Miracle-dz/UniFAR-FTUs huggingface dataset:
Modeling of Plug-in Hybrid Electric Vehicle Charging Demand in Probabilistic Power Flow Calculations

Millions of electric vehicles (EVs), especially plug-in hybrid EVs (PHEVs), will be integrated into the power grid in the near future. Due to their large quantity and complex charging behavior, the impact of substantial PHEVs charging on the power grid needs to be investigated. Since the charging behavior of PHEVs in a certain regional transmission network or a local distribution network is determined by different uncertain factors, their overall charging demand tends to be uncertain and in this situation probabilistic power flow (PPF) can be applied to analyze the impact of PHEVs charging on the power grid. However, currently there is no suitable model of the overall charging demand of PHEVs available for PPF calculations. In this paper, a methodology of modeling the overall charging demand of PHEVs is proposed. The proposed methodology establishes a single PHEV charging demand model, and then employs queuing theory to describe the behavior of multiple PHEVs. Moreover, two applications are given, i.e., modeling the overall charging demand of PHEVs at an EV charging station and in a local residential community, respectively. Comparison between PPF calculations and Monte Carlo simulation are made on a modified IEEE 30-bus system integrated with the two demand models proposed.
Cytochrome p-450 polymorphisms and response to clopidogrel.

BACKGROUND Clopidogrel requires transformation into an active metabolite by cytochrome P-450 (CYP) enzymes for its antiplatelet effect. The genes encoding CYP enzymes are polymorphic, with common alleles conferring reduced function. METHODS We tested the association between functional genetic variants in CYP genes, plasma concentrations of active drug metabolite, and platelet inhibition in response to clopidogrel in 162 healthy subjects. We then examined the association between these genetic variants and cardiovascular outcomes in a separate cohort of 1477 subjects with acute coronary syndromes who were treated with clopidogrel in the Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction (TRITON-TIMI) 38. RESULTS In healthy subjects who were treated with clopidogrel, carriers of at least one CYP2C19 reduced-function allele (approximately 30% of the study population) had a relative reduction of 32.4% in plasma exposure to the active metabolite of clopidogrel, as compared with noncarriers (P<0.001). Carriers also had an absolute reduction in maximal platelet aggregation in response to clopidogrel that was 9 percentage points less than that seen in noncarriers (P<0.001). Among clopidogrel-treated subjects in TRITON-TIMI 38, carriers had a relative increase of 53% in the composite primary efficacy outcome of the risk of death from cardiovascular causes, myocardial infarction, or stroke, as compared with noncarriers (12.1% vs. 8.0%; hazard ratio for carriers, 1.53; 95% confidence interval [CI], 1.07 to 2.19; P=0.01) and an increase by a factor of 3 in the risk of stent thrombosis (2.6% vs. 0.8%; hazard ratio, 3.09; 95% CI, 1.19 to 8.00; P=0.02). CONCLUSIONS Among persons treated with clopidogrel, carriers of a reduced-function CYP2C19 allele had significantly lower levels of the active metabolite of clopidogrel, diminished platelet inhibition, and a higher rate of major adverse cardiovascular events, including stent thrombosis, than did noncarriers.
PLGA 90/10 and caprolactone biodegradable nerve guides for the reconstruction of the rat sciatic nerve

The purpose of this study was to test in vivo two different nerve guides for promoting nerve regeneration across a 10‐mm gap of the rat sciatic nerve: 1) one made of PLGA in a novel proportion (90:10) of the two polymers poly(L‐lactide):poly(glycolide); 2) another made of (DL‐lactide‐ϵ‐caprolactone) copolyester (Neurolac®) tube, by comparing its healing efficacy with that of the more traditional methods of end‐to‐end nerve suture and autologous graft. Motor and sensory functional recovery were assessed throughout the healing period of 20 weeks, and the repaired nerves were processed for morphological and histomorphometrical analysis. Both motor and sensory functions improved significantly in all experimental nerve repaired groups. At the end of the 20‐week follow‐up, the end‐to‐end group showed better recovery of motor function when compared with the groups treated with guiding tubes. However, at this time point, the level of motor function in the Neurolac® and PLGA groups was similar to the one of the graft group. Nociception function also recovered faster in the end‐to‐end group compared with the Neurolac® and PLGA groups, and in this case, recovery was also delayed in the graft group. At the end of follow‐up, nociception was similar in all experimental groups. Morphological and histomorphometrical analysis showed that axon regeneration occurred in both PLGA and Neurolac® experimental groups, with no significant differences in the total number of regenerated fibers, but disclosed a different pattern of degradation of the two types of tubes with larger biodegradation of PLGA material by the end of 20 weeks. These results suggest that both types of biomaterials are a good substrate for preparing tubular nerve guides, and their different pattern of degradation does not seem to influence the degree of nerve regeneration. © 2007 Wiley‐Liss, Inc. Microsurgery, 2007.
Phylogenetic distribution and expression of a penicillin-binding protein homologue, Ear and its significance in virulence of Staphylococcus aureus.

PURPOSE Staphylococcus aureus is an opportunistic human pathogen that can cause serious infections in humans. A plethora of known and putative virulence factors are produced by staphylococci that collectively orchestrate pathogenesis. Ear protein (Escherichia coli ampicillin resistance) in S. aureus is an exoprotein in COL strain, predicted to be a superantigen, and speculated to play roles in antibiotic resistance and virulence. The goal of this study was to determine if expression of ear is modulated by single nucleotide polymorphisms in its promoter and coding sequences and whether this gene plays roles in antibiotic resistance and virulence. METHODOLOGY Promoter, coding sequences and expression of the ear gene in clinical and carriage S. aureus strains with distinct genetic backgrounds were analysed. The JE2 strain and its isogenic ear mutant were used in a systemic infection mouse model to determine the competiveness of the ear mutant.Results/Key findings. The ear gene showed a variable expression, with USA300FPR3757 showing a high-level expression compared to many of the other strains tested including some showing negligible expression. Higher expression was associated with agr type 1 but not correlated with phylogenetic relatedness of the ear gene based upon single nucleotide polymorphisms in the promoter or coding regions suggesting a complex regulation. An isogenic JE2 (USA300 background) ear mutant showed no significant difference in its growth, antibiotic susceptibility or virulence in a mouse model. CONCLUSION Our data suggests that despite being highly expressed in a USA300 genetic background, Ear is not a significant contributor to virulence in that strain.
Continuous flow peritoneal dialysis: first experience in children with acute renal failure.

BACKGROUND AND OBJECTIVES Acute renal failure can be treated with different dialysis modalities, depending on patient characteristics and hospital resources. Peritoneal dialysis (PD) can be first choice in situations like hypotension, disturbed coagulation, or difficult venous access. The main disadvantage of PD is the relatively limited efficacy. The aim of this study was to investigate whether continuous flow peritoneal dialysis (CFPD) is a more effective treatment than conventional PD in acute renal failure. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS A pilot study was performed at The Red Cross University Hospital in Cape Town in six patients. Patients were treated with both CFPD and conventional PD for 8 to 16 hours. CFPD was performed with two bedside-placed catheters. After initial filling, dialysate flow rate (100 ml/1.73 m2 per minute) was maintained with an adapted continuous venovenous hemofiltration machine. Ultrafiltration flow rate was set at 2.5 ml/1.73 m2 per minute. RESULTS Mean ultrafiltration was 0.20 ml/1.73 m2 per minute with conventional PD versus 1.8 ml/1.73 m2 per minute with CFPD. Mean clearances of urea and creatinine were 5.0 and 7.6 ml/1.73 m2 per minute with conventional PD versus 15.0 and 28.8 ml/1.73 m2 per minute with CFPD, respectively. No complications occurred. CONCLUSIONS In this first report of CFPD in six pediatric patients with acute renal failure, CFPD was on average three to five times more effective for urea and creatinine clearance and ultrafiltration than conventional PD, without any complications observed. CFPD has the ability to improve therapy for acute renal failure.
p53-independent apoptotic and necrotic cell deaths induced by adenovirus infection: suppression by E1B 19K and Bcl-2 proteins.

Adenovirus E1B 19K protein prevents premature death of adenovirus-infected cells. Viral mutants (19K mutants) defective in the 19K protein induce enhanced cell death, resulting in fragmentation of viral and cellular DNA. The 19K protein can also suppress the effects of certain external cell death-inducing stimuli, such as tumor necrosis factor alpha and various DNA-damaging agents that induce apoptosis. We have examined viral infection of permissive human cells and nonpermissive rat cells to determine if the 19K mutant induces apoptotic or necrotic type of cell death. Infection of normal rat kidney cells with an adenovirus type 2 19K deletion mutant induces internucleosomal DNA fragmentation and condensation of nuclear chromatin. Electron microscopic examination of these cells revealed the presence of condensed subnuclear bodies characteristic of apoptosis. In contrast, infection of human A549 cells induces random DNA fragmentation, and these cells do not exhibit characteristic condensation of the nuclear chromatin but contain enlarged nuclei loaded with virus particles. Therefore, it appears that adenovirus infection induces both apoptotic and necrotic types of cell death, depending on the cell type. Both types of cell death can be suppressed by E1B 19K protein. Similarly, a recombinant adenovirus expressing the human Bcl-2 protein but lacking the E1B proteins can efficiently suppress both apoptotic and necrotic cell death induced by adenovirus infection. The requirement of p53 tumor suppressor protein in adenovirus-induced cell death was investigated by infection of human Saos2 and mouse p53 nullizygous (p53-/-) cells lacking p53 tumor suppressor protein. (ABSTRACT TRUNCATED AT 250 WORDS)
A Wnt7b-dependent pathway regulates the orientation of epithelial cell division and establishes the cortico-medullary axis of the mammalian kidney

The mammalian kidney is organized into a cortex where primary filtration occurs, and a medullary region composed of elongated tubular epithelia where urine is concentrated. We show that the cortico-medullary axis of kidney organization and function is regulated by Wnt7b signaling. The future collecting duct network specifically expresses Wnt7b. In the absence of Wnt7b, cortical epithelial development is normal but the medullary zone fails to form and urine fails to be concentrated normally. The analysis of cell division planes in the collecting duct epithelium of the emerging medullary zone indicates a bias along the longitudinal axis of the epithelium. By contrast, in Wnt7b mutants, cell division planes in this population are biased along the radial axis, suggesting that Wnt7b-mediated regulation of the cell cleavage plane contributes to the establishment of a cortico-medullary axis. The removal of β-catenin from the underlying Wnt-responsive interstitium phenocopies the medullary deficiency of Wnt7b mutants, suggesting a paracrine role for Wnt7b action through the canonical Wnt pathway. Wnt7b signaling is also essential for the coordinated growth of the loop of Henle, a medullary extension of the nephron that elongates in parallel to the collecting duct epithelium. These findings demonstrate that Wnt7b is a key regulator of the tissue architecture that establishes a functional physiologically active mammalian kidney.
Role of Cardiolipin in Mitochondrial Signaling Pathways

The phospholipid cardiolipin (CL) is an essential constituent of mitochondrial membranes and plays a role in many mitochondrial processes, including respiration and energy conversion. Pathological changes in CL amount or species composition can have deleterious consequences for mitochondrial function and trigger the production of reactive oxygen species. Signaling networks monitor mitochondrial function and trigger an adequate cellular response. Here, we summarize the role of CL in cellular signaling pathways and focus on tissues with high-energy demand, like the heart. CL itself was recently identified as a precursor for the formation of lipid mediators. We highlight the concept of CL as a signaling platform. CL is exposed to the outer mitochondrial membrane upon mitochondrial stress and CL domains serve as a binding site in many cellular signaling events. During mitophagy, CL interacts with essential players of mitophagy like Beclin 1 and recruits the autophagic machinery by its interaction with LC3. Apoptotic signaling pathways require CL as a binding platform to recruit apoptotic factors such as tBid, Bax, caspase-8. CL required for the activation of the inflammasome and plays a role in inflammatory signaling. As changes in CL species composition has been observed in many diseases, the signaling pathways described here may play a general role in pathology.
The Growing Global Obesity Problem: Some Policy Options to Address It

The last few decades have seen fundamental changes in food consumption patterns around the world. These changes were characterized not only by an increase in overall calorie intakes but also by a shift in the composition of the diet towards more meat, eggs, dairy products as well as more fats and oils, i.e. a shift towards high calorie diets that are also much richer in saturated fats and cholesterol. The main drivers of this transition include factors such as: (i) rapidly falling real prices for food; (ii) urbanization with the development of new marketing channels and the spread of supermarkets into developing countries; (iii) and freer trade and globalization with the emergence of large, trans-nationally operating food companies. This diet transition also brought about a rapid increase in the prevalence of overweight, obesity and related non-communicable diseases (NCDs). Initially, these problems were limited to developed countries, but more recently, there are growing concerns that the adverse effects of a rapid nutrition transition could even be more severe in developing countries. The growing health concerns have also given rise to a intense debate about possible remedies to stop and reverse the obesity epidemic in developed countries, and, perhaps even more importantly, to prevent similar developments in developing countries. Some of these policy options are being examined in this paper. The instruments analysed include price interventions, both at the level of primary commodities and final consumer goods (tax on fat food), direct incentives to reduce and disincentives to maintain an excess body weight; finally the paper also presents some experience gathered with a combination of various measures in integrated nutrition programmes.
FADD, Caspase-3, and Caspase-8 and Incidence of Coronary Events

Objective— To investigate the relationship between 3 markers of apoptosis, that is, FADD (Fas-associated death domain–containing protein), caspase-3, and caspase-8, and incidence of coronary events (CEs) in a population-based cohort study. Approach and Results— In vitro experiments were performed to assess the response of the apoptotic biomarkers after Fas stimulation of peripheral blood mononuclear cells. The experiments showed significantly increased releases of FADD, caspase-3, and caspase-8 after Fas stimulation. The relationship between FADD, caspase-3, and caspase-8, respectively, and incidence of CEs was studied in 4284 subjects from the population-based Malmö Diet and Cancer Study. Cox’ proportional hazards regression was used to examine the association between the apoptotic biomarkers and incidence of CE over a mean follow-up of 19 years. A total of 381 individuals had CE during the follow-up. High FADD at baseline was significantly associated with incident CE. In the highest compared with the lowest quartile of FADD, the risk factor adjusted hazards ratio for CE was 1.82 (95% confidence interval, 1.35–2.46; P for trend <0.001). A significant association was also found between caspase-8 and CE; the hazards ratio (Q4 versus Q1) was 1.90 (95% confidence interval, 1.39–2.60; P for trend <0.001) after adjustment for risk factors. No association was found between caspase-3 and CEs. Conclusions— High levels of FADD and caspase-8, but not caspase-3, were associated with increased incidence of CE in subjects from the general population. The in vitro experiments support the view that these biomarkers could reflect activation of the extrinsic apoptotic pathway.
2003 Daniel McAlpine Memorial Lecture Increasing threat of diseases to exotic plantation forests in the Southern Hemisphere: lessons from Cryphonectria canker

Plantation forestry in the Southern Hemisphere has grown dramatically in the last hundred years. This has largely been due to the exceptional growth and performance of exotic species, particularly Pinus, Eucalyptus and Acacia. It is generally recognised that the success of these plantations has, at least in part, been due to the separation of the trees from their natural enemies. In this regard, the trees have performed similarly to weeds. Indeed, in some situations, species regarded as highly desirable for forestry are also recognised as noxious weeds. The artificial barrier between exotic plantation species and their pathogens is, however, crumbling. Despite intensive efforts to exclude pests and pathogens from countries now dependent on plantations of exotic trees, new and seriously damaging incursions are occurring with increasing frequency. Cryphonectria canker of Eucalyptus caused by Cryphonectria cubensis provides an important and interesting example and is used in this paper to illustrate emerging trends. These include evidence to suggest that native pathogens, previously thought to be relatively host specific and non-threatening, are adapting to infect exotic plantation trees. Other than the damage that these pathogens are causing to exotics, they now pose a serious threat to the same or related tree species in their areas of origin. This tremendous threat is only just being recognised and it is little understood. This is, at least in part, due to a poor understanding of the taxonomy and ecology of even some of the better known tree pathogens. Intensive efforts will be required to protect the sustainability of exotic plantation forestry. They will also be needed to ensure that ‘new pathogens’ do not lead to destruction of the same or related tree species in their areas of origin.
Retrospective analysis of surgically treated infective endocarditis cases.

BACKGROUND Prosthetic valve endocarditis (PVE) and native valve endocarditis (NVE) both cause high rates of morbidity and mortality and are significant health problems in our community. Optimal timing of the surgical intervention depends on the hemodynamic stability of the patient. In the present study, we retrospectively evaluated the clinical status, bacteriology, morbidity, and mortality parameters of infective endocarditis cases that were treated surgically. METHODS Thirty patients (20 male and 10 female) who underwent cardiac valve surgery between April 2001 and December 2006 were included in the study. The mean (SD) age of the patients was 36.5 +/- 5.42 years. Thirty-five surgical operations were conducted on 30 patients. We evaluated the patient demographic, etiologic, and surgical data retrospectively with respect to mortality and morbidity. RESULTS The mean time to develop PVE was 13 months. We recorded a mortality rate of 16.6% (2 deaths in NVE operations and 3 deaths in PVE operations). Repeat surgeries were performed in 2 aortic valve cases and 3 mitral valve cases in which paravalvular leakage was noticed in the prosthetic valves. CONCLUSION Despite significant medical and surgical advances, both NVE and PVE still continue to be causes of high mortality and morbidity rates in cardiac surgery.
Vasopressin modulates cerebrovascular responses to opioids in newborn pigs.

Vasopressin receptor blockade has been observed to attenuate the systemic vascular effects of dynorphin. This study was designed to determine the ability of vasopressin to modulate cerebrovascular responses to opioids in newborn pigs equipped with closed cranial windows. Topical dynorphin 13 increased pial arteriolar diameter during normotension (151 +/- 5, 171 +/- 4, 183 +/- 4 and 187 +/- 4 microns for control, 10(-10), 10(-8) and 10(-6) M dynorphin 13, respectively). During hypotension, however, responses to dynorphin 13 were reversed to concentration-dependent decreases in pial arteriolar diameter (184 +/- 3, 169 +/- 4, 165 +/- 4 and 159 +/- 4 microns for control 10(-10), 10(-8) and 10(-6) M dynorphin 13, respectively). Dynorphin 13-induced pial arteriolar dilation was potentiated by the V1 receptor antagonist [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid) 2(o-methyl)-Tyr-AVP] (MEAVP; 5 micrograms/kg i.v.; 14 +/- 1, 22 +/- 1 and 24 +/- 1% vs. 19 +/- 1, 26 +/- 1 and 30 +/- 1% increase for 10(-10), 10(-8) and 10(-6) M dynorphin 13 before and after MEAVP, respectively). In contrast, dynorphin 13-induced constriction during hypotension was markedly reduced by MEAVP (10 +/- 1, 15 +/- 1 and 16 +/- 2% vs. 1 +/- 1, 4 +/- 1 and 9 +/- 1% decrease for 10(-10), 10(-8) and 10(-6) dynorphin 13 before and after MEAVP, respectively). Dynorphin 8 and the synthetic kappa-opioid selective agonist, U5O,488H, elicited similar tone-dependent responses that were modified by MEAVP in a similar fashion. (ABSTRACT TRUNCATED AT 250 WORDS)