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For Modbus, this must correspond to the Unit Number used in the protocol addressing. This is the address configured in the device or by a dipswitch on the device. The range of Unit Number is 0 to 255 for Modbus. This Unit Number will appear on the System Status Display, Point Detail, user-built displays and tags to reference the status of this device. Changing only the Unit Number here will change the existing device. Changing both the Device Name and the Unit Number will make a copy of the device e.g. create another device.
Quilligan, E. J., Katigbak, E., Nowacek, C., and Czarnecki, N.: Correlation of Fetal Heart Rate Patterns and Blood Gas Volume. I. Normal Heart Rate Values. Am. J. Obst. & Gynec. 90: 1343 Dec. 15 ; , 1964. Herbert directed the BME graduate program at Boston U from 1982 to 1992 and oversaw the introduction of both M.S. and Ph.D. programs. Since 1995, Herbert has co-directed a National Science Foundation-sponsored program, Research Experiences for Undergraduates REU ; , at Boston U. He is also the author of a Whitaker Foundation grant currently supporting his department's Internship program. Beginning in 1992, Herbert served a three-year term as department chairman. During that time, he was elected Secretary of the national Council of Chairs of BME undergraduate programs. He received Boston U's College of Engineering Faculty Service Award in 2000. Herbert is the immediate past chair of the university's Faculty Council, where he successfully led the effort to allow faculty representation on the Board of Trustees. Herbert is President of Alpha Eta Mu Beta, the National Honor Society for BME and a past-president of the Biomedical Engineering Society BMES ; . He served for three years on the BMES Board of Directors and was co-chair of the 1995 BMES Fall Meeting hosted by Boston U. Herbert is widely recognized for his role in obtaining a million dollar Whitaker Foundation grant for BMES. He received the BMES's President's Award in 2003 and the Distinguished Service Award in 2004. Herbert is interested in the neural circuitry of the dorsal cochlear nucleus DCN ; . Using a variety of techniques including cross correlation of simultaneously recorded pairs of DCN units, intra-cellular recording and marking neurons in vivo, and computational modeling, he and his colleagues have provided a better understanding of this complex auditory nucleus. Herbert received his B.E. in electrical engineering from the City College of New York in 1974 and his Ph.D. in biomedical engineering from Johns Hopkins University in 1979. He spent a post-doctoral year at Hopkins before moving to Boston. He was elected to the Johns Hopkins Society of Scholars in 2003. Weight of animal kg ; x 0.05 mg kg hr predetermined pump delivery rate ml hr ; # mg nicardipine added to 1 ml sterile water In all treated animals, sufficient nicardipine was added to the pump to infuse throughout the 72 hour reperfusion period. The pumps were filled under sterile conditions and then incubated in sterile saline for 4 hours at 37 degrees C before subcutaneous insertion. In the PR group, the pump was inserted at the time of vertebral artery cautery, 24 hours before ischemia. In the PO group, the pump was inserted at the end of the 20 minute ischemic period. No pump was placed into control animals. The surgical method was otherwise identical in PO, PR, and control groups and placement of the pump in the PO and PR animals did not necessitate additional anesthesia, surgical time or trauma. The volume of nicardipine plus sterile water infused was 10 xl hr. This is a negligible volume and there was no difference in the subsequent state of hydration of treated and control animals. Plasma nicardipine levels were obtained in PR and PO rats at variable intervals after placement of the pump, usually 4, 24, 48, and 96 hours. In 10 rats, serial measurements were made during drug administration. Concentrations of nicardipine in samples of plasma were determined in the Department of Analytical and Metabolic Chemistry at Syntex Research, Palo Alto by means of a capillary column GC-ECD method which has a sensitivity of 1 ng nicardipine per ml of plasma.21 Somatosensory evoked potentials SEPs ; and brainstem auditory evoked potentials BEPs ; were performed 72 hours after ischemia in 10 control, 10 PR, and 10 PO animals using a Grass model 10ERSB evoked potential instrument Grass Instrument Co., Quincy, MA ; . Previous studies in our laboratory have shown changes in SEP amplitude as early as 24 hours following ischemia, but 72 hours was chosen for this study to correlate temporally with maximal neuropathological change. All calculations of SEP and BEP amplitude and latency were performed by an observer who was not aware of which treatment each rat had received. Rats were anesthetized with an intraperitoneal injection of chloral hydrate 0.5 mg gm ; prior to testing. Preliminary studies in our laboratory have shown that this anesthetic dose has no effect on either amplitude or latency of evoked potentials. Cortical SEPs were recorded from a platinum subdermal electrode just anterior to the interaural line "vertex" position ; . Preliminary studies in our laboratory have shown that a recording electrode at this position overlies the parietal cortex. Activity from this electrode was referenced to a distant subdermal electrode placed in the lumbar area, and a ground electrode was placed on a forelimb. Stimulating electrodes were inserted bilaterally in the perinasal area. Stimuli consisted of square wave electric pulses, 0.1 msec in duration at an intensity of 3.0 volts, delivered at a rate of 2 per second. Amplifier gain was adjusted to give a.

Cortisol levels surgical 7.70 + 3.53 nmol l; medical 8.66 + 4.68 nmol l ; t 21.01, df 75, P 0.32 ; . At follow-up, 66 85% ; of subjects completed the mood questionnaire EPDS ; by phone call or mail-in self-report; 48 women 62% ; returned a repeat saliva sample. There were no differences between procedure groups in the percentage of women with follow-up EPDS P 0.53 ; and cortisol levels P 0.74 ; . In the post-abortion assessment, 17% 7 42 ; of surgical and 21% 5 24 ; medical patients scored an EPDS ! 10 x2 0.18, df 1, P 0.67 ; . The mean EPDS of the surgical 5.24 + 6.02 ; and medical 6.25 + 5.39 ; groups were not significantly different z 0.59, P 0.56 ; . The overall reduction in the percentage of women with EPDS ! 10 McNemar's x2 5.26, df 1, exact P 0.03 ; and the reduction in mean EPDS by 2.68 z 3.48, P , 0.001 ; were significant. The predictors for elevated depression risk EPDS ! 10 ; at follow-up were past psychiatric history Fisher's exact P 0.05 ; and anxiety disorders Fisher's exact P 0.005 ; . At follow-up, the mean cortisol levels of the surgical 9.86 + 6.85 nmol l ; and medical groups 6.13 + 3.89 nmol l ; were not significantly different t 2.15, df 46, P 0.04 ; . However, the change in cortisol levels between baseline and follow-up was significant in the medical but not in the surgical group z 22.17, df 1, P 0.03 and nicorette. Calcium ions. In order to characterize the type s ; of voltage-dependent Ca2 + channels involved in the stimulussecretion coupling mechanism in the neurohypophysis of the jerboa, secretory responses were compared in the absence and presence of specific Ca2 + channel antagonists. Neural lobes were initially perifused with medium containing 40 mmol l 1 Na and secretion was triggered by increasing the extracellular K + concentration to 100 mmol l 1 for 6 min. After a 60 min recovery period in medium containing 40 mmol l 1 Na the neural lobes were again depolarized for 6 min in the presence experimental ; or absence control ; of Ca2 + channel antagonists that had been added to the perifusion medium 20 min before the onset of the second stimulation. Fig. 2 illustrates representative results. The addition of nicardipine 10 6 mol l 1 ; considerably reduced the amount of both AVP 67 % reduction, N 2 ; Fig. 2B ; and OT 78 % reduction, N 2 ; not shown ; released upon K + -induced depolarization. Furthermore, when -conotoxin 3 10 8 mol l 1 ; was added together with nicardipine 10 6 mol l 1 ; to the incubating medium, the secretory response was completely abolished Fig. 2C ; . Note that the AVP release induced by the Ca2 + ionophore A23187 was apparently unaffected by nicardipine, as the amount of AVP release, compared with controls, was not significantly different when the antagonist was added to the medium Fig. 2B ; . Secretory response of the neurohypophysis during sustained electrical stimulation Neurohypophyses from normal and dehydrated animals see Materials and methods ; were stimulated over a period of 2 h with 150 AVP-like bursts separated by 30 s intervals. The results are expressed as a rate constant of AVP release Fig. 3 ; . This has the advantage of allowing the amount of AVP released into the medium, at any given time, to be compared with the AVP content of the neural lobe. Of primary interest is the observation that the rate constant of AVP release from neurohypophyses of animals dehydrated for 54 days Fig. 3B ; did not differ, under these experimental conditions, from that calculated from control experiments Fig. 3A ; . In control animals, 150 AVP-like bursts separated by 30 s intervals induced the release of 42501272 pg of AVP per neural lobe S.E.M.; N 6 ; . This is equivalent to 28.3 pg of AVP per neural lobe per burst. In animals dehydrated for 54 days, the corresponding values were 60161390 pg of AVP per neural lobe S.E.M.; N 5; 40 pg AVP per neural lobe per burst ; . In an additional experiment, 200 AVP-like bursts separated by 30 s intervals induced the release of 5590 pg of AVP per neural lobe N 1; 28 pg AVP per neural lobe per burst ; . These experiments clearly show that neural lobes from dehydrated animals release as much AVP as those from control jerboas. Fig. 4 shows the release of OT under similar conditions. It can be seen that dehydration 54 days ; does not impair the secretory mechanism for OT. It should be noted that we systematically observed, during prolonged stimulation of the neural lobe from Jaculus orientalis, a large.

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