Silicon optical fiber.

Described herein are initial experimental details and properties of a silicon core, silica glass-clad optical fiber fabricated using conventional optical fiber draw methods. Such semiconductor core fibers have potential to greatly influence the fields of nonlinear fiber optics, infrared and THz power delivery. More specifically, x-ray diffraction and Raman spectroscopy showed the core to be highly crystalline silicon. The measured propagation losses were 4.3 dB/m at 2.936 microm, which likely are caused by either microcracks in the core arising from the large thermal expansion mismatch with the cladding or to SiO(2) precipitates formed from oxygen dissolved in the silicon melt. Suggestions for enhancing the performance of these semiconductor core fibers are provided. Here we show that lengths of an optical fiber containing a highly crystalline semiconducting core can be produced using scalable fiber fabrication techniques.

End-stage renal disease in specific ethnic and racial groups: risk factors and benefits of antihypertensive therapy.

During the past few years, it has become apparent that there are factors that place a person at greater risk for the development and progression of renal failure. This has been documented since the early 1980s by the United States Renal Data System that has collected data confirming that end-stage renal disease occurs at a greater rate in certain subpopulations of Americans. It is evident from an examination of the data that African Americans and American Indians have an incidence of end-stage renal disease that is not proportional to their percentage of the total population. In fact, African Americans and American Indians are reported to have at least a 4-fold greater incidence of end-stage renal disease than white Americans. There have been 5 factors identified: hypertension, glucose intolerance, insulin resistance, salt sensitivity, and hyperlipidemia, which may play a greater role in these subpopulations. In addition, as with other populations, lifestyle issues may serve to alter these primary risk factors or may act as direct modulators of renal disease progression. There is also a possibility that interactions between risk factors frequently occur that may modify the development or progression of the disease. This article reviews these risk factors and emphasizes the interaction between hypertension and the other factors. In addition, the effects of antihypertensive agents on risk factors and on renal outcome are emphasized. Where possible, issues specific to African Americans and American Indians are underscored; however, one must accept that the database on these populations is only now developing. This review should help the clinician make appropriate choices when prescribing antihypertensive therapy for patients who may be at risk of developing progressive renal failure.

Erythropoietin in preeclampsia.

To investigate the possible effect of preeclampsia on erythropoietin metabolism, we measured plasma and urine erythropoietin concentrations and complete blood count in 19 women with preeclampsia and nine healthy gravidas. Hemoglobin concentration and hematocrit values in the preeclamptic patients did not differ significantly from those of the normal pregnant controls. However, the plasma erythropoietin concentration tended to be higher in the preeclamptic group than in the normal pregnant controls (26.9 +/- 31.2 versus 11.2 +/- 9.9 mU/mL), though the difference was not statistically significant. Plasma erythropoietin concentration correlated negatively with both hemoglobin concentration and hematocrit (r = -0.85, P less than .01). The pattern and magnitude of the erythropoietin response to anemia paralleled that previously reported in individuals with iron deficiency anemia. No significant correlation was found between urinary erythropoietin excretion and blood pressure, qualitative albumin excretion, hematocrit, hemoglobin concentration, or plasma erythropoietin concentration. Based on our results, the erythropoietin response to anemia appears to be intact in preeclampsia, at least in the absence of renal failure.

Gonadotropin-releasing hormone agonist use in assisted reproduction cycles: the influence of long and short regimens on pregnancy rates.

OBJECTIVE: To compare the efficacy of GnRH agonists used in either the flare (short) or down-regulation (long) regimen as part of IVF or GIFT treatment cycles. DESIGN: Observational study. SETTING: Three IVF clinics. PATIENT(S): One thousand two hundred forty-four couples accepted for IVF or GIFT treatment at participating clinics. INTERVENTION(S): In vitro fertilization or GIFT protocols standard to each clinic were recorded. MAIN OUTCOME MEASURE(S): Treatment cycle characteristics and outcomes, including E2 level, number of oocytes retrieved, and clinical pregnancy rate. RESULT(S): At site 1, there were 146 clinical pregnancies in 980 flare cycles, for a pregnancy rate of 14.9%, compared with 148 clinical pregnancies in 650 down-regulation cycles, for a pregnancy rate of 22.8%. This difference persisted after adjustment for age, primary infertility diagnosis, GIFT or IVF therapy, and year of treatment, and appeared to be mediated largely by the number of oocytes retrieved (mean, 9.8 for downregulation and 8.7 for flare in the first cycle). Despite having fewer oocytes retrieved, women who received flare regimens had higher E2 levels before hCG administration. CONCLUSION(S): Women who received GnRH agonists in a flare regimen had 11% fewer oocytes retrieved and a 35% reduction in the clinical pregnancy rate compared with those who received them in a down-regulation regimen; this difference was not explained by patient selection factors.

Nitro containing L-arginine analogs interfere with assays for nitrate and nitrite.

We evaluated the effect of in vivo and in vitro administration of nitro-containing and nitro-deficient L-arginine-derived nitric oxide (NO) synthase inhibitors on the measurement of NO in plasma, urine and HEPES buffered physiologic salt solution (PSS) by ozone chemiluminescence and by the modified Griess reaction. In vivo administration of 1, 5, 25, 40 or 50 mg/kg of NG-nitro-L-or D-arginine methyl ester (LNAME, DNAME), NG-nitro-L-arginine (LNA) or aminoguanidine (AG) to rats and mice increased NO in urine and plasma as determined by chemiluminescence using 2.3% vanadium chloride in 2N HCI at 100 degrees C as the redox reagent. In vivo administration of 1 and 10 mg/kg/day of NG-imino-ethyl-L-ornithine (LNIO) or 3 amino-1,2,4 triazine (AT) reduced plasma and urine NO. Addition of LNAME, DNAME and LNA (100 nM to 1 mM) to the redox solution produced a concentration response curve for NO in the chemiluminescence assay similar to that produced by standard solutions of sodium nitrite and nitrate. LNMMA produced a small NO signal but only at concentrations equal to or exceeding 0.1 mM. LNIO, AT and AG did not give any NO signal even at concentrations exceeding 1 mM. Conversion of plasma or urine nitrate to nitrite with cadmium gave elevated values of plasma nitrite by the Greiss assay when LNAME or LNA was the NO synthase inhibitor. We conclude that in vivo and in vitro use of LNAME and LNA and in vivo use of high doses of aminoguanidine interfere with the assay of NO2- and NO3- with the modified Griess reaction and with chemiluminescence. We suggest that LNAME and LNA not be used in vivo or in vitro when total RNI is measured with these assays.

Parenteral hydralazine revisited.

Historical aspects of the development and application of the vasodilator hydralazine are reviewed. The pharmacology, pharmacokinetics, metabolism, and mechanism of action are discussed, with emphasis on the parenteral use of this drug. It is reiterated that parenteral hydralazine is the preferred drug for the treatment of severe preeclampsia, but its usefulness in other forms of accelerated hypertension is also addressed. Through comparisons with other established antihypertensive agents, the efficacy and pharmacoeconomic potential of hydralazine are stressed.

A unique hypertonic response to hypotonic infusion in the pregnant ewe.

OBJECTIVE: The purpose of this study was to compare the responses of the maternal ewe to intravenous volume expansion with either sufficient lactated Ringer's solution to elevate maternal venous pressure or sufficient hypotonic fluid to reduce blood osmolality. STUDY DESIGN: Chronically catheterized pregnant sheep were intravenously infused over 4 hours with either commercial lactated Ringer's solution (5.55 +/- 0.50 L/hr, 255 mOsm/kg, mildly hypotonic) or diluted Ringer's solution (2.04 +/- 0.27 L/hr, 150 mOsm/kg, markedly hypotonic). Data were statistically analyzed with two- and three-factor analyses of variance and bivariate regression analysis. RESULTS: During the mildly hypotonic infusion (n = 8) the maternal blood osmolality changes were -5.1 +/- 1.2, +2.7 +/- 1.0 and +6.8 +/- 1.1 mOsm/kg at 1 and 4 hours of infusion and 1 hour after the infusion. In four of the eight animals in this group profuse diarrhea developed. During the markedly hypotonic infusion (n = 11) the maternal blood osmolality changes were -9.9 +/- 1.1, -15.9 +/- 2.5, and -10.4 +/- 2.2 mOsm/kg at 1 and 4 hours of infusion and 1 hour after the infusion. Although urine osmolalities were significantly less than the osmolality of the infusate in both groups, only during the mildly hypotonic infusion was there a net loss of free water by the kidneys. The renal free water loss, the venous pressure increase, and the blood osmolality decrease were not significantly different whether diarrhea did or did not develop. CONCLUSION: The infusion of large volumes of mildly hypotonic Ringer's solution to the pregnant ewe produces a paradoxic increase in maternal plasma osmolality as a result of the excretion of large volumes of free water by the kidneys, and if the venous pressure is increased more than about 6 mm Hg with this infusion, diarrhea develops in the animals.

Fetal cardiovascular and fluid responses to maternal volume loading with lactated Ringer's or hypotonic solution.

To determine whether elevations in maternal vascular pressures or reductions in maternal osmolality would promote fluid transfer to the fetus, we intravenously infused either lactated Ringer's solution or diluted (hypotonic) lactated Ringer's solution continuously over 4 hours into late-gestation pregnant sheep. During the Ringer's solution infusion, the increases in maternal arterial (20.7 +/- 1.7 mm Hg, mean +/- SE) and venous (6.6 +/- 0.9 mm Hg) pressures were significantly greater (p less than 0.00001) than those during the hypotonic infusion (6.6 +/- 1.5 and 1.7 +/- 0.6 mm Hg, respectively). The maternal osmolality changes during the Ringer's infusion (-5.7 +/- 1.2 mOsm/kg at 1 hour and +6.8 +/- 1.1 mOsm/kg at 1 hour and -15.9 +/- 2.5 mOsm/kg at 5 hours). Fetal vascular pressures and blood volume were unchanged during either infusion. Fetal heart rate decreased by 15 to 20 beats/min by 1.5 hours of infusion in both groups but remained decreased only in the hypotonic group. Fetal urine flow decreased at the end of the Ringer's infusion and increased during the hypotonic infusion. These urine flow changes correlated with opposite changes in fetal plasma osmolality. The four-quadrant amniotic fluid index tended to increase in both groups, with an overall nonsignificant increase of 32% +/- 16% 1 hour after the infusions. In summary, our findings suggest that (1) acute increases in maternal vascular pressures do not appear to promote fluid transfer to the ovine fetus and (2) acute decreases in maternal osmolality result in a small shift of fluid into the fetus as evidenced by an increase in fetal urine flow.

Atrial natriuretic peptide and arginine vasopressin in pregnancy and pregnancy-induced hypertension.

Atrial natriuretic peptide (ANP) and arginine vasopressin concentrations were measured in 9 patients with pregnancy-induced hypertension. The results were compared to those found in 7 normal pregnant women matched for age, duration of pregnancy, and parity. Plasma ANP levels were significantly higher in the pregnancy-induced hypertension patients than in the control group. Plasma arginine vasopressin concentrations, however, were not significantly different in the two populations. The mechanism of the observed rise in ANP concentrations in the patients with pregnancy-induced hypertension is not known. However, it may be related to a rise in intra-atrial pressures secondary to hypertension, an increase in baroreceptor discharge as a result of hypertension, or, less likely, the ANP may be released from extracardiac sites.

Ethanol suppresses endotoxin but not platelet activating factor-induced hypotension and nitric oxide.

Ethanol (ETOH) inhibits the immune response to endotoxemia. The early stage of endotoxin (LPS)-induced shock is associated with an acute phase cardiovascular depression (APCD). Release of platelet activating factor (PAF) and tumor necrosis factor alpha (TNF alpha) with upregulation of nitric oxide (NO) production may initiate the APCD. Since ETOH inhibits induction of NO synthase (iNOS) mNRA by LPS, we postulate that ETOH may mask the APCD associated with endotoxemia. To test this, Sprague-Dawley rats (280-320 g, n = 5-6/group) were given LPS [0.75 mg/kg, intravenously (i.v.)] or PAF (10 to 150 micrograms/kg, i.v.) 30 min after administration of sterile saline (PBS), BN-5073 a mixed PAF antagonist (0.50 microgram/kg, i.v.), or ETOH [2.2-5.5 g/kg, intraperitoneally (i.p.)]. Cardiovascular parameters and plasma concentrations of nitrate and nitrite (RNI), ETOH, TNF alpha, and neutrophil (PMN) generation of RNI were measured. LPS and PAF both produced APCD. LPS-induced APCD was associated with tachycardia, elevated plasma TNF alpha and RNI, and ex vivo generation of RNI by PMNs. ETOH and BN-50730 prevented LPS-induced APCD and increases in RNI and TNF alpha. ETOH, however, increased the mortality associated with APCD. PAF produced only hypotension, bradycardia and elevated plasma levels of TNF alpha. ETOH and LNMMA did not affect PAF-induced APCD. BN-50730 inhibited PAF-induced APCD and plasma TNF alpha. We conclude that 1) ETOH inhibits the APCD and induction of NO characteristic of endotoxemia and 2) ETOH-induced suppression of LPS-mediated APCD may be mediated in part by suppression of release of intracellular PAF. Ethanol may increase the morbidity and mortality of endotoxemia by masking the hypotension and humoral changes characteristic of early endotoxemia thereby delaying appropriate therapy and by diminution of the protective effects of endogenous NO.

Acute maternal renal insufficiency in premature labor treated with indomethacin.

Three cases of acute renal insufficiency in pregnant women who were treated with indomethacin for premature labor are reported. At the time of presentation, all three women had normal renal function but within 30 hours of indomethacin therapy they were noted to have significant decreases in urine output and rising serum creatinines. The average time to recovery of renal function was 5 days. A consistent feature in all three women was the development of dyspnea associated with hypoxemia.

Effects of NO synthase inhibitors, arginine-deficient diet, and amiloride in pregnant rats.

This study tests the hypothesis that nitric oxide synthase (NOS) inhibition is linked to NG-nitro-L-arginine methyl ester (L-NAME)-mediated intrauterine growth retardation (IUGR) and fetal limb reduction deficits (LRD) in pregnant dams. Administration of L-NAME (1 mg/ml) or aminoguanidine (AG, 500 micrograms/ml) in the drinking water or intraperitoneal administration of L-N5-(1-iminoethyl)-ornithine (L-NIO, 10 mg.kg-1.day-1) on gestational days 13-20 decreased nitrite and nitrate plus nitrate (RNI) levels in the urine and plasma and decreased RNI in incubates of aorta and fetal limbs compared with pregnant rats given amiloride (50 micrograms/ml) or water (control). Although all drugs caused fetal IUGR, only L-NAME and amiloride caused fetal deaths and LRD. Urine and tissue levels of RNI were unchanged in rats fed and arginine-free diet (AFD) on gestational days 13-20, and yet fetal IUGR, deaths, and LRD were prevalent. L-NAME potentiated the fetal abnormalities and resorptions. Plasma arginine concentrations decreased with AFD > > L-NAME > L-NIO. Plasma ornithine, a precursor for polyamine synthesis, decreased with AFD and increased with L-NAME. Thus inhibition of NOS is not linked to LRD. The ability of L-NAME and amiloride to produce fetal IUGR and LRD may result from L-NAME-mediated modulation of amino acid delivery to the fetus and amiloride-mediated inhibition of protein synthesis. Finally, IUGR appears unrelated to LRD.