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ispartof: PHYSICAL REVIEW C vol:104 issue:2 status: published

ispartof: Physical Review C vol:101 issue:1 pages:014314-014314 status: published

©2017. The Authors. An ecologically and economically disruptive harmful algal bloom (HAB) affected much of the northeast Pacific margin in 2015, during a prolonged oceanic warm anomaly. Caused by diatoms of the genus Pseudo-nitzschia, this HAB produced the highest particulate concentrations of the biotoxin domoic acid (DA) ever recorded in Monterey Bay, California. Bloom inception followed strong upwelling during the spring transition, which introduced nutrients and eliminated the warm anomaly locally. Subsequently, moderate and intermittent upwelling created favorable conditions for growth and accumulation of HAB biomass, which was dominated by a highly toxigenic species, P. australis. High cellular DA concentrations were associated with available nitrogen for DA synthesis coincident with silicate exhaustion. This nutrient influence resulted from two factors: (1) disproportionate depletion of silicate in upwelling source waters during the warm anomaly, the most severe depletion observed in 24 years, and (2) silicate uptake by the dense diatom bloom.

Direct mass measurements of the low-spin 3/2(-) and high-spin 13/2(+) states in the neutron-deficient isotopes Po-195 and Po-197 were performed with the Penning-trap mass spectrometer ISOLTRAP at ISOLDE-CERN. These measurements allow the determination of the excitation energy of the isomeric state arising from the nu i(13/2) orbital in Po-195,Po-197. Additionally, the excitation energy of isomeric states of lead, radon, and radium isotopes in this region were obtained from alpha-decay chains. These excitation energies complete the knowledge of the energy systematics in the region and confirm that the 13/2(+) states remain isomeric, independent of the number of valence neutrons.

To induce proliferation of transplanted human cells in immunocompetent rats by administration of hepatotoxic doses of a selection agent. GFP-Huh7, a hepatocytederived cell line with low CYP2E1 expression, was used. Expression of CYP2E1, an enzyme responsible for conversion of acetaminophen (APAP) into hepatotoxic compounds, was quantitated by real-time PCR. To prevent rejection, immunological tolerance was induced by introduction of GFP-Huh7 cells into fetal rats in utero, prior to development of the immune system. After birth, GFP-Huh7 cells were transplanted and treated with pharmacological doses of APAP. ALT levels and histology were to detect liver damage. GFP (+) cells in rat livers were detected by real-time PCR and fluorescence microscopy. Expression of CYP2E1 in GFP-Huh7 cells was only 4% compared to control cells. Animals treated with APAP increased ALT to 210 IU/ml on day 1, followed by resolution by day 3. Histology confirmed patchy necrosis corresponding in time to the ALT peak. Fluorescence microscopy of livers from transplanted, APAP treated rats showed an increase of GFP (+) cells/field from 4±2 on day 2 to 45±10 on day 7. Real-time PCR confirmed a 10-fold increase of GFP mRNA in APAP treated rats. Control animals had no significant changes of GFP (+) cells or mRNA levels. In vivo, the difference in CYP2E1 gene expression between GFP-Huh7 and host hepatocytes provides a convenient and efficient pharmacological selection resulting in enrichment of GFP-Huh7 cells. Down regulation of CYPs by siRNA may permit application of the selection to other liver cell lines.

Pulmonary tumor embolism is a common finding at autopsy but is generally perceived as a difficult diagnosis to make ante mortem. After a retrospective review of 164 reported cases of pulmonary tumor embolism, we identified a typical profile of clinical, laboratory, and imaging features that may permit confident clinical diagnosis in most patients with this condition. The clinical features include a documented or suspected underlying malignancy, acute to subacute onset of dyspnea, and signs of cor pulmonale. Supportive laboratory features are hypoxemia or increased alveolar-arterial oxygen gradient, and invasive or noninvasive evidence of pulmonary artery hypertension. Typical imaging findings are normal chest radiographs; multiple, subsegmental, peripheral perfusion defects on ventilation-perfusion lung scans; and delayed filling with or without subsegmental filling defects but without a thrombus on pulmonary angiogram. Radiolabeled monoclonal antibody imaging and pulmonary microvascular cytology sampling techniques are promising diagnostic tests for early diagnosis of pulmonary tumor embolism.

The effects of parenteral vitamin E treatment on aspects of the pulmonary biochemical and morphologic response to 100% oxygen were studied in newborn rabbits manifesting chemical evidence of vitamin E deficiency. Pups treated with 2 mg/100 g body weight increased serum vitamin E levels from 0.39 to 2.17 mg/dl by 72 hr and lung tissue vitamin E content from 3.52 to 17 mg/mg wet weight of lung. In vitro lipid peroxidation in lung homoginates of animals in 100% oxygen for 72 hr was inhibited by approximately 80% in animals receiving 100% oxygen plus vitamin E. Hyperoxia-induced increases in the pulmonary antioxidant enzymes, superoxide dismutase, glutathione peroxidase, and glutathione reductase were diminished by vitamin E administration. Lungs from vitamin E-treated animals did not show the early lung epithelial injury seen in animals exposed to 100% oxygen but not treated with vitamin E. Mophometric analysis of lungs of animals in room air for 72 hr showed 81.6% of lung to be normal as compared with 43.3% normal lung in the group maintained in 100% oxygen for 72 hr. In the group treated with oxygen plus vitamin E, the lungs were similar to room air controls (82.6% normal). This study thus provides further evidence for a direct antioxident affect of vitamin E in lung.

We have developed a short-term organ culture model for the study of the biochemical and morphological development of late gestation fetal rat lung. Explants (1 mm3) of 19-day lung were cultured in an oxygen enriched environment in the presence of synthetic serum-free medium for 3 days. Morphological maturation continued in culture. The rate of incorporation of choline into disaturated phosphatidylcholine and the content of this phospholipid in the explants increased in vitro in a pattern very similar to that which occurs in vivo. The activities of choline kinase and cholinephosphotransferase were also similar in cultured lung and in vivo. Studies of glucose oxidation to CO2 provided additional evidence that the explants remained viable in culture. The explants retained the sensitivity of fetal lung to hormonal action. This was demonstrated by the stimulation of choline incorporation into phospholipid by cyclic AMP and an increase in the glycogen content after exposure to insulin.

Summary: 17β-Estradiol (0.44 to 4.4 μg/kg) was intramuscularly administered to pregnant rabbits on day 25 or 26 of gestation, and the fetuses were delivered by cesarean section 24 hr later. On light microscopy, the lungs from the treated group had larger alveoli and thinner interalveolar septa than did those from the controls at the same gestational age. The lumen:septa ratio was 0.62 ± 0.06 in the control group and 0.88 ± 0.05 in the treated group (P < 0.01). Blood vessels in the lungs of the treated group were also more mature than were those in the control group. Alveolar epithelial cells consisted of 52% undifferentiated, 21% type II, and 27% type I cells in the control group. In the estrogen-treated group, the corresponding distribution was 25, 29, and 45%. There were 0.82 ± 0.16 lamellar bodies per alveolar cell in the treated group compared to 0.38 ± 0.06 in the controls (P < 0.05). Estrogen decreased fetal lung glycogen content from 247 ± 15 μg/mg protein to 70 ± 9 on day 26 and from 103 ± 13 to 13 ± 2 on day 27 (P < 0.001). Estrogen administration increased the rate of incorporation of choline into phosphatidylcholine in fetal lung slices, decreased the rate of thymidine incorporation into DNA, but had no effect on the rates of incorporation of ethanolamine into phosphatidylethanolamine or of leucine into protein. These data indicate that estrogen accelerates the rate of fetal lung maturation. It appears to stimulate lung differentiation at the expense of lung growth. Speculation: Estrogen may be involved in the physiologic control of fetal lung maturation and pulmonary surfactant production.

Summary: The influence of insulin on the biochemical and morphologic maturation of 19-day fetal rat lung (term is 22 days) was studied in an organ culture system. Exposure to insulin for 24 hr resulted in a significant increase in the glycogen content and the rate of glucose oxidation to CO2. In association with this, there was morphologic evidence of delayed lung maturation as evidenced by a significant decrease in the number of lamellar bodies and type II cells in the explants. Insulin treatment had no effect on the rate of choline incorporation into phosphatidylcholine (PC) or disaturated PC and did not antagonize the dexamethasone-induced stimulation of choline incorporation into PC. When the incorporation of [3H]acetate into the various phospholipid fractions was examined, however, it was found that exposure to insulin resulted in a significant decrease in the percentage of phospholipid radioactivity in the disaturated PC fraction and an increase in the percentage of radioactivity in the “membrane” phospholipids, phosphatidylethanolamine, phosphatidylinositol plus phosphatidylserine, and sphingomyelin. There was no significant change in the unsaturated PC and phosphatidylglycerol fractions. Treatment with dexamethasone generally had the opposite effect to insulin with regard to acetate incorporation into the various phospholipid fractions, and when the two hormones were combined, this effect was diminished or abolished. The effects of insulin could not be accounted for on the basis of a change in activity of any of the enzymes of phospholipid synthesis that were examined. These findings suggest that insulin stimulates the synthesis of the cell membrane phospholipids while decreasing that of the surfactant phospholipid, disaturated PC. Speculation: Insulin stimulates lung cell growth while delaying lung cell differentiation.