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Biomedical subjects

L Jacobson

Publications and source records attributed to L Jacobson.

At least 73 records · Page 4Linked to original sources
PubMed1998

Excising the reexcision: stereotactic core-needle biopsy decreases need for reexcision of breast cancer.

There is debate regarding use of the stereotactic core-needle biopsy (SCNB) for highly suspicious mammographic lesions. This study compares a serial group of mammography-detected breast cancer patients treated before and after the use of SCNB. We studied 113 consecutive nonpalpable breast cancers between 1994 and 1996. Altogether 47 patients were diagnosed by wire-localized breast biopsy (wire group) and the next 66 consecutive breast cancer patients by SCNB (stereo group). Negative margins were found more often in the stereo group than in the wire group (77% vs. 38%, p < 0.001). Reexcision was required more frequently in the wire group than in the stereo group (68% vs. 21%, p < 0.001), and one-staged surgical procedures were done more often in the stereo group than the wire group (79% vs. 21%, p < 0.001). The volume of the initial wide excision was much larger in the stereo group than in the wire group (p = 0.002). Those in the wire group required 50% more operations per patient (1.8 vs. 1.2) than the stereo group. A significant cost savings can be estimated in the stereo group compared with the wire group. The use of SCNB was associated with breast excisions of larger volume, negative margins, and decreased need for reexcision. Simultaneous adjunct procedures resulted in one-stage operations, improving cost savings. The use of SCNB for nonpalpable breast cancer benefits the patient, the surgeon, and the payor. It should be undertaken prior to the first surgical procedure.

Biopsy, Needle↗
PubMed1998

Periventricular leukomalacia causes visual impairment in preterm children. A study on the aetiologies of visual impairment in a population-based group of preterm children born 1989-95 in the county of Värmland, Sweden.

PURPOSE: To determine the causes of visual impairment in a population-based group of visually impaired preterm children. METHODS: Ophthalmological examination and magnetic resonance imaging or computed tomography of the brain were performed in all visually impaired preterm children born 1989-95 in Värmland. RESULTS: Ten of 18 children had periventricular leukomalacia affecting the optic radiation, six had other lesions or malformations in the posterior visual pathways/cortex, but no child had visually impairing retinopathy of prematurity. CONCLUSION: We conclude that cerebral lesions or malformations are common causes of the visual functional deficit in visually impaired children born preterm. Brain damage should be suspected in a prematurely born child who presents with either of the signs: fixation difficulties, strabismus or nystagmus.

Adult↗
PubMed1998

Children with blindness due to retinopathy of prematurity: a population-based study. Perinatal data, neurological and ophthalmological outcome.

A population-based group of 27 children with total blindness due to retinopathy of prematurity (ROP), born in Sweden from 1980 to 1990, was examined. They constituted all but two of the total of 29 children with total blindness due to ROP known to the national register of visually impaired children when reviewed from 1980 to 1 January 1995. All children had a gestational age of less than 31 weeks and most had had a complicated perinatal period. The retinal disease was discovered late, most often after it had already progressed to bilateral retinal detachment. Repeated vitreoretinal surgery had been performed in most children, but postoperative visual function did not improve. Three-quarters of the group had major neurological impairment (mental retardation, cerebral palsy, or epilepsy) at age 4 to 14 years. There was an impression that extensive ophthalmological efforts delayed neurodevelopmental assessments and examinations as well as adequate habilitation.

Adolescent↗
PubMed1998

Nystagmus in periventricular leucomalacia.

BACKGROUND/AIMS: Periventricular leucomalacia (PVL) is a lesion in the immature brain involving the optic radiation. Children with PVL have visual problems including crowding, visual field defects, strabismus, and visual perceptual/cognitive deficits, together with nystagmus. They often have optic nerve hypoplasia seen either as small discs or as large cupping of normal sized optic discs. This study aimed to perform eye movement recordings in a group of children with PVL in order to characterise and classify the nystagmus. METHODS: 19 children with PVL on cerebral imaging underwent eye movement recordings with the Ober-2 infrared reflection technique. RESULTS: 16 of the 19 subjects had horizontal nystagmus. CONCLUSION: The present study shows that nystagmus is commonly seen in children with PVL.

Adolescent↗
PubMed1998

Relation between blindness due to retinopathy of prematurity and autistic spectrum disorders: a population-based study.

Children with blindness due to retinopathy of prematurity (ROP)--who are at greatly increased risk of cerebral damage--have been noted to have a high rate of autistic symptoms, but systematic controlled studies have been lacking. A controlled population-based study was performed; one group was blind due to ROP (N=27) and the other was congenitally blind due to hereditary retinal disease (N=14). Fifteen of the 27 children with ROP had autistic disorder. All these children were mentally retarded and about one-third of them had cerebral palsy. In the comparison group, two of the 14 children had autistic disorder. It is concluded that there is a strong association between ROP and autistic disorder. The association is most probably mediated by brain damage and is largely independent of the blindness per se.

Adolescent↗
PubMed1998

The role of dual energy x-ray absorptiometry in aiding the diagnosis of pediatric osteogenesis imperfecta.

The role of dual energy x-ray absorptiometry (DEXA) in the evaluation of the pediatric patient with multiple fractures has not been well established. We retrospectively examined the medical records of 45 patients who had presented to our institution with multiple fractures of unknown cause, who were not known to have osteogenesis imperfecta, and who had obtained DEXA as part of their evaluation. Of these, 26 patients had sufficient clinical data for inclusion in this study. Patients underwent DEXA of the anteroposterior spine and whole body. A z score was calculated to normalize the DEXA values for age. The diagnosis of osteogenesis imperfecta was correlated with the outcome of each DEXA scan to assess the validity of DEXA as a diagnostic tool. The DEXA of the anteroposterior spine had the highest sensitivity at 91.7%, while DEXA of the whole body had the highest specificity at 100.0%. Decreased bone mineral density may be associated with osteogenesis imperfecta, and DEXA is helpful in detecting low bone mineral density that may be missed on plain radiographs of children with milder forms of osteogenesis imperfecta.

Absorptiometry, Photon↗
PubMed1997

Impaired diurnal adrenal rhythmicity restored by constant infusion of corticotropin-releasing hormone in corticotropin-releasing hormone-deficient mice.

The normal pattern of daily glucocorticoid production in mammals requires circadian modulation of hypothalamicpituitary-adrenal axis activity. To assess both the factors responsible for imparting this diurnal profile and its physiologic importance, we have exploited corticotropin-releasing hormone (CRH)-deficient mice generated by homologous recombination in embryonic stem cells. CRH-deficient mice have lost normal circadian variations in plasma ACTH and glucocorticoid while maintaining normal circadian locomotor activity. Constant peripheral infusion of CRH produced marked diurnal excursions of plasma glucocorticoid, indicating that CRH acts in part as a permissive factor for other circadian modulators of adrenocortical activity. The presence of atrophic adrenals in CRH-deficient mice without an overt deficit in basal plasma ACTH concentration suggests that the diurnal increase in ACTH is essential to maintain normal adrenal function.

Adrenal Cortex↗
PubMed1997

Large cups in normal-sized optic discs: a variant of optic nerve hypoplasia in children with periventricular leukomalacia.

OBJECTIVE: To evaluate optic disc morphologic features in children with periventricular leukomalacia (PVL). PATIENTS AND METHODS: Seventeen children with PVL (patient group) were compared with 17 sex- and age-matched, full-term healthy control children (control group). Clinical ophthalmological examination and digital image analysis of fundus photographs were performed in all children. In children with PVL, cerebral imaging was performed. RESULTS: Children with PVL had larger optic disc cupping (P<.02) than did control children. A large proportion of the children with PVL had strabismus, nystagmus, and restricted visual fields. CONCLUSION: Our study indicates that optic nerve hypoplasia in children with PVL is often associated with a normal-sized optic disc with a large cup. This unusual form of optic nerve hypoplasia most likely results from transsynaptic degeneration of optic axons caused by the primary bilateral lesion in the optic radiation.

Adolescent↗
PubMed1997

Identification of phospholipase A2 and neurotoxic activities in the venom of the New Guinean small-eyed snake (Micropechis ikaheka).

The Papua New Guinean small-eyed snake (Micropechis ikaheka) is recognised as a cause of life-threatening envenoming in certain parts of New Guinea. The clinical features suggest the presence of toxins acting at the neuromuscular junction and on muscle. We have used the mouse phrenic nerve hemidiaphragm preparation, a phospholipase A2 assay, and 125I-neurotoxin-binding radioimmunoassays to look for toxic activities in the crude venom and in preliminary high-performance liquid chromatography (HPLC) fractions. Micropechis ikaheka venom at 1 and 3 micrograms/ml completely abolished nerve-evoked muscle twitch within 70 min at 37 degrees C. There was also a sustained contracture of the muscle and some reduction in twitch tension evoked by direct stimulation; these were explained by the presence of phospholipase A2 activity. The venom inhibited the binding of 125I-alpha-bungaro-toxin to detergent-extracted human muscle acetylcholine receptor (AChR), and inhibited acetylcholine receptor function in a muscle cell line. It also inhibited binding of 125I-omega-conotoxin GVIA to detergent-extracted human frontal cortex voltage-gated calcium channels, but this appeared to be dependent on the phospholipase A2 activity. Identification of the main neurotoxic fractions following HPLC are shown.

Animals↗
PubMed1997

Utrophin abundance is reduced at neuromuscular junctions of patients with both inherited and acquired acetylcholine receptor deficiencies.

Congenital myasthenic syndromes are a heterogeneous group of conditions in which muscle weakness resulting from impaired neuromuscular transmission is often present from infancy. One form of congenital myasthenic syndrome is due to a reduction of the number of acetylcholine receptors (AChRs) at the neuromuscular junction. We describe four new cases of AChR deficiency, characterized by a reduction in both miniature endplate potential amplitude and AChR abundance accompanied by elongation of the neuromuscular junction and some decrease in postsynaptic folding. A number of cytoplasmic proteins are normally associated with the postsynaptic membrane and may contribute to the clustering of AChRs at the neuromuscular junction. We therefore investigated the expression of several of these proteins in these AChR-deficiency patients. In each patient, immunolabelling of the neuromuscular junction for rapsyn, dystrophin, beta-dystroglycan and a form of beta-spectrin was strong but that for utrophin was markedly reduced or absent. This suggested that a defect in utrophin expression might underlie the congenital AChR deficiency. However, a reduction in utrophin labelling was also seen in three patients with adult acquired autoimmune myasthenia gravis in whom AChR loss results directly from the extracellular binding of autoantibodies. We conclude that the loss of AChRs in AChR deficiency does not result from the absence of rapsyn or beta-dystroglycan and that reduction of utrophin is probably secondary to the loss of AChRs. The possible role of AChRs and/or utrophin in determining the extent of postsynaptic folding is discussed.

Action Potentials↗
PubMed1997

Diverse Fab specific for acetylcholine receptor epitopes from a myasthenia gravis thymus combinatorial library.

The muscle weakness in myasthenia gravis (MG) is caused by heterogeneous high-affinity IgG autoantibodies to the nicotinic acetylcholine receptor (AChR), a complex ion channel glycoprotein. These antibodies are clearly responsible for reducing AChR numbers at the neuromuscular junction in myasthenia; however, the origins, diversity, specificity and pathogenicity of individual antibodies have not yet been established. We have cloned and characterized four different AChR-specific Fab from an MG patient's thymus by screening an IgG1/kappa gene combinatorial lambda phage library with soluble human AChR labeled with [125I] alpha-bungarotoxin. Unlike most previously cloned human antibodies, all four Fab immunoprecipitated soluble human muscle AChR. Two Fab strongly inhibited binding of mAb to the main immunogenic region on the alpha subunits and one Fab bound to an epitope on the fetal-specific gamma subunit. In sensitivity and fine specificity, these Fab resembled the anti-AChR antibodies found in many MG patients, including the donor. The closest germline counterparts for their heavy chains were in VH families 1, 3 and 4; however, there were many differences consistent with an antigen-driven response of diverse B cell clones. The combinatorial approach holds promise for further analysis of human autoantibodies.

Adult↗
PubMed1997

Prescription opiate abuse in chronic pain patients: clinical criteria, incidence, and predictors.

OBJECTIVES: Opiates are commonly used to treat patients with chronic nonmalignant pain. There is much controversy over the definition, incidence, and risk factors of prescription opiate abuse in chronic pain treatment. The present study, done at the Seattle VA Medical Center, was designed to create opiate abuse criteria, test inter-rater reliability of the criteria, apply the criteria to a group of chronic pain patients, and correlate the risk of opiate abuse with the results of alcohol and drug testing. DESIGN/OUTCOME MEASURES: A committee of experienced pain providers designed a five-point prescription opiate abuse checklist based on DSM-III-R parameters. The criteria were then applied to patients enrolled in the pain clinic. The reliability of the criteria were determined using two providers who were familiar with every patient in the clinic. Drug, alcohol, and psychosocial testing were correlated with the risk of opiate abuse. RESULTS: A total of 19% (76/403) of all pain clinic patients were using chronic opiates. Thirty-four percent (26/76) met one, and 27.6% (21/76) met three or more of the abuse criteria. The criteria had an inter-rater reliability of > 0.9. There were no differences between chronic opiate users (n = 76) and opiate abusers (n = 21) for a history of drug or alcohol abuse or on psychosocial testing. CONCLUSIONS: Prescription opiate abuse criteria for use in patients with chronic nonmalignant pain were designed. The criteria had good reliability and can be applied during normal clinic interactions. The percentage of chronic opiate users who become opiate abusers in pain treatment is within the range reported by others. Past opiate or alcohol abuse or psychosocial testing on clinic admission failed to predict who would become an opiate abuser. The criteria can be used to identify patients who will subsequently require more intensive treatment or intervention or can be used as an outcome to measure to test the effectiveness of treatment strategies.

Adult↗
PubMed1997

Protein malnutrition increases plasma adrenocorticotropin and anterior pituitary proopiomelanocortin messenger ribonucleic acid in the rat.

The mechanism by which protein malnutrition increases circulating glucocorticoids is unclear. To determine whether ACTH synthesis and secretion also increase in protein malnutrition, rats were sham adrenalectomized or adrenalectomized and replaced with varying amounts of corticosterone before dietary protein deprivation. Pair-fed rats served as controls for reduced voluntary food intake in protein-deprived rats. Dietary protein deficiency, but not pair-feeding, increased resting plasma corticosterone in sham-adrenalectomized rats. Restraint-induced ACTH secretion was not inhibited by the increased basal corticosterone levels in protein-deficient rats. When increases in corticosterone were eliminated by adrenalectomy or controlled by adrenalectomy with low level corticosterone replacement, increases in resting plasma ACTH and anterior pituitary POMC messenger RNA expression occurred with protein deprivation that could be statistically discriminated by regression analysis from changes due to caloric restriction (pair-feeding) and overt glucocorticoid feedback resistance. We conclude that protein malnutrition increases pituitary-adrenocortical activity at least in part by specifically increasing the drive for ACTH synthesis and secretion.

Adrenocorticotropic Hormone↗