bluuebunny/crossref_metadata_2025_split huggingface dataset:
Complement Dependency of Splenic Localization of Pneumococcal Polysaccharide and Conjugate Vaccines
Authors: Breukels M. A. , Zandvoort A. , Rijkers G. T. , Lodewijk M. E. , Klok P. A. , Harms G. , Timens W. 
Published: April 2005

AbstractThe immune response to polysaccharides is initiated when polysaccharides bind complement factor C3d, and these polysaccharide–C3d complexes subsequently localize on splenic marginal zone B cells strongly expressing CD21 (complement receptor 2). Infants and children under the age of 2 years have low or absent expression of CD21 on their marginal zone B cells, and consequently do not adequately respond to polysaccharides. In contrast, polysaccharide–protein conjugate vaccines are able to induce antibodies at this young age. Conjugate vaccines apparently overcome the necessity for CD21–C3d interaction for an antipolysaccharide immune response.We demonstrate in a rat model that localization of pneumococcal polysaccharides on splenic marginal zone B cells indeed is complement dependent. We also show that pneumococcal conjugates do not specifically localize on splenic marginal zone B cells and that splenic localization of polysaccharide conjugates is independent of the presence of complement. Thus, the induction of antipolysaccharide antibodies by conjugate vaccines apparently can occur independently of CD21–C3d interaction. These basic findings may explain the effectiveness of conjugated vaccines in young children and may open the way for their application in other patient groups.
Distinct Interethnic Differences in Immunoglobulin G Class/Subclass and Immunoglobulin M Antibody Responses to Malaria Antigens but not in Immunoglobulin G Responses to Nonmalarial Antigens in Sympatric Tribes Living in West Africa
Authors: Bolad A. , Farouk S. E. , Israelsson E. , Dolo A. , Doumbo O. K. , Nebié I. , Maiga B. , Kouriba B. , Luoni G. , Sirima B. S. , Modiano D. , Berzins K. , Troye‐Blomberg M. 
Published: April 2005

AbstractThe well‐established relative resistance to malaria observed in the Fulani as compared with other sympatric tribes in West Africa has been attributed to their higher levels of serum immunoglobulin (Ig) G antibodies to malarial antigens. In this study, we confirm and extend the previous findings by analyses of the levels of IgM, IgG and IgG subclasses of anti‐malarial antibodies in asymptomatic individuals of different sympatric tribes in Burkina Faso (Fulani/Mossi) and Mali (Fulani/Dogon). The Fulani showed significantly higher median concentrations of anti‐malarial IgG and IgM antibodies than the sympatric tribes at both locations. Although the overall subclass pattern of antibodies did not differ between the tribes, with IgG1 and IgG3 as dominant, the Fulani showed consistently significantly higher levels of these subclasses as compared with those of the non‐Fulani individuals. No significant differences were seen in the levels of total IgG between the tribes, but the Fulani showed significantly higher levels of total IgM than their neighbours in both countries. While the antibody levels to some nonmalarial antigens showed the same pattern of differences seen for antibody levels to malaria antigens, no significant such differences were seen with antibodies to other nonmalarial antigens. In conclusion, our results show that the Fulani in two different countries show higher levels of anti‐malarial antibodies than sympatric tribes, and this appears not to be a reflection of a general hyper‐reactivity in the Fulani.
Specific binding of amyloid‐β‐protein to IMR‐32 neuroblastoma cell membrane
Authors: Inaba S. , Okada T. , Konakahara T. , Kodaka M. 
Published: April 2005

Abstract:In flow cytometry using two detecting methods, we have found that amyloid‐β‐protein(1–40) [Aβ(1–40)] has high affinity to IMR‐32 neuroblastoma cell membrane when it is aggregated to form β‐sheet conformation, whereas random coil small Aβ‐species has low affinity. The difference in the binding ability to the cell membranes well accounts for the cytotoxicity of Aβ(1–40); namely, aggregated β‐sheet Aβ(1–40) gives cytotoxicity higher than random coil Aβ(1–40). Specific binding between Aβ(1–40) and ganglioside GM1 of the raft‐like domain in lipid membrane is suggested from a surface plasmon resonance (SPR) experiment.
CLARIFYING HOMOLOGIES IN THE MAMMALIAN CEREBRAL CORTEX: THE CASE OF THE THIRD VISUAL AREA (V3)
Authors: Rosa Marcello GP , Manger Paul R 
Published: April 2005

SUMMARY1. Experiments in mammalian models are the main source of information on the neural architecture underlying human visual perception, establishing scientific boundaries for the interpretation of experiments using non‐invasive techniques in humans and for the realistic modelling of visual processes. Thus, it is important to define the homology between visual areas in different species.2. To date, relatively few visual areas can be defined with certainty across mammalian Orders. Here, we review the evidence pointing to the fact that the third visual area (V3; or area 19) is a crucial node of a system involved in shape recognition that exists in most, if not all, eutherian mammals.3. The size and shape of area V3 are variable, even between species that belong to the same Order. Although some features of the visuotopic organization of V3 are constant (including the relative location of the representations of the upper and lower quadrant and correspondence between the anterior border and the representation of the vertical meridian of the visual field), others are variable between species and even individuals. A complex pattern of representation, involving topological discontinuities, can exist.4. In addition to its location in relation to the first (V1) and second (V2) visual areas, the identification of V3 homologues can be aided by certain other features, including low myelination, weak cytochrome oxidase reactivity, response properties that are indicative in the processing of stimulus shape, relationship to clusters of neurons forming interhemispheric connections and projections from the koniocellular (W‐cell‐like) components of the lateral geniculate nucleus.5. Recent research in primates has clarified the organization of the V3 homologue in members of this Order. Regions of cortex that were formerly thought to belong to V3 (including a densely myelinated region near the dorsal midline) are better considered as part of a separate dorsomedial area, involved in motion analysis and visuomotor integration. The redefined V3, which includes the ‘ventral posterior area’ and parts of the dorsolateral complex proposed by earlier studies, is very similar to V3 (area 19) of other species in terms of structure and function.
EUPHORBIA THYMIFOLIA SUPPRESSES HERPES SIMPLEX VIRUS‐2 INFECTION BY DIRECTLY INACTIVATING VIRUS INFECTIVITY
Authors: Yang Chien‐Min , Cheng Hua‐Yew , Lin Ta‐Chen , Chiang Lien‐Chai , Lin Chun‐Ching 
Published: April 2005

SUMMARY1. The ethyl acetate (EtOAc) extract and 3‐O‐galloyl‐4,6‐(S)‐hexahydroxydiphenoyl‐d‐glucose (3OG46HG) of Euphorbia thymifolia Linnea have been shown to exhibit anti‐herpes simplex virus (HSV)‐2 activity in vitro. In the present study, we investigated the mode of action of these two compounds in suppressing HSV‐2 multiplication.2. The results demonstrated that the EtOAc extract and 3OG46HG affected virus infectivity in a dose‐dependent manner. The EtOAc extract significantly reduced virus infectivity at a concentration of 4.0 µg/mL, whereas 3OG46HG obviously diminished virus infectivity at concentration of a 0.5 µg/mL. The virucidal ability of the EtOAc extract was affected by the incubation period, but not by the incubation temperature. In the case of the action of 3OG46HG against HSV‐2, the effects of incubation time and temperature were negligible.3. In summary, the EtOAc extract and 3OG46HG of E. thymifolia are concluded to inhibit HSV‐2 multiplication by reducing virus infectivity.
15‐F2t‐ISOPROSTANE and 5‐F2t‐ISOPROSTANE ARE NOT TRIGGERS OF MYOCARDIAL PRECONDITIONING
Authors: Arnaud Claire , Cracowski Jean‐Luc , Hakim Ahmed , Durand Thierry , Guy Alexandre , Godin‐Ribuot Diane , Bessard Germain , Ribuot Christophe 
Published: April 2005

SUMMARY1. Myocardial ischaemia–reperfusion in humans is associated with increased formation of 15‐F2t‐isoprostane and 5‐F2t‐isoprostane (15‐F2t‐IsoP and 5‐F2t‐IsoP, respectively). Whether this formation is relevant clinically remains controversial. The present study was performed in order to evaluate the ability of the isoprostanes 15‐F2t‐IsoP and 5‐F2t‐IsoP to reduce myocardial ischaemic injury in rat isolated heart.2. Rats were divided into six groups. Hearts were excised, perfused retrogradely and pretreated with vehicle (ethanol 5.10−7 and 2.10−9 mol/L; n = 6), subjected to ischaemic preconditioning (n = 8) or pretreated with the isoprostanes 15‐F2t‐IsoP (3.10−10 and 3.10−7 mol/L; n = 8) or 5‐F2t‐IsoP (10−9 mol/L; n = 8). After a 5 min treatment−5 min washout period, hearts were submitted to 30 min global ischaemia, followed by a 120 min reperfusion period.3. The infarct‐to‐ventricle zone ratio was significantly reduced in ischaemic preconditioned (20.6 ± 2.6%) compared with vehicle groups (44.5 ± 4.3 and 51.3 ± 2.5% in groups pretreated with 5.10−7 or 2.10−9 mol/L ethanol, respectively). Pretreatment with either isoprostane had no cardioprotective effect; the infarct‐to‐ventricle ratios were 43.1 ± 2.2, 49.4 ± 5.9 and 44.5 ± 5.0% for groups treated with 3.10−10 mol/L 15‐F2t‐IsoP, 3.10−7 mol/L 15‐F2t‐IsoP or 10−9 mol/L 5‐F2t‐IsoP, respectively.4. These data provide evidence that the isoprostanes 15‐F2t‐IsoP and 5‐F2t‐IsoP are not implicated in early myocardial preconditioning at concentrations similar to those found in the human coronary sinus following coronary angioplasty.
HYPERTENSION 2020: CONFRONTING TOMORROW'S PROBLEM TODAY
Authors: Reid Christopher M , Thrift Amanda G 
Published: April 2005

SUMMARY1. In developed countries, the major burden of disease is due to chronic diseases, such as heart disease and stroke. In contrast, the major burden of disease among people in developing countries has been due largely to diseases caused by malnutrition, poor sanitation and infection. In recent years, with increasing economic and demographic development, there has been a shift in developing countries from diseases caused by poverty towards chronic, non‐communicable, lifestyle‐related diseases. The rapid emergence of these chronic diseases has not occurred with a similarly rapid decline in infectious diseases. Therefore, these developing countries are experiencing high rates of both infectious and chronic diseases.2. The increase in chronic diseases in developing countries has been brought about by the increasing prevalence of risk factors, such as increased alcohol consumption, smoking, obesity, physical inactivity and low fruit and vegetable intake. In parallel with this, there is also increased evidence of high blood pressure and high cholesterol levels.3. The preventive strategies required to reverse this trend for these emerging diseases include the education of public health professionals, the introduction of surveillance activities to monitor changes in risk factors, the introduction of health promotion, the development of prevention research and improved advocacy for disease prevention programmes. Experience from other countries provides evidence that prevention programmes can work. The global challenge is to ensure that implementation of such programmes in the world's developing nations does not come too late.
MECHANISMS MEDIATING PRESSURE NATRIURESIS: WHAT WE KNOW and WHAT WE NEED TO FIND OUT
Authors: Evans Roger G , Majid Dewan SA , Eppel Gabriela A 
Published: April 2005

SUMMARY1. It is well established that pressure natriuresis plays a key role in long‐term blood pressure regulation, but our understanding of the mechanisms underlying this process is incomplete.2. Pressure natriuresis is chiefly mediated by inhibition of tubular sodium reabsorption, because both total renal blood flow and glomerular filtration rate are efficiently autoregulated. Inhibition of active sodium transport within both the proximal and distal tubules likely makes a contribution. Increased renal interstitial hydrostatic pressure (RIHP) likely inhibits sodium reabsorption by altering passive diffusion through paracellular pathways in ‘leaky’ tubular elements.3. Nitric oxide and products of cytochrome P450‐dependent arachidonic acid metabolism are key signalling mechanisms in pressure natriuresis, although their precise roles remain to be determined.4. The key unresolved question is, how is increased renal artery pressure ‘sensed’ by the kidney? One proposal rests on the notion that blood flow in the renal medulla is poorly autoregulated, so that increased renal artery pressure leads to increased renal medullary blood flow (MBF), which, in turn, leads to increased RIHP. An alternative proposal is that the process of autoregulation of renal blood flow leads to increased shear stress in the preglomerular vasculature and, so, release of nitric oxide and perhaps products of cytochrome P450‐dependent arachidonic acid metabolism, which, in turn, drive the cascade of events that inhibit sodium reabsorption.5. Central to the arguments underlying these opposing hypotheses is the extent to which MBF is autoregulated. This remains highly controversial, largely because of the limitations of presently available methods for measurement of MBF.
PATHOGENESIS OF HYPERTENSION IN RENAL FAILURE: ROLE OF THE SYMPATHETIC NERVOUS SYSTEM and RENAL AFFERENTS
Authors: Phillips Jacqueline K 
Published: April 2005

SUMMARY1. The kidney receives a dense innervation of sympathetic and sensory fibres and can be both a target of sympathetic activity and a source of signals that drive sympathetic tone. In the normal state, interactions between the kidney and sympathetic nervous system (SNS) serve to maintain blood pressure and glomerular filtration rate within tightly controlled levels. In renal failure, a defect in renal sodium excretory function leads to an abnormal pressure natriuresis relationship and activation of the renin–angiotensin–aldosterone system, contributing to the development of hypertension and progression of kidney disease.2. Evidence now strongly indicates a role for the SNS in the pathogenesis of hypertension in renal failure. Hypertension occurs commonly and early in renal disease and is paralleled by increases in SNS activity, as indicated by increased muscle sympathetic nerve activity and circulating catecholamines. This appears to be driven by the diseased kidneys, because nephrectomy or denervation has been shown to correct blood pressure and SNS activity in human and animal studies.3. Afferent signals from the kidney, detected by chemoreceptors and mechanoreceptors, feed directly into central nuclei of the SNS, including the hypothalamus and circumventricular organs, in addition to the stimulus provided by circulating and brain‐derived angiotensin II. Therefore, the pathogenesis of hypertension in renal failure is complex and arises from the interaction of haemodynamic and neuroendocrine factors.4. Increased SNS activity has significant implications with regard to increased risk of cardiovascular disease and is an important consideration in the treatment of renal failure.
LONG‐TERM REGULATION OF ARTERIAL BLOOD PRESSURE BY HYPOTHALAMIC NUCLEI: SOME CRITICAL QUESTIONS
Authors: Dampney Ral , Horiuchi J , Killinger S , Sheriff Mj , Tan Psp , McDowall Lm 
Published: April 2005

SUMMARY1. The long‐term level of arterial pressure is dependent on the relationship between arterial pressure and the urinary output of salt and water, which, in turn, is affected by a number of factors, including renal sympathetic nerve activity (RSNA). In the present brief review, we consider the mechanisms within the brain that can influence RSNA, focusing particularly on hypothalamic mechanisms.2. The paraventricular nucleus (PVN) in the hypothalamus has major direct and indirect connections with the sympathetic outflow and there is now considerable evidence that tonic activation of the PVN sympathetic pathway contributes to the sustained increased level of RSNA that occurs in conditions such as heart failure and neurogenic hypertension. The tonic activity of PVN sympathetic neurons, in turn, depends upon the balance of excitatory and inhibitory inputs. A number of neurotransmitters and neuromodulators are involved in these tonic excitatory and inhibitory effects, including glutamate, GABA, angiotensin II and nitric oxide.3. The dorsomedial hypothalamic nucleus (DMH) also exerts a powerful influence over sympathetic activity, including RSNA, via synapses with sympathetic nuclei in the medulla and, possibly, also other brainstem regions. The DMH sympathetic pathway is an important component of the phasic sympathoexcitatory responses associated with acute stress, but there is no evidence that it is an important component of the central pathways that produce long‐term changes in arterial pressure. Nevertheless, it is possible that repeated episodic activation of this pathway could lead to vascular hypertrophy and, thus, sustained changes in vascular resistance and arterial pressure.4. Recent studies have reactivated the old debate concerning the possible role of the baroreceptor reflex in the long‐term regulation of sympathetic activity. Therefore, central resetting of the baroreceptor–sympathetic reflex may be an important component of the mechanisms causing sustained changes in RSNA. However, little is known about the cellular mechanisms that could cause such resetting.
NITRIC OXIDE and SYMPATHETIC NERVE ACTIVITY IN THE CONTROL OF BLOOD PRESSURE
Authors: Ramchandra Rohit , Barrett Carolyn J , Malpas Simon C 
Published: April 2005

SUMMARY1. Endothelial dysfunction marked by impairment in the release of nitric oxide (NO) is seen very early in the development of hypertension and is considered important in mediating the impaired vascular tone evident in essential hypertensive patients.2. Recently, a hypothesis has emerged that NO acting as a neurotransmitter in the brain can modulate levels of sympathetic nerve activity and thereby blood pressure. The NO inhibition model of hypertension has been used to explore the possibility that a decrease in levels of NO can cause an increase in levels of sympathetic nerve activity that can mediate the hypertension.3. In the present review, we examine the literature regarding the role of NO in setting the mean level of sympathetic nerve activity and blood pressure. Although the acute effects of NO inhibition are well understood, the chronic interaction between the sympathetic nervous system and NO has only been investigated using indirect measures of sympathetic nerve activity, such as ganglionic blockade. This has led to inconsistent results regarding the role of NO in modulating sympathetic nerve activity chronically.4. Some of the conflicting results may be explained by differences in the ‘background’ levels of angiotensin (Ang) II. Evidence suggests that NO may interact with AngII and baroreceptor afferent inputs in the central nervous system to set the mean level of sympathetic nerve activity.5. We suggest chronic NO inhibition can increase sympathetic nerve activity if baroreceptor input is intact and AngII levels are elevated. Although studies exploring the actions of NO or AngII in isolation are useful for gathering initial information, future studies should focus on their interactions and their role in setting the long‐term levels of sympathetic activity and blood pressure.
ROLE OF THE CENTRAL NUCLEUS OF THE AMYGDALA IN THE CONTROL OF BLOOD PRESSURE: DESCENDING PATHWAYS TO MEDULLARY CARDIOVASCULAR NUCLEI
Authors: Saha S 
Published: April 2005

SUMMARY1. One of the key areas that links psychologically induced stress with the blood pressure‐regulatory system is the central nucleus of the amygdala (CeA). This is an integratory forebrain nucleus that receives input from higher centres in the forebrain and has extensive connections with the hypothalamus and the medulla oblongata, areas involved in the regulation of the cardiovascular reflexes.2. Based on studies using electrical or chemical stimulation or electrolytic lesions of the CeA, it has become clear that the CeA plays an important role in the regulation of blood pressure in response to stressful or fearful stimuli.3. Two important medullary areas known to receive projections from the CeA are the nucleus tractus solitarius (NTS) and the rostral ventrolateral medulla (RVLM). The NTS is the site of the first synapse for afferent fibres originating from baroreceptors, chemoreceptors and the heart, whereas the RVLM contains neurons that maintain resting blood pressure and sympathetic nerve activity via projections to sympathetic preganglionic neurons in the intermediolateral cell column of the thoracolumbar spinal cord.4. Electron microscopic studies using combined anterograde tracing and pre‐ and post‐embedding immunogold labelling have shown that the pathways originating from the CeA to the NTS are inhibitory and may use GABA as a neurotransmitter. The results of these studies suggest that blood pressure changes produced by activation of the CeA may be mediated by attenuation of baroreceptor reflexes through a GABAergic mechanism at the level of the NTS.5. Neuronal tract tracing combined with neurofunctional studies using the Fos protein as a marker of activated neurons indicate that the CeA projects directly to baroreceptive neurons in the NTS and RVLM that are activated by changes in blood pressure.6. In conclusion, studies that have examined the efferent pathways of the CeA suggest that CeA neurons with projections to medullary baroreceptive neurons may play a vital role in the reflex changes in sympathetic nerve activity that are involved in blood pressure regulation in response to stress or anxiety.
CHRONIC EFFECTS OF ANGIOTENSIN II and AT1 RECEPTOR ANTAGONISTS IN SUBFORNICAL ORGAN‐LESIONED RATS
Authors: Collister John P , Hendel Michael D 
Published: April 2005

SUMMARY1. Angiotensin (Ang) II is known to exert some of its effects centrally via circumventricular organs. These unique central nervous system areas lack the normal blood–brain barrier and, therefore, allow peptide hormones access to the brain. Of these, the subfornical organ (SFO) has been shown to be involved in many of the acute dipsogenic and pressor effects of AngII, but much less is known about the role of the SFO in the chronic effects of AngII. We hypothesized that the SFO is a central site involved in the chronic hypotensive effects of endogenous AT1 receptor blockade, as well as the chronic hypertensive effects of exogenously administered AngII.2. In order to test these hypotheses, SFO‐lesioned (SFOx) or sham Sprague‐Dawley rats were instrumented with venous catheters and radiotelemetric pressure transducers for intravenous administration of losartan or AngII and continuous measurement of blood pressure and heart rate. Rats were given 3 days of saline control infusion (7 mL/day of 0.9% NaCl) and were then infused with either losartan (10 mg/kg per day) or AngII (10 ng/kg per min) for 10 days.3. By day 4 of losartan treatment, arterial pressure had decreased 24 ± 2 and 18 ± 2 mmHg in sham (n = 9) and SFOx (n = 10) rats, respectively. Furthermore, by day 5 of AngII infusion, arterial pressure had increased 12 ± 3 mmHg in sham rats (n = 9), but only by 4 ± 1 mmHg in SFOx rats (n = 9). In each treatment group, these attenuated pressure responses in SFOx rats continued through day 10 of treatment.4. These results support the hypotheses that the SFO plays a role in both the hypotensive effects of chronic AT1 receptor blockade and the chronic hypertensive phase of exogenously administered AngII.