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Preterm labor is a major cause of perinatal mortality and morbidity, and in approximately 30% of cases a clinical cause is not identified. Acute chorioamnionitis is found histologically in a significant percentage of placentas from preterm deliveries, and the mother is often asymptomatic. Although such subclinical acute chorioamnionitis is known to play a role in preterm labor, this study explores the hypothesis that chronic deciduitis with plasma cells is seen more frequently in cases of preterm labor than in control placentas. Thirty-nine singleton placentas from patients with idiopathic preterm labor were examined microscopically and compared in a blinded fashion with 39 gestational age-matched control placentas. Cases of clinical acute chorioamnionitis and known chronic maternal diseases were excluded. Thirty-nine control singleton placentas were obtained from patients undergoing induction of labor for fetal structural abnormalities, excluding aneuploidy. The presence or absence of acute chorioamnionitis, acute fetal inflammatory response, chronic deciduitis, chronic villitis, infarction, and decidual vasculopathy was noted. Immunohistochemical staining was undertaken to further define leukocyte subtypes. Forty-one percent of cases and 15% of controls showed chronic deciduitis (P = 0.022). Forty-six percent of cases and 18% of controls showed histologic acute chorioamnionitis (P = 0.015). There were 8 cases demonstrating acute fetal inflammatory response but only 1 control (P = 0.029). Little difference was seen in the distribution of lymphocyte subsets between cases and control placentas. Our findings suggest that chronic deciduitis plays a role in the etiology of some cases of preterm labor.

Fetal breathing movements (FBM) are inhibited by both exogenous prostaglandin E 2 (PGE 2 ) and ethanol in sheep. Maternal ethanol exposure in late-gestation sheep also increases fetal [PGE 2 ]. However, during prolonged reduced uterine blood flow (RUBF) when [PGE 2 ] in fetal plasma is already elevated, FBM are not inhibited by ethanol. These experiments were designed, therefore, to test the hypothesis that the FBM response to PGE 2 is also diminished during RUBF. PGE 2 (594 ± 19 ng·min -1 ·kg -1 fetal body weight) was infused for 6 h into the jugular vein of RUBF (P O 2 = 14 ± 1 mmHg (1 mmHg = 133.3 Pa); n = 7) and control (P O 2 = 22 ± 1 mmHg (p < 0.01); n = 7) ovine fetuses, and the effect on FBM, electrocortical (ECoG), and electroocular activities was determined. The infusion of PGE 2 increased plasma [PGE 2 ] from 881 ± 162 to 1189 ± 114 pg·mL -1 in RUBF fetuses and from 334 ± 72 to 616 ± 118 pg·mL -1 (p < 0.05) in control fetuses. FBM were initially inhibited by PGE 2 from 22.5 ± 9.4 and 17.9 ± 6.5% of the time to 6.9 ± 2.4 and 0.5 ± 0.4% (p < 0.01) in RUBF and control fetuses, respectively. FBM remained inhibited in control fetuses throughout the infusion but returned to baseline incidence in RUBF fetuses in the last 2 h of the infusion. These results are consistent with the hypothesis that one component of the adaptative mechanisms of the fetus to prolonged RUBF is an altered response of FBM to exogenous PGE 2 . We speculate that the lack of a sustained inhibition in FBM during RUBF with infusion of PGE 2 may be a result of an alteration in brainstem receptor function or number or local PGE 2 removal.Key words: fetal breathing movements, prostaglandin E 2 , hypoxia, reduced uterine blood flow, ethanol, fetal behaviour.

Fetal breathing movements (FBM) are inhibited by both exogenous prostaglandin E2 (PGE2) and ethanol in sheep. Maternal ethanol exposure in late-gestation sheep also increases fetal [PGE2]. However, during prolonged reduced uterine blood flow (RUBF) when [PGE2] in fetal plasma is already elevated, FBM are not inhibited by ethanol. These experiments were designed, therefore, to test the hypothesis that the FBM response to PGE2 is also diminished during RUBF. PGE2 (594+/-19 ng.min(-1).kg(-1) fetal body weight) was infused for 6 h into the jugular vein of RUBF (PO2 = 14+/-1 mmHg (1 mmHg = 133.3 Pa); n = 7) and control (PO2 = 22+/-1 mmHg (p < 0.01); n = 7) ovine fetuses, and the effect on FBM, electrocortical (ECoG), and electroocular activities was determined. The infusion of PGE2 increased plasma [PGE2] from 881+/-162 to 1189+/-114 pg.mL(-1) in RUBF fetuses and from 334+/-72 to 616+/-118 pg.mL(-1) (p < 0.05) in control fetuses. FBM were initially inhibited by PGE2 from 22.5+/-9.4 and 17.9+/-6.5% of the time to 6.9+/-2.4 and 0.5+/-0.4% (p < 0.01) in RUBF and control fetuses, respectively. FBM remained inhibited in control fetuses throughout the infusion but returned to baseline incidence in RUBF fetuses in the last 2 h of the infusion. These results are consistent with the hypothesis that one component of the adaptative mechanisms of the fetus to prolonged RUBF is an altered response of FBM to exogenous PGE2. We speculate that the lack of a sustained inhibition in FBM during RUBF with infusion of PGE2 may be a result of an alteration in brainstem receptor function or number or local PGE2 removal.

  Last Thursday, on the day it was reported that Tory Health Secretary Jeremy Hunt had refused to give NHS nurses a pathetic 1% pay rise, I suffered a massive heart attack. [...]I would not be here today without the skill, commitment and care I received in a whirlwind three hours that went from initial diagnosis of a panic attack to an ambulance, lights flashing, rushing me straight to an operating theatre at Newcastle's Freeman Hospital.

  Last Thursday, on the day it was reported that Tory Health Secretary Jeremy Hunt had refused to give NHS nurses a pathetic 1% pay rise, I suffered a massive heart attack. [...]I would not be here today without the skill, commitment and care I received in a whirlwind three hours that went from initial diagnosis of a panic attack to an ambulance, lights flashing, rushing me straight to an operating theatre at Newcastle's Freeman Hospital.

Fetal breathing movements (FBM) occur 30-40% of the time in late gestation and are important for lung growth and development. FBM are inhibited by both acute hypoxia and ethanol exposure. During prolonged hypoxia, FBM return to normal incidence over 12-16 h. The neuromodulators prostaglandin E $\\sb2$(PGE $\\sb2$ ) and adenosine both inhibit FBM and have been implicated in hypoxia- and ethanol-induced inhibition of FBM. I have hypothesized that increased circulating concentration of PGE $\\sb2$during prolonged hypoxia alters the FBM response to ethanol and exogenous PGE $\\sb2$ , and that increased concentration of fetal PGE $\\sb2$and adenosine in the fetal brain mediate ethanol-induced inhibition of FBM. Prolonged fetal hypoxia was induced in chronically-catheterized fetal sheep by reducing uterine blood flow (RUBF). The effects of maternal ethanol administration (1 g/kg maternal body weight) or fetal PGE $\\sb2$administration (600 ng/kg fetal body weight/min) on FBM, eye movements, and electrocortical activity (ECoG) were then examined. In utero microdialysis was developed to determine effect of maternal ethanol infusion on the concentration of PGE $\\sb2$and adenosine the fetal cerebral extracellular fluid (ECF) with simultaneous measurements of FBM, eye movements and ECoG. During ethanol exposure, the effect of the selective adenosine A $\\sb1$receptor antagonist, 8-cyclopentyltheophylline (8-CPT) (4$\\mu$ g/kg fetal body weight/min) on FBM, eye movements and low-voltage (LV) ECoG re determined to examine the role of the adenosine A $\\sb1$receptor subtype in ethanol-induced inhibition of FBM. During RUBF, ethanol did not inhibit FBM, eye movements or low-voltage (LV) ECoG. Ethanol-induced inhibition of FBM in normoxic fetuses at 125 days' gestation was not associated with an increase in the concentration of PGE $\\sb2$in fetal plasma. Exogenous PGE $\\sb2$initially inhibited FBM and eye movements during RUBF, but the inhibition was not sustained for the full infusion period. In normoxic fetuses, ethanol-induced inhibition of FBM, eye movements and LV ECoG was associated with an increase in the concentration of adenosine and a decrease in the concentration of PGE $\\sb2$in the fetal cerebral ECF. Infusion of 8-CPT reversed ethanol-induced inhibition of FBM, with FBM returning to normal incidence, but 8-CPT had no effect on the incidence of eye movements or LV ECoG. I conclude from these studies that: (1) Prolonged RUBF, and the resultant increase in the concentration of PGE $\\sb2$in fetal plasma, leads to an inability of ethanol to inhibit FBM and an inability of exogenous PGE $\\sb2$to inhibit FBM throughout a 6-h infusion. (2) Adenosine mediates ethanol-induced inhibition of FBM via the A $\\sb1$receptor subtype in fetal sheep, but does not mediate the inhibition of eye movements LV and ECoG. (3) PGE $\\sb2$in the fetal brain does not mediate ethanol-induced inhibition of FBM in ovine fetuses younger than 130 days' gestation.

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Fetal breathing movements (FBM) are inhibited by both exogenous prostaglandin E 2 (PGE 2 ) and ethanol in sheep. Maternal ethanol exposure in late-gestation sheep also increases fetal [PGE 2 ]. However, during prolonged reduced uterine blood flow (RUBF) when [PGE 2 ] in fetal plasma is already elevated, FBM are not inhibited by ethanol. These experiments were designed, therefore, to test the hypothesis that the FBM response to PGE 2 is also diminished during RUBF. PGE 2 (594 ± 19 ng·min -1 ·kg -1 fetal body weight) was infused for 6 h into the jugular vein of RUBF (PO 2 = 14 ± 1 mmHg (1 mmHg = 133.3 Pa); n = 7) and control (PO 2 = 22 ± 1 mmHg (p < 0.01); n = 7) ovine fetuses, and the effect on FBM, electrocortical (ECoG), and electroocular activities was determined. The infusion of PGE 2 increased plasma [PGE 2 ] from 881 ± 162 to 1189 ± 114 pg·mL -1 in RUBF fetuses and from 334 ± 72 to 616 ± 118 pg·mL -1 (p < 0.05) in control fetuses. FBM were initially inhibited by PGE 2 from 22.5 ± 9.4 and 17.9 ± 6.5% of the time to 6.9 ± 2.4 and 0.5 ± 0.4% (p < 0.01) in RUBF and control fetuses, respectively. FBM remained inhibited in control fetuses throughout the infusion but returned to baseline incidence in RUBF fetuses in the last 2 h of the infusion. These results are consistent with the hypothesis that one component of the adaptative mechanisms of the fetus to prolonged RUBF is an altered response of FBM to exogenous PGE 2 . We speculate that the lack of a sustained inhibition in FBM during RUBF with infusion of PGE 2 may be a result of an alteration in brainstem receptor function or number or local PGE 2 removal.Key words: fetal breathing movements, prostaglandin E 2 , hypoxia, reduced uterine blood flow, ethanol, fetal behaviour.

The purpose of this study was to present a professional biography of Ethel Loroline Martus Lawther. The writer attempted to trace and identify the professional contributions of Ethel Loroline Martus Lawther and to show the resulting influences on physical education. To accomplish this objectiv