Showing papers by "University of Lausanne published in 1998"
TL;DR: A Brooks parsimony analysis produced an unrooted area phylogram, showing that: (i) the northern regions were colonized generally from the Iberic and Balkanic refugia; and (ii) the Italian lineages were often isolated due to the presence of the Alpine barrier.
Abstract: The Quaternary cold periods in Europe are thought to have heavily influenced the amount and distribution of intraspecific genetic variation in both animals and plants. The phylogeographies of 10 taxa, including mammals (Ursus arctos, Sorex spp., Crocidura suaveolens, Arvicola spp.), amphibians (Triturus spp.), arthropods (Chorthippus parallelus), and plants (Abies alba, Picea abies, Fagus sylvatica, Quercus spp.), were analysed to elucidate general trends across Europe. Only a small degree of congruence was found amongst the phylogeographies of the 10 taxa, but the likely postglacial colonization routes exhibit some similarities. A Brooks parsimony analysis produced an unrooted area phylogram, showing that: (i) the northern regions were colonized generally from the Iberic and Balkanic refugia; and (ii) the Italian lineages were often isolated due to the presence of the Alpine barrier. The comparison of colonization routes highlighted four main suture-zones where lineages from the different refugia meet. Some of the intraspecific genetic distances among lineages indicated a prequaternary divergence that cannot be connected to any particular cold period, but are probably related mainly to the date of arrival of each taxon in the European continent. As a consequence, molecular genetics so far appears to be of limited use in dating Quaternary events.
2,855 citations
TL;DR: Antibodies present in pooled human intravenous immunoglobulins (IVIG) blocked Fas-mediated keratinocyte death in vitro and indicated that IVIG may be an effective treatment for toxic epidermal necrolysis of TEN.
Abstract: Toxic epidermal necrolysis (TEN, Lyell's syndrome) is a severe adverse drug reaction in which keratinocytes die and large sections of epidermis separate from the dermis. Keratinocytes normally express the death receptor Fas (CD95); those from TEN patients were found to express lytically active Fas ligand (FasL). Antibodies present in pooled human intravenous immunoglobulins (IVIG) blocked Fas-mediated keratinocyte death in vitro. In a pilot study, 10 consecutive individuals with clinically and histologically confirmed TEN were treated with IVIG; disease progression was rapidly reversed and the outcome was favorable in all cases. Thus, Fas-FasL interactions are directly involved in the epidermal necrolysis of TEN, and IVIG may be an effective treatment.
1,020 citations
TL;DR: Only a few low molecular mass signals, including jasmonic acid, ethylene and salicylic acid, upregulate the expression of scores of defense-related genes, which fine-tunes its defense gene expression against aggressors.
1,008 citations
TL;DR: The results indicate that the mere trimerization of the Fas and TRAIL receptors may not be sufficient to trigger death signals, and the observation that sFasL is less cytotoxic than membrane-bound FasL may explain why in certain types of cancer, systemic tissue damage is not detected, even though the levels of circulating sFAsL are high.
Abstract: Human Fas ligand (L) (CD95L) and tumor necrosis factor (TNF)-α undergo metalloproteinase-mediated proteolytic processing in their extracellular domains resulting in the release of soluble trimeric ligands (soluble [s]FasL, sTNF-α) which, in the case of sFasL, is thought to be implicated in diseases such as hepatitis and AIDS. Here we show that the processing of sFasL occurs between Ser126 and Leu127. The apoptotic-inducing capacity of naturally processed sFasL was reduced by >1,000-fold compared with membrane-bound FasL, and injection of high doses of recombinant sFasL in mice did not induce liver failure. However, soluble FasL retained its capacity to interact with Fas, and restoration of its cytotoxic activity was achieved both in vitro and in vivo with the addition of cross-linking antibodies. Similarly, the marginal apoptotic activity of recombinant soluble TNF-related apoptosis-inducing ligand (sTRAIL), another member of the TNF ligand family, was greatly increased upon cross-linking. These results indicate that the mere trimerization of the Fas and TRAIL receptors may not be sufficient to trigger death signals. Thus, the observation that sFasL is less cytotoxic than membrane-bound FasL may explain why in certain types of cancer, systemic tissue damage is not detected, even though the levels of circulating sFasL are high.
825 citations
TL;DR: In this paper, the authors developed a simple model of corporate ownership structure in which costs and benefits of ownership concentration are analyzed and derived predictions for the trade and pricing of blocks, and provided criteria for the optimal choice of ownership structure.
Abstract: The paper develops a simple model of corporate ownership structure in which costs and benefits of ownership concentration are analyzed The model cornpares the liquidity benefits obtained through dispersed corporate ownership with the benefits from efficient management control achieved by some degree of ownership concentration The paper reexamines the free-rider problem in corporate control in the presence of liquidity trading, derives predictions for the trade and pricing of blocks, and provides criteria for the optimal choice of ownership structure THE RECENT INCOMPLETE CONTRACTING approach in corporate finance has considerably improved our understanding of how small firms determine their capital structure The basic setting considered in this line of research is one where a founder-manager seeks funding from one or several financiers The main premise is that the founder-manager, in her dealings with the financiers, is primarily concerned with maintaining her private benefits of control For small firms these are often quite large relative to the financial returns Thus, for a small firm the problem of determining the financial structure often reduces to the problem of how to obtain fundingr while giving away as little control as possible to the financiers Of course, most financiers insist on some form of protection, so that the final compromise reached in most financial contracts for small firms is one resembling a debt contract (or a venture capital contract), which protects the founder-manager's control as long as the firm is performing adequately' This perspective for small firms does not extend naturally to large firms because the private benefits of control of the managers for large firms are likely to be small relative to the firm's monetary returns, so that protection of these benefits is not an overriding consideration Moreover, large firms
751 citations
TL;DR: In this paper, the authors studied the joint distribution of the time of ruin, the surplus immediately before ruin, and the deficit at ruin, which can naturally be interpreted as discounting, and obtained explicit answers for zero initial surplus, very large initial surplus and arbitrary initial surplus if the claim amount distribution is exponential or a mixture of exponentials.
Abstract: This paper studies the joint distribution of the time of ruin, the surplus immediately before ruin, and the deficit at ruin. The time of ruin is analyzed in terms of its Laplace transforms, which can naturally be interpreted as discounting. Hence the classical risk theory model is generalized by discounting with respect to the time of ruin. We show how to calculate an expected discounted penalty, which is due at ruin and may depend on the deficit at ruin and on the surplus immediately before ruin. The expected discounted penalty, considered as a function of the initial surplus, satisfies a certain renewal equation, which has a probabilistic interpretation. Explicit answers are obtained for zero initial surplus, very large initial surplus, and arbitrary initial surplus if the claim amount distribution is exponential or a mixture of exponentials. We generalize Dickson’s formula, which expresses the joint distribution of the surplus immediately prior to and at ruin in terms of the probability of ult...
730 citations
TL;DR: The survey of the literature is complete to the end of 1996 and 63313 stars are included in this version as mentioned in this paper, which represents 36683 new measurements, and new precepts have been used to compute mean values.
Abstract: We present a new version of the uvby cata- logue. The survey of the literature is complete to the end of 1996 and 63313 stars are included in this version. This represents 36683 new measurements. New precepts have been used to compute mean values.
693 citations
TL;DR: A role for MyD88 as an adapter in IL-1 signal transduction is supported; MyD 88 forms homodimers in vivo through DD-DD and Toll-Toll interactions.
657 citations
TL;DR: A novel member of the TNF family designated APRIL (for a proliferation-inducing ligand) is described and it is suggested that APRIL may be implicated in the regulation of tumor cell growth.
Abstract: Members of the tumor necrosis factor (TNF) family induce pleiotropic biological responses, including cell growth, differentiation, and even death. Here we describe a novel member of the TNF family designated APRIL (for a proliferation-inducing ligand). Although transcripts of APRIL are of low abundance in normal tissues, high levels of mRNA are detected in transformed cell lines, and in human cancers of colon, thyroid, and lymphoid tissues in vivo. The addition of recombinant APRIL to various tumor cells stimulates their proliferation. Moreover, APRIL-transfected NIH-3T3 cells show an increased rate of tumor growth in nude mice compared with the parental cell line. These findings suggest that APRIL may be implicated in the regulation of tumor cell growth.
605 citations
TL;DR: In this paper, the presence of mRNA encoding for two monocarboxylate transporters, MCT1 and MCT2, was found to be consistent with the existence of an activitydependent astrocyte-neuron lactate shuttle for the supply of energy substrates to neurons.
Abstract: Mounting evidence from in vitro experiments indicates that lactate is an efficient energy substrate for neurons and that it may significantly contribute to maintain synaptic transmission, particularly during periods of intense activity. Since lactate does not cross the blood-brain barrier easily, blood-borne lactate cannot be a significant source. In vitro studies by several laboratories indicate that astrocytes release large amounts of lactate. In 1994, we proposed a mechanism whereby lactate could be produced by astrocytes in an activity-dependent, glutamate-mediated manner. Over the last 2 years we have obtained further evidence supporting the notion that a transfer of lactate from astrocytes to neurons might indeed take place. In this article, we first review data showing the presence of mRNA encoding for two monocarboxylate transporters, MCT1 and MCT2, in the adult mouse brain. Second, by using monoclonal antibodies selectively directed against the two distinct lactate dehydrogenase isoforms, LDH1 and LDH5, a specific cellular distribution between neurons and astrocytes is revealed which suggests that a population of astrocytes is a lactate 'source' while neurons may be a lactate 'sink'. Third, we provide biochemical evidence that lactate is interchangeable with glucose to support oxidative metabolism in cortical neurons. This set of data is consistent with the existence of an activity-dependent astrocyte-neuron lactate shuttle for the supply of energy substrates to neurons.
599 citations
TL;DR: The ability of IL-2 to enhance expression of a pro-apoptotic molecule, FasL, and to suppress an inhibitor of Fas signaling, FLIP, likely accounts for the role of this cytokine in potentiating T cell apoptosis.
TL;DR: FLIPs are highly expressed in tumor cells, T lymphocytes and healthy, but not injured, myocytes; this suggests a critical role of FLIPs as endogenous modulators of apoptosis.
TL;DR: In this paper, a low-temperature scanning tunneling microscope was used to study the electron scattering of isolated Ce adatoms on Ag(111) surfaces, and the dip spectrum was interpreted as a Fano interference for the limit where the $f$ orbital has a very small matrix element.
Abstract: Electron scattering of isolated Ce adatoms on Ag(111) surfaces was studied with a low-temperature scanning tunneling microscope. Tunneling spectra obtained on and near Ce reveal a characteristic dip around the Fermi energy which is absent for nonmagnetic Ag adatoms. This feature is detected over a few atomic diameters around Ce atoms at the surface. The transition matrix element from the localized $f$ electron to the tunnel-current carrying continuum states bears a strong resemblance to discrete autoionized states. We interpret the dip spectrum as a Fano interference for the limit where the $f$ orbital has a very small matrix element.
Journal Article•
TL;DR: The results suggest that the Melan-A(26-35) peptide analogue ELAGIGILTV may be more immunogenic than the natural peptides in HLA-A*0201 melanoma patients and should thus be considered as a candidate for future peptide-based vaccine trials.
Abstract: The Melan-A/MART-1 gene, which is expressed by normal melanocytes as well as by most fresh melanoma samples and melanoma cell lines, codes for Ags recognized by tumor-reactive CTL. HLA-A*0201-restricted Melan-A-specific CTL recognize primarily the Melan-A27-35 (AAGIGILTV) and the Melan-A26-35 (EAAGIGILTV) peptides. The sequences of these two peptides are not necessarily optimal as far as binding to HLA-A*0201 is concerned, since both lack one of the dominant anchor amino acid residues (leucine or methionine) at position 2. In this study we introduced single amino acid substitutions in either one of the two natural peptide sequences with the aim of improving peptide binding to HLA-A*0201 and/or recognition by specific CTL. Surprisingly, analogues of the Melan-A27-35 peptide, which bound more efficiently than the natural nonapeptide to HLA-A*0201, were poorly recognized by tumor-reactive CTL. In contrast, among the Melan-A26-35 peptide analogues tested, the peptide ELAGIGILTV was not only able to display stable binding to HLA-A2.1 but was also recognized more efficiently than the natural peptide by two short-term cultured tumor-infiltrated lymph node cell cultures as well as by five of five tumor-reactive CTL clones. Moreover, in vitro generation of tumor-reactive CTL by stimulation of PBMC from HLA-A*0201 melanoma patients with this particular peptide analogue was much more efficient than that observed with either one of the two natural peptides. These results suggest that the Melan-A26-35 peptide analogue ELAGIGILTV may be more immunogenic than the natural peptides in HLA-A*0201 melanoma patients and should thus be considered as a candidate for future peptide-based vaccine trials.
TL;DR: Exposure of human endotheliai cells to TNF and IFN-γ results in a reduced activation of integrin αVβ3, an adhesion receptor that plays a key role in tumor angiogenesis, leading to a decreased αV β3-dependent endothelioi cell adhesion and survival.
Abstract: Administration of tumor necrosis factor (TNF) and gamma interferon (IFN-gamma) to melanoma patients causes selective disruption of the tumor vasculature but the mechanism of this disruption is unknown. Here we report that exposure of human endothelial cells to TNF and IFN-gamma results in a reduced activation of integrin alphaVbeta3, an adhesion receptor that plays a key role in tumor angiogenesis, leading to a decreased alphaVbeta3-dependent endothelial cell adhesion and survival. Detachment and apoptosis of angiogenic endothelial cells was demonstrated in vivo in melanoma metastases of patients treated with TNF and IFN-gamma. These results implicate integrin alphaVbeta3 in the anti-vascular activity of TNF and IFN-gamma and demonstrate a new mechanism by which cytokines control cell adhesion.
TL;DR: The high and ubiquitous expression of PPARbeta suggests some fundamental role(s) that this receptor might play throughout development, and Interestingly, PPARalpha, -beta and -gamma are coexpressed at high levels in brown adipose tissue.
Abstract: The expression patterns of the three different peroxisome proliferator-activated receptor (PPAR) isotypes have been determined during rat embryonic development by in situ hybridization. The expression of PPARalpha starts late in development, with increasing levels in organs such as liver, kidney, intestine, and pancreas, in which it will also be present later in adulthood to regulate its specific target genes. PPARalpha is also transiently expressed in the embryonic epidermis and central nervous system. PPARgamma presents a very restricted pattern of expression, being strongly expressed in brown adipose tissue, in which differentiation it has been shown to participate. Like PPARalpha, it is also expressed transiently in the central nervous system. Interestingly, PPARalpha, -beta and -gamma are coexpressed at high levels in brown adipose tissue. Finally, the high and ubiquitous expression of PPARbeta suggests some fundamental role(s) that this receptor might play throughout development.
TL;DR: The results demonstrate the importance of NPY Y1 receptors in NPY-mediated cardiovascular response and in the regulation of body weight through central control of energy expenditure and are also indicative of a role for the Y1 receptor in the control of food intake.
Abstract: Neuropeptide Y (NPY) is a 36-amino-acid neurotransmitter which is widely distributed throughout the central and peripheral nervous system1. NPY involvement has been suggested in various physiological responses including cardiovascular homeostasis2 and the hypothalamic control of food intake3. At least six subtypes of NPY receptors have been described4,5. Because of the lack of selective antagonists, the specific role of each receptor subtype has been difficult to establish. Here we describe mice deficient for the expression of the Y1 receptor subtype. Homozygous mutant mice demonstrate a complete absence of blood pressure response to NPY, whereas they retain normal response to other vasoconstrictors. Daily food intake, as well as NPY-stimulated feeding, are only slightly diminished, whereas fast-induced refeeding is markedly reduced. Adult mice lacking the NPY Y1 receptor are characterized by increased body fat with no change in protein content. The higher energetic efficiency of mutant mice might result, in part, from the lower metabolic rate measured during the active period, associated with reduced locomotor activity. These results demonstrate the importance of NPY Y1 receptors in NPY-mediated cardiovascular response and in the regulation of body weight through central control of energy expenditure. In addition, these data are also indicative of a role for the Y1 receptor in the control of food intake.
TL;DR: It is shown that BB queens initiating reproduction are killed by workers, and that it is primarily Bb rather than BB workers that are responsible for these executions.
Abstract: A ‘green-beard’ gene is defined as a gene that causes a phenotypic effect (such as the presence of a green beard or any other conspicuous feature), allows the bearer of this feature to recognize it in other individuals, and causes the bearer to behave differently towards other individuals depending on whether or not they possess the feature1,2,3 Such genes have been proposed on theoretical grounds to be agents mediating both altruism and intragenomic conflicts1,2, but until now few, if any, of these genes have been identified4,5 Here we provide evidence of a green-beard gene in the red imported fire ant, Solenopsis invicta In polygyne (multiple-queen) colonies, all egg-laying queens are Bb heterozygotes at the locus Gp-9 (ref 6) Previous studies suggested that bb females die prematurely from intrinsic causes6; we now show that BB queens initiating reproduction are killed by workers, and that it is primarily Bb rather than BB workers that are responsible for these executions This implies that allele Gp-9b is linked to a green-beard allele that preferentially induces workers bearing the allele to kill all queens that do not bear it Workers appear to distinguish BB from Bb queens on the basis of a transferable odour cue
TL;DR: It is shown that the combination of pressure and oscillatory shear Stress can downregulate ecNOS levels, as well as upregulate transient expression of ET-1, compared with unidirectional shear stress.
Abstract: —In vivo, endothelial cells (ECs) are subjected to a complex mechanical environment composed of shear stress, pressure, and circumferential stretch. The aim of this study was to subject bovine aortic ECs to a pulsatile pressure oscillating from 70 to 130 mm Hg (mean of 100 mm Hg) in combination with pulsatile shear stresses from 0.1 to 6 dyne/cm2 (1 dyne/cm2=0.1 N/m2) with or without a cyclic circumferential stretch of 4% for 1, 4, and 24 hours. The effect of highly reversing oscillatory shear stress (range −3 to +3 dyne/cm2, mean of 0.3 dyne/cm2) typical of regions prone to the development of atherosclerotic plaques was also studied at 4 and 24 hours. Endothelin-1 (ET-1) and endothelial constitutive nitric oxide synthase (ecNOS) mRNA expression was time and mechanical force dependent. ET-1 mRNA was maximal at 4 hours and decreased to less than static culture expression at 24 hours, whereas ecNOS mRNA increased over time. Pressure combined with low shear stress upregulated ET-1 and ecNOS mRNA compared with static control. Additional increase in expression for both genes was observed under a combination of higher shear stress and pressure. A cyclic circumferential stretch of 4% did not induce a further increase in ET-1 and ecNOS mRNA at either low or high shear stress. Oscillatory shear stress with pressure induced a higher expression of ET-1 mRNA but lower expression of ecNOS mRNA compared with unidirectional shear stress and pressure. We have shown that the combination of pressure and oscillatory shear stress can downregulate ecNOS levels, as well as upregulate transient expression of ET-1, compared with unidirectional shear stress. These results provide a new insight into the exact role of mechanical forces in endothelial dysfunction in regions prone to the development of atherosclerosis.
TL;DR: In this paper, the authors reviewed the significance of the Brianconnais domain in the Alpine orogen in the light of data concerning its collision with the active Adriatic margin and the passive Helvetic margin.
TL;DR: Overexpression of CARDIAK induced the activation of both NF-kappa B and Jun N-terminal kinase (JNK) and this interaction correlated with the processing of pro-caspase-1 and the formation of the active p20 subunit of caspases 1 and 2.
Journal Article•
TL;DR: Apoptosis mediated by chemotherapeutic drugs and gamma irradiation was not affected by FLIP or the absence of Fas, indicating that these treatments can induce cell death in a Fas-independent and FLIP-insensitive manner.
Abstract: FLICE-inhibitory protein, FLIP (Casper/I-FLICE/FLAME-1/CASH/CLARP/MRIT), which contains two death effector domains and an inactive caspase domain, binds to FADD and caspase-8, and thereby inhibits death receptor-mediated apoptosis. Here, we characterize the inhibitory effect of FLIP on a variety of apoptotic pathways. Human Jurkat T cells undergoing Fas ligand-mediated apoptosis in response to CD3 activation were completely resistant when transfected with FLIP. In contrast, the presence of FLIP did not affect apoptosis induced by granzyme B in combination with adenovirus or perforin. Moreover, the Fas ligand, but not the perforin/granzyme B-dependent lytic pathway of CTL, was inhibited by FLIP. Apoptosis mediated by chemotherapeutic drugs (i.e., doxorubicin, etoposide, and vincristine) and gamma irradiation was not affected by FLIP or the absence of Fas, indicating that these treatments can induce cell death in a Fas-independent and FLIP-insensitive manner.
TL;DR: In this article, the authors defined two suites of the orogenic Wilson cycle, namely, the alkali-calcic monzonite-monzogranite-syenite and aluminous biotite-bearing suites.
TL;DR: It is suggested that gammaENaC facilitates neonatal lung liquid clearance and is critical for renal Na+ and K+ transport, and that low level Na+ transport may be sufficient for perinatal lungLiquid absorption but insufficient to maintain electrolyte balance by the distal nephron.
Abstract: Genetic evidence supports a critical role for the epithelial sodium channel (ENaC) in both clearance of fetal lung liquid at birth and total body electrolyte homeostasis. Evidence from heterologous expression systems suggests that expression of the alphaENaC subunit is essential for channel function, whereas residual channel function can be measured in the absence of beta or gamma subunits. We generated mice without gammaENaC (gammaENaC -/-) to test the role of this subunit in neonatal lung liquid clearance and total body electrolyte balance. Relative to controls, gammaENaC (-/-) pups showed low urinary [K+] and high urinary [Na+] and died between 24 and 36 h, probably from hyperkalemia (gammaENaC -/- 18.3 mEq/l, control littermates 9.7 mEq/l). Newborn gammaENaC (-/-) mice cleared lung liquid more slowly than control littermates, but lung water at 12 h (wet/dry = 5.5) was nearly normal (wet/dry = 5.3). This study suggests that gammaENaC facilitates neonatal lung liquid clearance and is critical for renal Na+ and K+ transport, and that low level Na+ transport may be sufficient for perinatal lung liquid absorption but insufficient to maintain electrolyte balance by the distal nephron. The gammaENaC (-/-) newborn exhibits a phenotype that resembles the clinical manifestations of human neonatal PHA1.
TL;DR: Consensus was reached regarding the significant intermediary roles of cell proliferation and PPAR-alpha receptor expression and activation in tumor formation and risk assessments based on tumor data may not be appropriate.
TL;DR: The consistency of the patterns observed indicate that, in this population, higher frequency of whole grain food intake is an indicator of reduced risk of several neoplasm at all sites, except thyroid.
Abstract: The relationship between frequency of consumption of whole grain food and risk of selected neoplasms has been analysed using data from an integrated series of case-control studies conducted in northern Italy between 1983 and 1996. The overall dataset included the following incident, histologically confirmed neoplasms: oral cavity and pharynx 181, oesophagus 316, stomach 745, colon 828, rectum 498, liver 428, gallbladder 60, pancreas 362, larynx 242, breast 3,412, endometrium 750, ovary 971, prostate 127, bladder 431, kidney 190, thyroid 208, Hodgkin's disease 80, non-Hodgkin's lymphomas 200, multiple myelomas 120. Controls were 7,990 patients admitted to hospital for acute, non-neoplastic conditions, unrelated to long-term modifications in diet and not likely to have been caused by tobacco or alcohol use. Odds ratios (OR) for subsequent scores (never/occasional/frequent) of whole grain food consumption were derived after allowance for age, sex, education, smoking, alcohol intake and body mass index. High intake of whole grain foods consistently reduced risk of neoplasm at all sites, except thyroid. The ORs for the highest category of consumption were 0.2–0.3 for upper digestive and respiratory tract neoplasms, 0.5 for stomach, colon and gallbladder, 0.7 for rectum, 0.6 for liver, 0.8 for pancreas and prostate, 0.9 for breast and endometrium, 0.6 for ovary, 0.4 for bladder and kidney, 1.3 for thyroid and around 0.5 for lymphomas and myeloma. The tests for trend in risks were significant for all neoplasms, except pancreas, endometrium, Hodgkin's disease and multiple myeloma. No significant heterogeneity was found across strata of age at diagnosis, sex, education, smoking habit, alcohol intake and body mass index. Thus, even in the absence of a univocal and satisfactory biological interpretation, the consistency of the patterns observed indicate that, in this population, higher frequency of whole grain food intake is an indicator of reduced risk of several neoplasms. Int. J. Cancer 77:24–28, 1998.© 1998 Wiley-Liss, Inc.
TL;DR: The gene (ptsK) encoding this serine/threonine protein kinase is identified, the purified protein product is characterized and the reported results advance the understanding of phosphorylation‐dependent carbon control mechanisms in Gram‐positive bacteria.
Abstract: HPr(Ser) kinase is the sensor in a multicomponent phosphorelay system that controls catabolite repression, sugar transport and carbon metabolism in gram-positive bacteria. Unlike most other protein kinases, it recognizes the tertiary structure in its target protein, HPr, a phosphocarrier protein of the bacterial phosphotransferase system and a transcriptional cofactor controlling the phenomenon of catabolite repression. We have identified the gene (ptsK) encoding this serine/threonine protein kinase and characterized the purified protein product. Orthologues of PtsK have been identified only in bacteria. These proteins constitute a novel family unrelated to other previously characterized protein phosphorylating enzymes. The Bacillus subtilis kinase is shown to be allosterically activated by metabolites such as fructose 1,6-bisphosphate and inhibited by inorganic phosphate. In contrast to wild-type B. subtilis, the ptsK mutant is insensitive to transcriptional regulation by catabolite repression. The reported results advance our understanding of phosphorylation-dependent carbon control mechanisms in Gram-positive bacteria.
TL;DR: Data on the lifespan of queens in ants and termites is reviewed because such data are highly relevant for comparative analyses on life-history.
Abstract: Comparative studies are increasingly used to identify factors responsible for the evolution of plant and animal phenotypes and social insects provide ideal systems for such studies as a result of their modular growth and their bewildering diversity in social organization. Here I review data on the lifespan of queens in ants and termites because such data are highly relevant for comparative analyses on life-history. Lifespan has been reported in 53 ant and 10 termite species. Information on the mode of colony founding and number of queens per colony is also provided for the 53 ant species. Finally, I suggest that students of social insects would greatly benefit if information on colony characteristics, individual phenotypes and behaviour would become available for a larger number of species, perhaps on a database that would be accessible on the web.
TL;DR: These mice develop myocardial hypertrophy without signs of fibrosis independently from the presence of hypertension, demonstrating that local Ang II production is important in mediating the hypertrophic response in vivo.
Abstract: —Cardiac hypertrophy is frequent in chronic hypertension. The renin-angiotensin system, via its effector angiotensin II (Ang II), regulates blood pressure and participates in sustaining hyp...