bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced Egress of Intracellular Eimeria tenella Sporozoites by Splenic Lymphocytes from Coccidian-Infected Chickens
Authors: Dong Xiaojuan , Abdelnabi Ghada H. , Lee Sung H. , Li Guangxing , Jin Hong , Lillehoj Hyun S. , Suo Xun 
Published: June 2011

ABSTRACT

Egress, which describes the mechanism that some intracellular parasites use to exit from parasitophorous vacuoles and host cells, plays a very important role in the parasite life cycle and is central to
Eimeria
propagation and pathogenesis. Despite the importance of egress in the intracellular parasite's life cycle, very little information is known on this process compared to other steps, e.g., invasion. The present study was conducted to investigate the interplay between the host adaptive immune system and
Eimeria
egression. Splenic lymphocytes or soluble immune factors were incubated with parasite-infected host cells for 3 or 5 h, and the percentage of egress was calculated according to an established formula. Viability of egressed parasites and host cells was tested using trypan blue exclusion and annexin V and propidium iodide staining, respectively. We found that premature egression of sporozoites from
Eimeria tenella
-infected primary chicken kidney cells or from chicken peripheral blood mononuclear cells occurred when the cells were cocultured
in vitro
with spleen lymphocytes from
E. tenella
-infected chickens but not when they were cocultured with splenocytes from uninfected chickens.
Eimeria
-specific antibodies and cytokines (gamma interferon [IFN-γ], interleukin-2 [IL-2], and IL-15), derived from
E. tenella
-primed B and T lymphocytes, respectively, were capable of promoting premature egress of sporozoites from infected host cells. Both egressed parasites and host cells were viable, although the latter showed reduced reinvasion ability. These results suggest a novel, immune-mediated mechanism that the host exploits to interrupt the normal
Eimeria
life cycle
in vivo
and thereby block the release of mature parasites into the environment.
Development and Application of a Mouse Intestinal Loop Model To Study the
In Vivo
Action of Clostridium perfringens Enterotoxin
Authors: Caserta Justin A. , Robertson Susan L. , Saputo Juliann , Shrestha Archana , McClane Bruce A. , Uzal Francisco A. 
Published: June 2011

ABSTRACT

Clostridium perfringens
enterotoxin (CPE) is responsible for causing the gastrointestinal symptoms of
C. perfringens
type A food poisoning, the second most commonly identified bacterial food-borne illness in the United States. CPE is produced by sporulating
C. perfringens
cells in the small intestinal lumen, where it then causes epithelial cell damage and villous blunting that leads to diarrhea and cramping. Those effects are typically self-limiting; however, severe outbreaks of this food poisoning, particularly two occurring in psychiatric institutions, have involved deaths. Since animal models are currently limited for the study of the CPE action, a mouse ligated intestinal loop model was developed. With this model, significant lethality was observed after 2 h in loops receiving an inoculum of 100 or 200 μg of CPE but not using a 50-μg toxin inoculum. A correlation was noted between the overall intestinal histological damage and lethality in mice. Serum analysis revealed a dose-dependent increase in serum CPE and potassium levels. CPE binding to the liver and kidney was detected, along with elevated levels of potassium in the serum. These data suggest that CPE can be absorbed from the intestine into the circulation, followed by the binding of the toxin to internal organs to induce potassium leakage, which can cause death. Finally, CPE pore complexes similar to those formed in tissue culture cells were detected in the intestine and liver, suggesting that (i) CPE actions are similar
in vivo
and
in vitro
and (ii) CPE-induced potassium release into blood may result from CPE pore formation in internal organs such as the liver.
Multigenic Control and Sex Bias in Host Susceptibility to Spore-Induced Pulmonary Anthrax in Mice
Authors: Yadav Jagjit S. , Pradhan Suman , Kapoor Renuka , Bangar Hansraj , Burzynski Benjamin B. , Prows Daniel R. , Levin Linda 
Published: June 2011

ABSTRACTMechanisms underlying susceptibility to anthrax infection are unknown. Using a phylogenetically diverse panel of inbred mice and spores ofBacillus anthracisAmes, we investigated host susceptibility to pulmonary anthrax. Susceptibility profiles for survival time and organ pathogen load differed across strains, indicating distinct genetic controls. Tissue infection kinetics analysis showed greater systemic dissemination in susceptible DBA/2J (D) mice but a higher terminal bacterial load in resistant BALB/cJ (C) mice. Interestingly, the most resistant strains, C and C57BL/6J (B), demonstrated a sex bias for susceptibility. For example, BALB/cJ females had a significantly higher survival time and required 4-fold more spores for 100% mortality compared to BALB/cJ males. To identify genetic regions associated with differential susceptibility, survival time and extent of organ infection were assessed using mice derived from two susceptibility models: (i) BXD advanced recombinant inbred strains and (ii) F2 offspring generated from polar responding C and D strains. Genome-wide analysis of BXD strain survival identified linkage on chromosomes 5, 6, 9, 11, and 14. Quantitative trait locus (QTL) analysis of the C×DF2 population revealed a significant QTL (designatedRpai1forresistance topulmonaryanthraxinfection, locus1) for survival time on chromosome 17 and also identified a chromosome 11 locus for lung pathogen burden. The striking difference between genome-wide linkage profiles for these two mouse models of anthrax susceptibility supports our hypothesis that these are multigenic traits. Our data provide the first evidence for a differential sex response to anthrax resistance and further highlight the unlikelihood of a single common genetic contribution for this response across strains.
Surface Export of GAPDH/SDH, a Glycolytic Enzyme, Is Essential for Streptococcus pyogenes Virulence
Authors: Jin Hong , Agarwal Shivangi , Agarwal Shivani , Pancholi Vijay 
Published: June 2011

ABSTRACT

Streptococcal surface dehydrogenase (SDH) (glyceraldehyde-3-phosphate dehydrogenase [GAPDH]) is an anchorless major multifunctional surface protein in group A
Streptococcus
(GAS) with the ability to bind important mammalian proteins, including plasmin(ogen). Although several biological properties of SDH are suggestive of its possible role in GAS virulence, its direct role in GAS pathogenesis has not been ascertained because it is essential for GAS survival. Thus, it has remained enigmatic as to “how and why” SDH/GAPDH is exported onto the bacterial surface. The present investigation highlights “why” SDH is exported onto the GAS surface. Differential microarray-based genome-wide transcript abundance analysis was carried out using a specific mutant, which was created by inserting a hydrophobic tail at the C-terminal end of SDH (M1-SDH
HBtail
) and thus preventing its exportation onto the GAS surface. This analysis revealed downregulation of the majority of genes involved in GAS virulence and genes belonging to carbohydrate and amino acid metabolism and upregulation of those related to lipid metabolism. The complete attenuation of this mutant for virulence in the mouse model and the decreased and increased virulence of the wild-type and mutant strains postcomplementation with SDH
HBtail
and SDH, respectively, indicated that the SDH surface export indeed regulates GAS virulence. M1-SDH
HBtail
also displayed unaltered growth patterns, increased intracellular ATP concentration and Hpr double phosphorylation, and significantly reduced pH tolerance, streptolysin S, and SpeB activities. These phenotypic and physiological changes observed in the mutant despite the unaltered expression levels of established transcriptional regulators further highlight the fact that SDH interfaces with many regulators and its surface exportation is essential for GAS virulence.

IMPORTANCE
Streptococcal surface dehydrogenase (SDH), a classical anchorless cytoplasmically localized glycolytic enzyme, is exported onto the group A
Streptococcus
(GAS) surface through a hitherto unknown mechanism(s). It has not been known why GAS or other prokaryotes should export this protein onto the surface. By genetic manipulations, we created a novel GAS mutant strain expressing SDH with a 12-amino-acid hydrophobic tail at its C-terminal end and thus were able to prevent its surface exportation without altering its enzymatic activity or growth pattern. Interestingly, the mutant was completely attenuated for virulence in a mouse peritonitis model. The global gene expression profiles of this mutant reveal that the surface exportation of SDH is mandatory to maintain GAS virulence. The ability of GAS as a successful pathogen to localize SDH in the cytoplasm as well as on the surface is physiologically relevant and dynamically obligatory to fine-tune the functions of many transcriptional regulators and also to exploit its virulence properties for infection.
Surviving Bacterial Sibling Rivalry: Inducible and Reversible Phenotypic Switching in Paenibacillus dendritiformis
Authors: Be’er Avraham , Florin E.-L. , Fisher Carolyn R. , Swinney Harry L. , Payne Shelley M. 
Published: June 2011

ABSTRACT

Natural habitats vary in available nutrients and room for bacteria to grow, but successful colonization can lead to overcrowding and stress. Here we show that competing sibling colonies of
Paenibacillus dendritiformis
bacteria survive overcrowding by switching between two distinct vegetative phenotypes, motile rods and immotile cocci. Growing colonies of the rod-shaped bacteria produce a toxic protein, Slf, which kills cells of encroaching sibling colonies. However, sublethal concentrations of Slf induce some of the rods to switch to Slf-resistant cocci, which have distinct metabolic and resistance profiles, including resistance to cell wall antibiotics. Unlike dormant spores of
P. dendritiformis
, the cocci replicate. If cocci encounter conditions that favor rods, they secrete a signaling molecule that induces a switch to rods. Thus, in contrast to persister cells,
P. dendritiformis
bacteria adapt to changing environmental conditions by inducible and reversible phenotypic switching.

IMPORTANCE
In favorable environments, species may face space and nutrient limits due to overcrowding. Bacteria provide an excellent model for analyzing principles underlying overcrowding and regulation of density in nature, since their population dynamics can be easily and accurately assessed under controlled conditions. We describe a newly discovered mechanism for survival of a bacterial population during overcrowding. When competing with sibling colonies,
Paenibacillus dendritiformis
produces a lethal protein (Slf) that kills cells at the interface of encroaching colonies. Slf also induces a small proportion of the cells to switch from motile, rod-shaped cells to nonmotile, Slf-resistant, vegetative cocci. When crowding is reduced and nutrients are no longer limiting, the bacteria produce a signal that induces cocci to switch back to motile rods, allowing the population to spread. Genes encoding components of this phenotypic switching pathway are widespread among bacterial species, suggesting that this survival mechanism is not unique to
P. dendritiformis
.
An Unusual Mechanism of Isopeptide Bond Formation Attaches the Collagenlike Glycoprotein BclA to the Exosporium of Bacillus anthracis
Authors: Tan Li , Li Mei , Turnbough Charles L. 
Published: June 2011

ABSTRACT

The outermost exosporium layer of spores of
Bacillus anthracis
, the causative agent of anthrax, is comprised of a basal layer and an external hairlike nap. The nap includes filaments composed of trimers of the collagenlike glycoprotein BclA. Essentially all BclA trimers are tightly attached to the spore in a process requiring the basal layer protein BxpB (also called ExsFA). Both BclA and BxpB are incorporated into stable, high-molecular-mass complexes, suggesting that BclA is attached directly to BxpB. The 38-residue amino-terminal domain of BclA, which is normally proteolytically cleaved between residues 19 and 20, is necessary and sufficient for basal layer attachment. In this study, we demonstrate that BclA attachment occurs through the formation of isopeptide bonds between the free amino group of BclA residue A20 and a side chain carboxyl group of an acidic residue of BxpB. Ten of the 13 acidic residues of BxpB can participate in isopeptide bond formation, and at least three BclA polypeptide chains can be attached to a single molecule of BxpB. We also demonstrate that similar cross-linking occurs
in vitro
between purified recombinant BclA and BxpB, indicating that the reaction is spontaneous. The mechanism of BclA attachment, specifically, the formation of a reactive amino group by proteolytic cleavage and the promiscuous selection of side chain carboxyl groups of internal acidic residues, appears to be different from other known mechanisms for protein cross-linking through isopeptide bonds. Analogous mechanisms appear to be involved in the cross-linking of other spore proteins and could be found in unrelated organisms.

IMPORTANCE
Isopeptide bonds are protein modifications found throughout nature in which amide linkages are formed between functional groups of two amino acids, with at least one of the functional groups provided by an amino acid side chain. Isopeptide bonds generate cross-links within and between proteins that are necessary for proper protein structure and function. In this study, we discovered that BclA, the dominant structural protein of the external nap of
Bacillus anthracis
spores, is attached to the underlying exosporium basal layer protein BxpB via isopeptide bonds formed through a mechanism fundamentally different from previously described mechanisms of isopeptide bond formation. The most unusual features of this mechanism are the generation of a reactive amino group by proteolytic cleavage and promiscuous selection of acidic side chains. This mechanism, which apparently relies only on short peptide sequences in protein substrates, could be a general mechanism
in vivo
and adapted for protein cross-linking
in vitro
.
The efficacy of frequency specific microcurrent therapy on delayed onset hamstring muscle soreness: Figure 31
Authors: Curtis D , Fallows S , Morris M , McMakin C 
Published: June 2011

IntroductionThe effects of frequency specific microcurrent (FSM) therapy versus sham therapy in delayed onset muscle soreness (DOMS) was studied to determine whether specific frequencies on two channels would produce better results than single channel single frequency microcurrent therapy which has been shown to be ineffective as compared to sham in DOMS. Frequency specific therapy is thought to operate by the effects of both microamperage current and resonance on tissues and biochemical bonds.Methods18 male and 17 female healthy participants (mean age 32 +/- 4.2 years) were recruited. Following a 15-minute treadmill warm-up and 5 sub-maximal eccentric muscle contractions, participants performed 5 sets of 15 maximal voluntary eccentric muscle contractions on a seated leg curl machine. Post-exercise, participants had one leg randomly assigned to a subsensory, silent treatment of 20 minutes of frequency specific microcurrent stimulation, while the other leg acted as non-treated control with the device turned off. (see figure 1) Participants were blinded to the treatment but the experimenter was not. Soreness was rated for each leg at baseline and at 24, 48 and 72 hours post exercise on a visual analogue scale (VAS), which ranged from 0 (no pain) to 10 (worst pain ever).Figure 31Frequency specific microcurrent stimulationResultsBoth groups were identical at baseline (p= 1.00). Post-exercise there was a significant difference (p=0.0005) at 24 hours in the treated (1.3 / 10 ± 1.0) versus non-treated leg (5.2 / 10 ± 1.3). At 48 hours the treated leg was 1.2 / 10 ± 1.1 versus the non-treated of 7.0 / 10 ± 1.1 (p= 0.0005). At 72 hours the treated group was 0.7 / 10 ± 0.6 and the non-treated was 4.0 /10 ± 1.6 (p= 0.0005).ConclusionFSM therapy provided significant protection from DOMS at all time points tested.
The influence of three 48-hour dietary protocols on metabolic parameters during the maximal incremental treadmill test
Authors: Čanaki Martina , Ružić Lana , Leko Goran 
Published: June 2011

IntroductionThere are no protocol recommendations per-taining to nutrition before the performance assessment. The aim of this study was to determine the influence of three vari-ous 48-hour dietary protocols on parameters obtained during three trials of the maximal incremental treadmill test.MethodsThirteen physically active subjects (age: 25.73±3.09) underwent all-out treadmill test using a breath-by-breath analyzer. During the 13-day experiment, the subjects were submitted to the three controlled 48-hour dietary protocols. The obtained data were divided in three subgroups with respect to dietary conditions that prevailed during each trial. Three 48-hour dietary protocols consisted of (1) a low carbohydrate (CHO) diet 1.06 gkg-1 body mass of CHO; (2) a mixed diet 2.6 gkg-1 body mass of CHO; and (3) a high carbohydrate diet 5 gkg-1 body mass of CHO.ResultsThe results confirmed the difference in the observed metabolic parameters after implementing the 48-hour high-carbohydrate diet. It is important to note that the metabolic indicators corresponding to the anaerobic threshold and maximal work load significantly change and reach higher values under the influence of a high-carbohydrate diet at maximal workload. Respiratory exchange ratio and blood lactate concentration contributed the most to the observed differences (p<0,03).ConclusionsEnergy sources pertaining to different nutri-ents have to be accurately defined and balanced during both competition but also functional testing. Otherwise, errors can occur in the given physiological parameters which serve as the guidelines for planning and programming the training process, which is a precondition for maximizing the com-petition performance. An athlete, before the physiological assessment, should take approximately the same amount of carbohydrate (>75%) and other nutrients, just like before a competition depending on duration and intensity of the sports activity.
Aspects of anthropometric and morphofunctional cardiac parameters in a lot of junior football players
Authors: Dinu V , Călina M L , Rusu L , Bieru D Enescu , Gusti A 
Published: June 2011

IntroductionPhysical exercises and sport activity induce myocardium and vascular tree important functional and morphologic adjustment changes, which mostly explain the aerobe performances improvement. The present work studied the anthropometric and morphofunctional cardiac parameters in 30 junior football players, with ages between 10 and 18 years, during specific training period.MethodsIn order to appreciate the athletes anthropometric profile, that have been measured the height, the weight, the body mass index, the thoracic perimeter and the Erismann harmony index.Was recorded the ECG for the 12 classic derivations using the HEART 112D device and also the blood pressure and the heart rate values. The parameters obtained through echocardiography using the SIEMENS Acuson CV/70 device were: the cardiac cavity diameters, the cardiac volumes, the ejection fraction and the interventricular septum dimensions.ResultsThe results were compared with the ones of a 30 subjects control group, having the same age but not practicing any performance sports. Anthropometric measurements reveal that 32.5% of the sportsmen were underweight, 62.5% had a normal weight and the others were overweight. The thoracic diameters were moderately statistically correlated (r = 0.42) with a slight increase of left ventricle telesystolic and telediastolic volumes. The cardiac volumes were within studied age specific limits, being correlated with the presence of pulmonary regurgitation and ejection fraction (r = 0.78).ConclusionsThe effort practice by the professional junior football players ameliorates the anthropometric parameters, but also the morphofunctional cardiac ones.
Midportion Achilles tendinosis and the plantaris tendon
Authors: Alfredson Håkan 
Published: June 2011

ObjectivesWhen re-operating patients with midportion Achilles tendinosis, having had a poor effect of ultrasound (US) and Doppler-guided scraping, the author found the involvement of the plantaris tendon to be a likely reason for the poor result. The aim of this study was to investigate the occurrence of a plantaris tendon in close relation to the Achilles tendon in consecutive patients with midportion Achilles tendinosis undergoing treatment with US and Doppler-guided scraping.Material and methodsThis study includes 73 consecutive tendons with chronic painful midportion Achilles tendinosis, where US+Doppler examination showed thickening, irregular tendon structure, hypo-echoic regions, and localised high blood flow outside and inside the ventral Achilles midportion. The tendons were treated with US+Doppler-guided scraping, via a medial incision. If there was a plantaris tendon located in close relation to the medial Achilles, it was extirpated.ResultsAn invaginated, or ‘close by located’, enlarged plantaris tendon was found in 58 of 73 (80%) tendons. Preliminary clinical results of the combined procedure, US + Doppler-guided surgical scraping and extirpation of the plantaris tendon, are very promising.ConclusionsA thickened plantaris tendon located in close relation to the medial Achilles seems common in patients with chronic painful midportion tendinosis. The role of the plantaris tendon in midportion Achilles tendinosis needs to be further evaluated and should be kept in mind when treating this condition.
Early marriage, poor reproductive health status of mother and child well-being in India
Authors: Prakash Ravi , Singh Abhishek , Pathak Praveen Kumar , Parasuraman Sulabha 
Published: June 2011

Background and methodologyEarly marriage, women's poor reproductive health and child well-being are important areas of concern, especially in developing countries like India. Data from the third wave of National Family Health Survey (NFHS, 2005–2006) was used to examine the effects of early marriage on the reproductive health status of women and on the well-being of their children. Bivariate analyses, multiple linear regression and logistic regression were used for analyses.ResultsThe results show that early age at marriage had detrimental effects on the reproductive health status of women. Women married at an early age were exposed to frequent childbearing, unplanned motherhood and abortions, which negatively affected their nutritional status. Children born to mothers with poor reproductive health had lower chances of survival and a higher likelihood of anthropometric failure (i.e. stunting, wasting and underweight).Discussion and conclusionsProgrammes should focus on delaying entry of adolescents into wedlock and motherhood through information, education and communication. More emphasis needs to be put on meeting the reproductive needs of poor adolescent mothers, and improving the nutritional status of their children, to break the vicious circle of poor reproductive health and poverty.