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H D Pomeranz

Publications and source records attributed to H D Pomeranz.

16 recordsLinked to original sources
PubMed2000

Palinopsia and polyopia in the absence of drugs or cerebral disease.

OBJECTIVE: To report the occurrence of palinopsia and polyopia in patients who neither used drugs nor had diseases of the cerebral hemispheres, a group in which these visual symptoms have not been reported. METHOD: The patient records in the database of an academic neuro-ophthalmology unit were reviewed. RESULTS: Seventeen patients were identified in the database with the diagnosis of palinopsia or polyopia, of whom eight had diseases of the cerebral hemispheres, leaving nine patients for analysis. No patients with a history of drug toxicity were identified. In one patient the symptoms presented during an initial episode of demyelinative optic neuritis in the absence of clinical or laboratory evidence of cerebral lesions. In another patient they developed immediately after laser treatment of diabetic macular edema. A third patient developed the symptoms in association with visual loss from Leber's hereditary optic neuropathy. The other six patients were healthy individuals. CONCLUSION: Palinopsia and related visual symptoms can occur in otherwise healthy individuals and in patients with disease apparently confined to the eye or the optic nerve.

Adult↗
PubMed1998

Radiation-associated cerebral blindness.

PURPOSE: To report a case of blindness caused by a white-matter injury after whole brain irradiation for metastatic renal cell carcinoma. METHODS: Case report. We performed comprehensive serial neuro-ophthalmologic examinations. RESULTS: Four to 5 months after resection of renal cell metastasis in the left occipital cortex, interleukin-2 therapy, and whole brain irradiation with 3,000 cGy plus a 1,500-cGy boost to the posterior third of the brain, the patient developed a progressive decline in visual acuity in both eyes to hand motions. Magnetic resonance imaging disclosed signal abnormalities without mass effect in the white matter of the parietal and occipital lobes bilaterally, including the optic radiations. CONCLUSION: This case is a unique example of cortical blindness secondary to radiation injury in the occipital lobes and optic radiations.

Blindness↗
PubMed1993

Neural crest-derived cells isolated from the gut by immunoselection develop neuronal and glial phenotypes when cultured on laminin.

The neural crest-derived cells that colonize the bowel are different from their predecessors in the premigratory crest. A procedure, which utilized the immunoselection of cells with a magnet, was thus devised to obtain crest-derived precursors from developing gut. Primary antibodies against cell surface antigens, NC-1 in chick, quail, and rat, or antibodies to a 110-kDa laminin binding protein (alpha-110) in mouse, were used in conjunction with secondary antibodies coupled to magnetic beads. Immediately after immunoselection with NC-1, almost all of the selected cells were NC-1-immunoreactive. Neurons and glia, identified immunocytochemically with antibodies to specific markers, developed preferentially in cultures of immunoselected cells. Some of the phenotypes expressed by neurons arising in vitro were appropriate for the bowel (serotonin- and vasoactive intestinal peptide-immunoreactive); however, catecholaminergic neurons, which are not present in the enteric nervous system, also differentiated in the cultures. Neuronal development, as well as neurite outgrowth, were promoted by laminin. Cells selected with alpha-110 from the fetal murine bowel preferentially gave rise in vitro to neurons and glia. These data suggest that the population of crest-derived cells that colonizes the gut is multipotent, that development of catecholaminergic neurons in situ is prevented by the intact enteric microenvironment, that laminin is important in the formation of enteric ganglia, and that the 110-kDa laminin binding protein is expressed on the surfaces of the immediate precursors of enteric neurons and glia.

Animals↗
PubMed1991

Expression of a neurally related laminin binding protein by neural crest-derived cells that colonize the gut: relationship to the formation of enteric ganglia.

In order to give rise to the enteric nervous system (ENS), cells migrating from the neural crest must find the bowel and cease migrating at appropriate locations within the gut. Previous studies of the development of the ENS in a mutant mouse have led to the hypothesis that laminin in the enteric mesenchyme may act as a signal to crest-derived cells to cease migrating and extend neurites (or glial processes). Implied in this hypothesis is the idea that crest-derived cells, as a prelude to their participation in ganglion formation, acquire a neurally related laminin receptor, which they do not express at pre-enteric stages of migration. As a partial test of this hypothesis, single and double label immunocytochemistry at light and electron microscopic (EM) levels were used to study the expression of cell surface laminin binding proteins by crest-derived cells in the process of migrating to or within the developing chick gut. Two antibodies (called 3070 and alpha-110) raised against neuronal cell surface laminin binding proteins were employed for this purpose. Laminin binding protein immunoreactivity was found to be expressed within the bowel and ganglion of Remak by a subset of crest-derived cells (identified immunocytochemically with NC-1/HNK-1 antibodies) and by all of those developing as neurons (identified immunocytochemically with antibodies to neurofilament-associated proteins). Laminin binding protein immunoreactivity was also found to be expressed in fixed neural structures elsewhere in the embryos, including cranial and spinal roots, nerves, and ganglia. In contrast, laminin binding protein immunoreactivity was not expressed by migrating crest-derived cells in the vicinity of the vagal or sacral regions of the neuraxis (from which the precursors of the ENS take origin); nor was it expressed by juxta-pharyngeal vagal crest-derived cells migrating to the foregut through the caudal branchial arches or by the caudal stream of sacral crest-derived cells approaching the hindgut. EM immunocytochemistry confirmed that laminin binding protein immunoreactivity in the bowel was located on the surfaces of crest-derived cells, and was exhibited both by those cells that could only be distinguished from their neighbors by their NC-1/HNK-1 immunoreactivity and by cells developing as neurons or glia. EM immunocytochemistry also revealed that the surfaces of crest-derived cells migrating through the enteric mesenchyme were contacted by many small osmiophilic "puffs" of laminin-immunoreactive extracellular material. These puffs coincided in location with membrane sites that expressed the immunoreactivity of the laminin binding protein. These observations are consistent with the hypothesis that laminin plays a role in the formation of enteric ganglia.

Animals↗
PubMed1991

Colonization of the post-umbilical bowel by cells derived from the sacral neural crest: direct tracing of cell migration using an intercalating probe and a replication-deficient retrovirus.

Experiments were done to test the hypothesis that the avian gut is colonized by cells derived from both vagal and sacral regions of the neural crest. A fluorescent dye, diI (1,1-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate), and a replication-deficient retrovirus (LZ10; Galileo et al. 1990) were employed as tracers. Since LZ10 was constructed with lacZ of E. coli as a reporter gene, infected cells were identified by demonstrating beta-galactosidase immunoreactivity. DiI and LZ10 were injected between the neural tube and surface ectoderm (before the migration of crest cells away from the injection sites) at vagal, truncal (diI only), or sacral axial levels. The bowel was examined 4 days later in order to allow crest-derived cells sufficient time to migrate to the gut. Following injections of either tracer into the vagal crest, labelled cells were found in the gizzard and duodenum. When diI or LZ10 was injected into the sacral crest, labelled cells were seen in the post-umbilical bowel and ganglion of Remak. In the hindgut, marked cells were concentrated in the mesenchyme, just internal to the serosa, and were never observed rostral to the umbilicus. No fluorescent cells were ever found in the bowel following truncal injections of diI, although such cells were observed in sympathetic ganglia. Labelled cells were always found in dorsal root ganglia, no matter which tracer or level of the crest was injected. In embryos injected with LZ10, infected cells in the gut and dorsal root ganglia displayed a neural crest marker (NC-1 immunoreactivity). These observations confirm that the gut is colonized by cells from the sacral as well as the vagal region of the neural crest and that the emigrés from the sacral crest are confined to the post-umbilical bowel.

Animals↗
PubMed1990

Distribution of laminin in the murine pituitary.

The distribution and cellular localization of the glycoprotein laminin were investigated by light and electron microscopic immunocytochemistry in the adult murine pituitary gland. Immunoblots confirmed that laminin was the only protein in the pituitary gland of the adult male mouse to react with antilaminin serum. Laminin immunoreactivity was demonstrated at the light microscopic level simultaneously with that of beta-follicle stimulating hormone (beta-FSH) and beta-luteinizing hormone (beta-LH). In addition to its distribution is basal laminae, laminin immunoreactivity was coincidently expressed in gonadotrophs with the immunoreactivities of beta-FSH and beta-LH. Electron microscopic immunocytochemistry was employed on aldehyde-fixed sections embedded in L.R. White. Sites of binding of primary antisera to laminin were identified with affinity-purified secondary antisera directly coupled to 20 nm particles of colloidal gold. Three antisera recognizing laminin were compared and found to result in an identical pattern of immunoreactivity. Laminin was found extracellularly only in formed basal laminae in all three lobes of the pituitary and was not found in extracellular matrices of connective tissue. Laminin immunoreactivity was also found intracellularly in gonadotrophs but in none of the other endocrine or non-endocrine cells of the anterior lobe. Within gonadotrophs, only secretory granules were labeled. The majority, but not all, secretory granules were labeled in each of the gonadotrophs examined, and the proportion of granules labeled with laminin could not be increased by doubling the concentration of anti-laminin serum. Laminin immunoreactivity segregated with the subset of secretory granules containing beta-FSH. In contrast, laminin immunoreactivity was absent in the smaller subset of secretory granules that contain serotonin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Colonization of the avian hindgut by cells derived from the sacral neural crest.

Studies were done to test the hypothesis that the chick hindgut is colonized by emigrés from the sacral region of the neural crest. Crest-derived cells were identified immunocytochemically with the monoclonal antibody, NC-1, and by their ability to give rise to neurons or glia in the bowel. Neurons were recognized by demonstrating acetylcholinesterase activity, neurofilament immunoreactivity, or the immunoreactivity of a neurofilament-associated protein, NAPA-73, with a monoclonal antibody, E/C8. The visualization of glial fibrillary acidic protein immunoreactivity was employed to detect enteric glia. Separate rostral and caudal populations of NC-1-immunoreactive cells were detected in stage 21 embryos (Day E3.5) that extended in continuous streams from the sacral crest to the hindgut. The rostral group, coexpressed neural markers, while the caudal population did not. The rostral, dually labeled cells appeared to become embedded in the mesenchyme of the dorsal bowel by Day E4 and then to enter the mesentery by Day E5 to give rise to the ganglion of Remak. The caudal NC-1-immunoreactive group, which did not express neural markers, appeared to ascend within the colorectum and, in contrast to the rostral cells, fully encircled the gut. NC-1-immunoreactive neurons and glia developed in organotypic tissue cultures and chorioallantoic membrane grafts of both dorsal and ventral halves of the postumbilical bowel explanted at Days E4 and 5, ages known to precede the colonization of the hindgut by cells from the vagal crest. These observations are consistent with the view that NC-1-immunoreactive cells, which do not express neural markers, migrate from the sacral crest to the hindgut. A subset of these cells appears to be capable of giving rise to neurons in vitro, explaining the development of neurons in the explants of the ventral halves of the gut; however, the fate of the sacral crest-derived cells in situ remains to be established.

Acetylcholinesterase↗
PubMed1988

Accumulation of components of basal laminae: association with the failure of neural crest cells to colonize the presumptive aganglionic bowel of ls/ls mutant mice.

Aganglionosis occurs in the terminal colon of the ls/ls mouse because an intrinsic defect of the presumptive aganglionic tissue prevents the entry and colonization of this portion of the bowel by migrating neural crest cells. The current study was undertaken to determine if abnormalities of the extracellular matrix could be identified in this segment that might account for migratory failure. Since basal laminae of the muscularis mucosa are overproduced in the aganglionic segment of adult ls/ls mice, we examined components of basal laminae in fetal gut from Day E 11 to Day E 16 of gestation. This period spans the time of enteric ganglion formation. Laminin and collagen type IV were studied by immunocytochemistry and proteoglycans by staining glycosaminoglycans with Alcian blue. Abnormalities of each of these components occur during development of the presumptive aganglionic bowel in the ls/ls mouse and could be detected as early as Day E 11. These defects consist mainly of an overabundance of these materials, both in defined basal laminae and throughout the extracellular space of the mesenchyme. Electron microscopic observations in the presumptive aganglionic ls/ls colon revealed a thickening of basal laminae and exceptionally wide intercellular spaces between smooth muscle myoblasts that contained an irregular fibrillar material, consisting of 4.5- to 6.0-nm filaments associated with 14- to 20-nm granules. Fibrillar and flocculant material was continuous with formed basal laminae, and was concentrated in the same areas found to have an overabundance of laminin immunoreactivity. These observations indicate that there is an accumulation of extracellular matrix material, including components of basal laminae, that (i) precedes the formation of enteric ganglia, (ii) is in the path through which enteric neural precursors from the crest would have to migrate, and (iii) is limited to the aganglionic and hypoganglionic ls/ls bowel. These data are consistent with the hypothesis that components of basal laminae contribute to the inability of crest cells to colonize the terminal bowel of ls/ls mice.

Animals↗
PubMed1987

Origin and morphology of nerve fibers in the aganglionic colon of the lethal spotted (ls/ls) mutant mouse.

The lethal spotted mutant mouse (ls/ls) develops congenital megacolon because of the absence of ganglia in the terminal colon. This aganglionosis results from a failure of neural crest cells to colonize this area during fetal life. We have postulated that the microenvironment of the aganglionic segment of bowel is abnormal. Our hypothesis suggests that this abnormal enteric microenvironment fosters the sprouting of neuritic processes. We further propose that neural and glial precursors cease to migrate once they have extended their definitive processes. As a result, the area distal to the site where neurite extension is favored does not become colonized by neural or glial precursors. A prediction of this hypothesis is that the aganglionic tissue should be innervated by axons from neurons located both in the more proximal ganglionated bowel and in ganglia located outside the gut. Neurons and their processes in control and ls/ls terminal gut were located by the histochemical demonstration of acetylcholinesterase (AChE) activity and their structure was classified as intrinsic (enteric) or extrinsic in type by electron microscopy. In ls/ls mice the submucosal plexus was much more severely affected than the myenteric plexus. No submucosal ganglia were found within 30 mm of the anus. In contrast, myenteric ganglia extended to within 4 mm of the anus on the mesenteric side of the gut and to within 15 mm on the antimesenteric side. Rostral to the areas that were absolutely aganglionic, both plexuses were hypoganglionic, especially the submucosal plexus, which was hypoganglionic throughout the entire colon. Both the aganglionic and caudal hypoganglionic zones of the ls/ls bowel were penetrated by large nerve trunks that had the ultrastructural characteristics of extra-enteric peripheral nerve. Unusual ganglia, outside the enteric musculature in the adventitia of the colon, were connected to these trunks. The location of the cell bodies of origin of the nerve fibers in the terminal colon of control mice and in the aganglionic segment of the bowel in ls/ls mice was determined by following the retrograde transport of tracers injected as close as possible to the anus. An extrinsic innervation originating from the inferior mesenteric ganglion and dorsal root ganglia (L6-S1) was found in both types of animal. In control but not ls/ls mice retrograde labeling was also observed in the sacral parasympathetic nucleus of the spinal cord. In addition, neuritic processes were traced to neurons in myenteric ganglia. In control mice, these labeled neurons were present in ganglia within the injection site as well as in bowel rostral and caudal to it.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic Fibers↗