Onshore-offshore patterns in the evolution of phanerozoic shelf communities.

Cluster analysis of Cambrian-Ordovician marine benthic communities and community-trophic analysis of Late Cretaceous shelf faunas indicate that major ecological innovations appeared in nearshore environments and then expanded outward across the shelf at the expense of older community types. This onshoreinnovation, offshore-archaic evolutionary pattern is surprising in light of the generally, higher species turnover rates of offshore clades. This pattern probably results from differential extinction rates of onshore as compared to offshore clades, or from differential origination rates of new ecological associations or evolutionary novelties in nearshore environments.

Sudden extinction of the dinosaurs: latest Cretaceous, upper Great Plains, USA.

Results of a three-year field study of family-level patterns of ecological diversity of dinosaurs in the Hell Creek Formation of Montana and North Dakota show no evidence (probability P < 0.05) of a gradual decline of dinosaurs at the end of the Cretaceous. Stratigraphic reliability was maintained through a tripartite division of the Hell Creek, and preservational biases were corrected for by comparison of results only from similar fades as well as through the use of large-scale, statistically rigorous survey and collection procedures. The findings are in agreement with an abrupt extinction event such as one caused by an asteroid impact.

Pathways of acetyl CoA production for lipogenesis from acetoacetate, beta-hydroxybutyrate, pyruvate and glucose in neonatal rat lung.

The rate of fatty acid synthesis from acetoacetate (AcAc) is 2-3 times greater than from glucose in developing rat lung. To determine the reason for this difference, we investigated the pathways of lipogenesis from [3-14C] AcAc, [3-14C] beta-hydroxybutyrate (beta OHB), [U-14C] glucose or [2-14C] pyruvate in minced lung tissue of 3- to 4-day-old rats. The addition of (-)hydroxycitrate, an inhibitor of ATP-citrate lyase, inhibited fatty acid synthesis from glucose, pyruvate, and beta OHB by 88%, 70% and 60%, respectively, but had no effect on that from AcAc. Benzene 1,2,3-tricarboxylate, an inhibitor of tricarboxylate translocase, inhibited fatty acid synthesis from all substrates by at least 50%. Incubation with aminooxyacetate, an inhibitor of aspartate aminotransferase, had no effect on lipid synthesis from glucose, pyruvate or AcAc, but increased lipid synthesis from beta OHB. Results indicate that for lipid synthesis in the neonatal lung, acetyl CoA from AcAc is derived predominantly from a cytoplasmic pathway involving AcAcCoA synthetase and AcAcCoA thiolase, whereas citrate is the major route of acetyl group transfer from glucose. Lipogenesis from beta OHB involves both the cytoplasmic and citrate pathways.

Pulmonary surfactant lipid synthesis from ketone bodies, lactate and glucose in newborn rats.

The contribution of acetoacetate (AcAc), beta-hydroxybutyrate (beta OHB), lactate and glucose to pulmonary surfactant lipid synthesis in three- to five-day-old rats was measured. Minced lung tissue was incubated with 3H2O and [3-14C]AcAc, [3-14C]beta OHB, [U-14C]lactate or [U-14C]glucose, and the radioactivity incorporated into surfactant lipids was measured. When expressed as nmol of substrate incorporated/g lung tissue per four hr, lactate was incorporated more rapidly than other substrates into total surfactant lipids and phosphatidylcholine (PC). There was no difference in the rates of incorporation of lactate, AcAc or glucose into disaturated PC (DSPC). Substrates other than glucose were incorporated almost exclusively into fatty acids, whereas 60-80% of glucose incorporated into surfactant phospholipids was found in fatty acids, with the remaining in glyceride-glycerol. When expressed as nmol acetyl units incorporated/g lung tissue per four hr, the rates of AcAc, lactate and glucose incorporation into total surfactant fatty acids were comparable. Glucose incorporation into DSPC and PC was greater than that of AcAc and lactate. When glucose was the only exogenous substrate added to the incubation medium, it contributed 37% of total surfactant fatty acids synthesized de novo. In the presence of other substrates, the contribution of glucose to de novo fatty acid synthesis dropped to 14-20%. In the presence of unlabeled glucose, 14C-labeled AcAc, lactate and beta OHB contributed 52%, 40% and 19%, respectively, of the total fatty acids synthesized de novo. The rate of beta OHB incorporation into surfactant lipids was only about 50% that of other substrates and was accompanied by low activity of beta-hydroxybutyrate dehydrogenase measured for newborn lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung lipid synthesis from acetoacetate and glucose in developing rats in vitro.

Acetoacetate (AcAc) and glucose were compared as energy sources and as precursors for lipid synthesis in the lungs of developing rats. Minced lung tissue was incubated with [3-14C]AcAc or [U-14C]glucose and the oxidation of each substrate to CO2 or its incorporation into tissue lipids was quantified. The highest rates of oxidation were obtained during the first 5 days for AcAc and the first 2 days of life for glucose and oxidation of AcAc was 3-4 times greater than that of glucose at all ages. Throughout postnatal development, the rates of nonsaponifiable lipid, fatty acid and hence total lipid (chloroform/methanol extractable) synthesis from AcAc were 2-3 times those of glucose. The highest rates of total lipid synthesis from AcAc and glucose were observed at birth. Glucose was utilized for glyceride-glycerol synthesis at a higher rate than AcAc. Similar patterns of incorporation of AcAc and glucose into various lipid classes were noted. Of the total lipids synthesized from AcAc and glucose, respectively, phospholipid plus monoglyceride accounted for 64% and 77%, triglyceride 13% and 13%, diglyceride plus cholesterol 11% and 4%, fatty acids 9% and 4%, and cholesteryl esters 3% and 1%. AT birth, the specific activities of all lipids except triglyceride derived from AcAc were greater than those from glucose. Rates of synthesis of all complex lipids declined with age. The results of these experiments demonstrate that AcAc is utilized more readily than glucose for energy production and lipid synthesis in developing rat lungs.

Preferential utilization of ketone bodies in the brain and lung of newborn rats.

Persistent mild hyperketonemia is a common finding in neonatal rats and human newborns, but the physiological significance of elevated plasma ketone concentrations remains poorly understood. Recent advances in ketone metabolism clearly indicate that these compounds serve as an indispensable source of energy for extrahepatic tissues, especially the brain and lung of developing rats. Another important function of ketone bodies is to provide acetoacetyl-CoA and acetyl-CoA for synthesis of cholesterol, fatty acids, and complex lipids. During the early postnatal period, acetoacetate (AcAc) and beta-hydroxybutyrate are preferred over glucose as substrates for synthesis of phospholipids and sphingolipids in accord with requirements for brain growth and myelination. Thus, during the first 2 wk of postnatal development, when the accumulation of cholesterol and phospholipids accelerates, the proportion of ketone bodies incorporated into these lipids increases. On the other hand, an increased proportion of ketone bodies is utilized for cerebroside synthesis during the period of active myelination. In the lung, AcAc serves better than glucose as a precursor for the synthesis of lung phospholipids. The synthesized lipids, particularly dipalmityl phosphatidylcholine, are incorporated into surfactant, and thus have a potential role in supplying adequate surfactant lipids to maintain lung function during the early days of life. Our studies further demonstrate that ketone bodies and glucose could play complementary roles in the synthesis of lung lipids by providing fatty acid and glycerol moieties of phospholipids, respectively. The preferential selection of AcAc for lipid synthesis in brain, as well as lung, stems in part from the active cytoplasmic pathway for generation of acetyl-CoA and acetoacetyl-CoA from the ketone via the actions of cytoplasmic acetoacetyl-CoA synthetase and thiolase.

Surfactant phospholipids and lavage phospholipase A2 in experimental Pneumocystis carinii pneumonia.

The effect of Pneumocystis carinii pneumonia on surfactant phospholipids and lavage phospholipase A2 was investigated. Pneumocystis carinii infection was induced in adult rats by immunosuppression with dexamethasone administered in the drinking water (2 mg/L) for 6 to 8 wk. Surfactant phospholipids were isolated from lung lavage and lung tissue. Dexamethasone administration significantly increased total lung and lavage phospholipids in corticosteroid-treated animals receiving prophylaxis against P. carinii with trimethoprim-sulfamethoxazole (TMP-SMZ) when compared with no treatment control animals. Lavage surfactant phospholipids from P. carinii-infected rats were 25% that of no treatment control rats and less than 10% that of corticosteroid control animals receiving TMP-SMZ. Phospholipid composition of lavage phospholipids was also altered in P. carinii pneumonia, with slight increase in the percentage of sphingomyelin and reduced percentage of total phosphatidylcholine. Postlavage tissue phospholipids of P. carinii-infected rats were 4 times that of no treatment control animals, although only about 50% that of corticosteroid control animals. There was no significant difference in lavage phospholipase A2 activity for the P. carinii-infected and corticosteroid control groups, although the enzyme activity was at least 4 times that of the no treatment control group. The surfactant changes were associated with abnormal excised lung pressure-volume curves and decreased deflation stability in the animals with P. carinii. These results indicate that the corticosteroids used in this model induce an increase in both lung surfactant phospholipids and phospholipase A2. Despite this increase in lavage phospholipids, P. carinii pneumonia in this model causes an alveolar surfactant phospholipid deficiency without significant increase in phospholipase A2 activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcass nitrogen as a predictor of protein requirement for mature female rats.

The minimal level of dietary protein required for maintenance of nitrogen equilibrium was investigated using Sprague-Dawley rats, 12 months of age. Rats were fed casein, supplemented with methionine, at levels ranging from 0.84 to 5.18% of the diet for 4, 8 or 12 weeks and were compared to a control group fed a similar diet containing 9.90% protein or to a baseline group fed a stock diet. The effect of dietary protein levels on total serum protein and on liver and carcass composition was assessed. Protein requirement levels with 95% confidence intervals were predicted by linear regression. Dietary protein levels of 2.14% or lower were not adequate to maintain body weight and serum protein levels, and animals fed these diets had elevated levels of liver lipid. Protein nutriture of rats fed 3.20% protein was generally intermediate between those fed 2.14% or less and those fed 3.62% or greater. Compared to carcass nitrogen, carcass water was not as reliable a parameter for determination of protein requirements. Using the baseline group for comparison and carcass nitrogen as the dependent variable, a dietary protein requirement was predicted for these animals of 3.91--4.19% with confidence intervals of 3.50--4.56% and 3.13--5.48%, respectively. This level is comparable to the maintenance protein requirement of 4% indicated by the National Research Council for adult rats.