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Biomedical subjects

D G Gardner

Publications and source records attributed to D G Gardner.

At least 109 records · Page 6Linked to original sources
PubMed1989

Expression of the atrial natriuretic peptide gene in human fetal heart.

Expression of the human atrial natriuretic peptide (hANP) gene was examined in tissues of 19 to 28-week-old human fetuses. As expected the fetal atria express the hANP gene at a high level, accruing substantial quantities of ANP immunoreactivity and ANP mRNA. The neonatal ventricle also expresses the hANP gene at a significant level. ANP mRNA levels in the ventricle were, on the average, about 20% of those in the right atria. ANP immunoreactivity in ventricle was less that 5% of that in the right atria, suggesting important differences in the way these tissues synthesize and store the ANP peptide. Much lower levels of hANP transcripts were also detected in the lung and aortic arch. Analysis of the 5' termini of cardiac hANP transcripts using three independent techniques suggests the presence of two transcription start sites. A major start site is located approximately 28 basepairs downstream from the primary TATA sequence. A second minor start site is positioned about 110 basepairs further upstream. Immunocytochemistry and in situ hybridization analysis indicate that the hANP gene is expressed in a homogeneous distribution throughout the atrial myocardium. Diffuse low level expression is also present within the ventricular myocardium. In addition, there are scattered foci of increased expression in the ventricle which tend to be concentrated in the subendocardium of that organ. These findings indicate that the developing human ventricles as well as the atria possess the capacity to express the hANP gene at a substantial level and suggest that the ventricle may contribute significantly to the circulating pool of plasma ANP.

Atrial Natriuretic Factor↗
PubMed1988

Upstream sequences confer atrial-specific expression on the human atrial natriuretic factor gene.

5'-Flanking sequences from the human atrial natriuretic factor (hANF) gene were subcloned into a reporter plasmid (pSVOCAT) and transfected into primary cultures of neonatal rat atrial cardiocytes. Hybrid hANFCAT genes containing either 2500 or 409 base pairs of 5'-flanking sequence DNA were expressed at similar levels. When sequences between -409 and -332 were deleted, reporter gene (CAT) activity decreased significantly. Expression of the hANFCAT constructs was specific for atrial cells, as no expression was detected in primary cultures of ventricular cardiocytes or nonmyocardial cells derived from the neonatal hearts. Correct transcription start sites for the transfected hANF genes were confirmed by S1 nuclease mapping and RNase protection analysis. A "gel shift" assay was used to identify a specific cardiac nuclear protein which bound to the 5'-flanking sequence of the hANF gene. A 192-base pair PvuII fragment (-400 to -208) associated with a protein in these extracts in a tissue- and sequence-specific fashion. These findings indicate that the DNA sequence between -409 and -332 in the hANF gene harbors a tissue-specific element whose activity may involve association with a cardiac-specific nuclear protein.

Animals↗
PubMed1988

Expression of the gene for the atrial natriuretic peptide in cardiac myocytes in vitro.

Primary cultures of neonatal cardiocytes express the gene for atrial natriuretic peptide (ANP). In general the levels of expression follow the rank order: atrial greater than ventricular much greater than nonmyocardial cells. Following the initial dispersion cardiocytes require 48 to 72 hours before ANP secretion and ANP mRNA accumulation approach a new steady-state level. In situ hybridization analysis indicates that ANP gene expression is concentrated in a subpopulation of cardiocytes in both the atrial and the ventricular cell cultures. These findings suggest that these primary cultures may be of value in defining the factors governing the expression of the ANP gene in the cardiac cell.

Animals↗
PubMed1988

An evaluation of reported cases of median mandibular cysts.

All English-language reports of median mandibular cysts and one German article were carefully studied. All but three of 20 such cases were readily interpreted as being various forms of odontogenic cysts. Tissue sections of two of the three others were obtained, and it was eventually concluded that all three probably also represented odontogenic cysts. The median mandibular cyst does not appear to exist as an entity. All cysts reported as such are probably odontogenic. In previous reports on median mandibular cysts, undue emphasis has been placed on the "vitality" of adjacent teeth, as determined by thermal or electrical pulp testing. These tests are not completely reliable. Mucous cells and cilia can be found in odontogenic cysts, and consequently their presence in lesions reported as median mandibular cysts does not preclude these cysts from being odontogenic.

Humans↗
PubMed1988

Inability to distinguish ameloblastomas from odontogenic cysts based on expression of blood cell carbohydrates.

This study was designed to confirm the report by Vedtofte and coworkers that the epithelium of ameloblastomas can be distinguished from that of nonneoplastic odontogenic cysts by differences in expressivity of cell surface carbohydrates with blood group specificity. Immunoperoxidase techniques were used to study four radicular cysts, seven dentigerous cysts, six ameloblastomas, and six examples of plexiform unicystic ameloblastoma. No consistent differences were found in the expressivity of the blood group carbohydrates A, B, and H type 2 in the nonneoplastic odontogenic cysts as compared to the ameloblastomas. Consequently, the demonstration of these blood group carbohydrates is of no value in the differential diagnosis of nonneoplastic odontogenic epithelium from ameloblastomas, including especially the plexiform unicystic ameloblastoma, the pattern that so closely resembles hyperplastic odontogenic epithelium.

ABO Blood-Group System↗
PubMed1988

Radiotherapy in the treatment of ameloblastoma.

There is a lack of well-documented evidence in the literature concerning the relative radioresponsiveness or radioresistance of ameloblastomas, although they are generally considered radioresistant. Most of the previous papers referring to this subject lack acceptable histopathologic proof of the diagnosis, adequate radiotherapeutic data, and/or follow-up information; many predate the use of megavoltage irradiation. The present article reports 5 cases of ameloblastoma that were treated by radiotherapy, 3 by megavoltage irradiation. All have been confirmed histologically by an oral pathologist, all have adequate radiotherapeutic data and, with one exception, adequate follow-up information. In addition, the reasons for our present lack of knowledge of this subject are discussed; objective criteria are presented for evaluating the results of radiotherapy on ameloblastomas; the only other series of ameloblastomas treated by megavoltage irradiation is analyzed. Although radiotherapy can reduce the size of an ameloblastoma, primarily that part of the tumor which has expanded the jaw or broken into the soft tissues, it does not appear to be an appropriate treatment for an operable ameloblastoma. Its main use is in inoperable cases, primarily in the posterior maxilla.

Adult↗
PubMed1988

Processing of the primary transcript for the rat growth hormone gene in vivo.

Processing of the rat growth hormone (rGH) gene primary transcript and the effects of thyroid and glucocorticoid hormones on rGH pre-mRNA levels have been studied using subcloned radiolabeled DNA fragments from each of the four introns of this gene as probes. Blot-hybridization analysis of poly(A)+RNA from GC cells, GH3 cells, and normal pituitary gland indicates that processing of intron sequences from the precursor transcript takes place in a qualitatively similar fashion in each of these cell types. The data indicate that, in general, those introns closest to the termini of the primary transcript are removed first followed by removal of the internal introns. The suggested order of removal is IA, ID, IC, and IB. This process is unaffected qualitatively by thyroid or glucocorticoid hormones, both of which increase the rate of transcription of the gene. In addition to the primary transcript and the partially processed intermediate transcripts, GC and GH3 cells were found to contain a heterogenous group of intron-containing polyadenylated rGH gene transcripts which cannot be accounted for by any combination of intron deletions. These transcripts could arise either from internal start sites in the gene, premature termination of transcription, or inefficient processing of rGH mRNA precursors in the transformed cells. Thyroid hormone rapidly increases the levels of intron C-containing transcripts with kinetics that parallel the binding of thyroid hormone receptor to nuclei, but does not alter the ratio of primary to partially processed transcripts. These data suggest that most of the stimulatory activity of this hormone is due to effects on rGH gene transcription and not on pre-mRNA processing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The glandular odontogenic cyst: an apparent entity.

This article reports 8 examples of a rare cyst of the jaws that appears to be a distinct entity and which we have named glandular odontogenic cyst because of its unusual histopathological features. This lesion occurs over a wide age range in both sexes, tends to recur, and may become very large. However, one example in this series remained small over a period of 9 years; another, somewhat atypical example, was associated with an ameloblastoma.

Adult↗
PubMed1988

Perinatal expression of the atrial natriuretic factor gene in rat cardiac tissue.

The expression of the atrial natriuretic factor (ANF) gene was examined in the perinatal rat ventricle. The late fetal ventricle (day -3 relative to parturition) demonstrated a modest level of ANF gene expression. This expression increased at the time of birth and peaked on day +1 after birth. Atrial ANF immunoreactivity (irANF) increased gradually during the postpartum period (day +1 to 2-3 wk of age), while ventricular irANF as well as ventricular ANF mRNA levels fell over the same interval. This decrease in ANF gene expression resulted from a decrease in activity of the same major transcription start site employed in the adult atria and ventricle. Plasma irANF levels were very high in the neonatal period and decreased over the ensuing 2-3 wk, a profile similar to that seen for ventricular ANF gene expression. In situ hybridization histochemistry revealed that, while adult rat ventricular ANF mRNA was predominantly confined to the subendocardial layer, neonatal ventricles expressed the ANF gene throughout approximately 50% of the inner wall thickness. These findings suggest that the ANF gene is responding to regulatory stimuli that appear at or near the time of parturition and dissipate in the early neonatal period.

Aging↗
PubMed1988

Vagal C-fiber blockade abolishes sympathetic inhibition by atrial natriuretic factor.

Administration of atrial natriuretic factor (ANF) to anesthetized rats decreases renal nerve activity (RNA), an effect prevented by vagotomy but not by atropine. We sought to determine whether afferent vagal C-fibers mediate the inhibition of sympathetic outflow. ANF (2.5 micrograms/kg iv) decreased mean arterial pressure (MAP) by 25 +/- 2 mmHg, RNA by 11 +/- 5%, and least splanchnic nerve activity (LSNA) by 10 +/- 4% in anesthetized rats with arterial baroreceptors intact, and by 40 +/- 3 mmHg, 28 +/- 7%, and 23 +/- 4%, respectively, in sinoaortic-denervated rats. Inhibition of RNA and LSNA by ANF was reduced slightly by cooling the vagi to 6 or 7 degrees C, a temperature at which conduction in A-fibers was blocked and that in C-fibers attenuated; inhibition was abolished when C-fibers were blocked by cooling to 0 degrees C. We conclude that the inhibition of RNA and LSNA by ANF was mediated by afferent vagal C-fibers. We also obtained evidence that the aortic nerves contribute to ANF-induced inhibition of RNA. Our results support the notion that ANF evokes a generalized decrease in sympathetic tone that contributes to the hypotension, cardiac inhibition, and natriuresis accompanying systemic administration of the peptide.

Animals↗
PubMed1988

Urinary cGMP as biological marker of the renal activity of atrial natriuretic factor.

Current evidence suggests guanosine 3',5'-cyclic monophosphate (cGMP) serves as the second messenger for atrial natriuretic factor (ANF) in the kidney in vivo. We examined whether extracellular cGMP accumulation quantitatively reflected the concentration of cGMP within renal cells and whether urinary excretion of cGMP correlated with the physiological action of ANF. cGMP egression was examined in renal epithelial LLC-PK1 cells. ANF augmented intracellular cGMP concentration and extracellular cGMP appearance. Extracellular cGMP was an excellent function of the time-integrated intracellular cGMP concentration. In clearance studies in awake rats, urinary cGMP was primarily of renal cellular origin and correlated with the natriuresis induced by ANF in a time-dependent and concentration-dependent fashion. Urinary cGMP excretion may be useful as a biological marker for the renal activity of ANF in vivo.

Animals↗
PubMed1988

Gene for the rat atrial natriuretic peptide is regulated by glucocorticoids in vitro.

Glucocorticoids regulate the expression of the gene for atrial natriuretic peptide (ANP) in neonatal cardiocytes. Dexamethasone (Dex) increased cytoplasmic ANP mRNA levels and media ANP immunoreactivity in a dose-dependent fashion. These effects were not shared by the other classes of steroid hormones and were reversed by the glucocorticoid antagonist RU 38486. The effect on ANP mRNA levels resulted, at least in part, from enhanced transcription of the gene. Dex effected a two-fold increase in ANP gene activity assessed using a run-on transcription assay. The turnover of the ANP transcript was approximated using a standard pulse-chase technique. The half-life of the ANP mRNA was 18 h in hormone-free media. In the presence of Dex this half-life increased modestly to 30 h, although the increase relative to the control did not reach statistical significance. The effect of Dex at the level of the individual myocardial cell was assessed by in situ hybridization analysis using a specific [3H]cRNA probe. These studies demonstrated a significant level of ANP expression within a subpopulation of cells in the cultures. Exposure of the cells to Dex for 24 h did not recruit additional cells into the expressing pool (27.3% cells/high power field vs. 31.3% for the control) but did increase the level of expression (i.e., grain density) within individual cells. These findings indicate that glucocorticoids stimulate expression of the ANP gene directly at the level of the myocardial cell. This results predominantly from transcriptional activation in cells already expressing the gene rather than through recruitment of previously quiescent cells.

Animals↗
PubMed1987

Teratoma of the maxilla.

This article presents a case report of an intraoral teratoma in an 11-year-old boy. The tumor contained cartilage, smooth muscle, respiratory epithelium, brain, and skeletal muscle. Two adjacent cervical lymph nodes exhibited reactive changes, but another had been largely replaced by brain tissue.

Child↗
PubMed1987

Plexiform unicystic ameloblastoma of the maxilla.

Plexiform unicystic ameloblastomas have a marked predilection for occurring in the posterior part of the mandible. This article presents the first report of such a lesion in the maxilla.

Ameloblastoma↗
PubMed1987

Identification of atrial natriuretic factor gene transcripts in the central nervous system of the rat.

Atrial natriuretic factor (ANF) gene transcripts have been identified in the hypothalamus, brainstem, and cerebral cortex of the rat. The hypothalamic transcripts are similar in overall size (approximately 1100 nucleotides), 5' terminus, 3' terminus, and nucleotide sequence to their counterparts synthesized in the cardiac atria. The 5' terminus of the hypothalamic transcripts, determined by both S1 nuclease and primer-extension analysis, was located approximately 20 nucleotides downstream from the TATAAAA sequence that is thought to dictate the start of transcription. Similar 5' termini were identified in RNA from the brainstem and cerebral cortex. The 3' termini of the hypothalamic transcripts mapped approximately 10 nucleotides downstream from each of two successive AATAAA sequences that are believed to provide the cleavage signal required for subsequent polyadenylylation. The same 3' termini were present in atrial, ventricular, lung, and pituitary RNA. To confirm the identity of the hypothalamic gene transcript, a partial-length cDNA clone encoding ANF was isolated from a hypothalamic cDNA library and sequenced. This hypothalamic clone was identical to an analogous atrial cDNA clone at each of its 612 nucleotide positions. These findings suggest that ANF peptides, previously identified in specific loci of the hypothalamus and pontine tegmentum, are synthesized locally in these tissues and support a role for this peptide in the central regulation of cardiovascular physiology.

Amino Acid Sequence↗
PubMed1987

Increased synthesis and release of atrial peptide during DOCA escape in conscious dogs.

The escape from the sodium-retaining effects of prolonged mineralocorticoid treatment in animals and humans was first noted over 40 yr ago, but despite intense study the mechanisms responsible for the escape phenomenon have not been identified. Putative "natriuretic hormones" have been proposed to account for the escape phenomenon. To determine whether atrial natriuretic peptides (ANP) could participate in the escape phenomenon, the mineralocorticoid deoxycorticosterone acetate (DOCA) was administered to conscious dogs for 14 days. Escape was accompanied by a doubling of plasma ANP concentration and four- to sevenfold increases in cardiac ANP messenger RNA. There were also significant increases in mean arterial blood pressure during the last 8 days of DOCA treatment. Thus increases in the synthesis and secretion of ANP and increases in atrial pressure may represent mechanisms that contribute to the escape from mineralocorticoid-induced sodium retention.

Animals↗
PubMed1987

The gene for the atrial natriuretic factor is expressed in the aortic arch.

The gene for atrial natriuretic factor is expressed within the adventitial cells of the rat aortic arch. Atrial natriuretic factor transcripts, similar in overall size (1100-1200 nucleotides) and 5'-termini to those found in the atria, were identified in the arch. Much lower levels (approximately 10-20%) of these transcripts were present in distal thoracic aorta. Atrial natriuretic factor peptide was localized by immunocytochemistry to the adventitia of the arch in regions thought to harbor the aortic baroreceptors. These data suggest a previously unsuspected role for the peptide in regulating systemic blood pressure through the baroreceptor reflex.

Animals↗