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S Flanders

Publications and source records attributed to S Flanders.

10 recordsLinked to original sources
PubMed2006

Fetal acidemia and electronic fetal heart rate patterns: is there evidence of an association?

OBJECTIVE: Despite the ubiquity of electronic fetal monitoring, the validity of the relationship between various fetal heart rate (FHR) patterns and fetal acidemia has not yet been established in a large unselected series of consecutive pregnancies. The aim of this study was to examine the published literature for evidence of such a relationship. METHODS: Four hypotheses based on assumptions in common clinical use were examined. The literature was searched for relationships between certain aspects of FHR patterns (e.g., degree of FHR variability, depth of decelerations), and fetal acidemia, or fetal vigor (5-minute Apgar score >or=7). We also attempted to relate duration of these patterns to the degree of acidemia. Using standardized FHR nomenclature we defined patterns based on baseline FHR variability, baseline rate, decelerations, and accelerations. RESULTS: The following relationships were observed: (1) Moderate FHR variability was strongly associated (98%) with an umbilical pH >7.15 or newborn vigor (5-minute Apgar score >or=7). (2) Undetectable or minimal FHR variability in the presence of late or variable decelerations was the most consistent predictor of newborn acidemia, though the association was only 23%. (3) There was a positive relationship between the degree of acidemia and the depth of decelerations or bradycardia. (4) Except for sudden profound bradycardia, newborn acidemia with decreasing FHR variability in combination with decelerations develops over a period of time approximating one hour. Most studies identified were observational and uncontrolled (grade III evidence of US Preventive Services Task Force); however, there was general agreement amongst the various studies, strengthening the validity of the observations. CONCLUSIONS: The validity of the relationship between certain FHR patterns and fetal acidemia and/or vigor, is supported by observations from the literature. In addition four assumptions commonly used in clinical management are supported. These conclusions need to be confirmed by a prospective examination of a large number of consecutive, unselected FHR patterns, and their relationship to newborn acidemia. Pending the completion of such studies, these observations can be used to justify certain aspects of current clinical management, and may assist in standardizing the diversity of opinions regarding FHR pattern management.

Acidosis↗
PubMed2001

Assessing homeostasis through circadian patterns.

An organism is thought to be in a dynamic state of homeostasis when each physiological and behavioral system reaches a delicate balance within the framework of other regulatory processes. Many biological systems target specific set-point variables and generate circadian patterns. In this article, we focus on specific measurements representative of two systems, namely deep-body temperature and activity counts. We examine data collected every 30 minutes in mice, assume there are underlying circadian patterns, and extend the approach presented in Brumback and Rice (1998, Journal of the American Statistical Association 93, 961-976) in order to obtain estimates in the presence of correlated data. We then assess homeostasis using these estimates and their statistical properties.

Animals↗
PubMed1999

Mechanisms of melatonin-induced vasoconstriction in the rat tail artery: a paradigm of weak vasoconstriction.

1. Vasoconstrictor effects of melatonin were examined in isolated rat tail arteries mounted either in an isometric myograph or as cannulated pressurized segments. Melatonin failed by itself to mediate observable responses but preactivation of the arteries with vasopressin (AVP) reliably uncovered vasoconstriction responses to melatonin with maxima about 50% of maximum contraction. Further experiments were conducted with AVP preactivation to 5-10% of the maximum contraction. 2. Responses to melatonin consisted of steady contractions with superimposed oscillations which were large and irregular in isometric but small in isobaric preparations. Nifedipine (0.3 microM) reduced the responses and abolished the oscillations. Charybdotoxin (30 nM) increased the magnitude of the oscillations with no change in the maximum response. 3. Forskolin (0.6 microM) pretreatment increased the responses to melatonin compared to control and sodium nitroprusside (1 microM) treated tissues. The AVP concentration required for preactivation was 10 fold higher than control in both the forskolin and nitroprusside treated groups. 4. In isometrically-mounted arteries treated with nifedipine, melatonin receptor agonists had the potency order 2-iodomelatonin > melatonin > S20098 > GR196429, and the MT2-selective antagonist luzindole antagonized the effects of melatonin with a low pK(B) of 6.1+/-0.1. 5. It is concluded that melatonin elicits contraction of the rat tail artery via an mt1 or mt1-like receptor that couples via inhibition of adenylate cyclase and opening of L-type calcium channels. Calcium channels and charybdotoxin-sensitive K channels may be recruited into the responses via myogenic activation rather than being coupled directly to the melatonin receptors. 6. It is proposed that the requirement of preactivation for overt vasoconstrictor responses to melatonin results from the low effector reserve of the melatonin receptors together with the tail artery having threshold inertia. Potentiative interactions between melatonin and other vasoconstrictor stimuli probably also result from the threshold inertia. A simple model is presented and a general framework for consideration of interactions between weak vasoconstrictor agonists and other vasoconstrictor stimuli is discussed.

Acetamides↗
PubMed1998

Transitions in health-related quality of life during the first nine months after diagnosis with prostate cancer.

Health-Related Quality of Life (HRQOL) is an important outcome measure in the study of prostate cancer. There are few data regarding the effect of sociodemographic variables, such as insurance status, educational level, marital status or income, on HRQOL. We examined whether these or other sociodemographic and clinical variables are predictive of HRQOL outcomes using an observational database of prostate cancer patients accrued from a wide array of clinical practice settings. We studied 131 patients with newly-diagnosed prostate cancer who had been followed for at least nine months. Patients were enrolled in CaPSURE(TM), a large, observational database of patients with prostate cancer. General and disease-specific HRQOL were measured with established, validated instruments at diagnosis and nine months later. Sociodemographic data and co-morbidity counts were recorded at baseline. Multivariate regression analysis was used to determine whether sociodemographic or clinical variables were predictive of baseline HRQOL or HRQOL changes during the study period. Several sociodemographic and clinical variables demonstrated significant associations with HRQOL. We found improvements in general and disease-specific domains of HRQOL during the nine months after diagnosis. For married patients, Emotional Well-Being and Family Functioning scores were better at baseline (+11.8, P<0.02), but Family Functioning declined over the nine month study period (-18.5, P=0.0006). Older patients had slightly better baseline performance in several domains of HRQOL, but experienced greater HRQOL decrements over time than did younger patients. Increasing comorbidity was associated with worse baseline general HRQOL. Early tumor stage was predictive of better scores in general HRQOL domains at baseline. Limited palpable disease stage (T2A/T2B) was predictive of worse Sexual Function and Sexual Bother at nine months (-8.6, P=0.04; -24, P=0.008). After initial decreases, patients appear to experience an improvement in general and disease-specific HRQOL within nine months of initial diagnosis with prostate cancer. Marital status is associated with better HRQOL, while advancing age is associated with more significant HRQOL declines over time. Patients with lower stage disease were noted to have better general HRQOL at baseline, although decreases in the physical domains were noted at nine months. These data shed new light on patients' experience with prostate cancer and suggest that HRQOL outcomes over time may occur in a predictable manner.

Journal Article↗
PubMed1996

Effect of cold storage in University of Wisconsin solution on the responses of porcine hepatic arteries to 5-hydroxytryptamine and bradykinin in vitro.

1. Responses to 5-hydroxytryptamine (5-HT), bradykinin and sodium nitroprusside (SNP) were examined in hepatic arteries of the pig 1 h after dissection (fresh) and following 24 h storage in either Ca(2+)-free Krebs solution or the cryopreservative University of Wisconsin (UW) solution. 2. In fresh arteries contracted to approximately 40% of the maximum response to potassium with U46619, a thromboxane A2-mimetic, concentration-response curves to 5-HT (10(-10)-10(-5) M) were biphasic, with relaxation at low concentrations (< 10(-8) M) and contraction at high concentrations. Bradykinin (10(-10)-10(-7) M) produced concentration-dependent relaxation of precontracted fresh arteries with no apparent constrictor response. 3. Following 24 h storage in Ca(2+)-free Krebs solution, relaxation responses to 5-HT and the sensitivity of the arteries to bradykinin were significantly reduced. Storage in UW solution did not affect relaxation responses to either 5-HT or bradykinin. Relaxation responses to SNP (10(-8)-10(-3) M) were unaffected by storage in either solution. 4. Treatment of fresh arteries with NG-nitro-L-arginine (L-NOARG, 10(-4) M) significantly attenuated the relaxation response to 5-HT and displaced the bradykinin concentration-response curve four fold to the right with no affect on its maximum relaxation. 5. From these results it is concluded that endothelial cell function is better preserved during cold storage in UW solution than in Ca(2+)-free Krebs solution.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗