Hydrocarbons obtained by pyrolysis of some precambrian rocks of minnesota

Drill core samples of 42 Precambrian sedimentary, igneous, and metamorphic rocks were analyzed by heating under partial vacuum at 100°C and at 400°C to release hydrocarbons and other volatile products.The core samples yielded methane in amounts ranging from traces to 3 microliters per gram, but averaged much less. By way of comparison, samples of Middle Devonian Marcellus black shale, from Pennsylvania, yielded methane in amounts up to 7ul/g.Other straight chain hydrocarbons up to C₁₁ were found in the volatile products, especially those obtained at 400°C, and benzene was a common product, also mainly in the 400°C experiments. Carbon dioxide and nitrogen appear to form a large part of the nonhydrocarbon volatiles in at least some of the samples.Spectral data indicate that the straight chain pyrolysis products of the Precambrian rocks are mainly alkenes, whereas those of the Devonian rocks, referred to above, are a mixture of alkanes and alkenes. Alkanes were however, obtained from several algae-bearing Middle Precambrian argillites. Available evidence indicates, although not conclusively, that the alkenes were contained in the rock rather than being produced from alkanes during pyrolysis.The writers believe that surface contamination in most of the drill cores was minimal owing to the low permeability of the rocks studied, and that contamination by drilling was also minimal.There is a reasonable possibility that the volatiles, if not formed from kerogen residues by the pyrolysis experiments, are in part juvenile igneous gases or are substances that were distilled out of the deeperlying rocks during intervals of folding and metamorphism, and subsequently accumulated at higher levels.     

Tissue distribution and kininogen gene expression after acute-phase inflammation

A kinin-directed monoclonal antibody to kininogens has been developed by the fusion of murine myeloma cells with mouse splenocytes immunized with bradykinin-conjugated hemocyanin. The hybrid cells were screened by an enzyme-linked immunosorbent assay (ELISA) and a radioimmunoassay (RIA) for the secretion of antibodies to bradykinin. Ascitic fluids were produced and purified by a bradykinin-agarose affinity column. The monoclonal antibody (IgG1) bound to bradykinin, Lys-bradykinin, Met-Lys-bradykinin, and kininogens in ELISA. Further, this target-directed monoclonal antibody recognized purified low and high molecular weight bovine, human, or rat kininogens and T-kininogen in Western blotting. After turpentine-induced acute inflammation, rat kininogen levels increased dramatically in liver and serum as well as in the perfused pituitary, heart, lung, kidney, thymus, and other tissues, as identified by the kinin-directed kininogen antibody in Western blot analyses. The results were confirmed by measuring kinin equivalents of kininogens with a kinin RIA. During an induced inflammatory response, rat kininogens were localized immunohistochemically with the kinin-directed monoclonal antibody in parenchymal cells of liver, in acinar cells and some granular convoluted tubules of submandibular gland, and in the collecting tubules of kidney. Northern and cytoplasmic dot blot analyses using a kinin oligonucleotide probe showed that kininogen mRNA levels in liver but not in other tissues increase after turpentine-induced inflammation. The results indicated that rat kininogens are distributed in various tissues in addition to liver and only liver kininogen is induced by acute inflammation. The target-directed kininogen monoclonal antibody is a useful reagent for studying the structure, localization, and function of kininogens or any protein molecule containing the kinin moiety.     

Lipid peroxidation in plumbagin administered rats

Plumbagin was administered to rats at a concentration of 1,2,4,8 and 16 mg per kg body weight. After 24 h lipid peroxide levels were found to decrease in subcellular fractions of liver. Plumbagin inhibited ascorbate and nicotinafde adenine dinucleotide phosphate (reduced) dependent lipid peroxidation but was without any effect on cumene hydroperoxide dependent lipid peroxidation. Injection of 16 mg of plumbagin per kg body weight was found to decrease liver total reduced glutathione and also fcrosomal glucose-6-phosphatase. The results are discussed with reference to the anti- and prooxidant properties of plumbagin.     

Seed development in Pisum

The Ih and lh _i alleles have been shown previously to reduce the level of endogenous gibberellin A₁ (GA₁) in shoots of pea (Pisum sativum L.), resulting in a dwarf phenotype compared with the wild type, cv. Torsdag (Lh). In addition, plants homozygous for the lh ⁱ allele have reduced seed yield compared with Lh (tall, wild type) and lh (dwarf) plants. In this paper we show that the lh ⁱ mutation is expressed in developing seeds and pods. Comparison of GA levels in young shoots and developing seeds of genotypes lh and lh ⁱ demonstrates that the relative severity of the two mutations varies in different tissues. Homozygous h ⁱ seeds have reduced GA levels, weigh less, and are less likely to develop to maturity when compared with Lh seeds. However, fertilization of lh ⁱ plants with Lh pollen increases seed GA levels, seed weight and seed survival, indicating that an increase in seed GA levels due to the presence of the Lh allele can restore normal seed growth. Pods developing on self-pollinated lh ⁱ plants are shorter than pods on Lh (wild type) plants, although this may be an indirect effect of the increased seed abortion of lh _i plants. Based on these results we suggest that endogenous GAs play an important role in the development of seeds of P. sativum L.Abbreviations GA_(n) gibberellin A_n We wish to thank Katherine McPherson, Peter Newman, Leigh Johnson and Peter Bobbi for technical assistance, Professor L. Mander (ANU, Canberra) and Professor B.O. Phinney (UCLA, USA) for labelled GA standards, and the Australian Research Council for financial support.     

Auto and transactivation of FGF expression: Potential mechanism for regulation of myogenic differentiation

Summary Fibroblast growth factors (FGFs) are potent inhibitors of myogenic differentiation. The recent observation that the endogenous expression of acidic and basic FGF by myogenic cells decreases coordinately with differentiation suggests a regulatory role for these growth factors in myogenesis. Inasmuch as other proteins known to influence myogenesis (e.g., MyoD1 and myogenin) activate their own expression as well as the expression of other members of their family, we hypothesized that the FGFs might be capable of similar autoregulation. We examined the effect of exogenously supplied FGF on the abundance of the mRNAs encoding acidic and basic FGF in Sol 8 myoblasts, and demonstrate that either acidic or basic FGF stimulate, through paracrine mechanisms, the accumulation of the mRNAs encoding both of these FGFs. Thus FGFs can auto- and transregulate their own expression in a manner analogous to that observed for the myogenic determination proteins. In addition, similar to that previously observed for MyoD1, both acidic and basic FGF suppress myogenin expression in myoblasts. These results suggest two mechanisms whereby endogenously produced FGFs participate in the maintenance of the undifferentiated state of myogenic cells. These data provide support for paracrine, and suggest potential autocrine, roles for FGFs in the regulation of myogenic differentiation.     

Size regulation of multiple organelles competing for a limiting subunit pool

How cells regulate the size of intracellular structures and organelles is a longstanding question. Recent experiments suggest that size control of intracellular structures is achieved through the depletion of a limiting subunit pool in the cytoplasm. While the limiting pool model ensures organelle-to-cell size scaling, it does not provide a mechanism for robust size control of multiple co-existing structures. Here we develop a generalized theory for size-dependent growth of intracellular structures to demonstrate that robust size control of multiple intracellular structures, competing for a limiting subunit pool, is achieved via a negative feedback between the growth rate and the size of the individual structure. This design principle captures size maintenance of a wide variety of subcellular structures, from cytoskeletal filaments to three-dimensional organelles. We identify the feedback motifs for structure size regulation based on known molecular processes, and compare our theory to existing models of size regulation in biological assemblies. Furthermore, we show that positive feedback between structure size and growth rate can lead to bistable size distribution and spontaneous size selection.