Miracle-dz/UniFAR-FTUs huggingface dataset:
Effect of Acute Hypoxia on Post-Exercise Parasympathetic Reactivation in Healthy Men

In this study we assessed the effect of acute hypoxia on post-exercise parasympathetic reactivation inferred from heart rate (HR) recovery (HRR) and HR variability (HRV) indices. Ten healthy males participated in this study. Following 10 min of seated rest, participants performed 5 min of submaximal running at the speed associated with the first ventilatory threshold (Sub) followed by a 20-s all-out supramaximal sprint (Supra). Both Sub and Supra runs were immediately followed by 15 min of seated passive recovery. The resting and exercise sequence were performed in both normoxia (N) and normobaric hypoxia (H; FiO2 = 15.4%). HRR indices (e.g., heart beats recovered in the first minute after exercise cessation, HRR60s) and vagal-related HRV indices [i.e., natural logarithm of the square root of the mean of the sum of the squared differences between adjacent normal R–R intervals (Ln rMSSD)] were calculated for both conditions. Difference in the changes between N and H for all HR-derived indices were also calculated for both Sub and Supra. HRR60s was greater in N compared with H following Sub only (60 ± 14 vs. 52 ± 19 beats min−1, P = 0.016). Ln rMSSD was greater in N compared with H (post Sub: 3.60 ± 0.45 vs. 3.28 ± 0.44 ms in N and H, respectively, and post Supra: 2.66 ± 0.54 vs. 2.65 ± 0.63 ms, main condition effect P = 0.02). When comparing the difference in the changes, hypoxia decreased HRR60s (−14.3% ± 17.2 vs. 5.2% ± 19.3; following Sub and Supra, respectively; P = 0.03) and Ln rMSSD (−8.6% ± 7.0 vs. 2.0% ± 13.3, following Sub and Supra, respectively; P = 0.08, Cohen’s effect size = 0.62) more following Sub than Supra. While hypoxia may delay parasympathetic reactivation following submaximal exercise, its effect is not apparent following supramaximal exercise. This may suggest that the effect of blood O2 partial pressure on parasympathetic reactivation is limited under heightened sympathetic activation.
Impact of Land Use on PM2.5 Pollution in a Representative City of Middle China

Fine particulate matter (PM2.5) pollution has become one of the greatest urban issues in China. Studies have shown that PM2.5 pollution is strongly related to the land use pattern at the micro-scale and optimizing the land use pattern has been suggested as an approach to mitigate PM2.5 pollution. However, there are only a few researches analyzing the effect of land use on PM2.5 pollution. This paper employed land use regression (LUR) models and statistical analysis to explore the effect of land use on PM2.5 pollution in urban areas. Nanchang city, China, was taken as the study area. The LUR models were used to simulate the spatial variations of PM2.5 concentrations. Analysis of variance and multiple comparisons were employed to study the PM2.5 concentration variances among five different types of urban functional zones. Multiple linear regression was applied to explore the PM2.5 concentration variances among the same type of urban functional zone. The results indicate that the dominant factor affecting PM2.5 pollution in the Nanchang urban area was the traffic conditions. Significant variances of PM2.5 concentrations among different urban functional zones throughout the year suggest that land use types generated a significant impact on PM2.5 concentrations and the impact did not change as the seasons changed. Land use intensity indexes including the building volume rate, building density, and green coverage rate presented an insignificant or counter-intuitive impact on PM2.5 concentrations when studied at the spatial scale of urban functional zones. Our study demonstrates that land use can greatly affect the PM2.5 levels. Additionally, the urban functional zone was an appropriate spatial scale to investigate the impact of land use type on PM2.5 pollution in urban areas.
Cricoid Pressure Does Not Increase the Rate of Failed Intubation by Direct Laryngoscopy in Adults

Background:Cricoid pressure (CP) is applied during induction of anesthesia to prevent regurgitation of gastric content and pulmonary aspiration. However, it has been suggested that CP makes tracheal intubation more difficult. This double-blind randomized study evaluated the effect of CP on orotracheal intubation by direct laryngoscopy in adults. Methods:Seven hundred adult patients undergoing general anesthesia for elective surgery were randomly assigned to have a standardized CP (n = 344) or a sham CP (n = 356) during laryngoscopy and intubation. After anesthesia induction and complete muscle relaxation, a 30-s period was allowed to complete intubation with a Macintosh No. 3 laryngoscope blade. The primary endpoint was the rate of failed intubation at 30 s. The secondary endpoints included the intubation time, the Cormack and Lehane grade of laryngoscopic view, and the Intubation Difficulty Scale score. Results:Groups were similar for demographic data and risk factors for difficult intubation. The rates of failed intubation at 30 s were comparable for the two groups: 15 of 344 (4.4%) and 13 of 356 (3.7%) in the CP and sham CP groups, respectively (P = 0.70). The grades of laryngoscopic view and the Intubation Difficulty Scale score were also comparable. Median intubation time was slightly longer in the CP group than in the sham CP group (11.3 and 10.4 s, respectively, P = 0.001). Conclusions:CP applied by trained personnel does not increase the rate of failed intubation. Hence CP should not be avoided for fear of increasing the difficulty of intubation when its use is indicated.
Decentralized Online Learning Algorithms for Opportunistic Spectrum Access

The fundamental problem of multiple secondary users contending for opportunistic spectrum access over multiple channels in cognitive radio networks has been formulated recently as a decentralized multi-armed bandit (D-MAB) problem. In a D-MAB problem there are M users and N arms (channels) that each offer i.i. d. stochastic rewards with unknown means so long as they are accessed without collision. The goal is to design a decentralized online learning policy that incurs minimal regret, defined as the difference between the total expected rewards accumulated by a model-aware genie, and that obtained by all users applying the policy. We make two contributions in this paper. First, we consider the setting where the users have a prioritized ranking, such that it is desired for the K-th-ranked user to learn to access the arm offering the K-th highest mean reward. For this problem, we present the first distributed policy that yields regret that is uniformly logarithmic over time without requiring any prior assumption about the mean rewards. Second, we consider the case when a fair access policy is required, i.e., it is desired for all users to experience the same mean reward. For this problem, we present a distributed policy that yields order-optimal regret scaling with respect to the number of users and arms, better than previously proposed policies in the literature. Both of our distributed policies make use of an innovative modification of the well known UCB1 policy for the classic multi-armed bandit problem that allows a single user to learn how to play the arm that yields the K-th largest mean reward.
Anomalous cellular morphology and growth characteristics of Neisseria meningitidis in subminimal inhibitory concentrations of penicillin G

The effects of subminimal inhibitory concentrations of penicillin G on Neisseria meningitidis in the presence and absence of selected stabilizers were examined. Subminimal inhibitory concentrations of penicillin G decreased cell numbers and altered both colonial and ultrastructural morphologies of this meningococcus. Although these levels of penicillin did not have immediate adverse effects on cell mass increase, deoxyribonucleic acid synthesis, or the incorporation of [3H]leucine into protein, they did significantly alter the division rate and the integrity of the cell envelope. The inability of many of the abnormal membranous cell types produced in subminimal inhibitory concentrations of penicillin to form either complete or properly oriented division septa and the overproduction of cell wall material at such sites was indicative of the disruptive effects of this antibiotic on functions necessary for maintaining the normal division process. The addition of the stabilizers polyvinylpyrrolidone-40 and horse serum to the test medium diminished the effects of penicillin G as evidenced by a fourfold increase in the minimal inhibitory concentration. Moreover, such stabilizers maintained the association of the outer membrane with the peptidoglycan and inner membrane.
Stress-induced hyperglycaemia and venous thromboembolism following total hip or total knee arthroplasty

Summary Stress-induced hyperglycaemia is common during orthopaedic surgery. In addition, hyperglycaemia activates coagulation. The aim of the study was to assess whether stress-induced hyperglycaemia is associated with symptomatic or asymptomatic venous thromboembolism (VTE) following orthopaedic surgery. We performed post-hoc analyses in the four RECORD studies (REgulation of Coagulation in major Orthopaedic surgery reducing the Risk of Deep venous thrombosis and pulmonary embolism). Separate analyses were performed for patients undergoing elective total hip or knee replacement. Outcome measures were symptomatic VTE and “total VTE” (defined as the composite of symptomatic VTE, asymptomatic DVT assessed by per protocol venography and all cause mortality). Glucose levels were measured pre-op and 6 hours post-op, categorised into quartiles, based on the distribution in the respective cohorts. The influence of glucose, adjusted for body mass index, age, gender and diabetes mellitus on VTE was assessed by logistic regression analyses. A total of 12,383 patients were eligible for assessment of symptomatic VTE, and 8,512 patients were eligible for assessment of total VTE. Increased glucose levels after total hip replacement were associated with total VTE; adjusted odds ratio (OR) highest versus lowest quartile 1.9 (95% confidence interval [CI] 1.3 to 3.0). Furthermore, increase in glucose levels during total hip replacement was associated with total VTE (OR highest versus lowest quartile 1.8 (95%CI 1.2 to 2.8). This was not observed in patients undergoing total knee replacement, probably due to differences in the applied surgical procedures.
Learning in Multi-Agent Systems

Learning agents acting in a multi agent environment can improve their performance. These agents might decide upon their course of action by learning about other agents with whom they interact. The learning agents can learn about the others’ information and rules of behavior. The agents will not need to plan their actions beforehand, each time they are asked to solve the same problem they have already solved or when dealing with similar problems. Our research focusses in finding learning algorithms for multi agent environments. In particular, we want to develop agents that learn how to cooperate with other agents and learn how to become experts. I am studying these themes in several domains to achieve a more broader understanding of how learning is influenced by different multi-agent domains and thus how learning algorithms can be developed. The research aims at answering the following questions: 1. How do agents learn how to act? I am looking at
BCL-2 family member BOK promotes apoptosis in response to endoplasmic reticulum stress

Significance The role of B-cell lymphoma-2 (BCL-2) ovarian killer (BOK) in apoptosis regulation has been a long-standing enigma. Despite the homology to BAX and BAK, BOK has yet to be linked to a definitive physiologic function in the classical apoptotic pathway. Here, we report a selective role for BOK in promoting mitochondrial apoptosis in response to endoplasmic reticulum stress. B-cell lymphoma 2 (BCL-2) ovarian killer (BOK) is a BCL-2 family protein with high homology to the multidomain proapoptotic proteins BAX and BAK, yet Bok−/− and even Bax−/−Bok−/− and Bak−/−Bok−/− mice were reported to have no overt phenotype or apoptotic defects in response to a host of classical stress stimuli. These surprising findings were interpreted to reflect functional compensation among the BAX, BAK, and BOK proteins. However, BOK cannot compensate for the severe apoptotic defects of Bax−/−Bak−/− mice despite its widespread expression. Here, we independently developed Bok−/− mice and found that Bok−/− cells are selectively defective in their response to endoplasmic reticulum (ER) stress stimuli, consistent with the predominant subcellular localization of BOK at the ER. Whereas Bok−/− mouse embryonic fibroblasts exposed to thapsigargin, A23187, brefeldin A, DTT, geldanamycin, or bortezomib manifested reduced activation of the mitochondrial apoptotic pathway, the death response to other stimuli such as etoposide, staurosporine, or UV remained fully intact. Multiple organs in Bok−/− mice exhibited resistance to thapsigargin-induced apoptosis in vivo. Although the ER stress agents activated the unfolded protein response, both ATF4 and CHOP activation were diminished in Bok−/− cells and mice. Importantly, BAX and BAK were unable to compensate for the defective apoptotic response to ER stress observed in SV40-transformed and primary Bok−/− cells, and in vivo. These findings support a selective and distinguishing role for BOK in regulating the apoptotic response to ER stress, revealing—to our knowledge—the first bona fide apoptotic defect linked to Bok deletion.
Differential Control of Mincle-Dependent Cord Factor Recognition and Macrophage Responses by the Transcription Factors C/EBPβ and HIF1α

Trehalose-6,6-dimycolate (TDM), the mycobacterial cord factor, and its synthetic analog Trehalose-6,6-dibehenate (TDB) bind to the C-type lectin receptors macrophage-inducible C-type lectin (Mincle) and Mcl to activate macrophages. Genetically, the transcriptional response to TDB/TDM has been defined to require FcRγ-Syk-Card9 signaling. However, TDB/TDM-triggered kinase activation has not been studied well, and it is largely unknown which transcriptional regulators bring about inflammatory gene expression. In this article, we report that TDB/TDM caused only weak Syk-phosphorylation in resting macrophages, consistent with low basal Mincle expression. However, LPS-priming caused MYD88-dependent upregulation of Mincle, resulting in enhanced TDB/TDM-induced kinase activation and more rapid inflammatory gene expression. TLR-induced Mincle expression partially circumvented the requirement for Mcl in the response to TDB/TDM. To dissect transcriptional responses to TDB/TDM, we mined microarray data and identified early growth response (Egr) family transcription factors as direct Mincle target genes, whereas upregulation of Cebpb and Hif1a required new protein synthesis. Macrophages and dendritic cells lacking C/EBPβ showed nearly complete abrogation of TDB/TDM responsiveness, but also failed to upregulate Mincle. Retroviral rescue of Mincle expression in Cebpb-deficient cells restored induction of Egr1, but not of G-CSF. This pattern of C/EBPβ dependence was also observed after stimulation with the Dectin-1 ligand Curdlan. Inducible expression of hypoxia-inducible factor 1α (HIF1α) also required C/EBPβ. In turn, HIF1α was not required for Mincle expression, kinase activation, and Egr1 or Csf3 expression, but critically contributed to NO production. Taken together, we identify C/EBPβ as central hub in Mincle expression and inflammatory gene induction, whereas HIF1α controls Nos2 expression. C/EBPβ also connects TLR signals to cord factor responsiveness through MYD88-dependent upregulation of Mincle.
Sickness and in Health The story of health as told by an augmented Solow growth model and cross-country dynamic panel data

This paper tests whether the Solow model augmented with multiple forms of human capitals can explain cross-country difference in growth and investigates the effect of health on the growth of per capita income. Following Knowles and Owen (1995), we introduce both education human capital and health human capital into the textbook Solow model and extend their cross-section analysis to a dynamic panel data analysis to control for omitted variable and endogeneity biases, using a robust and consistent system GMM estimator. By adopting the latest available data for a sample of 111 developed and developing countries over 1960-2004 and various health indicators, as well as splitting our data into sub-samples, We find firstly, the GMM estimators provide relatively more consistent results. The augmented MRW model provides a fairly good account of international variation in economic growth. Conditional convergence, with a speed of around 2 percent per annum, has been found in either the full sample or sub-samples. Secondly, the role of education capital measured as average years of schooling has been partially identified in the extended Solow model incorporating both education and health capitals, rather than the original MRW model. Finally, both the stock of health, and the investment or accumulation of health capital appears strongly associated with the output growth, particularly for low income countries. The effects of health on economic growth largely vary with different samples of countries.
Labor Supply of New York City Cabdrivers: One Day at a Time

Life-cycle models of labor supply predict a positive relationship between hours supplied and transitory changes in wages. We tested this prediction using three samples of wages and hours of New York City cabdrivers, whose wages are correlated within days but uncorrelated between days. Estimated wage elasticities are significantly negative in two out of three samples. Elasticities of inexperienced drivers average approximately −1 and are less than zero in all three samples (and significantly less than for experienced drivers in two of three samples). Our interpretation of these findings is that cabdrivers (at least inexperienced ones): (i) make labor supply decisions "one day at a time" instead of intertemporally substituting labor and leisure across multiple days, and (ii) set a loose daily income target and quit working once they reach that target.
Fourfold increased detection of Lynch syndrome by raising age limit for tumour genetic testing from 50 to 70 years is cost-effective.

BACKGROUND Recognising colorectal cancer (CRC) patients with Lynch syndrome (LS) can increase life expectancy of these patients and their close relatives. To improve identification of this under-diagnosed disease, experts suggested raising the age limit for CRC tumour genetic testing from 50 to 70 years. The present study evaluates the efficacy and cost-effectiveness of this strategy. METHODS Probabilistic efficacy and cost-effectiveness analyses were carried out comparing tumour genetic testing of CRC diagnosed at age 70 or below (experimental strategy) versus CRC diagnosed at age 50 or below (current practice). The proportions of LS patients identified and cost-effectiveness including cascade screening of relatives, were calculated by decision analytic models based on real-life data. RESULTS Using the experimental strategy, four times more LS patients can be identified among CRC patients when compared with current practice. Both the costs to detect one LS patient (€9437/carrier versus €4837/carrier), and the number needed to test for detecting one LS patient (42 versus 19) doubled. When family cascade screening was included, the experimental strategy was found to be highly cost-effective according to Dutch standards, resulting in an overall ratio of €2703 per extra life-year gained in additionally tested patients. CONCLUSION Testing all CRC tumours diagnosed at or below age 70 for LS is cost-effective. Implementation is important as relatives from the large number of LS patients that are missed by current practice, can benefit from life-saving surveillance.
Duality and evolving set bounds on mixing times.

This survey is an in-depth development of the theoretical aspects of the method of Evolving Sets, a method which has been used in several of my papers. It is fairly esoteric as to a large degree it stems from my efforts to ascertain whether Evolving sets is provably stronger than other isoperimetric methods (answer: yes, with qualifications). For an introduction to the method please see Chapter 4 of my book "Mathematical aspects of mixing times in Markov chains" with Prasad Tetali, or the paper "Evolving sets, mixing and heat kernel bounds" by Morris and Peres.
Clonal Expansion of T Cells in Abdominal Aortic Aneurysm: A Role for Doxycycline as Drug of Choice?

Most reported studies with animal models of abdominal aortic aneurysm (AAA) and several studies with patients have suggested that doxycycline favourably modifies AAA; however, a recent large long-term clinical trial found that doxycycline did not limit aneurysm growth. Thus, there is currently no convincing evidence that doxycycline reduces AAA expansion. Here, we critically review the available experimental and clinical information about the effects of doxycycline when used as a pharmacological treatment for AAA. The view that AAA can be considered an autoimmune disease and the observation that AAA tissue shows clonal expansion of T cells is placed in the light of the well-known inhibition of mitochondrial protein synthesis by doxycycline. In T cell leukaemia animal models, this inhibitory effect of the antibiotic has been shown to impede T cell proliferation, resulting in complete tumour eradication. We suggest that the available evidence of doxycycline action on AAA is erroneously ascribed to its inhibition of matrix metalloproteinases (MMPs) by competitive binding of the zinc ion co-factor. Although competitive binding may explain the inhibition of proteolytic activity, it does not explain the observed decreases of MMP mRNA levels. We propose that the observed effects of doxycycline are secondary to inhibition of mitochondrial protein synthesis. Provided that serum doxycycline levels are kept at adequate levels, the inhibition will result in a proliferation arrest, especially of clonally expanding T cells. This, in turn, leads to the decrease of proinflammatory cytokines that are normally generated by these cells. The drastic change in cell type composition may explain the changes in MMP mRNA and protein levels in the tissue samples.
Osteonecrosis in Children Treated for Lymphoma or Solid Tumors

Purpose The purpose of this study was to find out the incidence of and clinical risk factors for magnetic resonance imaging (MRI)-detected osteonecrosis (ON) in children treated for lymphoma or solid tumors. Patients and Methods The development of ON was studied in 32 childhood cancer patients who underwent MRI scanning of the lower extremities at the end of their treatment. The underlying malignancy was Wilms tumor in 8 patients, non-Hodgkin lymphoma (NHL) in 8, Hodgkin disease (HD) in 7, rhabdomyosarcoma in 6, and other occasional solid tumors in 3 patients. Results Six of the 32 patients (19%) had ON. The mean age of the patients with ON at diagnosis was 12.7 years compared with 5.8 years for the patients without ON (P<0.001). All the patients with ON had either HD (4 patients) or NHL (2 patients). Two (33%) of the patients with ON were symptomatic. Conclusions ON in MRI was found to be a common complication in children after treatment for HD or NHL. The risk for ON seems to be very low in patients with other solid tumors even when they receive high cumulative doses of dexamethasone.