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Biomedical subjects

H A Miller

Publications and source records attributed to H A Miller.

At least 19 recordsLinked to original sources
PubMed2000

The late nonfunctioning duodenal atresia repair--a second look.

BACKGROUND/PURPOSE: In 1986, the authors reported on 3 newborns who had repair of their duodenal atresia, and between 6 and 18 months postoperatively an anastomotic obstruction developed in each suddenly. After prolonged medical and surgical treatments it became apparent that the duodenal atresia repair was functionally obstructed and plication of the dilated atonic proximal duodenum was curative. Since then, 2 more patients became so obstructed at 5 and 24 years postoperatively. The aim of this study was to report the very late occurrence of a functional obstruction of a newborn duodenal atresia repair. METHODS: The 2 additional histories and surgical repairs were reviewed. RESULTS: The 5-year old boy was cured immediately with plication only of his dilated proximal duodenum. The 24-year-old nurse had a very stormy 2-year course with several bypass operations, which did not relieve her abdominal pain and bile vomiting until they were taken down and her dilated proximal duodenum was plicated, after which she made a good recovery. Both remain well. CONCLUSION: An uncommon, very late, sudden, apparently anastomotic, postoperative, newborn, duodenal atresia repair obstruction caused by proximal, dilated, duodenal atony, and dysfunction can occur many years later and responds to duodenal plication alone.

Adult↗
PubMed1999

Modulation of endogenous GABA release by an antagonistic adenosine A1/dopamineD1 receptor interaction in rat brain limbic regions but not basal ganglia.

Behavioral and biochemical studies suggest that a negative interaction exists between adenosine A(1) and dopamine D(1) receptors in the brain and that this may contribute to the psychomotor effects of adenosine receptor agonists and antagonists. We examined the functional significance of A(1) and D(1) receptor subtypes in modulating electrically evoked endogenous GABA release from slices/punches of rat basal ganglia (striatum, globus pallidus, striatum containing globus pallidus, and substantia nigra reticulata) and limbic regions (ventral pallidum and nucleus accumbens). In basal ganglia, stimulation of A(1) receptors with the selective agonist R-PIA (1-100 nM) resulted in a concentration-dependent decrease in GABA release. The selective A(1) antagonist DPCPX (10-100 nM) increased GABA release, suggesting that endogenous adenosine tonically inhibits GABA release. However, in basal ganglia, consistent dopamine D(1) receptor modulation of GABA, release was not observed in response to either D(1) agonists or antagonists. Furthermore, the A(1) receptor-mediated inhibition of GABA release was not changed by concurrent activation of D(1) receptors, thus confirming the lack of D(1) receptor modulation under these conditions. In contrast, in ventral pallidum and nucleus accumbens, stimulation of D(1) receptors with SKF-82958 (1 microM) increased GABA release significantly. The D(1) receptor-mediated increase in GABA release was attenuated by concurrent activation of adenosine A(1) receptors. These results are consistent with the hypothesis that an antagonistic A(1)/D(1) receptor interaction may be important in modulating GABA release in limbic regions.

Adenosine↗
PubMed1999

Partial tracheal obstruction due to chondromas in ball pythons (Python regius).

Over a 9-mo period, three adult ball pythons (Python regius) (one male, two females) were evaluated for severe dyspnea. Partial obstructions of the tracheal lumen were identified radiographically and/or visualized with a 3.0-mm rigid laparoscope inserted into the tracheal lumen in all three snakes. Administration of systemic antibiotics and nebulization resulted in partial improvement of the dyspnea. In two snakes, the tracheal lesions were removed with a rigid laparoscope and a flexible biopsy instrument inserted into the tracheal lumen. The other snake died and was necropsied. Histologically, the lesions from two snakes were determined to be benign chondromas. The chondromas were composed of a variably disorganized chondroid matrix populated by quiescent, normal-appearing chondrocytes within lacunae, although the chondrocytes were increased in density compared with normal hyaline cartilage and contained rare mitotic figures. The tracheal masses in one snake grew by expansion, not invasion, and were focally continuous with a mineralized cartilage tracheal ring, suggesting a benign nature. This is the second report of tracheal chondroma in ball pythons. Tracheal chondromas are exceedingly rare in humans and domesticated animals, suggesting a possible predisposition of ball pythons for this neoplasm.

Animals↗
PubMed1998

On the possible role of positive end-expiratory pressure ventilation in the treatment of chylothorax caused by blunt chest trauma.

Recent reports on the treatment of chylothorax postulate a benefit to ventilator therapy, especially using positive end-expiratory pressure (PEEP). This report describes the use of mechanical ventilation with PEEP in the management of a 24-year-old male motorcyclist who sustained a ligamentous Chance fracture of the thoracic spine at the T6-7 level with bilateral traumatic chylothorax. Treatment of the chylothorax consisted of high PEEP ventilation, bilateral chest tube thoracostomies, and total parenteral nutrition. The chylothoraces resolved within 4 days of treatment and mechanical ventilation was stopped. Ventilator therapy of traumatic chylothorax and the physiologic grounds for its use are discussed. A review of the literature and experimental evidence seem to suggest that ventilator treatment of traumatic chylothoraces is effective.

Accidents, Traffic↗
PubMed1996

Expression and modulation of 5-hydroxytryptamine1A receptors in P11 cells.

P11 cells were transfected with DNA for the human 5-hydroxytryptamine1A (5-HT1A) receptor. These cells stably expressed the 5-HT1A receptor coupled to the inhibition of adenylyl cyclase, and not to the stimulation of phosphoinositide hydrolysis. Homologous and heterologous regulation of the 5-HT1A receptor was studied in this cell system. Pretreatment of P11-5HT1A cells with the 5-HT1 receptor agonist 5-carbox-amidotryptamine (5-CT) resulted in a 3-fold increase in both basal and forskolin-stimulated cAMP accumulation, and desensitization of the 5-HT1A receptor as indicated by a decrease in the potency of 8-hydroxydipropylaminotetralin (8-OH-DPAT) to inhibit forskolin-stimulated cAMP accumulation (vehicle-treated cells: EC50 = 2.3 +/- 0.8 nM; 5-CT-treated cells: 9.9 +/- 0.4 nM). The sensitization of adenylyl cyclase as a result of chronic agonist exposure was prevented by the 5-HT1A antagonist WAY100635, which indicated that the effect of 5-CT pretreatment on basal and forskolin-stimulated cAMP accumulation was mediated by 5-HT1A receptor activation. Pretreatment of cells with pertussis toxin abolished the inhibition of forskolin-stimulated cAMP accumulation mediated by 5-HT1A receptor activation and prevented the sensitization of adenylyl cyclase as a result of chronic 5-HT1A receptor agonist exposure. Pretreatment of P11-5HT1A cells with the phorbol ester, phorbol 12-myristate 13-acetate (PMA), also resulted in desensitization of the 5-HT1A receptor, as indicated by a marked decrease in the potency and intrinsic activity of 8-OH-DPAT. No change in the binding characteristics (i.e., Kd or Bmax) of [3H]8-OH-DPAT to 5-HT1A receptor sites was observed after 5-CT or PMA treatments. Activation of alpha-1 adrenergic receptors, but not 5-HT2A receptors, had effects on 5-HT1A receptor responsiveness similar to those seen with PMA pretreatment. In P11-5HT1A cells, homologous regulation of the 5-HT1A receptor was characterized by sensitization of adenylyl cyclase and a decrease in agonist potency, whereas heterologous regulation of the 5-HT1A receptor was characterized by a greater decrease in agonist potency, as well as a marked decrease in intrinsic activity.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Expression of the human 5-hydroxytryptamine1A receptor in Sf9 cells. Reconstitution of a coupled phenotype by co-expression of mammalian G protein subunits.

The possibility that Spodoptera frugiperda (Sf9) cells can provide an intact cell setting for reconstitution of the human 5-hydroxytryptamine1A (5-HT1A) receptor with mammalian G protein subunits was explored. The 5-HT1A receptor was found to assume an uncoupled phenotype when expressed alone in Sf9 cells at relatively high levels (5-34 pmol of receptor/mg of membrane protein), i.e. agonist-binding to the receptor was characterized by a relatively high Kd and an insensitivity to GTP. Co-expression of the receptor with members of the alpha i "family" together with various combinations of beta 1 and gamma subunits increased the affinity for agonists to that observed for the coupled form of receptor in mammalian cells, concomitant with conferrance of guanosine 5'-(beta,gamma-imino)triphosphate sensitivity. The agonists employed were [3H]8-hydroxy-N,N-dipropyl-2-aminotetralin ([3H]8-OH-DPAT) and [125I]R(+)-trans-8-hydroxy-2-[N-n-propyl-N-(3'-iodo-2'-propenyl) amino]tetralin ([125I]8-OH-PIPAT). The binding of an antagonist, [125I]4-(2'-methoxyphenyl)-1-[2'-[N-(2"- pyridinyl)-p-iodobenzamido]ethyl]piperazine ([125I]p-MPPI), was unaffected by co-expression of G protein subunits. Both alpha and beta gamma subunits were required for optimal coupling. No differences were evident among alpha i1, alpha i2, alpha i3, alpha o, and alpha z when expressed with beta 1 gamma 2 in this regard, nor among most permutations of beta 1 gamma subunits when expressed with alpha i1 (beta 1 gamma 2 approximately beta 1 gamma 3 approximately beta 1 gamma 5 > beta 1 gamma 1). Alpha s and alpha q expressed with beta 1 gamma 2 did not participate in coupling. These data support the conclusion that normal interactions between a mammalian receptor and a select array of G proteins can be established in intact Sf9 cells, and extend previous observations of 5-HT1A receptor coupling to G(o) and the pertussis toxin-insensitive G protein Gz.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Dexamethasone recruits atrial natriuretic peptide secretory cells in the rat left atrium and apex of the ventricle.

The response of the atrial natriuretic peptide (ANP) secreting cells from both rat atria and the apex of the ventricles to dexamethasone (DEX) was analyzed by the plaque assay. In right atrial cardiocytes, 25% of the cells secreted ANP basally; DEX treatment did not alter this percentage. However, in the left atrial secretory population, a discordance between the basal (15%) and DEX stimulated (25%) percent plaque formation was found. ANP secreting cells from the ventricular apex responded similarly to DEX exposure (26%), with 8% of the cells basally releasing the hormone. These data suggest that in both the left atria and apex of the rat ventricles, exposure to DEX recruits ANP secretory cells from a non-secreting population. Consequently, the release of ANP from these tissues would increase after glucocorticoid stimulation.

Animals↗
PubMed1995

Proportions of rat ANP-secreting cells that are cardiomyocytes and that synthesize the hormone.

Atrial natriuretic peptide (ANP) is released from the heart and participates in regulating blood pressure and volume. We recently developed a reverse hemolytic plaque assay to measure the release of ANP from individual rat atrial cardiocytes. This assay determines the total proportion of atrial cardiocytes committed to releasing ANP. We combined the plaque assay with immunocytochemistry (IC) and in situ hybridization (IS). Combining the plaque assay with IC for myosin revealed that 13.5 +/- 0.9% (%myosin+ and plaque forming; mean +/- SE, n = 4) of atrial cardiocytes are cardiomyocytes that release ANP. Combination of the plaque assay with IS for ANP mRNA showed that 16.6 +/- 0.6% (%in situ+ and plaque forming; mean +/- SE, n = 4) of the cardiocytes in the rat atria synthesize and release the hormone. Incubation of atrial cardiocytes with dexamethasone to stimulate ANP gene expression did not alter the total proportion of in situ-positive ANP-secreting cells. These data suggest that, within the total ANP-secreting population of the rat atria, only 33% of the secreting cells are cardiomyocytes. In addition, 68% of the ANP-secreting cells do not appear to synthesize the hormone. These results imply that muscle and nonmuscle cells are involved in secreting ANP and that cardiomyocytes synthesize the hormone.

Animals↗
PubMed1995

Induction of an acute phase response in lambs causes an increase in plasma levels of GH and IGF-I.

GH and IGF-I plasma concentrations were measured in lambs during an acute phase response induced by an intrathoracic injection of yeast. The acute phase response was indicated by reduced feed intake, weight loss and an increase in plasma concentrations of the acute phase protein haptoglobin. Intensive blood sampling on day 1 revealed elevated basal concentrations of GH in the yeast-injected group compared with concentrations in pair weight and ad libitum fed control lambs. This suggests that at the beginning of an acute phase response there is an increase in either GH secretion or the half life of GH. No evidence of a specific GH-binding protein in sheep plasma could be detected. IGF-I concentrations in the yeast-injected group remained constant for 3 days then increased to a peak level at day 6. In contrast, plasma IGF-I concentrations were depressed from days 3 to 6 in the pair weight control group and they were unchanged in the ad libitum fed controls. When the IGF-I concentrations were elevated in the yeast-injected group, this group had a higher daily weight gain despite their lower feed intake compared with the ad libitum fed controls. These results suggest that IGF-I may be associated with the increase in weight in the late stage of an acute phase response during recovery from an infection or injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Reaction↗
PubMed1994

Unsuspected tracheal rupture in blunt thoracic trauma.

The purpose of this report is to describe the discovery and management of an unanticipated injury during fibreoptic tracheal intubation. A 23-yr-old man sustained blunt cervical, thoracic and abdominal trauma in a motor vehicle accident. He was brought to the operating room for urgent management of his abdominal and cervical spine injuries. Examination of his airway during awake fibreoptic tracheal intubation revealed an unexpected tracheal injury. Surgical repair of the trachea was uneventful. The diagnosis and airway management of tracheal rupture are discussed. This case illustrates the importance of a full diagnostic examination during invasive anaesthetic procedures such as tracheal intubation.

Abdominal Injuries↗
PubMed1992

Dexamethasone stimulates release of an ANP-like substance from rainbow trout cardiocytes.

A substance that cross-reacts with antiserum to human atrial natriuretic peptide (ANP) is found in fish hearts. This ANP-like material increases sodium output from the gill and kidney while inhibiting sodium uptake in the gut. Mammalian ANP secretion is stimulated by glucocorticoids, and cortisol injection increases sodium output in salt-loaded fish. Therefore, we wanted to determine if the release of ANP in fish is sensitive to dexamethasone. Ventricle cardiocytes from the rainbow trout Oncorhynchus mykiss were treated with various doses of dexamethasone for 18 or 72 h. Single ventricle cells were then assayed for ANP release using a reverse hemolytic plaque assay and antiserum to human alpha-ANP. Incubation with 100 microM dexamethasone almost doubled the population of ventricle cells committed to ANP release (basal, 15.0 +/- 0.3% vs. Dexamethasone, 28.3 +/- 1.4%; values are percent plaque formation +/- SE). Stimulation of ANP secretion was dependent on dose and time of exposure to dexamethasone. These results suggest that ANP secretion in fish is regulated by glucocorticoids.

Animals↗
PubMed1990

Release of atrial natriuretic peptide from individual rat cardiocytes.

Atrial natriuretic peptide (ANP) is released from the atria and acts to regulate blood volume and pressure. The release of ANP appears to be stimulated by atrial distension, initiated by stretch on the cardiocytes. The purpose of the present study was to develop an assay that would allow for the detection of ANP release from single, isolated cells in the absence of distension. Using the reverse hemolytic plaque assay and antibody raised against human-alpha ANP, the release of ANP was detected from trypsin dissociated rat atrial cells. The specificity of the assay was demonstrated by a 67% reduction in ANP plaque forming cells detected following preabsorption of the anti-sera with rat-alpha ANP. The assay also proved efficient in monitoring changes in ANP secreting cell populations, where an acute treatment with dexamethasone resulted in a doubling of the percentage of atrial cardiocytes detected within a 4 hour antibody incubation. Finally, the assay established that about 52% of the dispersed atrial cardiocytes release ANP. The establishment of a plaque assay for ANP release should assist in addressing questions concerning what hormones may regulate ANP secretion directly and also allow for the determination of ANP secreting cell population dynamics.

Animals↗
PubMed1989

Ontogeny of prolactin secretion in the neonatal rat is regulated posttranscriptionally.

PRL-secreting cells first appear in appreciable numbers on day 4 of neonatal life in rats. In the present study, we attempted to ascertain whether the ontogenic appearance of PRL mRNA and hormone release were temporally coordinated or discordant. Our results show that the PRL gene is expressed at least 3 days before the onset of secretion in newborn rats. Moreover, steady state levels of PRL mRNA in neonates are at least as high as those found in 10-day-old rats, in which 15-17% of all pituitary cells secret the hormone. This apparent blockage of translation is attributable to a lack of association of PRL message with ribosomes in the neonate. Taken together, these data indicate that the ontogeny of PRL secretion in rats is regulated translationally as well as transcriptionally.

Animals↗
PubMed1988

Attenuation of growth hormone gene expression in desensitized somatotropes.

The effects of GRF-induced desensitization of somatotropes on GH gene expression were investigated on pituitary cells derived from male rats. Pretreatment of monodispersed cells for 18 hr with GRF abolished both the acute release of GH and the stimulation of GH gene expression in response to a subsequent 4 hr challenge with GRF. Concomitant preincubation with GRF and SS resulted in restoration of the ability of GRF to stimulate release of GH but not to augment GH gene expression. These results demonstrate that desensitization by GRF affects both the release of GH and GH gene expression, whereas the resensitizing effects of SS appear to be directed exclusively at the release mechanism.

Animals↗
PubMed1988

Evidence for a cAMP-dependent nuclear factor capable of interacting with a specific region of a eukaryotic gene.

Nuclear extracts prepared from the livers of rats treated with or without 8-bromo-cAMP were tested for their ability to bind to various fragments from the flanking region of the gene encoding phosphoenolpyruvate carboxykinase (GTP) [GTP: oxaloacetate carboxy-lyase (transphosphorylating), EC 4.1.1.32] known to contain the element that confers transcriptional regulation by cAMP. Using the nitrocellulose-filtration method, concentration-dependent, apparently saturable binding was seen that is both specific and cAMP dependent. Analysis of various fragments pinpointed the active binding region to positions within the -67 to -111 region, which coincides with the functional regulatory element as shown by recent transfection studies. Formation of an apparently single complex between a synthetic oligomer containing the region from -67 to -111 of the phosphoenolpyruvate carboxykinase gene and a factor in nuclear extracts from cAMP-treated rat liver was visualized by the gel-retardation method. Complex formation is both concentration and cAMP dependent and can be prevented by excess specific but not nonspecific competitor DNA. The congruity of the results with the two different methods suggests that the factor we have detected has properties consistent with a possible role as mediator of the transcriptional control exerted by cAMP in eukaryotic cells.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Liver tissue from lactating rats produces a factor that stimulates prolactin release and gene expression.

Liver tissue from nursing rats produces a substance, termed liver lactogenic factor (LLF), that potently stimulates casein release from isolated mammary cells. Inasmuch as the production of LLF is dependent on PRL, we decided to determine whether it could influence the release of the hormone by dissociated pituitary cells in culture. This was accomplished by measuring PRL release with a reverse hemolytic plaque assay and PRL gene expression with a DNA probe complementary to PRL mRNA. Treatment of pituitary cells from day 10 lactating rats with liver slice incubates from the same type of animal caused a 35.3 +/- 4.3% increase in PRL release during a 3-h incubation. Likewise, the same dose of LLF activity markedly increased (3.5-fold) the steady state levels of PRL mRNA. The responses were reasonably specific for PRL, since neither GH plaque development nor gene expression was affected by identical treatment. Taken together these results demonstrate that LLF can act directly at the pituitary level to exert positive feedback effects on both PRL release and gene expression.

Animals↗