bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is there really a ‘J‐shaped’ curve in the association between alcohol consumption and symptoms of depression and anxiety? Findings from the Mater‐University Study of Pregnancy and its outcomes*
Authors: Alati Rosa , Lawlor Debbie A. , Najman Jake M. , Williams Gail M. , Bor William , O'Callaghan Michael 
Published: April 2005

ABSTRACTAims  To determine the nature of the association between alcohol consumption and symptoms of anxiety and depression in women.Design  Prospective cohort study of women (n = 4527) who received antenatal care at a major public hospital (Mater Misericordiae Hospital) in South Brisbane between 1981 and 1984 and who have follow‐up data on alcohol use, depressive and anxiety symptoms over a 14‐year period.Findings  At the 5‐year follow‐up there was a ‘J‐shaped’ association between alcohol consumption and both symptoms of depression and of anxiety. However, at the baseline assessment and the 14‐year follow‐up alcohol consumption was linearly and positively associated with depressive symptoms with increasing prevalence of symptoms with greater consumption. At the 5‐year follow‐up the prevalence of depressive and anxiety symptoms among those who were abstainers at both baseline and 5‐year follow‐up was similar to that among those who had been previous drinkers and then become abstainers (P = 0.67). Similarly, the prevalence of these symptoms was the same at the 14‐year follow‐up comparing those who had been abstainers at baseline, 5‐year and 14‐year follow‐up to those who had previously consumed alcohol but were then abstainers.Conclusions  The nature of the association between alcohol consumption and symptoms of depression and anxiety may vary across their life course in women. Previous drinkers who become abstainers do not appear to be at any higher risk of symptoms of depression or anxiety compared to those who always abstained, suggesting that increased symptoms in abstainers at age 30 is not due to ‘sick quitters’. The association of high alcohol consumption with symptoms of depression and anxiety may be confounded by low income and smoking.
Marijuana use and car crash injury
Authors: Blows Stephanie , Ivers Rebecca Q. , Connor Jennie , Ameratunga Shanthi , Woodward Mark , Norton Robyn 
Published: April 2005

ABSTRACTAims  To investigate the relationship between marijuana use prior to driving, habitual marijuana use and car crash injuryDesign and setting  Population based case–control study in Auckland, New Zealand.Participants  Case vehicles were all cars involved in crashes in which at least one occupant was hospitalized or killed anywhere in the Auckland region, and control vehicles were a random sample of cars driving on Auckland roads. The drivers of 571 case and 588 control vehicles completed a structured interview.Measurements  Self reported marijuana use in the 3 hours prior to the crash/survey and habitual marijuana use over the previous 12 months were recorded, along with a range of other variables potentially related to crash risk. The main outcome measure was hospitalization or death of a vehicle occupant due to car crash injury.Findings  Acute marijuana use was significantly associated with car crash injury, after controlling for the confounders age, gender, ethnicity, education level, passenger carriage, driving exposure and time of day (OR 3.9, 95% CI 1.2–12.9). However, after adjustment for these confounders plus other risky driving at the time of the crash (blood alcohol concentration, seat‐belt use, travelling speed and sleepiness score), the effect of acute marijuana intake was no longer significant (OR 0.8, 95% CI 0.2–3.3). There was a strong significant association between habitual use and car crash injury after adjustment for all the above confounders plus acute use prior to driving (OR 9.5, 95% CI 2.8–32.3).Conclusions  This population‐based case–control study indicates that habitual use of marijuana is strongly associated with car crash injury. The nature of the relationship between marijuana use and risk‐taking is unclear and needs further research. The prevalence of marijuana use in this driving population was low, and acute use was associated with habitual marijuana use, suggesting that intervention strategies may be more effective if they are targeted towards high use groups.
Activation of both acfA and acfD transcription by Vibrio cholerae ToxT requires binding to two centrally located DNA sites in an inverted repeat conformation
Authors: Withey Jeffrey H. , DiRita Victor J. 
Published: April 2005

SummaryThe Gram‐negative bacterium Vibrio cholerae is the infectious agent responsible for the disease Asiatic cholera. The genes required for V. cholerae virulence, such as those encoding the cholera toxin (CT) and toxin‐coregulated pilus (TCP), are controlled by a cascade of transcriptional activators. Ultimately, the direct transcriptional activator of the majority of V. cholerae virulence genes is the AraC/XylS family member ToxT protein, the expression of which is activated by the ToxR and TcpP proteins. Previous studies have identified the DNA sites to which ToxT binds upstream of the ctx operon, encoding CT, and the tcpA operon, encoding, among other products, the major subunit of the TCP. These known ToxT binding sites are seemingly dissimilar in sequence other than being A/T rich. Further results suggested that ctx and tcpA each has a pair of ToxT binding sites arranged in a direct repeat orientation upstream of the core promoter elements. In this work, using both transcriptional lacZ fusions and in vitro copper‐phenanthroline footprinting experiments, we have identified the ToxT binding sites between the divergently transcribed acfA and acfD genes, which encode components  of the accessory colonization factor required for efficient intestinal colonization by V. cholerae. Our results indicate that ToxT binds to a pair of DNA sites between acfA and acfD in an inverted repeat orientation. Moreover, a mutational analysis of the ToxT binding sites indicates that both binding sites are required by ToxT for transcriptional activation of both acfA and acfD. Using copper‐phenanthroline footprinting to assess the occupancy of ToxT on DNA having mutations in one of these binding sites, we found that protection by ToxT of the unaltered binding site was not affected, whereas protection by ToxT of the mutant binding site was significantly reduced in the region of the mutations. The results of further footprinting experiments using DNA templates having +5 bp and +10 bp insertions between the two ToxT binding sites indicate that both binding sites are occupied by ToxT regardless of their positions relative to each other. Based on these results, we propose that ToxT binds independently to two DNA sites between acfA and acfD to activate transcription of both genes.
The PilC adhesin of the Neisseria type IV pilus – binding specificities and new insights into the nature of the host cell receptor
Authors: Kirchner Marieluise , Meyer Thomas F. 
Published: April 2005

SummaryType IV pili of Neisseria gonorrhoeae and Neisseria meningitidis mediate the first contact to human mucosal epithelial cells, an interaction which is also critical for the interaction with vascular endothelial cells. The PilC proteins have been characterized as the principal pilus‐associated adhesin. Here we show that PilC2 exhibits a defined cell and tissue tropism, as it binds to human epithelial and endothelial cell lines, but not to human T cells or fibroblasts. Piliated gonococci and PilC2 exhibit similar patterns of binding to human epithelial and endothelial cells, supporting the function of PilC as the key pilus adhesin. Although CD46 has previously been suggested to be a pilus receptor, several observations indicate that neisserial type IV pili and the pilus adhesin PilC2 interact with epithelial cells in a CD46 independent manner. Biochemical approaches were used to characterize the nature of host cell factors mediating binding of piliated gonococci and PilC2 protein. Our data indicate that the putative host cell receptor for gonococcal pili and the PilC2 pilus adhesin is a surface protein. Glycostructures were found to not be involved in binding. Moreover, we observed the uptake of purified PilC2 protein together with its receptor via receptor‐mediated endocytosis and subsequent receptor re‐exposure on the cell surface. Our data support the existence of a specific pilus receptor and provide intriguing information on the nature of the receptor.
Iron limitation induces SpoT‐dependent accumulation of ppGpp in Escherichia coli
Authors: Vinella Daniel , Albrecht Christian , Cashel Michael , D’Ari Richard 
Published: April 2005

SummaryIn Escherichia coli the β‐lactam mecillinam specifically inhibits penicillin‐binding protein 2 (PBP2), a peptidoglycan transpeptidase essential for maintaining rod shape. We have previously shown that PBP2 inactivation  results  in  a  cell  division  block  and  that an increased concentration of the nucleotide ppGpp, effector of the RelA‐dependent stringent response, confers mecillinam resistance and allows cells to divide as spheres in the absence of PBP2 activity. In this study we have characterized an insertion mutation which confers mecillinam resistance in wild‐type and ΔrelA strains but not in ΔrelAΔspoT strains, devoid of ppGpp. The mutant has an insertion in the fes gene, coding for enterochelin esterase. This cytoplasmic enzyme hydrolyses enterochelin–Fe3+ complexes, making the scavenged iron available to the cells. We show that inactivation of the fes gene causes iron limitation on rich medium plates and a parallel SpoT‐dependent increase of the ppGpp pool, as judged by the induction of the iron‐regulated fiu::lacZ fusion and the repression of the stringently controlled P1rrnB::lacZ fusion respectively. We further show, by direct ppGpp assays, that iron starvation in liquid medium produces a SpoT‐dependent increase of the ppGpp pool, strongly suggesting a role for iron in the balance of the two activities of SpoT, synthesis and hydrolysis of (p)ppGpp. Finally, we present evidence that ppGpp exerts direct or indirect positive control on iron uptake, suggesting a simple homeostatic regulatory circuit: iron limitation leads to an increased ppGpp pool, which increases the expression of iron uptake genes, thereby alleviating the limitation.
A role for the Plasmodium falciparum RESA protein in resistance against heat shock demonstrated using gene disruption
Authors: Silva Monica Diez , Cooke Brian M. , Guillotte Micheline , Buckingham Donna W. , Sauzet Jean‐Pierre , Scanf Cecile Le , Contamin Hugues , David Peter , Mercereau‐Puijalon Odile , Bonnefoy Serge 
Published: April 2005

SummaryDuring erythrocyte invasion, the Plasmodium falciparum Ring‐infected erythrocyte surface antigen (RESA) establishes specific interactions with spectrin. Based on analysis of strains with a large chromosome 1 deletion, RESA has been assigned several functions, none of which is firmly established. Analysis of parasites with a disrupted resa1 gene and isogenic parental or resa3‐disrupted controls confirmed the critical role of RESA in the surface reactivity of immune adult sera on glutaraldehyde‐fixed ring stages. Absence of RESA did not influence merozoite invasion or erythrocyte membrane rigidity, was associated with a modest increase of cytoadhesion to CD36 under conditions of flow, but resulted in marked susceptibility to heat shock. resa1‐KO‐infected erythrocytes were prone to heat‐induced vesiculation like uninfected erythrocytes, whereas parental or resa3‐KO infected erythrocytes remained undamaged. Furthermore, a 6 h exposure of ring stages at 41°C resulted in 33% culture inhibition of resa1‐KO parasites while marginally impacting parental and resa3‐KO parasite growth. This points to a role for RESA in protecting the infected erythrocyte cytoskeleton during febrile episodes. Infection patterns of resa1‐KO and parental parasites in Saimiri sciureus indicated that RESA does not, at least on its own, modulate virulence in the squirrel monkey, as had been previously suggested.
The Autoreactivity of Therapeutic Intravenous Immunoglobulin (IVIg) Preparations Depends on the Fractionation Methods Used
Authors: Djoumerska I. , Tchorbanov A. , Pashov A. , Vassilev T. 
Published: April 2005

AbstractNatural immunoglobulin G (IgG) autoantibodies are present in the plasma of healthy individuals and, as a result, in pooled therapeutic intravenous immunoglobulin (IVIg) preparations. The production processes of commercial IVIg preparations involve different fractionation and virus‐inactivation steps that include in some cases treatments at extreme conditions. Different physical and chemical treatments are known to augment greatly the reactivity of natural autoantibodies to self‐antigens. It is not clear to what extent the self‐reactivity of IVIg preparations is due to the presence of natural IgG antibodies in the plasma pools used for fractionation, and to what extent it is due to the treatments that the IgG molecules have been subjected to during the fractionation process. We compared the binding of seven different commercial IVIg preparations to human liver antigens. All studied IVIg's could be clearly separated into two distinct groups: those that possess significant self‐reactivity and those with low binding to self‐antigens. Increased self‐binding was seen in the preparations produced using a fractionation step at low pH. The treatment of IVIg at low pH resulted in increasing the inhibitory effect of the pooled IgG on PHA‐induced proliferation of human peripheral blood mononuclear cells. IVIg's with high and low self‐binding may have different immunomodulating activities when infused to autoimmune patients.
Allogeneic Dendritomas Induce Anti‐tumour Immunity Against Metastatic Colon Cancer
Authors: Xu F. , Ye Y.‐J. , Cui Z.‐R. , Wang S. 
Published: April 2005

AbstractColon cancer (CC) is one of the most common malignancies in the Western world. Although surgical resection is the first choice worldwide, at this point an effective approach for the treatment of patients with metastasis and cancer recurrence post‐operation has not yet been found. The aim of this study was to investigate the role of the allogeneic dendritomas from fusion of dendritic cells (DC) and metastatic CC cells in the activation of anti‐tumour immunity against metastatic CC. Dendritomas were generated by fused allogeneic human peripheral blood DC with metastatic CC cells using 50% polyethylene glycol. The proliferation of the T cells and the toxicity of the cytotoxic T lymphocytes were observed after T cell pulsed with allogeneic dendritomas. The activated ratios of CD4+T helper 1 and CD8+Tc1 cells were about 51.55 and 65.60% after T cells were mixed with fusions for 24 h, which higher than those of controls. The proliferation of T cells were significantly higher than those of control after T cell pulsed with dendritomas (P < 0.01). Significantly, the activated CD8+ T lymphocytes effectively lysed the CC cells. These results demonstrate that allogeneic dendritomas activate T‐cell responses against metastatic CC cells.
In Vivo Transduction of Thymic Dendritic Cells with Adenovirus and Its Potential Use in Acute Inflammatory Diseases
Authors: Oberholzer C. , Tschoeke S. K. , Bahjat K. , LaFace D. , Hutchins B. , Clare‐Salzler M. J. , Moldawer L. L. , Oberholzer A. 
Published: April 2005

AbstractDendritic cells (DC) represent a potential target for gene therapy. In their ability to process antigens and present them to T cells, DC have been allocated a unique role as initiators of the immune response in both the innate and acquired immunity. Recent in vitro studies have showed the feasibility of DC transduction with adenoviral recombinants. In cancer therapy, targeting of DC with adenovirus has been proved to be effective in inhibiting tumour growth, as well as in reducing the number of tumour metastases. The aim of our study is to evaluate the feasibility of in vivo transduction of DC in a murine lymphocyte‐rich compartment (thymus) as a potential treatment for acute inflammatory diseases. Nearly 50% of the total thymic DC were transduced with a first‐generation adenoviral construct following intrathymic injection, and post‐transductional inflammation was neglectable. Transduction of thymic cells with adenoviral recombinants was able to induce the expression of an intracellular protein (β‐galactosidase, green fluorescent protein), as well as the secretion of human interleukin‐10, within the local compartment. Furthermore, this induction of the latter significantly decreased thymic apoptosis in the applied model of acute bacterial peritonitis (cecal ligation and puncture).
BRAIN PHARMACOKINETICS OF LIGNOCAINE BEFORE and FOLLOWING INTRAVENOUS PERFLUOROCARBON EMULSION INFUSION IN SHEEP
Authors: Doolette David J , Upton Richard N , Martinez Allison M 
Published: April 2005

SUMMARY1. Perfluorocarbon emulsions have potential medical applications, particularly as temporary oxygen carriers and are likely to be coadministered with other intravenous drugs. It is possible that perfluorocarbon emulsions may alter the disposition of other drugs in the body.2. In the present study, we examined the brain pharmacokinetics of a 5 min infusion of 100 mg lignocaine in three chronically instrumented sheep before and after the administration of a new investigational perflurocarbon emulsion (Oxygent™; Alliance Pharmaceutical, San Diego, CA, USA).3. The rate constant for the blood : brain equilibration of lignocaine was larger after perflubron administration. This change could not be attributed to a change in brain blood flow and, therefore, may be the result of a change in the free fraction of lignocaine in the blood.
ANGIOTENSIN II–NITRIC OXIDE INTERACTION IN GLOMERULAR ARTERIOLES
Authors: Patzak Andreas , Lai EnYin , Persson Pontus B , Persson A Erik G 
Published: April 2005

SUMMARY1. Resistance changes of the afferent and efferent arterioles determine blood flow and filtration rate in the kidney. The tone of both vessels results from the influence of nerves and humoral and paracrine factors, through a balance of constrictor and dilator systems. Angiotensin (Ang) II and nitric oxide (NO) are important factors determining vascular tone.2. In the present review, we show that, in addition to the basal production of NO, a specific and significant AngII‐induced release of NO occurs in glomerular arterioles. Data from investigations of arteriolar contraction, as well as from fluorescence measurements of NO, in the presence of selective angiotensin AT1 and AT2 receptor antagonists indicate an AT1 receptor‐stimulated release of NO in afferent arterioles.3. The AngII‐induced liberation of NO could prevent glomerular arterioles from a marked constriction, particularly in situations of high AngII levels in the kidney.
LONG‐TERM RECORDING OF SYMPATHETIC NERVE ACTIVITY: THE NEW FRONTIER IN UNDERSTANDING THE DEVELOPMENT OF HYPERTENSION?
Authors: Guild Sarah‐Jane , Barrett Carolyn J , Malpas Simon C 
Published: April 2005

SUMMARY1. With increasing evidence that the sympathetic nervous system plays a critical role in the development of hypertension, focus is turning to how these signals translate to a chronic increase in arterial pressure.2. The kidney's role in the control of salt and water homeostasis makes it an obvious target for such investigations. However, to date, many studies have been restricted to experiments lasting only a few hours or, at most, a few days, whereas others may use indirect methods of assessing sympathetic activity rather than direct recordings.3. We review current approaches used to determine the effects of renal sympathetic nerve activity (SNA) on arterial pressure and suggest possible avenues of future investigation. We propose that although afferent inputs, such as from chemoreceptors and baroreceptors, are important for the short‐term control of blood pressure via regulation of SNA to multiple organs, it is highly likely that alternative signals are important for setting the long‐term level of renal SNA.4. Emerging evidence indicates circulating angiotensin II is hormone that may act on the central nervous system to regulate renal SNA, renal function and, thus, blood pressure.5. We propose that an integral part of future studies seeking an understanding of the genesis of hypertension should include chronic direct recordings of renal SNA.
CARDIOVASCULAR ALTERATIONS BY CHRONIC INTERMITTENT HYPOXIA: IMPORTANCE OF CAROTID BODY CHEMOREFLEXES
Authors: Prabhakar Nanduri R , Peng Ying‐Jie , Jacono Frank J , Kumar Ganesh K , Dick Thomas E 
Published: April 2005

SUMMARY1. Humans experiencing intermittent hypoxia (IH) owing to recurrent apnoea syndromes exhibit serious cardiovascular morbidity, including high blood pressure, increased sympathetic nerve activity, cardiac arrhythmia and myocardial infarction. Although apnoeas are accompanied by a simultaneous decrease in arterial O2 (hypoxia) and an increase in CO2 (hypercapnia), studies on experimental animals suggest that hypoxia, rather than hypercapnia, is the primary stimulus for developing hypertension and enhanced sympathetic nerve activity. Enhanced hypoxic‐sensing ability of the carotid bodies and the ensuing reflex activation of the sympathetic nervous system have been suggested to play a critical role in cardiorespiratory alterations resulting from recurrent apnoeas.2. The purpose of the present review is to highlight recent studies demonstrating the effects of IH on carotid body sensory activity and its consequences on sympathetic activation in a rodent model of chronic IH. Adult rats exposed to chronic IH (15 s of 5% O2 followed by 5 min of 21% O2, nine episodes per h, 8 h/day for 10 days) exhibited selective enhancement of carotid body sensory response to hypoxia. In addition, chronic IH induced a novel form of sensory plasticity in the carotid body, manifested as sensory long‐term facilitation (LTF). Functional changes in the carotid body occurred in the absence of morphological changes in the chemoreceptor tissue.3. Acute hypoxia increased expiratory modulated splanchnic nerve activity (SNA) and acute IH‐induced LTF in SNA. Hypoxia‐induced SNA activation was prevented by bilateral sectioning of the sinus nerves. Rats exposed to chronic IH exhibited enhanced hypoxia‐induced sympathetic activation and augmented LTF of the SNA. Bilateral sectioning of the sinus nerves abolished these responses, suggesting chronic IH‐induced alterations in carotid body sensitivity contribute to LTF in SNA and the subsequent cardiovascular alterations.
HYPOTHESIS: THE SYSTEMIC CIRCULATION AS A REGULATED FREE‐MARKET ECONOMY. A NEW APPROACH FOR UNDERSTANDING THE LONG‐TERM CONTROL OF BLOOD PRESSURE
Authors: Fink Gregory D 
Published: April 2005

SUMMARY1. The purpose of the present paper is to discuss the long‐term regulation of arterial blood pressure. Current thinking on the topic favours the theory that tight regulation is achieved through the action of a central (or primary) controller, usually assumed to be in either the brain or kidneys.2. Here, an alternative explanation is considered; namely, that the average long‐term level of arterial pressure is an emergent property of a decentralized control system. The goal of the system is to deliver nutrient‐rich blood to distinct vascular regions based on their energy demand.3. Specifically, the circulation is conceptualized as a free‐market economy where tissues ‘compete’ for a scarce resource (the energy contained in blood) supplied by the heart–lung unit; the ‘price’ of the resource (analogous to the reciprocal of arterial pressure) is determined primarily by the dynamic relationship between supply and demand, not by a central mechanism.4. Based on this concept of the circulation as an energy market, economic analogies are used to suggest novel mechanisms by which the brain and kidney may affect the long‐term control of blood pressure.5. Market‐based control, a process derived from quantitative theoretical analysis of the performance of economic markets, is proposed as a new, potentially useful strategy for mathematically modelling the behaviour of the circulation.