Cyclonic and anticyclonic contributions to atmospheric energetics.

Migratory cyclones and anticyclones account for most of the day-to-day weather variability in the extratropics. These transient eddies act to maintain the midlatitude jet streams by systematically transporting westerly momentum and heat. Yet, little is known about the separate contributions of cyclones and anticyclones to their interaction with the westerlies. Here, using a novel methodology for identifying cyclonic and anticyclonic vortices based on curvature, we quantify their separate contributions to atmospheric energetics and their feedback on the westerly jet streams as represented in Eulerian statistics. We show that climatological westerly acceleration by cyclonic vortices acts to dominantly reinforce the wintertime eddy-driven near-surface westerlies and associated cyclonic shear. Though less baroclinic and energetic, anticyclones still play an important role in transporting westerly momentum toward midlatitudes from the upper-tropospheric thermally driven jet core and carrying eddy energy downstream. These new findings have uncovered essential characteristics of atmospheric energetics, storm track dynamics and eddy-mean flow interaction.

Cerebral hemodynamics during the induction of antenatal periventricular leukomalacia by hemorrhagic hypotension in chronically instrumented fetal sheep.

OBJECTIVE: Our purpose was to determine the characteristics of cerebral ischemia during the induction of antenatal periventricular leukomalacia by hemorrhagic hypotension in premature fetal sheep. STUDY DESIGN: The hemorrhage group received an acute withdrawal of 40% of the fetoplacental blood volume (n = 7), whereas an isovolemic exchange transfusion was performed in the control group (n = 7). Changes in the total hemoglobin, oxy-hemoglobin, and deoxy-hemoglobin levels in the cerebral tissue were assessed with the use of near-infrared spectroscopy and compared statistically. RESULTS: Of 7 fetuses in the hemorrhage group, 5 exhibited periventricular leukomalacia but none in the control group (P < .05). In the hemorrhage group, both brain total-hemoglobin and deoxy-hemoglobin decreased seriously after insult, and the decreased levels persisted even after recovery of systemic blood pressure, whereas such drastic changes were not observed in the control group, suggesting the occurrence of reperfusion failure in the fetal brain in the hemorrhage group. CONCLUSION: The no-reflow phenomenon and successive reperfusion injuries after cerebral ischemia could be closely involved in the induction of antenatal periventricular leukomalacia in this experimental condition.

Two sibling cases of hydrops fetalis due to alloimmune anti-CD36 (Nak a) antibody.

Two female sibling cases, who were born to a CD36 deficient mother, were presented with Coombs' test-negative hydrops. The alloimmune anti-CD36 (Nak(a)) antibody was accidentally found in the mother's serum after an episode of anaphylactic shock with thrombocytopenia, which occurred in an individual receiving fresh frozen plasma prepared from the mother's donated blood. The mother was then diagnosed as having type II CD36 deficiency, lacking CD36 on both platelets and monocytes, while both of her daughters were CD36 positive. Analyses of the CD36 gene revealed that the mother was a compound heterozygote for the CD36 gene mutation with a novel C --> T transition at nt 1366 in exon 12, corresponding to Arg386Trp, and a known 12bp deletion at nt 1438-1449 in exon 13. On the other hand, both patients, who showed half the normal level of CD36 on platelets and monocytes, were heterozygote with one mutation at Arg386Trp. The anti-CD36 antibody in the mother seemed to be responsible for the hydrops fetalis observed in her daughters, because the IgG isolated from the mother's serum showed suppressive effects on the CFU-E colony formation of CD34+ cells from a control donor. This is the first case report of hydrops fetalis caused by an alloimmune anti-CD36 antibody.

A rat model for arrest of alveolarization induced by antenatal endotoxin administration.

A possible association between intrauterine inflammation and impairments of lung development has been suggested. The purpose of this study is to determine the influence of a potent proinflammatory agent, intra-amniotic lipopolysaccharide (LPS), on lung development. At 21 d gestation, an intra-amniotic injection of 1 microg LPS was administered to two subgroups of WKAH rats. One subgroup received only LPS and the other received LPS plus a fetal intraperitoneal dose of 0.25 microg granulocyte-colony stimulating factor (hrG-CSF) to produce peripheral blood neutrophilia. A third subgroup received hrG-CSF only, and a control group received maternal intraamniotic and fetal intraperitoneal normal saline. All pups were delivered by cesarean section at 22 d (term, 22.5 d) and maintained under identical conditions. Left upper lungs were obtained for morphometric analysis at 1, 3, 7, 14, 21, 45, and 60 d of age. Morphometric analysis indicated that changes in alveolar surface density (Sv), average alveolar radius (r), and numerical density of alveoli (nv) all showed that there were fewer and larger alveoli in rat lungs that had been exposed to LPS, but not to hrG-CSF alone or saline. LPS-exposed alveoli showed fewer secondary septa, suggesting an arrest of alveolarization. No destructive changes were observed in any alveoli. We concluded that these changes could be caused purely by intra-amniotic LPS. These abnormalities closely mimic those of new bronchopulmonary dysplasia. The LPS damage model may be applicable to further studies of the pathophysiology of new BPD.

Successful treatment of congenital pulmonary alveolar proteinosis with intravenous immunoglobulin G administration.

The authors report a female patient with congenital pulmonary alveolar proteinosis (PAP). She had two brothers who died from the same disease. BAL did not improve her progressive respiratory failure. After intravenous immunoglobulin G (IVIG) administration for complicated hypogammaglobulinemia, she recovered from respiratory failure. The efficacy of IVIG was confirmed by recovery from deterioration in respiratory status and improvement in chest CT findings on two separate occasions. Subsequently, the patient remains free from respiratory symptoms for more than 3 years on an ongoing regimen of monthly IVIG. She had no surfactant protein (SP) B deficiency. Alveolar macrophages (AM) obtained from her BAL fluid were small and showed decreased phagocytotic activity. Immunostaining revealed weak expression of PU.1 in her AM, a key protein in AM maturation. All nucleotide sequences of granulocyte-macrophage colony stimulating factor (GM-CSF), GM-CSF-receptor and PU.1 were normal. Endotoxin-induced GM-CSF release from peripheral mononuclear cells (PMNC), and proliferation of PMNC in response to GM-CSF were normal. In addition, an antibody against GM-CSF, as seen in adult patients with idiopathic PAP, was not detected in the serum or BAL fluid. Although the patient's PMNC secreted only small amounts of IgG and IgM, an EB virus-derived cell line of her B cells secreted IgM as much as normal control cells. In a flow cytometric study, IgM was expressed on the cell surface. In conclusion, an abnormality in a single gene may have decreased secretion of immunoglobulin from the B cells and the AM phagocytotic activity in the patient.

Synthesis of optically active organoantimony compounds having an (S)-alpha-methylbenzyldimethylamine group and its evaluation for asymmetric reaction.

Novel, enantiomerically pure organoantimony compounds having a C-chiral amine moiety, (S)-(alpha-methyl-2-di-p-tolylstibanobenzyl)dimethylamine [AMSb] (2) and its (eta(6)-arene)chromium complex [AMSb-Cr(CO)(3)] (4), were prepared from common (S)-(alpha-methylbenzyl)dimethylamine (1) via its ortho-lithiated intermediates in short steps. The catalytic activity and enantioselectivity of the ligands 2 and 4 for asymmetric reaction are evaluated, and the optically active (eta(6)-arene)chromium complex 4 has been shown to be an effective ligand for rhodium-catalyzed asymmetric hydrosilylation of ketones.

Analyses of factors contributing to vulnerability to antenatal periventricular leukomalacia induced by hemorrhagic hypotension in chronically instrumented fetal sheep.

Our purpose was to determine factors contributing to vulnerability to antenatal periventricular leukomalacia (PVL) induced by hemorrhagic hypotension in premature fetal sheep. Systemic hypotension was induced in 10 fetal sheep by acutely withdrawing 35% to 40% of the fetoplacental blood volume at 113 d gestation. Brains were processed for histologic analysis 6 d after the insult. Statistical comparisons of physiologic parameters between fetuses suffering from PVL (n = 5) and those without PVL (n = 5) were performed. Significant correlations were found between induction of PVL and fetal brain weight, changes in fetal mean blood pressure over time, base excess, oxygen content, hematocrit, and plasma arginine vasopressin (AVP) levels in fetal abdominal aortic blood. Brain developmental stage, the magnitude of induced systemic hypotension, and baseline blood oxygen content were important intrinsic factors in the induction of antenatal PVL by hemorrhagic hypotension in premature fetal sheep.