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Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.
The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.
Electrochemical and spectroscopic characterization of the novel charge-transfer ground state in diimine complexes of ytterbocene.
The novel charge-transfer ground state found in alpha,alpha'-diimine adducts of ytterbocene (C(5)Me(5))(2)Yb(L) [L = 2,2'-bipyridine (bpy) and 1,10-phenanthroline (phen)] in which an electron is spontaneously transferred from the f(14) metal center into the lowest unoccupied (pi*) molecular orbital (LUMO) of the diimine ligand to give an f(13)-L(*)(-) ground-state electronic configuration has been characterized by cyclic voltammetry, UV-vis-near-IR electronic absorption, and resonance Raman spectroscopies. The voltammetric data demonstrate that the diimine ligand LUMO is stabilized and the metal f orbital is destabilized by approximately 1.0 V each upon complexation for both bpy and phen adducts. The separation between the ligand-based oxidation wave (L(0/-)) and the metal-based reduction wave (Yb(3+/2+)) in the ytterbocene adducts is 0.79 V for both bpy and phen complexes. The UV-vis-near-IR absorption spectroscopic data for both the neutral adducts and the one-electron-oxidized complexes are consistent with those reported recently, but previously unreported bands in the near-IR have been recorded and assigned to ligand (pi*)-to-metal (f orbital) charge-transfer (LMCT) transitions. These optical electronic excited states are the converse of the ground-state charge-transfer process (e.g., f(13)-L(*-) <--> f(14)-L(0)). These new bands occur at approximately 5000 cm(-1) in both adducts, consistent with predictions from electrochemical data, and the spacings of the resolved vibronic bands in these transitions are consistent with the removal of an electron from the ligand pi* orbital. The unusually large intensity observed in the f --> f intraconfiguration transitions for the neutral phenanthroline adduct is discussed in terms of an intensity-borrowing mechanism involving the low-energy LMCT states. Raman vibrational data clearly reveal resonance enhancement for excitation into the low-lying pi* --> pi* ligand-localized excited states, and comparison of the vibrational energies with those reported for alkali-metal-reduced diimine ligands confirms that the ligands in the adducts are reduced radical anions. Differences in the resonance enhancement pattern for the modes in the bipyridine adduct with excitation into different pi* --> pi* levels illustrate the different nodal structures that exist in the various low-lying pi* orbitals.
Can mosquitoes help to unravel the community structure of Plasmodium species?
There has been a recent revival in attempts to understand changes in patterns of abundance of Plasmodium spp. that infect humans. This has been driven by the purportedly beneficial effects of co-infection on clinical pathology and the recognition of Plasmodium vivax as a public health problem in its own right. In contrast to the attention given to mixed-species infections in humans, parasite infections and interactions within the mosquito vector remain poorly documented, even though the distribution of vector-borne parasites such as Plasmodium spp. depends on vector-vertebrate and, crucially, vector-parasite interactions. To understand malaria epidemiology and to design appropriate control measures, this gap must be re-addressed.
Molecular phylogenetic evidence refuting the hypothesis of Batoidea (rays and skates) as derived sharks.
Early morphological studies regarding the evolutionary history of elasmobranchs suggested sharks and batoids (skates and rays) were respectively monophyletic. More modern morphological cladistic studies, however, have tended to suggest that batoids are derived sharks, closely related to sawsharks and angelsharks, a phylogenetic arrangement known as the Hypnosqualea hypothesis. Very few molecular studies addressing interordinal relationships of elasmobranchs have been published; the few that do exist, are very limited in terms of both taxon representation and/or aligned sequence positions, and are insufficient to answer the question of whether batoids are derived sharks. The purpose of this study was to address this issue with more complete taxon representation, concomitant with a reasonable number of aligned sequence positions. The data set included a 2.4-kb segment of the mitochondrial 12S rRNA-tRNA valine-16S rRNA locus, and in terms of taxa, representatives of two orders of Batoidea, at least one representative of all orders of sharks, and as an outgroup, the widely recognized sister group to elasmobranchs-Holocephali. The results provide the first convincing molecular evidence for shark monophyly and the rejection of the Hypnosqualea hypothesis. Our phylogenetic placement of batoids as a basal elasmobranch lineage means that much of the current thinking regarding the evolution of morphological and life history characteristics in elasmobranchs needs to be re-evaluated.
Communicating about expected course and re-consultation for respiratory tract infections in children: an exploratory study.
Acute respiratory tract infection is the commonest reason for children consulting, and about one-fifth re-consult for the same illness episode. Fifty-nine audiotape recordings from nine general practitioners (GPs) consulting with children with acute respiratory tract infections were examined. Prognosis was mentioned in only 22 consultations, with GPs predicting a brief course in 11, a possibly longer than expected course in six, and with predicted duration not made explicit in five. Carers were invited to re-consult if they were 'unhappy' with the child's condition in 11 consultations, and specific triggers to re-consult were provided in 15. A patient information leaflet was given out only once. Providing carers with an evidence-based account of the likely clinical course and communicating specific triggers to re-consult may help them manage more of these illness episodes without re-consulting.
Glutamate leakage from a compartmentalized intracellular metabolic pool and activation of the lipoxygenase pathway mediate oxidative astrocyte death by reversed glutamate transport.
Astrocytes have essential roles for neuron survival and function, so that their demise in neurodegenerative insults, such as ischemia, deserves attention. A major event of the cell death cascade in ischemia is the reversed operation of excitatory amino acid transporters (EAAT), releasing glutamate. Cytotoxicity is conventionally attributed to extracellular glutamate accumulation. We previously reported that mimicking such dysfunction by EAAT substrate inhibitors, whose uptake induces glutamate release by heteroexchange, triggers glutathione (GSH) depletion and oxidative death of differentiated astrocytes in culture. Here we demonstrate that astrocyte death, although correlated with glutamate release, is not resulting from high extracellular glutamate-mediated toxicity. L-glutamate per se was gliotoxic only at concentrations much higher than the maximum reached with the potent EAAT substrate inhibitor L-trans-pyrrolidine-2,4-dicarboxylate (PDC), and toxicity was lower. Moreover, high glutamate concentrations offered protection against PDC. Protection was also provided by L-aspartate, which is both transported by EAAT and metabolized into glutamate, and by inhibiting glutamine synthetase, which uses transported glutamate to synthesize glutamine. Neither D-aspartate, a metabolically inert EAAT substrate, nor compounds that can provide glutamate intracellularly but are not EAAT substrates offered protection. Interestingly, only the compounds providing protection prevented PDC-induced GSH depletion. These data strongly suggest that reversed uptake-mediated astrocyte death results from the leakage of glutamate from a compartmentalized intracellular metabolic pool specifically fuelled by EAAT, crucial for preserving GSH contents. In addition, we provide evidence for a minor contribution of the cystine-glutamate antiporter x(c) (-) but a major role of the 5-lipoxygenase pathway in this death mechanism.
Re: UPDRS: Status and recommendations.
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A simple, dynamic measure of antiretroviral therapy adherence predicts failure to maintain HIV-1 suppression.
BACKGROUND: High levels of antiretroviral therapy adherence are important for human immunodeficiency virus type 1 (HIV-1) suppression, yet the magnitude of adherence required to maintain it is less well characterized. Furthermore, methods to accommodate changes in adherence over time are lacking. In the present study, our objective was to determine the magnitude of antiretroviral therapy adherence needed to maintain HIV-1 suppression by use of a time-updated adherence measure that has the potential to be of use in a clinical setting. METHODS: We examined a population-based cohort of HIV-1-infected subjects > or =18 years of age, residing in British Columbia, Canada, who started receiving antiretroviral therapy between 1 August 1996 and 30 September 2003, who had at least 2 consecutive viral loads <500 copies/mL and who had prescriptions filled at least 3 times during a follow-up period ending 30 September 2004. Virological failure was defined as the second of 2 consecutive viral loads >1000 copies/mL. Cox proportional hazards model was used to determine the relationship between virological failure and refill-based, time-updated surrogate measure of adherence. RESULTS: Among the 1634 participants > or =18 years of age who initiated triple combination therapy during the study, 606 virological failure events were identified. In multivariate analyses, subjects with < or =95% adherence were 1.66 (95% confidence interval, 1.38-2.01) times more likely to experience virological failure than those with >95% adherence. CONCLUSIONS: The highest levels of antiretroviral therapy adherence are associated with higher rates of maintained virological suppression. This simple, dynamic surrogate measure of adherence overcomes the limitation of single-point-in-time calculations of adherence and may be useful in real time to determine whether an individual is exhibiting incomplete adherence.
Re: Emmanuel David-Montefiore, Jean-Louis Frobert, Marielle Grisard-Anaf, Jean Lienhart, Karine Bonnet, Christophe Poncelet and Emile Daraï. Peri-operative complications and pain after the suburethral sling procedure for urinary stress incontinence: a French prospective randomised multicentre study comparing the retropubic and transobturator routes. Eur urol 2006;49:133-8.
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Re-wilding: introductions could reduce biodiversity.
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Graft failure from severe recurrent primary sclerosing cholangitis following orthotopic liver transplantation.
UNLABELLED: Speculation that primary sclerosing cholangitis (PSC) may recur in the transplanted liver is based on the relative increase in frequency of biliary abnormalities and histologic evidence of periportal fibrosis without other causes. A recent study demonstrated almost 9% of patients undergoing liver transplantation (OLT) for primary sclerosing cholangitis (PSC) develop recurrent sclerosing cholangitis although the patient and graft survival is not different from those in whom recurrence does not develop. Most reports of PSC recurrence post-OLT estimate rates of 1% to 14%, but to date, no center has reported rapidly progressive fibro-obliterative cholangitis leading to graft failure. CASE REPORT: DV was a 39-year-old white man with ulcerative colitis, since age 21, who developed jaundice and pruritus in 1992. ERCP and liver biopsy were consistent with PSC, and he developed thrombocytopenia and bleeding esophageal varices. He underwent an uneventful OLT in May 1994 with an ABO-compatible organ and normal ischemic times. There was no evidence of postoperative cytomegalovirus infection, hepatic artery thrombosis, or rejection. In October 1994, mild abnormalities of liver function tests (LFTs) led to liver biopsy that revealed inflammatory infiltrate in triad with spillover into lobules and mild periportal fibrosis. LFTs normalized without any treatment, but in February 1995 repeat liver biopsy for increased LFTs revealed moderate periportal fibrosis with inflammatory cells in triads and lobules. Viral shell and CMV titers were negative. No evidence of infectious etiology or rejection was noted. The patient was started on ursodeoxycholic acid at that time and percutaneous transhepatic cholangiogram (PTC) revealed marked narrowing of the intrahepatic ducts. Esophagogastroduodenoscopy (EGD) revealed esophageal varices. Hepatic arteriogram and Doppler ultrasound were negative. He developed progressive graft failure, and died at home while awaiting re-transplant. CONCLUSIONS: Although most series report mild recurrence of PSC following OLT, this case illustrates that early, severe recurrence of PSC may occur, leading to graft failure and need for re-transplantation.
Both L-Lactyl and D-Lactyl Enantiomers Modify Histones in Mouse Testis.
Dynamic histone posttranslational modifications are crucial to precisely orchestrate gene expression programs. The recently discovered histone lysine lactylation has already been explored in various pathological contexts, but less in normal tissues. This modification exists as two enantiomers, L- and D-lactylation; the former may more likely modify histones due to abundant L-lactate produced by glycolysis. Here, we report the identification by proteomics of L- and D-lactylation on lysines of histones H3 and H4 in mouse testis. We developed a targeted proteomic analysis of histone peptides using synthetic sequences modified by L- or D-lactyl, to acquire reliable identification and quantification data. Some histone peptides bearing either enantiomer are separated by reversed-phase chromatography. Interestingly, despite the fact that L-lactate is much more abundant than D-lactate in mouse testis, we estimated abundance ratios of L-over D-lactylation to lie between 0.4 and 1.6 on seven residues of histones H3 and H4. Next, targeted proteomic analyses were performed on histones extracted from meiotic and postmeiotic male germ cells (spermatocytes and round spermatids, respectively), which are known to use L-lactate as a main source of energy. Nonetheless, residues 18 and 23 of histone H3 (H3K18 and H3K23) were reliably quantified and shown to harbor balanced amounts of both enantiomers. The stoichiometry of lactylation is low over the whole sequence of H3 and H4, representing about 0.01 to 0.44%: this contrasts with acetylation which exists at up to 25 to 35% relative abundances on some N-terminal lysines. Yet, lactylation appears to be more abundant than acetylation on the C-terminal half of H3 and H4, where the latter modification is scarce. Collectively, our results suggest a mechanism producing a mixture of the two enantiomers of lactate, or of a more direct substrate for lactylation, that leads to the modification of histones by L- and D-lactylation.
You're the flight surgeon. WPW ECG pattern.
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Re-based heterogeneous catalysts for olefin metathesis prepared by surface organometallic chemistry: reactivity and selectivity.
Herein we describe the catalytic activity of 1, a well-defined Re alkylidene complex supported silica, in the reaction of olefin metathesis. This system is highly active for terminal and internal olefins with initial rates up to 0.7 mol per mol Re per s. It also catalyses the self-metathesis of methyl oleate (MO) without the need of co-catalysts. The turnover numbers can reach up to 900 for MO, which is unprecedented for a heterogeneous Re-based catalyst. Moreover the use of silica as a support can bring major advantages, such as the possibility to use branched olefins like isobutene, which are usually incompatible with alumina-based supports; therefore, the formation of isoamylene from the cross-metathesis of propene and isobutene can be performed. All these results are in sharp contrast to what has been found for other silica- or alumina-supported rhenium oxide systems, which are either completely inactive (silica system) or typically need co-catalysts when functionalised olefins are used. Finally the initiation step corresponds to a cross-metathesis reaction to give a 3:1 mixture of 3,3-dimethylbutene and trans-4,4-dimethylpent-2-ene, and make this catalyst the first generation of well-defined Re-based heterogeneous catalysts.
Eosinophilic gastroenteritis mimicking pancreatic cancer.
Eosinophilic gastroenteritis is a condition characterised by eosinophilic infiltration of the gastrointestinal tract. Biliary obstruction is an unusual presentation. A case where the initial investigations were consistent with carcinoma of the head of pancreas but the resection specimen showed no malignancy is presented. The diagnosis was suspected from a review of the patient's past history and confirmed by re-examination of the histology.
Effects of chronic cysteamine treatment on growth enhancement and insulin-like growth factor I and II mRNA levels in common carp tissues.
Insulin-like growth factors (IGF) belong to a family of growth factors with structural homology to proinsulin. In our previous studies, we found that both IGF-I and IGF-II gene expression showed growth hormone (GH) dependence in the brain and liver of juvenile common carp when treated in vivo with GH for a short time. This present work aimed to study the effects of both the short-term and long-term GH induction of IGF gene expression using cysteamine (CSH) and fasting/re-feeding. CSH is an agent that can deplete somatostatin to increase circulating GH level. IGF mRNA levels in the flesh (muscle) and liver of common carp were determined using real-time PCR. The chronic treatment of common carp with CSH was carried out for 63 d, with growth enhancement of the treated fish noted. Hepatic IGF-I and IGF-II mRNA levels increased in a dose-dependent manner with short-term CSH treatment, whereas IGF-I decreased and IGF-II increased in the liver after chronic CSH treatment. IGF-I and IGF-II mRNA levels in muscle were found to be elevated with the high-dose, long-term CSH treatment. Under the experimentally induced catabolic states of fasting, both hepatic IGF-I and IGF-II gene expression were significantly reduced, whereas they showed no change in muscle. After re-feeding, the hepatic expression of IGF-I in liver and muscle rebounded significantly. The hepatic IGF-II expression level showed no rebound after re-feeding, but the IGF-II level in muscle rebounded to the level of the fed group after re-feeding.
Tissue processing re-visited: a shifting paradigm in surgical pathology.
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