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PubMed2005

Validity and reproducibility of arterial pulse wave velocity measurement using new device with oscillometric technique: a pilot study.

BACKGROUND: Availability of a range of techniques and devices allow measurement of many variables related to the stiffness of large or medium sized arteries. There is good evidence that, pulse wave velocity is a relatively simple measurement and is a good indicator of changes in arterial properties. The pulse wave velocity calculated from pulse wave recording by other methods like doppler or tonometry is tedious, time-consuming and above all their reproducibility depends on the operator skills. It requires intensive resource involvement. For epidemiological studies these methods are not suitable. The aim of our study was to clinically evaluate the validity and reproducibility of a new automatic device for measurement of pulse wave velocity that can be used in such studies. METHODS: In 44 subjects including normal healthy control and patients with coronary artery disease, heart brachial, heart ankle, brachial ankle and carotid femoral pulse wave velocities were recorded by using a new oscillometric device. Lead I and II electrocardiogram and pressure curves were simultaneously recorded. Two observers recorded the pulse wave velocity for validation and one observer recorded the velocity on two occasions for reproducibility. RESULTS AND DISCUSSION: Pulse wave velocity and arterial stiffness index were recorded in 24 control and 20 coronary artery disease patients. All the velocities were significantly high in coronary artery disease patients. There was highly significant correlation between the values noted by the two observers with low standard deviation. The Pearson's correlation coefficient for various velocities ranged from (r = 0.88-0.90) with (p < 0.0001). The reproducibility was also very good as shown by Bland-Altman plot; most of the values were lying within 2 SD. The interperiod measurements of pulse wave velocity were also significantly correlated (r = 0.71-0.98) (P < 0.0001). Carotid-femoral pulse wave velocity was found to correlate significantly with heart brachial, heart ankle, brachial ankle pulse wave velocity and arterial stiffness index values. Reproducibility of our method was good with very low variability in both interobserver and interperiod analysis. CONCLUSION: The new device "PeriScope" based on oscillometric technique has been found to be a simple, non-invasive and reproducible device for the assessment of pulse wave velocity and can be used to determine arterial stiffness in large population based studies.

Adult↗
PubMed2002

GnRH pulse frequency modulation of gonadotropin subunit gene transcription in normal gonadotropes-assessment by primary transcript assay provides evidence for roles of GnRH and follistatin.

We examined the time course of action of GnRH pulse frequency on gonadotropin subunit gene transcription and assessed the roles of GnRH, follistatin (FS), and activin on differential transcription of the LHbeta and FSHbeta genes. GnRH-deficient male rats were pulsed with 25 ng GnRH either every 30 min (fast frequency) or every 240 min (slow frequency) for 1-24 h. Both GnRH frequencies increased alpha primary transcript (PT) 5-fold within 6 h, but only fast frequency GnRH increased alpha mRNA. Only fast frequency GnRH pulses affected LHbeta PT, resulting in 6- to 9-fold increases between 1-24 h. Fast frequency GnRH pulses transiently increased FSHbeta PT at 1 and 6 h (4- and 2-fold, respectively); but by 24 h FSHbeta PT had returned to control levels and was correlated to a 5- to 9-fold increase in FS mRNA. In contrast, slow GnRH pulses increased FSHbeta PT 3- and 6-fold at 8 and 24 h, respectively, which was correlated with a decline in FS mRNA. Activin mRNA did not change significantly after either GnRH frequency, but tended to fall after fast pulses. To test whether activin was required for the effects of GnRH on FSHbeta transcription, rats were treated with GnRH pulses every 240 min for 8 h +/- FS. FS treatment alone markedly decreased basal FSHbeta PT. GnRH in the presence of FS increased FSHbeta PT 8-fold but did not restore FSHbeta transcription to control or GnRH alone values. In summary, whereas alpha-subunit transcription is independent of frequency, an increase in alpha mRNA requires fast frequency GnRH pulses. Fast frequency GnRH pulses increased both LHbeta and FSHbeta transcription, but the response of FSHbeta was transient. The sustained rise in FSHbeta transcription and mRNA expression required slow frequency GnRH pulses and was correlated to low FS mRNA. Neutralization of pituitary activin by exogenous FS markedly reduced basal FSHbeta PT and mRNA but did not prevent the stimulation of FSHbeta transcription by slow frequency GnRH pulses. These studies suggest that the frequency regulation of FSHbeta transcription involves both direct actions of GnRH and indirect effects, via changes in pituitary FS expression.

Activins↗
PubMed1986

Evidence that the physiological pulse frequency of glucagon secretion optimizes glucose production by perifused rat hepatocytes.

We have reported that glucagon administered to perifused rat hepatocytes as a series of pulses at 15-min intervals is a more effective stimulus for hepatocyte glucose production (HGP) than is continuous glucagon infusion. To test whether the efficiency of HGP depends upon the frequency of pulsatile glucagon delivery, we administered glucagon to perifused rat hepatocytes as a series of pulses of fixed amplitude [922 +/- 30 (+/- SE) pg/ml] at eight separate pulse intervals ranging from 3-45 min. Compared to continuous infusion of the same total amount of hormone, pulsatile glucagon administration clearly enhanced HGP in a frequency-dependent fashion. At pulse intervals between 10 and 20 min, pulsatile HGP exceeded continuous HGP by a factor of 1.5-2. This range of optimal intervals compared favorably with the glucagon secretory period of 10 min observed in nonhuman primates and that of 13-20 min observed in humans. We noted a desensitization of the hepatocyte response to glucagon that was directly proportional to the log of the time-averaged hormone concentration. Since the magnitude of the desensitization elicited by pulsatile glucagon delivery exceeded the desensitization elicited by continuous hormone delivery regardless of pulse frequency, differential desensitization could not explain the frequency dependency of the pulse enhancement effect. A mathematical simulation of our data demonstrated that the asymmetry of the HGP waveform elicited by a brief glucagon pulse could account for the observed frequency dependency of HGP. Pulse to pulse summation and the desensitization phenomenon modulated both the magnitude of the pulse enhancement effect and the frequency range over which the effect was manifest. We conclude that the enhancement of HGP by glucagon pulses is a frequency-dependent phenomenon and that the physiological glucagon secretory period optimizes HGP.

Animals↗
PubMed1990

Testosterone differentially modulates gonadotropin subunit messenger ribonucleic acid responses to gonadotropin-releasing hormone pulse amplitude.

Testosterone (T) inhibits GnRH secretion and can also modulate the effects of GnRH on gonadotropin synthesis and secretion. To assess the effect of T on GnRH stimulation of alpha, LH beta, and FSH beta mRNA expression, we replaced T at three levels to reproduce low (1.5 +/- 0.5 ng/ml), medium (3.5 +/- 0.3 ng/ml), and high (6.2 +/- 0.6 ng/ml) physiological plasma concentrations. Additionally, as peripheral conversion to dihydrotestosterone (DHT) or estradiol (E2) may mediate T action, the effects of GnRH pulses in the presence of DHT and E2 were also studied. Male rats were castrated, and steroids were replaced via implants containing either T (three doses) or DHT or E2 (two doses each). GnRH pulses (10-250 ng/pulse) were administered iv at 30-min intervals for 48 h. Pituitary subunit mRNA concentrations, gonadotropin content, and LH and FSH secretion were determined. The patterns of alpha, LH beta, and FSH beta mRNA responses to increasing GnRH pulse amplitude were similar at all concentrations of plasma T. Alpha mRNA concentrations were increased 2- to 4-fold by GnRH pulses. At the same plasma T concentration, all doses of GnRH produced similar increases in alpha mRNA, but the response tended to be lower at the higher (6.2 ng/ml) levels of T. LH beta mRNA showed a clear dependence on GnRH pulse amplitude, with the maximum responses (2- to 3-fold) occurring after 10- to 25-ng GnRH pulses. At the higher (3.5 and 6.2 ng/ml) T concentrations, the dose-response curve was shifted to the left. The lowest GnRH pulse dose (10 ng) produced maximum responses, and LH beta mRNA increments in response to the higher GnRH doses were suppressed. FSH beta mRNA concentrations were increased by T in saline-pulsed controls. FSH beta mRNA responses were similar (2- to 3-fold) after all GnRH doses and at all concentrations of T. Increasing GnRH pulse doses reduced the pituitary content of both LH and FSH at all levels of T. Acute LH secretion was maximal after 10- and 25-ng pulses of GnRH when plasma T was low, but increased progressively with GnRH dose at the highest plasma T concentrations. Plasma FSH did not show any differential responsiveness to GnRH pulse dose or to increasing plasma T. Thus, LH synthesis and secretion are affected more than those of FSH by changing plasma concentrations of T. T may modulate posttranslational events in LH secretion. The higher GnRH doses effected LH release without increasing LH beta mRNA in the presence of higher physiological concentrations of T.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Dynamics of gonadotropin-releasing hormone release during a pulse.

This study examined the nature of the GnRH signal that travels down the pituitary portal vessels and causes an LH pulse. Individual GnRH pulses were described in terms of abruptness of increase and decrease, amplitude, duration, and amount of GnRH released. Pituitary portal blood was obtained at 30-sec intervals for 2.5 or 5 h from five short-term ovariectomized ewes. Jugular blood was sampled every 10 min for LH. We examined 13 GnRH pulss; each produced an LH pulse. The contour of most GnRH pulses approximated a square wave. The rising edge of the GnRH pulse was very abrupt; GnRH secretion increased as much as 50-fold within 1 min. The mean peak amount of GnRH collected during pulses (24 pg/min, range 2-66) was 70-fold greater than the interpulse baseline (0.2-0.5 pg/min). The release period was sustained an average of 5.5 min; thereafter, GnRH fell to prepulse levels within 3 min. Overall, the larger and more prolonged pulses of GnRH were associated with higher amplitude LH pulses. To assess the distortion of the GnRH signal by the collection procedure, samples were obtained in vitro using the same technique during application of 4- and 7-min square wave GnRH pulses by means of a syringe pump. Signals were carried as square-waves through the sampling operation with minimal distoration, with the exception that amplitude decreased during the collection procedure. Our findings indicate the square-wave pulses observed in vivo are an accurate description of the dynamics of GnRH release during a pulse in short-term overiectomized ewes.

Animals↗
PubMed1995

Homologous desensitization of gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone secretion in vitro occurs within the duration of an endogenous GnRH pulse.

A pulsatile GnRH signal is required for the maintenance of LH and FSH secretion. Studies in animals and in perifused pituitary cells have shown that continuous exposure to GnRH leads to decreased gonadotropin secretion and a blunted secretory response to subsequent pulses of GnRH, a process referred to as homologous desensitization. In the current study, we demonstrate that the duration of continuous GnRH exposure required to desensitize the gonadotrope in vitro is less than the durations of most in vivo GnRH pulses. Perifused male rat pituitary cells were tested with 20-sec pulses of 100 nM GnRH at 5-min intervals before, immediately upon termination of, and after GnRH infusions of varying concentration and duration. Desensitization in response to a GnRH infusion was calculated as the decrease in the LH response to the pulse of GnRH immediately after the infusion (Dsn pulse) compared to the mean LH response to GnRH pulses before and after the infusion. Gonadotropes were completely desensitized after a 2-min infusion of 10 nM GnRH (P < 0.05), the shortest duration tested. Endogenous GnRH pulses, by contrast, average more than 5 min in length. When the duration of GnRH infusion was held constant at 4 min, a concentration response for GnRH-induced desensitization was observed. Gonadotropes were desensitized by GnRH concentrations as low as 1 nM (P < 0.05), and maximal desensitization was observed with 5 nM GnRH. To determine the recovery period for GnRH-induced desensitization, a second series of experiments was performed. Experiments were conducted as described above, except the cells were perifused with medium that did not contain GnRH (recovery) for varying periods between the GnRH infusion and the Dsn pulse. A small response (16% of control) to the Dsn pulse of GnRH was observed after 1 min of recovery, and the response was not different from the control value (P > 0.05) after a 3-min recovery period. This recovery period is consistent with the ability to respond to endogenous GnRH pulses, which rarely exceed two per h. We conclude that GnRH-induced secretory desensitization and recovery occur within endogenous GnRH pulse durations and interpulse intervals, respectively. These data raise the possibility that homologous desensitization occurs under some in vivo conditions, providing an unexpected mechanism for physiological regulation of gonadotropin secretion.

Animals↗
PubMed1995

Gonadotropin-releasing hormone (GnRH) pulse pattern regulates GnRH receptor gene expression: augmentation by estradiol.

GnRH acts via a single cell surface receptor (GnRH-R), and the number of pituitary GnRH-R increases on proestrus, after gonadectomy, or in response to pulsatile GnRH in the rat. Estradiol (E2) is known to exert a transient positive action to increase GnRH-R number, and the rise in plasma E2 contributes to initiation of the midcycle LH surge. The present study was designed to determine the effect of GnRH pulse amplitude and frequency on GnRH-R messenger RNA (mRNA) levels and to assess the relative contributions of GnRH and gonadal steroids to increasing GnRH-R gene expression. These studies were conducted in vivo using previously characterized GnRH-deficient male (castrate testosterone-replaced) and ovariectomized phenoxybenzamine-treated female models. To investigate the effect of GnRH pulse amplitude, adult male and female rats received GnRH iv (5-250 ng/pulse at 30-min intervals; saline pulses to controls) for 12 or 24 h. In males, GnRH-R mRNA was increased by all pulse doses, with maximal effects (3-fold) at 5-25 ng/pulse. In contrast, only lower doses (5-10 ng/pulse) were effective in females (2-fold increase). In a subsequent study, GnRH pulses (25 ng for males; 10 ng for females) were given at 8-, 30-, or 240-min intervals for 12 or 24 h. Some animals received a continuous GnRH infusion (200 ng/h). In males, GnRH-R mRNA levels were stimulated by all GnRH pulse intervals (maximal after 30-min pulses), whereas continuous GnRH was ineffective. In females, only 30- and 240-min pulse intervals increased GnRH-R mRNA levels, with faster (8-min) pulses or continuous GnRH being ineffective. To determine the relative roles of ovarian steroids and GnRH, ovariectomized phenoxybenzamine-treated female animals received GnRH (10 ng/pulse, 30-min interval), E2 (via sc implants; plasma E2 levels, approximately 50 pg/ml), or their combination for 12-24 h (saline pulses to controls). In the absence of E2, GnRH-R concentrations fell by 70% between 12-24 h. E2 alone tended to increase GnRH-R mRNA at 12 h, with a 2-fold rise observed after 24 h. Pulsatile GnRH alone increased GnRH-R mRNA by 50% at 12 h (compared to saline-pulsed controls; P < 0.05) and by 6-fold after 24 h. When GnRH and E2 were combined, the magnitude of the increase (vs. saline controls) was greater than that seen for either GnRH or E2 alone.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

Count and spark? The echo response of the weakly electric fish Gnathonemus petersii to series of pulses.

Weakly electric fish of the pulse type electrolocate objects in the dark by emitting discrete electric organ discharges (EODs) separated by intervals of silence. Two neighbouring pulse-type fish often reduce the risk of discharging simultaneously by means of an 'echo response': one fish will respond to a neighbour's EOD with a discharge of its own following at a fixed short latency so that its EOD will occur long before the next EOD of its neighbour. Although working elegantly for two partners, this simple strategy should fail in larger groups because two fish could discharge in response to the same EOD of a third fish. Here, I show that the mormyrid fish Gnathonemus petersii could use a simple mechanism to reduce this problem. Individuals were stimulated with two closely spaced pulses, the second following so as to coincide with an echo given in response to the first. All the fish examined were able to respond more to the second pulse so that most of their echoes did not collide with the second pulse. An analysis was made of how echoing more to the second pulse depends on (i) the delay at which the stimulus followed the last spontaneous EOD, (ii) the spontaneous firing rate, (iii) the intensity of the stimulus, (iv) the number of stimulus pulses, (v) the interval between stimulus pulses, and (vi) the level of previous stimulation with double pulses. The results suggest that echoing more in response to the second pulse is probably because the first pulse causes an after-effect whose inferred properties would be compatible with the properties of the mormyromast afferences thought to be involved in the echo response.

Animals↗
PubMed1976

Delayed initiation of SS1 pulses in the sea anemone Calliactis parasitica: evidence for a fourth conducting system.

1. Single electrical shocks to the column sometimes elicit a series of 1-6 pulses in the SS1 (ectodermal slow system) but the first pulse does not appear until 5-28 s after stimulation. These pulses occur in addition to the early SS1 pulse which follows every shock and which has a conduction delay of less than 1 s. 2. The threshold of the delayed SS1 response is different from the thresholds of the three known conducting systems (through-conducting nerve net, SS1, and SS2). 3. In the case of stimulation of the column, the delayed SS1 pulses do not arise at the point of stimulation but probably originate in the tentacles or upper column. The pulse origin can shift during a single burst. 4. The pathway from the point of stimulation to the site of origin of delayed SS1 pulses is endodermal. We propose that this pathway represents a fourth conducting system (Delayed Initiation System--DIS). The DIS must connect, across the mesogloea, with the ectodermal SS1. The long pulse delay and repetitive firing may derive from pacemaker activity in the DIS. The DIS pacemakers closely resemble the pacemakers connected to the through-conducting nerve net. The DIS may be neuronal. 5. Delayed SS1 pulse bursts from unattached anemones showed an earlier onset, and more pulses/burst, than those from attached anemones. 6. Delayed SS1 pulses can also be evoked by electrical, and in some cases mechanical, stimulation of the pedal disc, tentacles, and pharynx, but there are regional differences in the number of pulses evoked, in their delay, and in their site of origin.

Action Potentials↗
PubMed1989

LHRH pulse frequency in normal and infertile men.

The aim of this study was to examine the hypothesis that decreased LHRH pulse frequency may be responsible for the preferential rise in FSH in infertile men. The LH pulse pattern was determined as an index of hypothalamic LHRH secretion in 21 infertile patients with idiopathic azoospermia or oligoasthenozoospermia and 14 fertile age-matched controls by frequent blood sampling at 10-min intervals for 24 h. The infertile patients were further divided into three groups according to their relative concentrations of FSH and LH: (1) normal FSH and LH, (2) raised FSH but normal LH, and (3) raised FSH and LH. LH pulses were detected by a computerized algorithm (Munro) validated against a threshold method. Concentrations of FSH, testosterone, sex hormone-binding globulin and oestradiol were measured in pooled plasma. Luteinizing hormone pulse frequencies in normal men were not significantly different from the infertile group as a whole. Similarly, mean LH pulse frequencies in infertile subgroups 1, 2 and 3 were not significantly lower than normal. Pulse interval, however, was increased in subgroup 1 compared with normal. Mean 24 h LH in group 2 was significantly higher than normal, but still within the normal range. The total testosterone, but not the free testosterone index was significantly decreased in the infertile group compared with normal. There was no correlation between mean FSH and LH pulse frequency or interval. In conclusion, our results show that in patients with seminiferous tubular dysfunction, the typical pattern of raised plasma FSH, increased LH pulse amplitude, raised FSH: LH ratio and normal or marginally low testosterone was not associated with any significant deviations in LHRH pulse frequency from the range observed in normal fertile men. This is not compatible with the hypothesis that decreased LHRH pulse frequency is associated with or the cause of the preferential rise in FSH in men with idiopathic infertility. Thus unlike anovulatory infertility in females, functional defects of hypothalamic LHRH secretion remain an uncommon finding in male infertility. Attempts to treat idiopathic oligozoospermia by altering LHRH pulse frequency is therefore unlikely to yield any clinical benefit.

Adult↗
PubMed1996

Reduction of radiation dose in pediatric patients using pulsed fluoroscopy.

OBJECTIVE: The purpose of this study was to determine if pulsed fluoroscopy reduces radiation exposure to pediatric patients undergoing conventional fluoroscopy. SUBJECTS AND METHODS: Four hundred one consecutive patients were nonrandomly divided into pulsed fluoroscopy and conventional fluoroscopy study groups. Two control groups were also assembled: 474 patients evaluated with conventional fluoroscopy before the study and 138 patients evaluated with pulsed fluoroscopy after the study. RESULTS: We found no difference in fluoroscopy times across the groups. Although the number of digital spot films was slightly higher for the pulsed fluoroscopy study group than for the conventional fluoroscopy study group, we found no difference in the number of digital spot films for the pulsed fluoroscopy study group and for the conventional fluoroscopy control group. Furthermore, the difference in the number of digital spot films was also insignificant for the pulsed fluoroscopy control group and the conventional fluoroscopy study group. The radiation exposure in the pulsed fluoroscopy study group was 50% lower (mean, 0.6 R) than in the conventional fluoroscopy study group. When using pulsed fluoroscopy in the 7.5 pulses-per-second mode, we were able to reduce radiation exposure by 75% of that from conventional fluoroscopy. CONCLUSION: Pulsed fluoroscopy reduces fluoroscopic radiation exposure to pediatric patients undergoing conventional fluoroscopy. Despite minor image degradation, pulsed fluoroscopy is the technique of choice at our institution.

Arthrography↗
PubMed1986

A comparison of local and remote masking on tactile pulse detection using different masking patterns.

Forward and backward masking functions were obtained for the detection of a 2-msec. tactile "test" pulse using two different masking patterns (5- or 10-pulse sequences) under conditions of both local and remote masking. Twelve ISIs (interval between "test" pulse and onset of the masking sequence) ranging from 10 to 76 msec. were used. A two-interval forced-choice (2-IFC) procedure was used in which observers were presented with two successive trains of tactile pulses, one having the "test" pulse at varying intervals prior (backward masking) to or after (forward masking) the masking sequence and one train having only a masking sequence. Observers were asked to report in which train of pulses they detected the "test" pulse. With local masking, i.e., when "test" pulse and masking sequence were presented to the same locus, there was substantially more forward than backward masking, and the 10-pulse sequence resulted in consistently greater amounts of masking than the 5-pulse mask. When the "test" pulse and masking sequence were delivered to different loci, i.e., the remote masking, the results were much less systematic. The data suggest that both peripheral and central factors contribute to the obtained masking functions and that both integration and interruption are producing the masking interference.

Discrimination Learning↗
PubMed1999

Pulsed-dose-rate and low-dose-rate brachytherapy: comparison of sparing effects in cells of a radiosensitive and a radioresistant cell line.

Pulsed-dose-rate regimens are an attractive alternative to continuous low-dose-rate brachytherapy. However, apart from data obtained from modeling, only a few in vitro results are available for comparing the biological effectiveness of both modalities. Cells of two human cell lines with survival fractions of 80% (RT112) and 10% (HX142) after a single dose of 2 Gy and with different halftimes for split-dose recovery and low-dose recovery were used. The cells were irradiated with a continuous low dose rate (80 cGy per hour) or with pulsed dose rate. Two different pulsed dose rates were tested: 4.25 Gy/h and 63 Gy/h. The effects of dose per pulse and the length of the interval between the pulses were investigated while keeping the overall treatment time constant. Survival after low-dose-rate irradiation was indistinguishable from that after pulses of 4.25 Gy/h in cells of both cell lines. Survival decreased with increasing dose per pulse. When the dose rate during the pulses was increased, survival decreased even further. This effect was most pronounced for the radiosensitive HX142 cells. In clinical pulsed-dose-rate brachytherapy, iridium sources move stepwise through the implant and deliver pulses at a high dose rate locally. These high-dose-rate pulses produce greater biological effectiveness compared to continuous low dose rate; this should be taken into account.

Brachytherapy↗
PubMed2000

Next-generation pulse oximetry. Focusing on Masimo's signal extraction technology.

Pulse oximeters are used to determine trends in patients' blood oxygen saturation and to warn of dangerous saturation levels. But conventional pulse oximetry has some inherent limitations. For example, it has difficulty monitoring patients who are moving or who have poor perfusion; it is also subject to interference from certain visible and infrared light sources. Over the past several years, a number of companies have developed advanced signal-processing techniques that allow pulse oximeters to overcome many of these limitations. We refer to such new technologies as next-generation pulse oximetry. In this Evaluation, we focus on the first next-generation technology to have reached the market: Masimo Corporation's Signal Extraction Technology (SET). We designed our study of Masimo SET to address the main question that needs to be asked of any next-generation technology: How well does it compare to conventional pulse oximetry? Specifically, how well does it perform when a patient is moving or being moved, when a patient is poorly perfused, or when certain types of light strike the sensor while it is attached to or detached from the patient? We also examined one type of sensor used with this product, comparing it to conventional tape-on sensors for comfort and durability. Several other next-generation pulse-oximeter products have become available since we began this study. We are currently evaluating these products and will publish our findings in the near future. A list of the products, including a brief description of each, is included in this article. Pulse oximeters are used to determine trends in patients' blood oxygen saturation and to warn against dangerous saturation levels. These monitors are often vital in helping to ensure patient safety, especially for critically ill patients, pediatric patients, and neonates. But conventional pulse oximetry has some inherent limitations--most significantly, it has difficulty monitoring patients who are moving or who have poor perfusion. Although gradual improvements have been made to the technology, only recently has it advanced to the point where it has really begun to overcome these limitations. A number of manufacturers have developed advanced signal-processing algorithms that allow pulse oximeters to "read through" motion and conditions of poor perfusion. The first of these "next-generation" pulse-oximeter technologies that reached the market was Masimo Corporation's Signal Extraction Technology (SET). We tested that product in this Evaluation. In this Overview, we'll tell you about conventional pulse oximetry and its shortfalls, next-generation technology and how it's designed to improve on the old methods, and how we approached our Evaluation of Masimo SET.

Adult↗
PubMed2005

[Induction of active antitumor immune response by myeloma idiotype protein-pulsed dendritic cells].

BACKGROUND & OBJECTIVE: Most multiple myeloma (MM) patients could not be cured by high-dose chemotherapy and bone marrow transplantation. This study was designed to investigate in vitro killing effect of tumor-specific cytotoxic T lymphocytes (CTLs) stimulated by idiotype protein (Id)-pulsed dendritic cells (DCs) on autologous MM cells. METHODS: DCs were generated from peripheral blood monocytes of 6 MM patients using interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF). After cultured for 5 days, immature DCs were pulsed with Idû tumor necrosis factor-alpha (TNF-alpha) was added at the 7th day. Id-pulsed DCs were cocultured with autologous T cells for 3 days to induce tumor-specific CTLs. MTT assay was used to detect proliferation of autologous T cells, and evaluate killing effect of CTLs on autologous MM cells. RESULTS: Mature DCs were successfully induced. Id-pulsed DCs markedly increased proliferation of autologous T cells in a dose-dependent manner; stimulation index (SI) of Id-pulsed DCs was the highest [(39.1+/-6.0)%] when the radio of DCs to T cells was 10:1, which was significantly higher than those of unpulsed mature DCs [(19.3+/-7.7)%], Id-pulsed immature DCs [(15.9+/-6.1)%], and unpulsed immature DCs [(11.4+/-4.9)%] (P < 0.01). Id-pulsed DCs induced anti-MM activity of CTLs in a dose-dependent manner. Unpulsed mature DCs also induced cytotoxicity of CTLs against autologous MM cellsû however, when DC:T was 30:1, killing rate of MM cells was significantly higher in Id-pulsed mature DCs group than in unpulsed mature DCs group [(70.1+/-7.9)% vs. (40.8+/-7.8)%,P < 0.05]. KRN7000-pulsed mature DCs stimulated proliferation of allogeneic T cells in a dose-dependent manner; when DC:T was 1:10, SI was significantly higher in KRN7000-pulsed mature DCs group than in unpulsed mature DCs group [(38.5+/-5.7)% vs. (20.2+/-5.7)%, P < 0.05]. CONCLUSIONS: Mature DCs could be induced and Id with biological activity could be extracted from peripheral blood of MM patients. Id-pulsed DCs could induce antitumor immune response. KRN7000 could improve the immune function of in vitro cultured DCs.

Adult↗
PubMed1990

[Effect of methylprednisolone pulse therapy in patients with lupus nephritis assessed by WHO morphologic classification].

To determine indications for treatment with high-dose intravenous methylprednisolone pulse therapy in lupus nephritis, we retrospectively assessed the response to pulse therapy over oral prednisolone administration in 120 biopsy proven lupus nephritis patients according to WHO morphologic classification. In the pulse group, 1 g of methylprednisolone was administered on three consecutive days and oral steroid therapy (40-30 mg) was started. In many occasions in treating class III and IV-b, repeated pulse therapy was performed. In control oral prednisolone group, middle-dose steroid therapy (50-30 mg) was started. In patients with minor glomerular abnormalities and mesangial lupus nephritis, rapid improvement of serological activities was observed in pulse group assessed by serum complement level, anti-DNA antibodies, and anti-nuclear antibodies. In patients with focal lupus nephritis, rapid rise in serum complement level and fall in proteinuria was observed in the pulse group. In patients with diffuse proliferative lupus nephritis with active necrotizing lesions, faster rise in serum complement level and proteinuria were observed in the pulse group. In patients with membranous lupus nephritis there was no significant difference between two groups. In comparison with the effect of pulse therapy among each morphologic class, the rise of serum complement level was slowest in class IV-b. Both group of IV-b and V manifested nephrotic syndrome and by pulse therapy the decrease in urinary protein was faster and more significant in class IV-b compared with class V. No significant adverse effect of methylprednisolone was observed during about 150 times of pulse therapy. Bacterial, viral infections such as herpes zoster and fungal infections were observed in pulse group as often as control group.

Administration, Oral↗
PubMed1995

Considerations for human exposure standards for fast-rise-time high-peak-power electromagnetic pulses.

Development of new emitter systems capable of producing high-peak-power electromagnetic pulses with very fast rise times and narrow pulse widths is continuing. Such directed energy weapons systems will be used in the future to defeat electronically vulnerable targets. Human exposures to these pulses can be expected during testing and operations. Development of these technologies for radar and communications purposes has the potential for wider environmental exposure, as well. Current IEEE C95.1-1991 human exposure guidelines do not specifically address these types of pulses, though limits are stated for pulsed emissions. The process for developing standards includes an evaluation of the relevant bioeffects data base. A recommendation has been made that human exposure to ultrashort electromagnetic pulses that engender electromagnetic transients, called precursor waves, should be avoided. Studies that purport to show the potential for tissue damage induced by such pulses were described. The studies cited in support of the recommendation were not relevant to the issues of tissue damage by propagated pulses. A number of investigations are cited in this review that directly address the biological effects of electromagnetic pulses. These studies have not shown evidence of tissue damage as a result of exposure to high-peak-power pulsed microwaves. It is our opinion that the current guidelines are sufficiently protective for human exposure to these pulses.

Animals↗
PubMed1993

L-2-amino-4-phosphonobutanoic acid and 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid reduce paired-pulse depression recorded from medial perforant path in the dentate gyrus of rat hippocampal slices.

The perforant path is the major excitatory cortical projection to the hippocampal dentate gyrus. Field potentials from the medial perforant path exhibit paired-pulse depression when evoked at interstimulus intervals of 40 to 800 msec. We found that an early component of paired-pulse depression recorded at interstimulus intervals of 40 to 100 msec from slices of rat hippocampus was reduced by L-2-amino-4-phosphonobutanoic acid (L-AP4) (20 microM) without a change in the size of the first field potential in the pair. Paired-pulse depression evoked at intervals of 200 to 800 msec was not reduced. 1S,3R-1-Aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD), DL-2-amino-3-phosphonopropionic acid and carbachol also reduced paired-pulse depression in a manner similar to L-AP4. Picrotoxin, phaclofen, theophylline or atropine did not reduce paired-pulse depression. Furthermore, paired-pulse depression (40-100 msec) does not appear to involve glutamate uptake or N-methyl-D-aspartate receptors as L-alpha-aminoadipate did not alter paired-pulse depression and neither trans-L-pyrrolidine-2,4-dicarboxylate and L-alpha-aminoadipate nor D-2-amino-5-phosphonopropionic acid blocked the effect of L-AP4 on paired-pulse depression. 4-Aminopyridine inhibits a potassium current that has a similar time course to the L-AP4-induced reduction of paired-pulse depression, however, paired-pulse depression was increased with exposure to 4-aminopyridine. These results indicate that the mechanism underlying paired-pulse depression consists of two components, the early component being reduced by L-AP4, 1S,3R-ACPD, DL-2-amino-3-phosphonopropionic acid and carbachol.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminobutyrates↗