bluuebunny/crossref_metadata_2025_split huggingface dataset:
Down regulation of Hsp70 expression level prolongs the duration of heat‐induced male sterility in Drosophila buzzatii
Authors: SARUP P. , DAHLGAARD J. , NORUP A.‐M. , JØRGENSEN K. T. , HEBSGAARD M. B. , LOESCHCKE V. 
Published: May 2004

Summary

The relationship between heat shock protein Hsp70 expression level and the duration of heat‐induced male sterility was investigated in four populations of Drosophila buzzatii Patterson and Wheeler. The effect of heat hardening on the duration of sterility was further examined after flies developed at either 25 or 31 °C. In addition, Hsp70 expression was measured in testes after development at three different thermal regimes.
Four main hypotheses were tested: (i) Hsp70 is expressed in testes of D. buzzatii males even at non‐stressful temperatures, and the level of expression increases with increasing rearing temperature. (ii) Hsp70 expression level differs between populations and is negatively correlated with the duration of poststress sterility. (iii) Experimentally induced Hsp70 expression at the pupal stage shortens the sterility period of flies reared above the temperature threshold of sterility. (iv) In contrast, a hardening treatment during the pupal stage of flies reared at 25 °C results in a longer time to fertility.
The results matched the hypotheses, leading to the conclusion that higher Hsp70 expression reduces the duration of heat‐induced male sterility.
Does testis size track expected mating success in yellow dung flies?
Authors: BLANCKENHORN W. U. , HELLRIEGEL B. , HOSKEN D. J. , JANN P. , ALTWEGG R. , WARD P. I. 
Published: May 2004

Summary

We quantitatively compare the fitness function linking male mating success in the field to body size and the allometric relationship linking testis length (estimating sperm production) to body size, both empirically derived, for the yellow dung fly Scathophaga stercoraria (Diptera: Scathophagidae).
We find that both relationships are similarly non‐linear (quadratic) and increasing. The most parsimonious interpretation of this congruence is that the evolution of testis size (and hence sperm numbers) evolutionarily ‘tracks’ the number of copulations a male of a given size can expect, resulting in the particular non‐linear testis size‐body size allometry evident.
We offer a general, two‐tiered statistical approach for this kind of quantitative comparison.
Net spinning caddisflies as stream ecosystem engineers: the influence of Hydropsyche on benthic substrate stability
Authors: CARDINALE B. J. , GELMANN E. R. , PALMER M. A. 
Published: May 2004

Summary

Organisms that physically modify or create habitat (ecosystem engineers) can have a profound influence on community and ecosystem dynamics.
Here evidence is presented that one of the most abundant and widely distributed lotic insects could act as an ecosystem engineer in streams by increasing the stability of benthic substrates during flooding.
Natural densities of larval net spinning caddisflies (Hydropsychidae) were established in stream channels that had standardized physical properties. The mobility of three particle sizes were measured during simulated flooding and the fraction of particles eroded compared with that of control streams.
Larvae increased the initial velocity required to erode sediments by 10–30%. At velocities sufficient to scour 87% of particles from control channels, 57–100% remained stable in channels colonized by larvae.
Assuming larvae have similar effects in natural streams, caddisflies could be expected to increase the recurrence interval of a substrate scouring flood from 1·67 year to 2·41 year, corresponding to a 17% decrease in the probability of bed scour per year.
Our study suggests these insects could play an important role in generating the spatial ‘refuges’ that moderate the resistance of lotic communities to flooding. It is argued that, as has occurred in marine systems, a better understanding of how freshwater organisms engineer their physical environment has much potential to complement our historical focus on the abiotic forces that constrain populations and communities.
Sex‐specific differences in cardiovascular performance of a centrarchid fish are only evident during the reproductive period
Authors: COOKE S. J. 
Published: May 2004

Summary

Although in birds and mammals sex‐specific differences in organismal performance and physiology are well documented, comparatively little is known about the influence of sex or reproductive status on fish performance or metabolism.
In this study, the resting cardiovascular performance of male and female Largemouth Bass Micropterus salmoides was contrasted across three seasons and different reproductive states including the spring when nesting males provide sole parental care. Doppler flow probes were used to monitor resting cardiac output (Q) and its two components (heart rate, fH and stroke volume, SVH).
During the spring when Largemouth Bass were engaged in reproduction (at 21 °C), parental male nesting fish had heightened resting cardiovascular rates (both Q and fH) relative to non‐nesting males and females. In the summer at higher water temperatures (24 °C), and in the autumn at water temperatures similar to the reproductive period (21 °C), resting cardiovascular variables were similar between sexes.
This study found that there are sex‐based differences in fish physiological performance. However, the sex‐specific differences were evident only during the reproductive period, and in particular for male fish actively engaged in the nesting phase of parental care, indicating a likely role of the endocrine system.
Endocrinology & Dialysis. Testosterone Metabolism and Replacement Therapy in Patients with End‐Stage Renal Disease
Authors: Holley JL , Johansen Kirsten L. 
Published: May 2004

ABSTRACTHypogonadism is common among men with end‐stage renal disease (ESRD), beginning before the need for dialysis and not improved with the initiation of dialysis. Many of the manifestations of hypogonadism, such as bone disease and muscle wasting, are also frequently seen among dialysis patients. There have been few studies of testosterone replacement therapy in this patient population, but available data suggest that testosterone can be administered without adjustment of the doses used in hypogonadal men with normal renal function. Extrapolation from results of treatment of hypogonadal older men with normal renal function suggests that testosterone replacement could improve libido and could have salutary effects on muscle mass and bone mineral density in patients with kidney disease. However, caution is warranted because of the potential side effects of testosterone therapy, and further research is needed to more precisely define the balance of risk and benefit in patients with chronic kidney disease. Specifically it will be important to determine the prevalence and clinical significance of hypogonadism in ESRD patients in the modern era and to measure the effects of replacement therapy on various symptoms of hypogonadism as well as on overall quality of life, physical functioning, and survival.
Hypothesis: The Body Mass Index Paradox and an Obesity, Inflammation, and Atherosclerosis Syndrome in Chronic Kidney Disease
Authors: Beddhu Srinivasan 
Published: May 2004

ABSTRACTThe association of high body mass index (BMI) with better survival in chronic kidney disease (CKD) is considered a “risk factor paradox” or “reverse epidemiology.” Since malnutrition is a powerful predictor of death and cardiovascular disease is its leading cause, it has been suggested that malnutrition and atherosclerosis must be associated. Thus the current paradigm is that malnutrition is a risk factor for atherosclerosis and obesity is protective in CKD patients. We recently showed that high‐BMI patients with inferred high body fat have an increased prevalence of atherosclerosis and subsequent cardiovascular and all‐cause mortality. Prior cross‐sectional studies also showed that high BMI in CKD is associated with higher C‐reactive protein (CRP) levels and increased coronary calcification on electron beam computed tomography (CT) scan. These apparently conflicting data on better survival but increased inflammation and atherosclerosis in high‐BMI CKD patients could be explained as follows. It is hypothesized that nutrition exerts a much stronger influence on survival than atherosclerosis in CKD. Malnutrition strongly augments the hazard of death from coexistent diseases, while better nutrition has the opposite effect. Thus the risk of death is highest in malnourished patients (low muscle and low fat mass) and lowest in well‐nourished patients (high BMI, high muscle mass). Obesity (high BMI, high fat mass) is associated with inflammation and atherosclerosis. The risk of death from obesity and atherosclerosis is increased, but not so much as occurs with malnutrition. Therefore high body fat patients have intermediate survival. Thus it is postulated that an association of obesity, inflammation, and atherosclerosis (OIA syndrome) might exist in CKD.
Fellows’ Forum in Dialysis. Depression: A Common but Underrecognized Condition Associated with End‐Stage Renal Disease
Authors: Perazella Mark A. , Wang Pei‐Li , Watnick Suzanne G. 
Published: May 2004

ABSTRACTWe describe a patient with end‐stage renal disease (ESRD) who developed depression over the period of dialysis initiation. Depression is an extremely common but underrecognized disorder in the dialysis population, which is one of the rationales for this case report. Here we present the epidemiology, mechanisms for diagnosis, associations with medical morbidity, and treatment modalities specifically for patients on dialysis.
Improved Survival with Higher Hematocrits: Where is the Evidence?
Authors: Cotter Dennis J. , Stefanik Kevin , Zhang Yi , Thamer Mae 
Published: May 2004

ABSTRACTThe Centers for Medicare and Medicaid Services (CMS) is reviewing Medicare coverage policy for recombinant human erythropoietin (epoetin) therapy. CMS officials are concerned that “Medicare spending on EPO may be higher than necessary without resulting in optimal patient benefit.” Approximately 190 end‐stage renal disease (ESRD) patients die each day—a mortality rate that has remained essentially unchanged since 1994—despite improvements in the “adequacy of dialysis, vascular access, and anemia management”. To date, the evidence cited in support of a survival benefit of epoetin confuses the relationship between treatment response and outcomes with a causal effect of epoetin. A variety of mechanisms may account for a non‐causal association between hematocrit and mortality can occur. We conclude that there is no basis for inferring the survival benefits (or detriments) of increasing a patient's hematocrit by adjusting the dosing of epoetin. Furthermore, we note that caution is required in administering large doses of epoetin to unresponsive patients in order to achieve the target hematocrit. A better understanding of the epoetin/survival relationship, well‐grounded in science, is needed to provide a basis for CMS to improve its current epoetin policies, and may help to improve patient mortality.
Heat‐shock induced nuclear retention and recycling inhibition of importin α
Authors: Furuta Maiko , Kose Shingo , Koike Makiko , Shimi Takeshi , Hiraoka Yasushi , Yoneda Yoshihiro , Haraguchi Tokuko , Imamoto Naoko 
Published: May 2004

Heat‐shock induces a strong stress response and modifies all aspects of cellular physiology, which involves dynamic changes in the nucleocytoplasmic distributions of a variety of proteins. Many distinct nucleocytoplasmic transport pathways exist in eukaryotic cells, but how a particular transport pathway is regulated under different cellular conditions remains elusive. The finding of this study indicate that conventional nuclear import, which is mediated by importin α/β, is down‐regulated, while the nuclear import of 70 kD heat‐shock cognate protein is up‐regulated in heat‐shock cells. Among the factors involved in the mediation of the conventional nuclear import, significant levels of importin α accumulate in the nucleus in response to heat‐shock. An analysis of the behaviour of importin α with fluorescence recovery after photobleaching and fluorescence loss in photobleaching studies show that nuclear importin α becomes less mobile and its nucleocytoplasmic recycling is impaired in heat‐shock cells. These data coincided well with biochemical and cytological studies. Our present data show that heat‐shock induces the nuclear accumulation, nuclear retention, and recycling inhibition of importin α, resulting in the suppression of conventional nuclear import. This suggests a new regulatory mechanism for the adaptation of cells to environmental changes, such as heat‐shock.
Transcriptional co‐activator activity of SYT is negatively regulated by BRM and Brg1
Authors: Ishida Michiko , Tanaka Shinya , Ohki Misao , Ohta Tsutomu 
Published: May 2004

The t(X;18)(p11.2;q11.2) translocation found in synovial sarcomas results in the fusion of the SYT gene on chromosome 18 to the SSX gene on chromosome X. Although the SYT‐SSX fusion proteins may trigger synovial sarcoma development, the biological functions of SYT, SSX and SYT‐SSX genes are unclear. Transfections of Gal4 DNA binding domain fusion protein constructs demonstrate that SYT protein acts as a transcriptional co‐activator at the C‐terminal domain and that the activity is repressed through the N‐terminus. The N‐terminal 70 amino acids of SYT bind not only to BRM, but also to Brg1, both of which are subunits of SWI/SNF chromatin remodelling complexes. Here, we have investigated the functions of BRM and Brg1 on the repression of SYT activity. The negative regulation of SYT transcriptional co‐activator activity is dependent on the ATP‐hydrolysis of BRM and Brg1 in the protein complexes. This indicates that the SWI/SNF protein complexes regulate SYT activity using the chromatin remodelling activity.
Over-expression of TATA binding protein (TBP) and p53 and autoantibodies to these antigens are features of systemic sclerosis, systemic lupus erythematosus and overlap syndromes
Authors: Chauhan R , Handa R , Das T P , Pati U 
Published: May 2004

Summary
The aim of this study was to determine the expression levels of p53 and TATA binding protein (TBP) and the presence of autoantibodies to these antigens in Asian Indian patients with systemic sclerosis (SSc), overlap syndromes (OS) and systemic lupus erythematosus (SLE). Fifty patients with SSc, 20 with OS, including mixed connective tissue diseases (MCTD), 20 with SLE, 10 disease controls (DC) and 25 controls (C) were studied. The over-expression of p53 and TBP antigen was determined quantitatively by sandwich enzyme-linked immunosorbent assay (ELISA), varies between four- and sevenfold higher in patients with SSc, OS and SLE, in comparison to DC and C. The expressed protein antigens were not present as free antigens but as immune-complexes. Autoantibodies to p53 were detected by ELISA in 78% subjects with SSc, 100% with OS and 80% with SLE. Autoantibodies to TBP were observed in 28% patients with SSc, 25% with OS and 15% with SLE. In comparison to healthy controls, the titre of antibodies to p53 was significantly higher in patients with SSc (P = 0·00001) than the patients with OS (P = 0·00279) and SLE (P = 0·00289), whereas the titre of antibodies to TBP was higher in patients with OS (P = 0·00185) than the SLE (P = 0·00673) and the SSc (P = 0·00986) patients. Autoantibodies to p53 and TBP were detected in all these patients and the levels of these two autoantibodies showed weak negative correlation with each other. We propose that the over-expression of these antigens might be due to hyperactive regulatory regions in the p53 and TBP gene.
Expression and subcellular distribution of toll-like receptors TLR4, TLR5 and TLR9 on the gastric epithelium in Helicobacter pylori infection
Authors: SCHMAUßER B , ANDRULIS M , ENDRICH S , LEE S K , JOSENHANS C , MÜLLER-HERMELINK H-K , ECK M 
Published: May 2004

SUMMARY
Toll-like receptors (TLRs) expressed by mucosal epithelium play an essential role in the defense against microbes by recognizing conserved bacterial molecules. For the first time TLR4, TLR5 and TLR9 have been microanatomically localized in patients with noninflamed gastric mucosa and Helicobacter pylori gastritis by immunohistochemistry. Because polarized expression of TLRs in apical and basolateral epithelial compartments is thought to modulate mucosal immunity, subcellular TLR distribution by gastric epithelium was investigated using confocal microscopy. TLR4, TLR5 and TLR9 were expressed by gastric epithelium in antrum and corpus of all patients with H. pylori gastritis (n = 14) and with noninflamed gastric mucosa (n = 5). TLR4 was expressed at the apical and the basolateral pole of the gastric epithelium as well in noninflamed gastric mucosa as in H. pylori gastritis. TLR5 and TLR9 expression in the noninflamed gastric mucosa was identical to that of TLR4 with localization at the apical and the basolateral epithelial pole. However, in H. pylori gastritis TLR5 and TLR9 expression on the gastric epithelium changed to an exclusive basolateral localization without detectable expression at the apical pole. In the human stomach, the gastric epithelium expressed TLR4, TLR5 and TLR9, which gives it the possibility to interact with H. pylori. Furthermore, gastric epithelial TLR4 expression is highly polarized in an apical and a basolateral compartment, whereas TLR5 and TLR9 polarization seems to be a process dynamically influenced by H. pylori infection. This polarized and dynamically regulated gastric epithelial expression of TLRs supports a sentinel role for these receptors in the mucosal immunity to H. pylori.
Constitutive expression of Interleukin-18 and Interleukin-18 receptor mRNA in tumour derived human B-cell lines
Authors: LOREY S L , HUANG Y C , SHARMA V 
Published: May 2004

SUMMARYInterleukin-18 (IL-18) is a pro-inflammatory cytokine involved in the Th1 immune response and expressed by a variety of cell types. IL-18 is a member of the IL-1 family and plays an important role in autoimmune diseases and inflammation. Using reverse transcriptase-polymerase chain reaction (RT-PCR) mRNA expression of IL-18, IL-18 receptor alpha (IL-18Rα), and beta (IL-18Rβ) were studied in tumour derived human B-cell lines. Furthermore, we investigated IL-18 protein secretion by using enzyme linked immunosorbent assay (ELISA). The results, as presented in this report, suggest that IL-18, IL-18Rα, and IL-18Rβ mRNA are constitutively and ubiquitously expressed in human B-cell lines, but secretion of the functional protein does not occur. We therefore speculate that IL-18 possibly affects B-cells through paracrine actions.
Langerhans cells from human oral epithelium are more effective at stimulating allogeneic T cellsin vitrothan Langerhans cells from skin
Authors: HASSÉUS B , JONTELL M , BERGENHOLTZ G , DAHLGREN U I 
Published: May 2004

SUMMARYThis report is focused on the functional capacity of Langerhans cells (LC) in the epithelium of skin and oral mucosa, which both meet different antigenic challenges. The capacity of LC from human oral and skin epithelium to provide co-stimulatory signals to T cells in vitro was compared. LC in a crude suspension of oral epithelial cells had a significantly enhanced T cell co-stimulatory capacity compared to skin epithelial cells. This applied both to cultures with concanavalin A (con-A)-stimulated syngeneic T cells and to a mixed epithelial cell lymphocyte reaction involving allogeneic T cells. The co-stimulatory capacity of oral and skin epithelial cells was reduced by &gt;70% if monoclonal antibodies against HLA-DR, -DP and -DQ were added to the cultures with allogeneic T cells, indicating the involvement of HLA class II expressing LC. Immunohistochemistry revealed that 6% of the epithelial cells were CD1a + LC in sections from both oral and skin epithelium. Interleukin (IL)-8 production was higher in cultures of oral epithelial cells and con-A stimulated T cells than in corresponding cultures with skin epithelial cells as accessory cells. The results suggest that LC in human oral epithelium are more efficient at stimulating T cells than those of skin.
Redox status and immune function in type I diabetes families
Authors: MATTEUCCI E , MALVALDI G , FAGNANI F , EVANGELISTA I , GIAMPIETRO O 
Published: May 2004

SUMMARYBecause abnormalities in redox balance cluster in type I diabetes families and the intracellular thiol redox status seems to modulate immune function, we aimed to investigate the relationship between oxidative stress and immunological features. We measured oxidative markers, serum proinflammatory cytokines, soluble cytokine receptors and subsets of peripheral blood lymphocytes (by varying combinations of CD4, CD8, CD23 or low-affinity IgE receptor, and CD25 or IL-2 receptor) from 38 type I patients, 76 low-risk (i.e. without underlying islet autoimmunity) non-diabetic first-degree relatives of diabetic patients, and 95 healthy subjects. In type I diabetes families, protein and lipid oxidation was confirmed by the presence of reduced sulphhydryl groups, increased advanced oxidation protein products, and increased plasma and erythrocyte malondialdehyde. Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25+ cells in peripheral blood. Patients with TIDM had similar defects and, in addition, showed decreased counts of peripheral CD4+CD8+ lymphocytes and increased serum levels of soluble receptors for interleukin (IL)-6 and IL-2. Abnormal indicators of oxidative stress were related in part to immune abnormalities. In the whole study group, we found a correlation (multiple R 0·5, P &lt; 0·001) of CD23+CD25+ cells with blood counts of monocytes, CD4+CD8+ cells, CD25+ cells, basal haemolysis and plasma levels of thiols. In type I diabetics, anti-GAD65 antibody levels were associated (multiple R 0·6, P = 0·01) positively with sIL-6R, negatively with duration of diabetes and CD23+CD25+ counts; plasma creatinine correlated positively (multiple R 0·6, P &lt; 0·001) with both sIL-2R and tumour necrosis factor (TNF)-α concentration. Our study reports the first evidence that the oxidative stress observed in type I families is related to immunological hallmarks (decreased peripheral numbers of monocytes as well as cells bearing a CD4+CD8+, CD23+CD25+ and CD25+ phenotype) from which the involvement of some immunoregulatory mechanisms could be suspected. It remains to be elucidated the course of events culminating in the loss of physiological immune homeostasis and disease pathology.
Anti-mannose binding lectin antibodies in sera of Japanese patients with systemic lupus erythematosus
Authors: TAKAHASHI R , TSUTSUMI A , OHTANI K , GOTO D , MATSUMOTO I , ITO S , WAKAMIYA N , SUMIDA T 
Published: May 2004

SUMMARYMannose-binding lectin (MBL) is a key element in innate immunity with functions and structure similar to that of complement C1q. It has been reported that MBL deficiency is associated with occurrence of systemic lupus erythematosus (SLE). We hypothesized that anti-MBL antibodies, if present, would affect the occurrence or disease course of SLE, by reduction of serum MBL levels, interference of MBL functions, or binding to MBL deposited on various tissues. To address this hypothesis, we measured the concentration of anti-MBL antibodies in sera of 111 Japanese SLE patients and 113 healthy volunteers by enzyme immunoassay. The titres of anti-MBL antibodies in SLE patients were significantly higher than those in healthy controls. When the mean + 2 standard deviations of controls was set as the cut off point, individuals with titres of anti-MBL antibodies above this level were significantly more frequent in SLE patients (9 patients) than in controls (2 persons). One SLE patient had an extremely high titre of this antibody. No associations of titres of anti-MBL antibodies and (i) genotypes of MBL gene, (ii) concentrations of serum MBL, or (iii) disease characteristics of SLE, were apparent. Thus, we have confirmed that anti-MBL antibodies are indeed present in sera of some patients with SLE, but the significance of these autoantibodies in the pathogenesis of SLE remains unclear.