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Hormones, the ectopic rat PDX-1 induced the endogenous human PDX-1 transcript and many pancreatic transcription factors, such as Beta-2, Nkx6.1, Nkx2.2, Ngn3, Isl-1, Pax4 and Pax6, in PDX-1- and SF-treated TAHL cells Fig. 3 ; . Although these nuclear factors should be analyzed further by protein detection assays, their inSapir et al.
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Creases in S-cell excitability Fig. 3E ; . Changes in AP pulse post hoc P 0.001 ; , first ISI P 0.05 ; , and slope P 0.05 ; in the 5-HT GDP S group were significantly different from those treated with 5-HT alone but not significantly different from the saline group. The same result was observed in S-cells treated with GDP S alone Fig. 3E; post hoc results: AP pulse, P 0.05; 1st ISI, P 0.01; slope, P 0.01 ; . No significant difference in S-cell membrane potential threshold or input resistance was observed among the 5-HT GDP S, GDP S, 5-HT, or saline groups Fig. 3E ; . Next, the involvement of a cAMP PKA second-messenger cascade was examined. 5-HT-induced increases in S-cell excitability properties were blocked when 50 M Rp-cAMP was included in the perfusate Fig. 3F; 5HT Rp-cAMP ; . Changes in AP pulse post hoc P 0.005 ; , first ISI P 0.05 ; , and slope P 0.01 ; in the 5-HT Rp-cAMP group were significantly different from those treated with 5-HT alone but not significantly different from the saline group. The same result was observed in S-cells treated with Rp-cAMP alone Fig. 3F ; , indicating that the drug did not affect S-cell excitability directly post hoc results: AP pulse, P 0.0005; 1st ISI, P 0.05; slope, P 0.01 ; . No significant difference in S-cell membrane potential threshold or input resistance was observed among the 5-HT Rp-cAMP, Rp-cAMP, 5-HT, or saline groups Fig. 3F ; . If 5-HT modulation of excitability does require the activity of a cAMP PKA second-messenger system, then increasing the intracellular level of cAMP should mimic the effects of 5-HT on this interneuron. A 5-min perfusion of the S-cell with 50 M db-cAMP produced increases in AP pulse and slope and decreases in first ISI that were statistically indistinguishable from those of 5-HT Fig. 3F ; but statistically different from the saline group post hoc results: AP pulse, P 0.001; 1st ISI, P 0.05; slope, P 0.05 ; . No significant difference in S-cell membrane potential threshold or input resistance was observed between the db-cAMP, 5-HT, or saline groups Fig. 3F ; . Together, the results from the Rp-cAMP and db-cAMP experiments demonstrate that 5-HT-induced increases in S-cell excitability require activation of a cAMP PKA second-messenger cascade. Sensitization is blocked by treatments that inhibit 5-HT modulation of excitability To examine whether sensitization-induced increases in Scell excitability are the result of serotonergic modulation, sensitization training was carried out under conditions that block potentiation of excitability by 5-HT. Specifically, semiintact preparations were treated with either 100 M methysergide or 50 M Rp-cAMP during sensitization training. In addition, the effects of these treatments on sensitization of whole-body shortening and the accompanying increase in Scell activity during shortening were examined. The intensity of the whole-body shortening reflex more than doubled after delivery of the sensitizing stimuli Fig. 4, B and C ; in preparations that underwent sensitization training in normal saline sens saline group ; . S-cell activity during shortening also increased relative to presensitization levels Fig. 4, B and D ; . No change in either the shortening reflex or S-cell activity was observed in preparations from sensitization control experiments in which delivery of the sensitizing stimuli was.
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Sophia - b. 1808: came to NB and first settled at Little Shemogue, Botsford Parish in Westmorland County, then in Shediac Parish, Westmorland County: Children are listed in an estimated order: 1 ; Frederick Chapman b. at Little Shemogue: 2 ; Bowden Chapman b. 12 Apr 1826 at Little Shemogue, died 20 Feb 1899, married Anna Marie Clarke: 3 ; possibly, Susan Chapman b. Feb 1831 at Little Shemogue: 4 ; Ann Chapman b. 1833: 5 ; Sophia Chapman b. 1833: 6 ; possibly, John C. Chapman b. 7 Jun 1834 at Little Shemogue: 7 ; Philip P. Chapman b. 1837: 8 ; Rosline E. Chapman b. c1840, died 1966, possibly m. James Webster of Shediac, NB: 9 ; Mary Chapman b. 1842, possibly married R.W. Abercrombie of Shediac: 10 ; Miss Chapman b. - , married James Wilbur of Shediac, NB. Source: MC2852 Purdy-Carter genealogical collection, MS2: on microfilm reel F20987: see sheet for Philip Chapman and midodrine.
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Strated that ['251]iodopindololprovides an excellent probe of adrenergic receptor function in skeletal muscle membranes from the rat 9 ; . In this study, a saturation curve and Scatchard analysis of ['251]iodopindolol binding to rat skeletal muscle sarcolemma are shown Fig. 9 ; . Saturation of the specific high affinity binding sites occurred at an [1251]iodopindolol concentration of 0.8 nM. By Scatchard analysis a single population of binding sites was found which had a KD of 0.10 nM, and a receptor density of 52fmol mg of membrane protein. These values agree closely with data reported previously 9 ; . Specificity of [1251]iodopindolol binding to rat sarcolemma was next examined by studying the relative ability of various adrenergic and serotonergic agonists and antagoniststo compete for [1251]iodopindololbinding sites. The representative results are depicted in Fig. lOA, which shows inhibition of ['251]iodopindololbinding by various -adrenergic antagonists and by stereoisomers of isoproterenol, a adrenergic agonist. Stereospecificity of the receptor to which iodopindolol binds is shown by the different inhibitory potentials of d- and 1-isoproterenol and d- and 1-propranolol. In both instances, the I-stereoisomer was a more potent inhibitor of ['251]iodopindololbinding. With propranolol, the d-stereoisomer required an approximately 100-fold greater concentration of antagonist to produce equal diminution of ['251]iodopindolol binding, whereas with isoproterenol, an approximately 10-fold greater concentration of the d-stereoisomer was required to produce equal displacement of binding as compared tothe 1-stereoisomer. -Adrenergic antagonists such as I-propranolol and oxprenolol were highly potent in competing for specific iodopindolol binding sites, whereas practolol a pl-selective antagonist ; was less so in competing for these binding sites. In contrast and as shown in Fig. 10B, serotonergic antagonists such as methysergide and cyproheptadine showed an extremely low potency with respect to displacement of [ '251]iodopindolol binding. Adrenergic agonists Fig. lOC ; showed an order of potency of isoproterenol epinephrine norepinephrine. Studies were also performed on the inhibition of [1251] iodoLSD binding to ratsarcolemma by these same adrenergic and serotonergic agonists and antagonists Fig. 11 ; . The physiologically relevant stereoisomers of P-adrenergic ligands such as I-isoproterenol and 1-propranolol as well as oxprenolol, practolol, and pindolol had low affinity for the LSD receptor and mifepristone.
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When cats were pretreated, 30 min before the pentagastrin with a 5-HT antagonist, methysergide 1 0 mg kg ; or cyproheptadine 0.4 mg kg ; Table 1 ; , the response to an infusion of pentagastrin became similar to that of histamine, rising to a maximum secretion at 150-180 min. This is clearly seen in Fig. 2. As the results for pentagastrin after cyproheptadine were so similar to those obtained for pentagastrin after methysergide, the former results have been omitted from the Figure. The results were in contrast to those obtained with pentagastrin alone since the peak secretion at 45 min was eliminated by both methysergide and cyproheptadine and the secretion increased to a slightly increasing plateau which was.
| Methysergide ingredientsWere rendered agglutinable by mild trypsin treatment and then incubated with 3o' g ml Con A Table 1 ; . Such cells do not cap their Con A receptors Fig. 4E ; . As shown in Fig. 4F, H-jw dB ; cells rendered agglutinable by mild trypsinization and then incubated with Con A show no obvious reduction in the number, size or distribution of microvilli suggesting that the Con A effect observed in Fig. 4A may be associated with lectin-receptor capping and not Con A-initiated cell agglutination and miglitol.
Innovations especially since it was possible for FDA to adopt some of the most important innovations, such as the interactive and proactive approaches and project management, regardless of whether Pilot Drug still existed. Pilot Drug pioneered many excellent changes at FDA, but Dr. Woodcock felt it was no longer needed or worth the cost.830 Dr. Murray Lumpkin, Deputy Center CDER ; Director for Review Management, is Dr. Woodcock's Deputy with direct management responsibility for all drug review divisions within FDA, with 980 people reporting to him. He stated that Pilot Drug was eliminated strictly for management reasons related in part to meeting PDUFA goals and in part to concerns over the "cowboy mentality" of Pilot Drug which resulted in Pilot Drug's failure to follow standard regulations, not permissible in a regulatory agency. 831 By 1995, Dr. Lumpkin and Dr. Woodcock ; realized that any delays in meeting PDUFA goals for timely review were no longer going to be caused at the initial review levels, since there were more staff to handle the workload. The bottleneck in the NDA review process that they saw was at the Office level.832 Before the 1995 reorganization, FDA was organized into 10 review divisions reporting to 2 Offices, with the Directors of each Office required to review and approve all NDA applications. In order to address this bottleneck, CDER was reorganized by Dr. Woodcock into 15 review divisions under 5 Offices. This effectively divided up the workload at the upper management level. During the course of this reorganization, Pilot Drug was eliminated and its portfolio was reallocated. Dr. Lumpkin believed that there was no reason to keep Pilot Drug intact to test innovations in the drug review process. While Pilot Drug had implemented many "very good, very important innovations, " primarily its focus on the interactive process, FDA needed to and was able to spread the valuable innovations pioneered by Pilot Drug throughout FDA.833 834 Dr. Woodcock's most serious critique of the quality of Pilot Drug's reviews stemmed from an experience she had when she was called in as a consultant to help Pilot Drug review several sclerederma and rheumatic drugs. 835 She said that there was even a and methysergide.
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