Miracle-dz/UniFAR-FTUs huggingface dataset:
Impact of controlled burns on the abundance of Ixodes scapularis (Acari: Ixodidae).

Information on the effect of vegetative destruction by controlled burns in reducing the abundance of the blacklegged tick, Ixodes scapularis Say, the vector for the agents of Lyme disease, human babesiosis, and human granulocytic ehrlichiosis, is limited. Therefore, the abundance of nymphal, larval, and adult I. scapularis was monitored by dragging the vegetation at 2 separate 4-ha tracts in Cockaponset State Forest in Connecticut following a single controlled burn on 15 April or 21 May 1992. The burn at the April burn site was rated as light to moderate with a flame height of 0.3 m and consumed approximately 67% of the surface leaf litter. The burn at the May burn site was rated moderate to severe with a flame height of 0.6-0.9 m. , which consumed vegetation < 5 cm in diameter and approximately 100% of the surface leaf litter. The impact of the burn was strongly influenced by the intensity and timing of the burn. Burning of the vegetation resulted in a reduction of the abundance of nymphal I. scapularis by 74% at the moderately burned site and 97% at the severely burned site, compared with adjacent unburned woodland. No larvae were recovered later in the summer from the severely burned tract. However, judging by the comparable abundance of adult I. scapularis in the fall at the burned and unburned woodlands, the effect of the burns was temporary. Burning the vegetation for the control of I. scapularis appears limited in effect and could be applied only on a large scale in areas with little or no human habitations.
SDF-1 Recruits Cardiac Stem Cell-Like Cells that Depolarize In Vivo

Prolongation or reestablishment of stem cell homing through the expression of SDF-1 in the myocardium has been shown to lead to homing of endothelial progenitor cells to the infarct zone with a subsequent increase in vascular density and cardiac function. While the increase in vascular density is important, there could clearly be other mechanisms involved. In a recent study we demonstrated that the infusion of mesenchymal stem cells (MSC) and MSC that were engineered to overexpress SDF-1 led to significant decreases in cardiac myocyte apoptosis and increases in vascular density and cardiac function compared to control. In that study there was no evidence of cardiac regeneration from either endogenous stem cells or the infused mesenchymal stem cells. In this study we performed further detailed immunohistochemistry on these tissues and demonstrate that the overexpression of SDF-1 in the newly infracted myocardium led to recruitment of small cardiac myosin-expressing cells that had proliferated within 2 weeks of acute MI. These cells did not differentiate into mature cardiac myocytes, at least by 5 weeks after acute MI. However, based on optical mapping studies, these cells appear capable of depolarizing. We observed greater optical action potential amplitude in the infarct border in those animals that received SDF-1 overexpressing MSC than observed in noninfarcted animals and those that received control MSC. Further immunohistochemistry revealed that these proliferated cardiac myosin-positive cells did not express connexin 43, but did express connexin 45. In summary, our study suggests that the prolongation of SDF-1 expression at the time of acute MI leads to the recruitment of endogenous cardiac myosin stem cells that may represent cardiac stem cells. These cells are capable of depolarizing and thus may contribute to increased contractile function even in the absence of maturation into a mature cardiac myocyte.
Prediction of incipient pasture-associated laminitis from hyperinsulinaemia, hyperleptinaemia and generalised and localised obesity in a cohort of ponies.

REASONS FOR PERFORMING STUDY The ability to predict ponies at increased risk of laminitic episodes, when exposed to nutrient dense pasture, would facilitate management to avoid disease. OBJECTIVES To identify variables and clinically useful cut-off values with reproducible diagnostic accuracy for the prediction of ponies that subsequently developed laminitis when exposed to nutrient dense pasture. METHODS A cohort of predominantly Welsh and Dartmoor ponies from a closed herd was evaluated in March 2006 (n = 74) and March 2007 (n = 57). Ponies were categorised as never laminitic or previously laminitic according to reported laminitic history and as clinically laminitic (CL) if laminitis was observed within 3 months following evaluation. Body condition score (BCS), cresty neck score (CNS), girth and neck circumferences (NC), withers height, blood pressure and hoof surface temperature, and plasma insulin, glucose, triglyceride, leptin, cortisol, ACTH, uric acid and TNF-alpha concentrations were measured. Analysis of sensitivity, specificity and receiver operating characteristic curves was used to evaluate the diagnostic accuracy for a variable to predict CL ponies. RESULTS Variables with diagnostic accuracy for the prediction of CL ponies included insulin, leptin, BCS, CNS, and NC:height ratio. Specific cut-off values of insulin (>32 mu/l), leptin (>73 ng/ml), BCS (> or = 7), CNS (> or = 4) and NC:height ratio (>0.71) had reproducible diagnostic accuracy for the prediction of laminitis. Combining tests did not result in higher diagnostic accuracy than individual tests of insulin or leptin during either evaluation. CONCLUSIONS Tests of insulin and leptin concentrations and measures of generalised (BCS) and localised (CNS or NC:height ratio) obesity were beneficial in the prediction of laminitic episodes. POTENTIAL RELEVANCE These results highlight the importance of monitoring and reducing insulin concentration, and generalised and regional obesity in ponies to reduce risk of laminitis.
Current Understanding of Pathogenesis and Treatment of TMJ Osteoarthritis

Osteoarthritis is a common disease that can cause severe pain and dysfunction in any joint, including the temporomandibular joint (TMJ). TMJ osteoarthritis (TMJOA) is an important subtype in the classification of temporomandibular disorders. TMJOA pathology is characterized by progressive cartilage degradation, subchondral bone remodeling, and chronic inflammation in the synovial tissue. However, the exact pathogenesis and process of TMJOA remain to be understood. An increasing number of studies have recently focused on inflammation and remodeling of subchondral bone during the early stage of TMJOA, which may elucidate the possible mechanism of initiation and progression of TMJOA. The treatment strategy for TMJOA aims at relieving pain, preventing the progression of cartilage and subchondral bone destruction, and restoring joint function. Conservative therapy with nonsteroidal anti-inflammatory drugs, splint, and physical therapy, such as low-energy laser and arthrocentesis, are the most common treatments for TMJOA. These therapies are effective in most cases in relieving the signs and symptoms, but their long-term therapeutic effect on the pathologic articular structure is unsatisfactory. A treatment that can reverse the damage of TMJOA remains unavailable to date. Treatments that prevent the progression of cartilage degradation and subchondral bone damage should be explored, and regeneration for the TMJ may provide the ideal long-term solution. This review summarizes the current understanding of mechanisms underlying the pathogenesis and treatment of TMJOA.
Horizontal-vertical guidance of Quadrotor for obstacle shape mapping

A real-time guidance algorithm for obstacle shape mapping is proposed. A stereo vision system and an ultrasonic sensor are assumed to be mounted on a quadrotor to obtain the shape information of an obstacle. The depth map acquired by the stereo vision system is utilized to detect and map the obstacle. Mapping the obstacle is performed by utilizing obstacle data points acquired from the depth map. States of the quadrotor are used to generate a path for obstacle mapping in real time. The quadrotor moves around the obstacle to map the overall shape of the obstacle while avoiding collisions. The quadrotor also performs vertical maneuvers if the image plane of the vision system cannot cover the entire obstacle. The horizontal and vertical maneuvers are performed in sequence to develop a systematic scheme to efficiently map the obstacle. Finally, numerical simulations are performed to demonstrate the performance of the proposed guidance algorithm.
Control of simian virus 40 DNA replication by the HeLa cell nuclear kinase casein kinase I

The initiation of simian virus 40 (SV40) DNA replication is regulated by the phosphorylation state of the viral initiator protein, large T antigen. We describe the purification from HeLa cell nuclei of a 35-kDa serine/threonine protein kinase that phosphorylates T antigen at sites that are phosphorylated in vivo and thereby inhibits its ability to initiate SV40 DNA replication. The inhibition of both origin unwinding and DNA replication by the kinase is reversed by protein phosphatase 2A. As determined by molecular weight, substrate specificity, autophosphorylation, immunoreactivity, and limited sequence analysis, this kinase appears to be identical to casein kinase I, a ubiquitous serine/threonine protein kinase that is closely related to a yeast kinase involved in DNA metabolism. The HeLa cell phosphorylation cycle that controls the initiation of SV40 DNA replication may also play a role in cellular DNA metabolism.
Population pharmacokinetics and effects of efavirenz in patients with human immunodeficiency virus infection

The reverse transcriptase inhibitor efavirenz is currently used at a fixed dose of 600 mg/d. However, dosage individualization based on plasma concentration monitoring might be indicated. This study aimed to assess the efavirenz pharmacokinetic profile and interpatient versus intrapatient variability in patients who are positive for human immunodeficiency virus, to explore the relationship between drug exposure, efficacy, and central nervous system toxicity and to build up a Bayesian approach for dosage adaptation.
Replication and amplification of novel vesicular stomatitis virus minigenomes encoding viral structural proteins

We have developed a system in which vesicular stomatitis virus (VSV) minigenomes encoding viral structural proteins can be expressed from plasmids. These RNAs can be replicated, transcribed, and packaged into infectious particles when coexpressed with the other VSV proteins. The minigenomes contain either the glycoprotein (G protein) gene (GMG [stands for G minigenome]) or both the G and matrix (M) protein genes (GMMG [stands for G/M minigenome]) from the Indiana serotype of VSV flanked by the trailer and leader regions from the wild-type VSV genome. Northern (RNA) blot analysis showed that the minigenome RNAs were replicated and that a positive-sense replicative intermediate was synthesized when coexpressed with the nucleocapsid (N) protein and the two VSV polymerase proteins (phosphoprotein [P] and the large catalytic subunit [L]) in vivo. In addition, functional mRNAs were transcribed from the minigenome templates, and the appropriate encoded proteins were expressed. Expression of the G and M proteins from GMMG resulted in the assembly and release of infectious particles that could be passaged on cells expressing the N, P, and L proteins only. Amplification occurred during successive passages, and after four passages approximately 30% of the cells expressed both the G and M proteins. Analysis of the RNAs produced in the GMMG-infected cells also showed that the minigenomes accurately reproduced all of the replicative and transcriptional events that normally occur in a VSV-infected cell. GMMG is therefore a novel type of defective particle which encodes functional viral proteins critical to its own propagation.
Expression of DNA Damage Checkpoint Protein Hus1 in Epithelial Ovarian Tumors Correlates With Prognostic Markers

Summary Hus1 and Rad9 are proteins involved in DNA damage checkpoint regulation, which is required for the maintenance of genomic stability. In addition to checkpoint activation, mammalian cells also use apoptosis to eliminate cells with severe DNA damage. Interestingly, Rad9 was shown to be directly involved in apoptosis as well. Despite the knowledge of molecular mechanisms on how Hus1 and Rad9 act in response to DNA damage, little is known about the role of these 2 proteins in cancer progression. In this study, we analyzed the expression of Rad9 and Hus1 in epithelial ovarian tumors and correlated them to clinopathological parameters and apoptotic biomarkers (p53, Bcl-2, and Bax). Histological sections from 114 primary ovarian epithelial tumors were stained with antibodies using the streptavidin-biotin method. In addition, mitotic and apoptotic indices (both hematoxylin-eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin end labeling assay) were also measured. We found that Rad9 expression correlated closely to significance only with the apoptotic and mitotic indices (P = 0.056 and 0.059, respectively). Hus1 levels correlated significantly with the clinicopathologic factors of bad prognosis, including FIGO (International Federation of Gynecology and Obstetrics) stage (P < 0.002) and with the p53 expression (P < 0.001), Bax expression (P < 0.008), mitotic index (P < 0.001), and apoptotic index (P < 0.003).
[Inhibitory effect of angiotensin blockade on hepatic fibrosis in common bile duct-ligated rats].

BACKGROUNDS AND AIMS Angiotensin receptors are found on hepatic stellate cells, which participate in hepatic fibrosis. Therefore, it is presumed that angiotensin has a role in hepatic fibrosis. The aim of this study was to evaluate the effects of angiotensin blockade on inhibition of hepatic fibrosis in cirrhotic rat model. MATERIAL AND METHODS Cirrhosis with portal hypertension was produced by common bile duct ligation (BDL) in the adult Sprague-Dawley rats. They were classified into 4 groups (each group n=6) as follows; G1: BDL without drug, G2: BDL+captopril 100 mg/kg/day beginning 2 weeks after BDL, G3: BDL+captopril 100 mg/kg/day, starting just after BDL, G4: BDL+losartan 10 mg/kg/day, starting just after BDL. After 4 weeks following BDL, hepatic fibrosis was histomorphologically analyzed by Batts & Ludwig score. alpha smooth muscle actin by immunohistochemical stain, hydroxyproline contents of liver tissue by spectrophotometry and expression of collagen, procollagen, and TGF-beta by real-time PCR were measured. RESULTS Batts & Ludwig score were 3.8, 3.0, 2.6,and 2.6 in G1, G2, G3, and G4, respectively. The expression of alpha-SMA was significantly lower in G3 and G4 than in G1; 11.9%, 10.9%, 2.6%, and 1.1% in G1, G2, G3, and G4, respectively (p<0.05). The concentration of hydroxyproline (microg/g liver tissue) was lower in G3 and G4 compared with G1 (p<0.05). Also, the administration of angiotensin blockade just after BDL significantly reduced the expression of collagen, procollagen, and TGF-beta mRNA. CONCLUSIONS Angiotensin blockades are effective in the prevention of hepatic fibrosis in BDL rats.
In vivo emergence of a novel mutant L159F/L320F in the NS5B polymerase confers low-level resistance to the HCV polymerase inhibitors mericitabine and sofosbuvir.

BACKGROUND Resistance to mericitabine (prodrug of HCV NS5B polymerase inhibitor PSI-6130) is rare and conferred by the NS5B S282T mutation. METHODS Serum HCV RNA from patients who experienced viral breakthrough, partial response, or nonresponse in 2 clinical trials in which patients received mericitabine plus peginterferon alfa-2a (40KD)/ribavirin were analyzed by population and clonal sequence analysis as well as phenotypic assay for assessment of in vivo mericitabine resistance. RESULTS Among 405 patients treated with mericitabine plus peginterferon alfa-2a/ribavirin in PROPEL and JUMP-C, virologic breakthrough or nonresponse were not observed; 12 patients experienced a partial response. The NS5B S282T resistance mutation was not observed in any patient. A number of treatment-associated NS5B changes were observed and characterized. A novel double mutant (L159F/L320F) with impaired replication capacity was detected in one HCV genotype 1b-infected patient. Introduction of double mutant L159F/L320F into genotype 1a (H77) and 1b (Con-1) replicons, respectively, increased the EC50 for mericitabine by 3.1- and 5.5-fold and the EC90 by 3.1- and 8.9-fold. The double mutant also decreased susceptibility to sofosbuvir (GS-7977) and GS-938 but not setrobuvir, relative to wild-type. CONCLUSIONS A novel and replication-deficient double mutation (L159F/L320F) confers low-level resistance to mericitabine and cross-resistance to both sofosbuvir and GS-938. CLINICAL TRIALS REGISTRATION NCT00869661, NCT01057667.
Chronic Physiological Shear Stress Inhibits Tumor Necrosis Factor–Induced Proinflammatory Responses in Rabbit Aorta Perfused Ex Vivo

Background—Regions in the vasculature exposed to steady laminar flow have a lower likelihood for atherosclerosis than regions exposed to disturbed flow with low shear stress. We previously found that laminar flow of short duration inhibited tumor necrosis factor (TNF)-&agr;–mediated proinflammatory signaling in cultured endothelial cells (ECs). However, mechanisms responsible for the atheroprotective effects of physiological shear stress remain undefined. Therefore, we examined the effects of chronic shear stress on TNF-&agr;–induced inflammatory responses using an ex vivo perfusion organ culture system. Methods and Results—Rabbit aortas were exposed to low or normal shear stress (0.4 or 12 dyne/cm2) at a constant pressure for 24 to 26 hours. EC and vascular smooth muscle cell (VSMC) proteins were selectively purified. After exposure to low shear stress, TNF-&agr; (50 ng/mL, 6 hours) specifically stimulated vascular cell adhesion molecule (VCAM)-1 expression in ECs but not VSMCs. TNF-&agr;–stimulated VCAM expression was inhibited significantly by preexposure to normal shear stress. Normal shear stress inhibited TNF (15 minutes) activation of mitogen-activated protein (MAP) kinases (c-Jun NH2-terminal kinase [JNK], p38, extracellular signal–regulated kinase [ERK]) in ECs. Specific pharmacological inhibitors of JNK and p38 but not ERK significantly inhibited TNF-induced VCAM expression. Normal shear stress prevented the association of TNF receptor (TNFR)-1 with TNFR-associated factor (TRAF)-2. There was no effect of low or normal shear stress on TNF-&agr;–induced nuclear factor-&kgr;B activation. A nitric oxide synthesis inhibitor, NG-nitro-l-arginine methyl ester, did not reverse the inhibitory effects of shear stress on VCAM expression. Conclusions—These results suggest that physiological shear stress is antiinflammatory by specifically inhibiting MAP kinase signaling and inhibiting TRAF-2 interaction with TNFR-1.
Measles virus genotype B2 is not inactive: Evidence of continued circulation in Africa

This study describes two measles outbreaks—one in Cape Town, South Africa in November 2002, and the other in Luanda, Angola in March 2003. The outbreaks were notable because they were caused by closely related genotype B2 viruses. This genotype was first described in an outbreak in Libreville, Gabon in the 1980s and was labeled as inactive by the World Health Organization in 2003 because it had not been detected for over 15 years. As the first three cases in the Cape Town outbreak were Angolan citizens who recently arrived from Angola, it appears likely that the source of the virus was Angola. Molecular analysis of specimens collected during the outbreak in Luanda provided direct evidence for the circulation of genotype B2 measles virus (MV) in Angola. This study clearly demonstrates that there is still active circulation of genotype B2 in Africa, and we propose that its apparent inactivity is merely the result of insufficient virologic/molecular surveillance in the region. These findings highlight the need for expanded molecular surveillance in Africa. J. Med. Virol. 77:550–557, 2005. © 2005 Wiley‐Liss, inc.
Hierarchical Game Theory for System-Optimal Control: Applications of Reverse Stackelberg Games in Regulating Marketing Channels and Traffic Routing

Complex decision-making problems have two common features: 1) they involve agents (firms, drivers, countries) with interdependent payoffs, that is, the action of one agent affects the others' rewards, and 2) they are inherently dynamic, that is, the agents compete or cooperate repeatedly over time, and their actions have an impact on the evolution of the state of the system [1]-[3]. An example can be found in road-traffic networks, where a driver affects the other drivers' travel time by selecting a particular route and a particular speed profile. When too many drivers opt for a popular connection at the same time, congestion results [4], [5]. Fisheries provide another, similar example. Overfishing means fewer fish are available for others in the short run, and the long-term sustainability of the fishery is put at risk [6]. These situations illustrate how the lack of coordination between parties in a system may result in a highly suboptimal use of scarce resources. While it is in the parties' common interest that some players act in an individually suboptimal manner, for instance, by taking unpopular routes that are not the shortest in distance, there is no mechanism that guarantees the behavior of the other parties. As a result, all parties act selfishly and face the suboptimal result of a severe traffic jam or a shortage of fish. For an illustration of this dilemma, see "The Wardrop Equilibrium Principles and the Braess Paradox. "
Challenges and Opportunities to Conduct Cancer Care Research in China: Experience from a Pilot Project.

BACKGROUND Cancer has become the leading cause of death in China. Effective cancer control and population science research programs are desperately needed in China. China Medical Board (CMB) funding has provided us with an opportunity to build a research team specializing in cancer care utilization and access research and demonstrate the usefulness of the accrued data. Their CMB project will describe patterns of cancer screening, incidence, and treatment in Shandong Province in China and enable the researchers to understand possible causes of disparities in cancer control in China. Yao initiated his research of cancer care in China as a PhD student when he was at The Pennsylvania State University but could not find any cancer related public data. FINDINGS Although CMB projects do not provide salary support for American faculty, they do provide Chinese scholars in the US an excellent opportunity to help improve health care in China. There are many challenges and opportunities in health care service and utilization research. For example, public data for this type of research does not exist. They had to acquire secondary data from several governmental organizations. They have reconciled regional variations in data management. Once they acquired all the data, They could create the most comprehensive cancer access, utilization, and outcomes research database to date in China and possibly expand this research in Shandong and other provinces. Students and analysts need to be trained to ensure the confidentiality of data linked to personal identifiers of patients and providers. They have also discovered holes in the data. Students and analysts will need to learn to manipulate and analyze large scale, messy, secondary data. DISCUSSION They hope that their key findings will identify innovative scientific opportunities to improve cancer control and reduce inequities in communities. They intend to write Chinese articles and reports to disseminate findings to communities, policy makers, and health care providers and to the scientific community. From the policy perspective, this study is a demonstration project drawing policy makers' attention to the importance of comprehensive cancer prevention and control data collection, both for accurate assessment and informed decision making with a high likelihood to effect desired change.