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Biomedical subjects

R Schiff

Publications and source records attributed to R Schiff.

At least 37 records · Page 2Linked to original sources
PubMed1994

Inhibition of CNS myelin development in vivo by implantation of anti-GalC hybridoma cells.

Implantation of hybridoma cells that secrete a monoclonal antigalactocerebroside into the dorsal columns of < or = 9-day-old rat spinal cord results in failure of development of dorsal column myelin in the vicinity of the implant. Clusters of apparently undamaged amyelinated axons remain among the hybridoma cells. Ventral myelin is unaffected. These in vivo results support antibody-mediated inhibition of myelin formation as a potential mechanism underlying failure of remyelination in multiple sclerosis.

Animals↗
PubMed1993

Myelin formation by mouse glia in myelin-deficient rats treated with cyclosporine.

Previous attempts to generate myelin in the myelin-deficient rat spinal cord by transplanting mouse glia were not successful. In order to determine whether this result was due to graft rejection or to interspecies mismatch of cellular or molecular components at the axoglial junction, we have repeated the experiment in cyclosporine-treated rats. Our results show that in the immunosuppressed hosts, foetal glial xenografts form an abundance of myelin within the dorsal columns at or near the injection site about two weeks after the operation. In some cases, myelination extends virtually across the entire width of the dorsal columns. Ultrastructurally, the myelin sheaths are normal in all respects, including the presence of the 'radial component'. The lateral edges of the myelin lamellae form typical paranodal axoglial junctions, some displaying periodic 'transverse bands'. We infer that previous mouse to rat xenograft failures reflect host immune response rather than mismatch of heterologous junctional components. We also compared foetal, early post-natal and adult xenografts. Foetal donor cells, containing an abundance of precursors but virtually no mature oligodendrocytes, are more effective than neonatal donor cells in forming myelin, and after adult grafts, we found no myelin formation. Thus, in xenografts, as in allografts, foetal precursor cells are far more suitable than glia from mature donors in generating significant amounts of myelin.

Animals↗
PubMed1993

Expression and cellular localization of uterine side-chain cleavage cytochrome P450 messenger ribonucleic acid during early pregnancy in mice.

Very little is known about steroidogenic capacities in the uterus during the early stages of pregnancy in rodents. Cholesterol side-chain cleavage cytochrome P450 (P450scc) is the enzyme catalizing the first and key regulatory reaction controlling the production of steroid hormones. Using a cRNA probe, we made use of in situ hybridization analysis to evaluate the spatial and temporal patterns of P450scc mRNA expression in the mouse uterus until midgestation. Unexpectedly, we found that upon implantation on day 4.5, maternal cells of both decidua capsularis and decidua basalis expressed P450scc mRNA. Only later, and no earlier than day 6.5 of gestation, were high levels of P450scc mRNA also detected in the trophoblast giant cells surrounding the embryonal cavity. Analysis of pseudopregnant mice revealed that the induction of P450scc mRNA can be coupled to the decidual reaction evoked by intrauterine injection of mineral oil. These results, therefore, unambiguously confirmed the capacity of the decidualized cells of maternal origin to express P450scc mRNA and, thus, ruled out any direct role of the blastocyst involvement in P450scc induction. The dual localization of P450scc mRNA in maternal and trophoblast cells, expressing this cytochrome earlier than the previously suspected onset of uterine steroidogenesis, suggests an unexpected role for steroid hormones locally produced at the site of implantation and the surrounding milieu of the embryo during the first half of pregnancy.

Animals↗
PubMed1991

Sonographic abnormalities of the thyroid gland in longterm survivors of Hodgkin disease.

We studied the thyroid gland in 18 long term survivors of Hodgkin Disease, all of whom received radiation therapy (2400-4000 cGy, mean 3434). Evaluation included clinical examination, thyroid function tests, ultrasound, as well as selective use of nuclear scintigraphy. The time interval post radiation was 1-16 years (mean 6.4 years). Clinical evaluation and thyroid function tests were insensitive in detecting abnormalities and most nodules were non palpable. Ultrasound detected abnormalities in 16 patients (89%) including diffuse atrophy (n = 6), solitary nodules (n = 4), multiple nodules (n = 5) and gland heterogeneity with calcification in one patient. Cold nodules on nuclear scintigraphy (n = 4) were subjected to biopsy. Multiple foci of papillary carcinoma were found in one patient. There was a tendency for nodules to increase in number as the post radiation interval also increased. We recommend frequent sonographic evaluation and early suppression of thyroid stimulation in an attempt to arrest the development of neoplastic changes.

Adolescent↗
PubMed1991

Transcriptional activation of mouse retrotransposons in vivo: specific expression in steroidogenic cells in response to trophic hormones.

Transcription of cellular retrotransposons is induced by a variety of physiological stimuli. We have used in situ hybridization analysis to determine the cell types in which mouse retrotransposons are transcriptionally activated in vivo under physiological conditions. Here, we report that VL30 retrotransposons are specifically expressed in steroidogenic cells within all four endocrine tissues engaged in synthesis of steroid hormones in response to the respective pituitary-derived trophic hormones. These tissues include ovarian steroidogenic theca cells and lutein cells of the corpus luteum, testosterone-producing Leydig cells of the testis, steroidogenic cells confined to the zona reticularis of the adrenal cortex, and progesterone-producing cells of the placenta. In the course of preovulatory follicular development and maturation, the profile of cells expressing the retrotransposon shifted in parallel to the changing profiles of the leutinizing hormone (LH)-induced steroidogenic output of the respective cells. Expression of VL30 in both male and female gonads was shown to be greatly stimulated by external administration of gonadotropins. In vitro studies using a LH-responsive Leydig cell line have confirmed that expression of the resident retrotransposons is gonadotropin dependent. Run-off transcription assays have indicated that activation is at the transcriptional level. To allow molecular access to gonadotropin-activated transcription units, the long terminal repeat (LTR) regulatory domains were cloned from VL30 cDNAs of LH-induced ovaries. Through the use of reporter gene constructs and transfection experiments it was shown that expression of these elements in steroidogenic cells is LH dependent. Furthermore, cAMP, a known mediator of trophic hormone responses, could replace the hormone for inducibility. Transfection studies have also shown that the retrotransposon LTRs may function as hormone-activated enhancers conferring a LH-dependent phenotype on a surrogate transcription unit. These studies have thus demonstrated that the transcriptional activation of resident retrotransposons in vivo is a dynamic process that can be modulated by gonadotropins and have the potential of imposing this phenotype on adjacent cellular genes.

Animals↗
PubMed1990

Monozygotic twins with trisomy 18: a report of discordant phenotype.

The predicted incidence of liveborn monozygotic trisomy 18 twins is one per million births. The first case of liveborn monozygotic trisomy 18 twins was reported in 1989 and we report a second case in which striking phenotypic discordance existed. The probability of monozygotic trisomy 18 twinning and the mechanisms for phenotypic discordance in trisomic twins is discussed.

Abnormalities, Multiple↗
PubMed1990

Local regulation within the female reproductive system and upon embryonic implantation: identification of cells expressing proenkephalin A.

The detection of proenkephalin A (PEA) mRNA and encoded peptides in various regions of the female reproductive system raised the possibility that opioid peptides might act as local regulators within this system. Assignment of a specific role for locally synthesized enkephalins has been hampered, however, by the unknown identity of the cells that produce PEA. Using in situ hybridization analysis we have now identified the cell types that express PEA mRNA in the reproductive system of female mice. In the ovary, PEA mRNA was localized primarily in theca cells of preovulatory follicles, and to a lesser extent, in follicular granulosa cells. In the oviducts, where PEA mRNA is most abundant, expression was confined to the secretory and ciliated epithelium of the mucosa. In the uterus, the site of PEA mRNA expression was the deep glandular layer of the endometrium. When pregnancy ensues, and upon decidual transformation, PEA expression by the same uterine cells was dramatically elevated. Elevated levels of PEA mRNA were detected predominantly in the vicinity of the implantation site, suggesting that signaling by the implanted embryo play a role in stimulating PEA expression. Based on these results, possible physiological roles for PEA-encoded peptides as autocrine/paracrine regulators within the female reproductive system are suggested.

Animals↗
PubMed1989

Myelin formation in myelin-deficient rat spinal cord following transplantation of normal fetal spinal cord.

Previous studies of the myelin-deficient rat spinal cord have suggested that astrocytes may play a role in preventing the formation of myelin in this mutant, or causing its breakdown. Comparison of mutant and normal littermate spinal cords shows a marked hypertrophy of astrocytes in the mutant in both gray matter and fiber tract regions. Nevertheless, when normal fetal spinal cord fragments are transplanted into mutant host spinal cord, clusters of normal-looking myelin sheaths develop with no sign of attack by host astrocytes.

Animals↗
PubMed1987

Treatment of adenosine deaminase deficiency with polyethylene glycol-modified adenosine deaminase.

We treated two children who had adenosine deaminase deficiency and severe combined immunodeficiency disease by injecting bovine adenosine deaminase modified by conjugation with polyethylene glycol. The modified enzyme was rapidly absorbed after intramuscular injection and had a half-life in plasma of 48 to 72 hours. Weekly doses of approximately 15 U per kilogram of body weight maintained plasma adenosine deaminase activity at two to three times the level of erythrocyte adenosine deaminase activity in normal subjects. The principal biochemical consequences of adenosine deaminase deficiency were almost completely reversed. In erythrocytes, adenosine nucleotides increased and deoxyadenosine nucleotides decreased to less than 0.5 percent of total adenine nucleotides. The activity of S-adenosylhomocysteine hydrolase, which is inactivated by deoxyadenosine, increased to normal in red cells and nucleated marrow cells. Neither toxic effects nor hypersensitivity reactions were observed. In vitro tests of the cellular immune function of each patient showed marked improvement, along with an increase in circulating T lymphocytes. Clinical improvement was indicated by absence of infection and resumption of weight gain. We conclude that from the standpoints of efficacy, convenience, and safety, polyethylene glycol-modified adenosine deaminase is preferable to red-cell transfusion as a treatment for adenosine deaminase deficiency. Patients with other inherited metabolic diseases in which accumulated metabolites equilibrate with plasma could benefit from treatment with the appropriate polyethylene glycol-modified enzyme.

Adenosine Deaminase↗
PubMed1986

Determination of right ventricular pressure in the presence of a ventricular septal defect using continuous wave Doppler ultrasound.

Continuous wave Doppler ultrasound was employed in 38 patients with ventricular septal defects, many with associated lesions, to measure the velocity (V) of the shunted blood. Using the modified Bernoulli equation (delta P = 4V2) the pressure difference (delta P) between the ventricles was determined. In 22 patients both right ventricular and either left ventricular or ascending aortic pressure were measured at the time shunt velocity was determined. In another 16 patients these measurements were not obtained simultaneously but in most they were done within 24 hours of each other. In the entire group, measured pressure differences between the ventricles (or aorta and right ventricle) ranged from 0 to 97 mm Hg (mean 52 +/- 24). On the basis of velocity measurements the pressure difference ranged from 7 to 112 mm Hg (mean 51 +/- 24). A close correlation was found between the two methods (r = 0.95, SEE = 7.8 mm Hg). This accuracy was not altered by associated lesions. These findings indicate that by the use of continuous wave Doppler interrogation right ventricular pressure can be accurately measured in the presence of a ventricular septal defect.

Adolescent↗
PubMed1986

Ultrastructural localization of laminin in rat sensory ganglia.

We adapted immunocytochemical methods for localization of laminin to examine its disposition in neural tissue at the ultrastructural level. In dorsal root ganglia, laminin was found in basal laminae of the satellite and Schwann cells ensheathing neuronal perikarya and nerve fibers, respectively, and around blood vessels. Within the basal lamina, the immunostain was found in the lamina lucida and lamina densa. Occasional immunostained coated pits were identified in satellite and Schwann cells, but virtually no intracellular label was seen even in freeze-thawed/detergent-permeabilized specimens. In the perineurium, only the basal lamina of the inward-facing surface of the inner-most cell layer was usually stained.

Animals↗