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Biomedical subjects

B Meyerson

Publications and source records attributed to B Meyerson.

At least 37 records · Page 2Linked to original sources
PubMed1992

Isolation of a hemoglobin-derived opioid peptide from cerebrospinal fluid of patients with cerebrovascular bleedings.

The hemorphins are peptides with opioid activity, which are enzymatically released from hemoglobin. A decapeptide identical to the sequence 32-41 of the beta-, delta-, gamma- or epsilon-chains of hemoglobin has been isolated from human ventricular cerebrospinal fluid (CSF). The peptide, designated LVV-hemorphin-7, was recovered in relatively high amounts (115-300 pmol per ml) from samples of patients with cerebrovascular bleedings, but was not detectable in control CSF. Its identity with the hemoglobin fragment was confirmed by mass spectrometry and gas-phase sequencing.

Amino Acid Sequence↗
PubMed1991

[Spinal cord stimulation in chronic neuropathic pain].

Seventeen years' experience of spinal cord stimulation in the treatment of chronic pain has shown it to be effective only in the case of neuropathic pain--in particular, pain due to lesions in peripheral nerves or posterior roots. In such cases, pharmacological treatment is often unsuccessful, and transcutaneous electrical nerve stimulation is only useful in certain cases. In a retrospective study of 84 patients followed for up to 16 years, 56 patients were still using their stimulators and reported continued pain relief. The majority suffered from peripheral neuralgia due to trauma or surgery and 72 per cent in that group enjoyed satisfactory relief. Trial stimulation via a temporary extension lead for at least 4-5 days is a prerequisite of good long-term results. It is concluded that spinal cord stimulation is an indispensable tool for treating chronic neuropathic pain, and it merits to be used more frequently.

Adult↗
PubMed1991

Intraputaminal infusion of nerve growth factor to support adrenal medullary autografts in Parkinson's disease. One-year follow-up of first clinical trial.

Experimental studies in rodents show that beta-nerve growth factor can increase the survival, neurite outgrowth, and functional effect of grafts of adrenal chromaffin cells to the basal ganglia. We, therefore, have begun to investigate whether treatment with nerve growth factor might also increase the functional effect of autografts of adrenal medullary tissue in patients with Parkinson's disease. Previous studies have shown that stereotactic implantation of adrenal tissue pieces produces a transient functional improvement that lasts for a few months. This report describes a trial of grafting of adrenal chromaffin tissue into the putamen, supported by infusion of nerve growth factor. The patient is a 63-year-old woman with a 19-year history of Parkinson's disease, now complicated by on-off phenomena and drug-induced hyperkinesia, despite optimized medical management. The left adrenal gland was removed, and the medulla was dissected into 1- to 2-mm3 pieces in a solution containing nerve growth factor purified from mouse submandibular gland. Pieces were implanted in six tracts 3 to 4 mm from a previously placed cannula in the left putamen. Through the cannula, nerve growth factor was infused for 23 days for a total dose of 3.3 mg. Clinical assessment consisted of global ratings for rigidity and/or hypokinesia and for drug-induced hyperkinesia. Measures of gait and fine-motor control were also made. The motor readiness potential and auditory evoked potentials were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1991

Functional changes in GABAA receptor stimulation during the oestrous cycle of the rat.

1. Slices of rat cuneate nucleus were used to study whether or not gonadal steroids influence the gamma-aminobutyric acid (GABA) system in vivo. Females in different stages of the oestrous cycle as well as steroid-treated (oestrogen, progesterone or both) ovariectomized animals were used. 2. Functional changes in the GABAA receptors were assayed using the effects of potentiators (benzodiazepine, barbiturate) and antagonists (picrotoxin) on the muscimol control dose-response curves. 3. The potentiating effect of the benzodiazepine, flurazepam was unchanged during the oestrous cycle, and the hormone treatments did not alter this effect. 4. During oestrus, an increase was seen in the potentiating effect of the barbiturate (pentobarbitone). This suggests a synergistic effect between barbiturates and gonadal steroids. Progesterone treatment also increased the effect of pentobarbitone. 5. The antagonistic action of picrotoxin was unaffected during the oestrous cycle. However, progesterone (or progesterone and oestrogen) treatment reduced the potency of picrotoxin. 6. This study supports the idea that endogenous steroids (presumably progesterone) affect the GABAA receptors during the oestrous cycle by a mechanism associated with the barbiturate site of the GABAA receptor complex.

Animals↗
PubMed1991

Behavioral effects of an intrauterine or neonatal diabetic environment in the rat.

Maternal diabetes during pregnancy may cause lasting effects on the psychoneurological development in the offspring. The aim of the present study was to investigate possible effects of an intrauterine or neonatal exposure to a diabetic environment on behavior during infancy and adulthood. On days 4 and 6 of age, offspring of streptozotocin-diabetic rats emitted higher numbers of ultrasound calls compared to control offspring. Neonatally streptozotocin-treated rats explored their environment by diminished sniffing and rearing intensity compared to control rats. However, in adult life neither of these rat groups displayed behavioral differences compared to their respective control group. The results suggest that development of basic behavioral patterns in the rat proceed almost normally despite exposure to a diabetic environment in the early embryonic period or in early infancy.

Animals↗
PubMed1987

Oestrogen induced suppression of collagen arthritis: I. Long term oestradiol treatment of DBA/1 mice reduces severity and incidence of arthritis and decreases the anti type II collagen immune response.

Experimental animal models can be used to help understand how oestrogen modulates autoimmune arthritis. We have previously shown that castration of female DBA/1 mice exaggerates arthritis induced with type II collagen. This report shows that treatment of castrated DBA/1 mice with low doses (0.2 micrograms twice a week) of beta-oestradiol reduces the incidence (37% vs 78% in controls) and severity (3.9 vs 5.6 mean scores) of arthritis. Levels of IgG anti type II collagen antibodies are decreased whereas levels of IgM antibodies are increased in the beta-oestradiol treated mice. The T cell response, as measured by a 3H-thymidine assay, is reduced in the beta-oestradiol treated mice. The results suggest that treatment with low doses of beta-oestradiol exerts a suppressive effect on both development of collagen arthritis as well as T cell dependent immune reactivity towards type II collagen.

Animals↗
PubMed1983

Postmortem changes in binding to the muscarinic receptor from human cerebral cortex.

The effects of storage at 4 degrees C on the antagonist and agonist binding properties of the muscarinic acetylcholine receptor from fresh surgical and frozen autopsy samples from human cerebral cortex were studied. The number of L-[3H]3-quinuclidinyl benzilate binding sites and their affinities were stable up to 51 h, both when stored as pieces of intact nonfrozen tissue and as a homogenate. The agonist binding properties as measured by the ability of the muscarinic agonist carbachol to compete with L-[3H]3-quinuclidinyl benzilate were also stable up to 51 h when the tissue was stored in the form of pieces. The affinity for carbachol decreased when the tissue was stored as a homogenate. The frozen autopsy samples showed no significant differences in binding properties in comparison with fresh neurosurgical tissue.

Aged↗
PubMed1982

Pre- and postsynaptic muscarinic receptors in surgical samples from human cerebral cortex.

The present study was carried out using fresh surgical material from human cerebral cortex of patients who were not medicated with atropine or other drugs known to affect the cholinergic system. The concentration of [3H]L-quinuclidinyl benzilate binding sites was 0.45 /+- 0.05 pmol/mg protein and the Kd-value of the receptor-[3H]L-QNB-complex was 0.038 /+- 0.005 nM. Agonist binding was studied by varying the concentration of carbamylcholine (10(-8) to 10(-2) M) in the presence of a constant concentration (0.2nM) of [3H]L-quinuclidinyl benzilate. The data revealed the existence of two populations of binding sites for carbamylcholine with different affinities and capacities. Presynaptic muscarinic receptors were studied in slices of the cerebral cortex, which were loaded with [3H]choline. The muscarinic antagonist, atropine (10(-6) and 10(-7) M) acting at the presynaptic muscarinic receptors enhanced the release of [3H] acetylcholine. It was also shown that muscarinic stimulation leads to elevation of cyclic GMP levels in the human cerebral cortical slices.

Acetylcholine↗