, associated with severe metabolic acidosis. Muscle cytochrome C oxidase was abnormally low. This boy displayed the classical clinical and biochemical features of MELAS syndrome, namely Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes. Treatment included carnitine, vitamin C, vitamin K, riboflavin, coenzyme Q10, and corticosteroids. He died at the age of 14 years following an episode of seizures, coma, and gastrointestinal hemorrhage. This is the first reported case of MELAS syndrome in Israel.

Child, Preschool↗
PubMed1994

Computerized respiratory muscle training in children with Duchenne muscular dystrophy.

The present study describes the use of simple video games for a 5-week regimen of respiratory muscle training in 15 patients with Duchenne muscular dystrophy (DMD) at various stages of the disease. The games were re-arranged to be operated and driven by the respiratory efforts of the patient and to incorporate accurate ventilation and time measurements. Improvement in respiratory performance was determined by maximum voluntary ventilation (MVV), maximal achieved ventilation (VEmax) during a progressive isocapnic hyperventilation manoeuvre (PIHV) and the PIHV duration. The actual training period was 23 +/- 4 days (mean +/- S.D.) at ventilatory effort of 46 +/- 6% MVV, for 10 +/- 3 min day-1. Patients with moderate impairment of lung function tests (LFT) showed an improvement in MVV, VEmax, and duration of PIHV of 12 +/- 7% (p < 0.02), 53 +/- 25% (p < 0.001) 57 +/- 21% (p < 0.01), respectively. Improvements correlated with actual training time and ventilation level, %MVV, but negatively correlated with years of immobilization and with the initial MVV. We conclude that computerized respiratory games may be applied for breathing exercises and may improve respiratory performance in recently immobilized children with DMD who have moderate impairment of LFT.

Adolescent↗
PubMed1994

Therapeutic time window and dose response of the beneficial effects of ketamine in experimental head injury.

BACKGROUND AND PURPOSE: The aim of this study was to determine the time and dose response of the therapeutic effects of the N-methyl-D-aspartate receptor antagonist ketamine in experimental head injury. METHODS: Sixty-six male Sprague-Dawley rats were divided into eight groups. Groups A, B, and C were surgically prepared but received no trauma. Groups D through H received a nonpenetrating impact to the left cranium. Group A (n = 7) received no treatment. Groups B (n = 4) and C (n = 5) received 60 and 120 mg/kg IP ketamine, respectively. Group D (n = 8) received no treatment. Groups E (n = 8) and F (n = 7) received 120 and 180 mg/kg IP ketamine, respectively, 1 hour after head trauma. Groups G (n = 7) and H (n = 9) were treated with 180 mg/kg IP ketamine 2 and 4 hours after head trauma, respectively. Neurological severity score (NSS, 0 through 25 from no injury to severe injury) was determined at 1, 24, and 48 hours after head trauma. After death at 48 hours, cortical slices were taken adjacent to the lesion on the traumatized hemisphere and from comparable sites in the contralateral hemisphere for determination of tissue specific gravity and water content. Brains were then placed in 4% formaldehyde, and the volume of hemorrhagic necrosis was measured 4 days later. NSS was compared within and between groups using the Kruskal-Wallis test for repeated measurements and Mann-Whitney U test for post hoc testing. Water content, specific gravity, and hemorrhagic necrosis were compared within and between groups using two-way ANOVA followed by Fisher's protected least significant difference procedure. A value of P < .05 was considered statistically significant. RESULTS: Head trauma alone increased NSS, decreased specific gravity, increased water content, and caused cerebral infarction in the injured hemisphere. Ketamine given in two time-dose regimens, 180 mg/kg IP at 2 hours (group G) and 120 mg/kg IP at 1 hour (group F) after trauma, improved NSS from 11.6 +/- 1.7 and 14.4 +/- 0.8 at 1 hour to 4.4 +/- 1.3 and 8.0 +/- 1.4 (mean +/- SEM) at 48 hours, respectively (P < .03). Compared with the untreated group (group D), 180 mg/kg IP ketamine given at 2 and 4 hours after head trauma decreased the volume of hemorrhagic necrosis from 37.1 +/- 9.5 mm3 to 10.1 +/- 3.8 and 15.3 +/- 3.6 mm3, respectively (P < .05). Brain tissue specific gravity and water content at 48 hours were not significantly different between treated and untreated groups. There was no difference in rectal and temporalis muscle temperature between groups. CONCLUSIONS: We conclude that 180 mg/kg IP ketamine was effective in ameliorating neurological dysfunction after head trauma in rats when the administration time was delayed for 1 hour to 2 hours but not after 4 hours. When given at 1 hour after head trauma, ketamine at 120 mg/kg but not 60 mg/kg is effective in reducing neurological damage after head trauma.

Analysis of Variance↗
PubMed1994

Effect of mannitol on cerebrospinal fluid dynamics and brain tissue edema.

Mannitol is used widely to decrease intracranial pressure (ICP); however, the mechanism by which this effect occurs is unclear. This study was designed to examine the effects of mannitol on cerebrospinal fluid (CSF) formation rate (Vf), resistance to reabsorption of CSF (Ra), and brain tissue water content (BTWC). Eighteen New Zealand White rabbits were allocated into one of three groups and studied at baseline and at two sequential doses of 20% mannitol: 0.75 g/kg followed by 4.4 mg.kg-1.min-1, and 2.0 g/kg (1.25 g/kg added to the initial dose of 0.75 g/kg) followed by 8.6 mg.kg-1.min-1. In Group 1, closed ventriculocisternal perfusion (VCP) was performed to determine changes in ICP due to mannitol. In Group 2, the increase in CSF osmolality due to mannitol was determined. In Group 3, mock CSF was used for open VCP to determine Vf and Ra. At the conclusion of each study, brain tissue samples were taken for determination of BTWC. Mannitol increased CSF and plasma osmolality. Ra was increased by 104% with the low dose of mannitol and not significantly changed by the high dose. Mannitol decreased BTWC, Vf (by 49% with the high dose), ICP, and hematocrit. The authors conclude that two of the mechanisms contributing to decreased ICP with mannitol are: 1) decreased CSF volume as indicated by decreased Vf, and 2) decreased brain tissue volume as indicated by decreased BTWC.

Animals↗