Nutrient and biomass allocation in Solidago altissima: effects of two stem gallmakers,fertilization, and ramet isolation

Summary The allocations of biomass, N, P, and K were determined by standard methods in goldenrod ramets (1) parasitized by dipteran and lepidopterous gallmakers, (2) from fertilized and unfertilized plots, and (3) whose rhizome connections to their parental clone were severed. The presence of ball galls and their larvae increased allocation to stem but decreased allocation to leaves and seed production, and reduced the number of new rhizomes. There was a marked magnification of N and P concentrations going up the food chains; from goldenrods to gallmakers to the gallmaker's parasitoid/inquiline guild. Nutrient budgets expressed as flow diagrams indicated that N and P costs of gall presence were similar to energy costs under conditions where nutrients did not limit plant growth. Our data do not indicate that the growth of the galls of these gallmakers is limited by either N or P. Ramets from fertilized plots contained more N and P than controls but decreased the percentage of biomass allocated to leaves and inflorescences; ramets isolated by rhizome-cutting compensated their loss by increased allocation to roots, current rhizomes, and new rhizomes but at a cost of lower allocation to seed production and leaves. Gallmakers have a negative impact on host plant fitness characteristics. This may be especially important to establishing perennial hosts, given that herbivore effects would reduce clonal expansion and hence the ultimate clone size, thereby decreasing lifetime plant fitness.     

Mepacrine (quinacrine) inhibition of thrombin-induced platelet responses can be overcome by lysophosphatidic acid

Addition of thrombin to human platelets results in production of lysophosphatidic acid. Such synthesis of lysophosphatidic acid can be inhibited by mepacrine, an inhibitor of the phospholipase A2 which attacks phosphatidic acid to give lysophosphatidic acid. In the present study, mepacrine was used at a concentration of 2.5-20 microM, sufficient to block aggregation and lysophosphatidic acid formation induced by 0.1 U/ml thrombin. Mepacrine, at this concentration, also blocked thrombin-induced phosphorylation of platelet myosin light chain and a 47 kDa protein, thrombin-induced secretion and thrombin-induced release of arachidonic acid from platelet phospholipids. However, mepacrine also partly inhibited the formation of phosphatidic acid in response to thrombin, consistent with some simultaneous inhibition of phospholipase C. Lysophosphatidic acid (2.5-22 microM) overcame the mepacrine block in thrombin-stimulated aggregation, protein phosphorylation and secretion without stimulating the release of arachidonic acid from platelet phospholipids or the formation of lysophosphatidic acid, and only slightly increasing phosphatidic acid formation. The results suggest that lysophosphatidic acid primarily acts distal to mepacrine inhibition of phospholipase A2 and phospholipase C and are consistent with the possibility that lysophosphatidic acid might be a mediator of part of the effects of low-dose thrombin on human platelets.     

Evolutionary impacts of the goldenrod ball gallmaker on Solidago altissima clones

Summary Three ramet clones of Solidago altissima were grown under greenhouse conditions to determine the effects of varying levels of attack by the goldenrod ball gallmaker (Eurosta solidaginis) on biomass allocation, leaf senescence rate and rhizome connections among ramets. The results, examined at both the individual ramet level and the clone level, showed that galled ramets became isolated from their clone through deterioration of rhizome connections. Gall effects were only observed at the ramet level although rhizome connection effects were detected at both the ramet and clone levels. The goldenrod ball gallmaker may therefore have little evolutionary impact on large clones but could appreciably affect newly established clones.     

Identification of two minor subunits in the pilus of Haemophilus influenzae.

Haemophilus influenzae type b (Hib) organisms produce pili, which mediate attachment to human cells and are multimeric structures composed of a 24-kDa subunit called pilin or HifA. Although pili from other organisms contain additional proteins accessory to pilin, no structural components other than pilin have been identified in Hib pili. Previous analysis of a Hib pilus gene cluster, however, suggested that two genes, hifD and hifE, may encode additional pilus subunits. To determine if hifD and hifE encode pilus components, the genes were overexpressed in Escherichia coli and the resulting proteins were purified and used to raise polyclonal antisera. Antisera raised against C-terminal HifD and HifE fragments reacted with H. influenzae HifD and HifE proteins, respectively, on Western immunoblots. Western immunoblot analysis of immunoprecipitated Hib pili demonstrated that HifD and HifE copurified with pili. In enzyme-linked immunosorbent assays, antisera raised against a recombinant HifE protein that contained most of the mature protein reacted more to piliated Hib than to nonpiliated Hib or to a mutant containing a hifE gene insertion. Immunoelectron microscopy confirmed that the HifE antiserum bound to pili and demonstrated that the antiserum bound predominantly to the pilus tips. These data indicate that HifD and HifE are pilus subunits. Adherence inhibition studies demonstrated that the HifE antiserum completely blocked pilus-mediated hemagglutination, suggesting that HifE mediates pilus adherence.     

Clinical management of patients with invasive cervical cancer following a negative Pap smear

Among 535 patients with invasive cervical carcinoma seen between January 1975 and June 1986, 26 were found to have developed the disease within six months (65 percent), 35 within 12 months (88 percent), 37 within 13 months (93 percent), and three developed the disease within 17 months after a negative Pap smear. Eighty-eight percent of these 40 patients were under age 40 at diagnosis. Rapidly progressive cancers are highly resistant to radiation therapy. Seven stage IB patients treated only with radiation died within nine to 29 months after initial therapy. By contrast, 15 patients treated by radical hysterectomy and four by radical hysterectomy and post-surgical radiation were alive with no evidence of disease from six to 109 months after surgery (median, 30 months). Six of nine patients with stage II to IV disease treated with radiation have died; the remaining three are alive. One patient is well 14 months after therapy, but two others have developed metastases seven and 12 months after treatment. Surprisingly, 37 of 40 patients had symptoms of pain, bleeding, and discharge at the initial diagnosis, but their physicians had a false sense of security because of a recent negative Pap smear. Early biopsy diagnosis and radical hysterectomy with bilateral pelvic lymphadenectomy is the most effective management for this cancer.     

History of Ichnology: The Correspondence Between the Reverend Henry Duncan and the Reverend William Buckland and the Discovery of the First Vertebrate Footprints

The Reverend Henry Duncan (1774–1846), clergyman, philosopher, writer, politician, archeologist, poet, educator, social reformer, and the founder of savings banks, was indeed a Man for All Seasons. In 1824, while Minister of the Church of Scotland at Ruthwell, Dumfriesshire, he was presented with a slab of red sandstone from the Corncockle Muir quarry in Annandale, exhibiting a set of footprints on it. Although Duncan felt from the start that he was dealing with the tracks of an animal, he wrote to the Reverend William Buckland, Reader in Mineralogy and Geology at the University of Oxford, to solicit his opinion on the origin of these curious markings. Buckland was at first skeptical, but after receiving casts of the markings from Duncan, he became convinced that they did in fact represent footprints. Duncan and Buckland maintained a correspondence about the footprints, and on January 7, 1828, Duncan described the Corncockle Muir footprints to the Royal Society of Edinburgh and quoted Buckland's findings. Duncan's paper was not published by the Society until 1831, but it aroused considerable interest—“Footsteps before the Flood”!—and was reported in several newspapers. This was the first scientific report of a fossil track; although a schoolboy, Pliny Moody, had found fossil footprints in Connecticut in 1802, they were not scientifically described until 1836. The Scottish tracks are now considered to be not reptilian but of synapsid origin and the rocks containing them are now known to be of Permian age.     

Saikosaponin-d,a novel SERCA inhibitor,induces autophagic cell death in apoptosis-defective cells

Autophagy is an important cellular process that controls cells in a normal homeostatic state by recycling nutrients to maintain cellular energy levels for cell survival via the turnover of proteins and damaged organelles. However, persistent activation of autophagy can lead to excessive depletion of cellular organelles and essential proteins, leading to caspase-independent autophagic cell death. As such, inducing cell death through this autophagic mechanism could be an alternative approach to the treatment of cancers. Recently, we have identified a novel autophagic inducer, saikosaponin-d (Ssd), from a medicinal plant that induces autophagy in various types of cancer cells through the formation of autophagosomes as measured by GFP-LC3 puncta formation. By computational virtual docking analysis, biochemical assays and advanced live-cell imaging techniques, Ssd was shown to increase cytosolic calcium level via direct inhibition of sarcoplasmic/endoplasmic reticulum Ca²⁺ ATPase pump, leading to autophagy induction through the activation of the Ca²⁺/calmodulin-dependent kinase kinase–AMP-activated protein kinase–mammalian target of rapamycin pathway. In addition, Ssd treatment causes the disruption of calcium homeostasis, which induces endoplasmic reticulum stress as well as the unfolded protein responses pathway. Ssd also proved to be a potent cytotoxic agent in apoptosis-defective or apoptosis-resistant mouse embryonic fibroblast cells, which either lack caspases 3, 7 or 8 or had the Bax-Bak double knockout. These results provide a detailed understanding of the mechanism of action of Ssd, as a novel autophagic inducer, which has the potential of being developed into an anti-cancer agent for targeting apoptosis-resistant cancer cells.