A new classification scheme for the family Araliaceae

The present paper deals with the following three aspects: 1. It attempts to discuss the problems on primitive forms of the family Araliaceae. The genus Tupidanthus Hook. f. & Thoms. was considered by H. Harms (1894) and H. L. Li (1942) as primitive, whilst another genus Plerandra A. Gray was regarded as primitive by R. H. Eyde & C. C. Tseng in 1971. Having made a detailed comparison of the taxonomical characters of these two genera, the present authors believe that both genera are not the most primitive in the Araliaceae. Their affinit yis not close enough and they possibly evolved in parallel lines from a common ancestor which is so far unknown yet. 2. By studying the systems of the past, the present authors believe that none of them is entirely satisfactory. Bentham (1867) recognized five ‘series’ (in fact, equivalent to ‘tribe’ with the ending-eae of names) based on the petaline arrangement in the bud, the numbers of stamen and the types of endospem. This is a plausible fundamental treatment for the Araliaceae, but choosing the endosperm as a criteria in dividing tribe is artifical. As we know today, both ruminate and uniform endosperm are usually presente in the same genus. Seemann’s system (1868) divided the Hederaceae (excl. Trib. Aralieae) into five tribes, in addition to the locules of ovary. The criteria are essentially the same as Bentham’s. The system of Hams (1894) divided the family into three tribes. Two tribes, Aralieae and Mackinlayeae, of Bentham are retained, but other groups were combined in the Trib. Schefflereae. However, Harms did not retain one of those three oldest legitimate names which had named by Bentham, that is contrary to the law of priority in the International Code of Botanical Nomenelature. Hutchinson (1967) adopted seven tribes for the family. The criteria essentially follow those of Bentham, but the inflorescence is overstressed. The inflorescence is an artifical taxonomical character in dividing tribes, because of some dioecious plants, such as Meryta sinclairii (Hook. f.) Seem., have two types of inflorescence in male and female plants. According to Hutchinson’s arrangement, the male and female plants would be put in separate tribes. 3. The present authors are of the opinion that in the study of a natural classification of plant groups emphasis should be laid not only on the characters of the reproductive organs, but on those of vegetative organs as well. The present revised system is based principally upon the characters of both flowers and leaves of the five tribes as follows: Trib. 1. Plerandreae Benth. emend. Hoo & Tseng Trib. 2. Tetraplasandreae Hoo & Tseng Trib. 3. Mackinlayeae Benth. Trib. 4. Aralieae Benth. Trib. 5. Panaceae Benth. emend. Hoo & Tseng     

Role of M-line proteins in sarcomeric titin assembly during cardiac myofibrillogenesis

A rat polyclonal anti-M-line protein antiserum and three mouse monoclonal anti-titin antibodies (E2, F3, and A12) were used to study the spatiotemporal relationship between M-line proteins and titin during myofibril assembly in cultured chicken cardiomyocytes by immunofluorescence microscopy. In day 2 cultures, M-line proteins and titin were detected as punctate staining in most cardiomyocytes, which possessed many nonstriated fibrils. At a late stage (day 3 cultures), M-line proteins were incorporated into dot-like structures along nonstriated fibrils, while titin staining was continuous on these structures. As development progressed, M-line proteins were registered in periodic pattern in the mid-A band. In cardiomyocytes from day 5 cultures, the titin bands were separated by an unstained region, and achieved their adult doublet pattern. Thus, the organization of titin in the sarcomere appears to occur later than that of M-line proteins in the M-line. Our morphological data indicate that the early registration of M-line proteins in primitive myofibrils may guide titin filament alignment via interaction between M-line proteins and titin. In order to investigate the role of M-line proteins in the assembly of titin filaments, anti-M-line protein or anti-titin antibodies were introduced into cultured cardiomyocytes by electroporation to functionally bind the respective proteins, and the profile of myofibril assembly was examined. Cardiomyocytes from day 2–3 cultures with incorporated anti-M-line protein antibodies became shrunk, and exhibited defective myofibrillar assembly, as shown by the failure of titin to assemble into a typical sarcomeric pattern. Incorporation of anti-titin antibody E2, which recognizes the M-line end domain of titin, resulted in the failure of M-line proteins organized into the M-line structure, as shown by random, sporadic staining with anti-M-line protein antibody. These studies confirm the essential role of M-line proteins in the organization of titin filaments in the sarcomere and that the interaction between titin and M-line proteins is crucial to the formation of the M-line structure. J. Cell. Biochem. 71:82–95, 1998. © 1998 Wiley-Liss, Inc.     

Gain of C-Ala enables AlaRS to target the L-shaped tRNAAla

Unlike many other aminoacyl-tRNA synthetases, alanyl-tRNA synthetase (AlaRS) retains a conserved prototype structure throughout biology. While Caenorhabditis elegans cytoplasmic AlaRS (CeAlaRS_c) retains the prototype structure, its mitochondrial counterpart (CeAlaRS_m) contains only a residual C-terminal domain (C-Ala). We demonstrated herein that the C-Ala domain from CeAlaRS_c robustly binds both tRNA and DNA. It bound different tRNAs but preferred tRNA^Ala. Deletion of this domain from CeAlaRS_c sharply reduced its aminoacylation activity, while fusion of this domain to CeAlaRS_m selectively and distinctly enhanced its aminoacylation activity toward the elbow-containing (or L-shaped) tRNA^Ala. Phylogenetic analysis showed that CeAlaRS_m once possessed the C-Ala domain but later lost most of it during evolution, perhaps in response to the deletion of the T-arm (part of the elbow) from its cognate tRNA. This study underscores the evolutionary gain of C-Ala for docking AlaRS to the L-shaped tRNA^Ala.     

Deposition of monomeric, not oligomeric, Abeta mediates growth of Alzheimer's disease amyloid plaques in human brain preparations.

Senile plaques composed of the peptide Abeta contribute to the pathogenesis of Alzheimer's disease (AD), and mechanisms underlying their formation and growth may be exploitable as therapeutic targets. To examine the process of amyloid plaque growth in human brain, we have utilized size exclusion chromatography (SEC), translational diffusion measured by NMR, and in vitro models of Abeta amyloid growth to identify the oligomerization state of Abeta that is competent to add onto an existing amyloid deposit. SEC of radiolabeled and unlabeled Abeta over a concentration range of 10(-)(10)-10(-)(4) M demonstrated that the freshly dissolved peptide eluted as a single low molecular weight species, consistent with monomer or dimer. This low molecular weight Abeta species isolated by SEC was competent to deposit onto preexisting amyloid in preparations of AD cortex, with first-order kinetic dependence on soluble Abeta concentration, establishing that solution-phase oligomerization is not rate limiting. Translational diffusion measurements of the low molecular weight Abeta fraction demonstrate that the form of the peptide active in plaque deposition is a monomer. In deliberately aged (>6 weeks) Abeta solutions, a high molecular weight (>100 000 M(r)) species was detectable in the SEC column void. In contrast to the active monomer, assembled Abeta isolated from the column showed little or no focal association with AD tissue. These studies establish that, at least in vitro, Abeta exists as a monomer at physiological concentrations and that deposition of monomers, rather than of oligomeric Abeta assemblies, mediates the growth of existing amyloid in human brain preparations.     

A novel double-membrane system for simultaneous nitrification and denitrification in a single tank

A novel biological treatment system, which contains two types of membrane modules in a single tank, was developed for simultaneous nitrification and denitrification. Both of the modules were fed with the substrates on the tube side of the silicone tubes by diffusing them to the biofilms which form on the surface of the tubes. One module was fed with methanol for denitrification and the other one was fed with pure oxygen for nitrification. As a result, the interference of organic carbon on nitrification, and that of oxygen on denitrification, were both hindered by the diffusion barriers (biofilms), thereby allowing two different niches for nitrifiers and denitrifiers to coexist in a single tank. Besides saving space and the amount of alkalinity required for nitrification, this system also produced low residual chemical oxygen demand (COD) and high nitrogen removal rates (2.9-3.4 gN m-2 d-1 of surface area of membrane).     

Oxidative stress regulates expression of VEGFR1 in myeloid cells: link to tumor-induced immune suppression in renal cell carcinoma

Metastatic renal cell carcinoma (RCC) associates with overproduction of vascular endothelial growth factor (VEGF) due to the mutation/inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene. Herein we demonstrate that implantation of human RCC tumor cells into athymic nude mice promotes the appearance of VEGF receptor 1 (VEGFR1)/CD11b double-positive myeloid cells in peripheral blood. Avastin-mediated VEGF neutralization was capable of significantly reducing the numbers of circulating VEGFR1+ myeloid cells. Conversely, up-regulation of VEGFR1 by myeloid cells could also be achieved in vitro by coculturing bone marrow cells with RCC-conditioned medium or by short-term exposure of naive myeloid cells to oxidative stress. Treatment of myeloid cells with H2O2, lipid peroxidation product 4-hydroxy-2(E)-nonenal, or an inhibitor of thioredoxin reductase all resulted in increased expression of VEGFR1. Furthermore, after exposure to oxidative stress, myeloid cells acquire immunosuppressive features and become capable of inhibiting T cell proliferation. Data suggest that tumor-induced oxidative stress may promote both VEGFR1 up-regulation and immunosuppressive function in bone marrow-derived myeloid cells. Analysis of tumor tissue and peripheral blood from patients with metastatic RCC revealed that VEGFR1+ cells can be also found in cancer patients. Restoration of immunocompetence in metastatic RCC patients by pharmacological elimination of VEGFR1+ cells may have a significant impact on the therapeutic efficacy of cancer vaccines or other immune-based therapies.     

HMMatch: peptide identification by spectral matching of tandem mass spectra using hidden Markov models.

Peptide identification by tandem mass spectrometry is the dominant proteomics workflow for protein characterization in complex samples. The peptide fragmentation spectra generated by these workflows exhibit characteristic fragmentation patterns that can be used to identify the peptide. In other fields, where the compounds of interest do not have the convenient linear structure of peptides, fragmentation spectra are identified by comparing new spectra with libraries of identified spectra, an approach called spectral matching. In contrast to sequence-based tandem mass spectrometry search engines used for peptides, spectral matching can make use of the intensities of fragment peaks in library spectra to assess the quality of a match. We evaluate a hidden Markov model approach (HMMatch) to spectral matching, in which many examples of a peptide's fragmentation spectrum are summarized in a generative probabilistic model that captures the consensus and variation of each peak's intensity. We demonstrate that HMMatch has good specificity and superior sensitivity, compared to sequence database search engines such as X!Tandem. HMMatch achieves good results from relatively few training spectra, is fast to train, and can evaluate many spectra per second. A statistical significance model permits HMMatch scores to be compared with each other, and with other peptide identification tools, on a unified scale. HMMatch shows a similar degree of concordance with X!Tandem, Mascot, and NIST's MS Search, as they do with each other, suggesting that each tool can assign peptides to spectra that the others miss. Finally, we show that it is possible to extrapolate HMMatch models beyond a single peptide's training spectra to the spectra of related peptides, expanding the application of spectral matching techniques beyond the set of peptides previously observed.