Miracle-dz/UniFAR-FTUs huggingface dataset:
Ecological Factors Characterizing the Prevalence of Bacterial Tick-Borne Pathogens in Ixodes ricinus Ticks in Pastures and Woodlands

ABSTRACT Ecological changes are recognized as an important driver behind the emergence of infectious diseases. The prevalence of infection in ticks depends upon ecological factors that are rarely taken into account simultaneously. Our objective was to investigate the influences of forest fragmentation, vegetation, adult tick hosts, and habitat on the infection prevalence of three tick-borne bacteria, Borrelia burgdorferi sensu lato, Anaplasma phagocytophilum, and Rickettsia sp. of the spotted fever group, in questing Ixodes ricinus ticks, taking into account tick characteristics. Samples of questing nymphs and adults were taken from 61 pastures and neighboring woodlands in central France. The ticks were tested by PCR of pools of nymphs and individual adults. The individual infection prevalence was modeled using multivariate regression. The highest infection prevalences were found in adult females collected in woodland sites for B. burgdorferi sensu lato and A. phagocytophilum (16.1% and 10.7%, respectively) and in pasture sites for Rickettsia sp. (8.7%). The infection prevalence in nymphs was lower than 6%. B. burgdorferi sensu lato was more prevalent in woodlands than in pastures. Forest fragmentation favored B. burgdorferi sensu lato and A. phagocytophilum prevalence in woodlands, and in pastures, the B. burgdorferi sensu lato prevalence was favored by shrubby vegetation. Both results are probably because large amounts of edges or shrubs increase the abundance of small vertebrates as reservoir hosts. The Rickettsia sp. prevalence was maximal on pasture with medium forest fragmentation. Female ticks were more infected by B. burgdorferi sensu lato than males and nymphs in woodland sites, which suggests an interaction between the ticks and the bacteria. This study confirms the complexity of the tick-borne pathogen ecology. The findings support the importance of small vertebrates as reservoir hosts and make a case for further studies in Europe on the link between the composition of the reservoir host community and the infection prevalence in ticks.
Repair in the rat lens after threshold ultraviolet radiation injury.

PURPOSE To investigate the development and recovery of lens damage after in vivo close-to-threshold exposure to ultraviolet B radiation. METHODS One eye of young, female Sprague-Dawley rats was exposed to 5 kJ/m2 narrowband ultraviolet radiation (UVR) (lambda(max) = 302 nm) for 15 minutes. Groups of rats were killed 1, 7, and 56 days after exposure. The structure of the exposed and nonexposed lenses was examined with light microscopy, scanning electron microscopy, transmission electron microscopy, freeze-fracture, fluorescent membrane staining, and Fourier transform analysis. RESULTS One day after UVR exposure the lens surface had flakelike opacities. Seven days after exposure, the lens surface appeared opaque and corrugated, and the equatorial cortex had small opacities. At 56 days postexposure, the surface and equator appeared clear, but the cortex had a subtle shell-shaped opacity. At 1 day postexposure, apoptotic cell death occurred in the lens epithelium, but the cortical fibers were normal. At 7 days postexposure, the epithelium and the fibers between the 10th and 40th growth shell below the capsule contained extracellular spaces of different sizes. After 56 days, the epithelial layer appeared normal, and the extracellular spaces had disappeared; but abnormal fibers were found between the 60th and 100th growth shell below the capsule. Fibers above and below the damaged growth shells appeared fully normal. CONCLUSIONS A close-to-threshold dose of UVR causes cataract, which is largely reversible. The UVR exposure leads to apoptosis in the lens epithelium, and after a latency period of several days, lens fibers are abnormal. Extracellular spaces develop in the epithelium and fibers. Within several weeks after exposure, the epithelium fully recovers and new fibers develop normally. The originally affected fibers are repaired. However, this repair is incomplete, leaving a small zone of enhanced light scattering in the equatorial cortex.
Heat generation required by information erasure.

Landauer argued that the erasure of 1 bit of information stored in a memory device requires a minimal heat generation of ${\mathit{k}}_{\mathit{B}}$T ln2 [IBM J. Res. Dev. 5, 183 (1961)], but recently several articles have been written to dispute the validity of his argument. In this paper, we deal with a basic model of the memory, that is, a system including a particle making the Brownian motion in a time-dependent potential well, and show that Landauer's claim holds rigorously if the random force acting on the particle is white and Gaussian. Our proof is based on the fact that the analogue of the second law of thermodynamics dQ\ensuremath{\le}${\mathit{k}}_{\mathit{B}}$TdS holds rigorously by virtue of the Fokker-Planck equation, even if the potential is not static. Using the above result, we also discuss the counterargument of Goto et al. to Landauer's claim based on the quantum flux parametron.
AMPA receptor‐mediated toxicity in oligodendrocyte progenitors involves free radical generation and activation of JNK, calpain and caspase 3

The molecular mechanisms underlying AMPA (α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate) receptor‐mediated excitotoxicity were characterized in rat oligodendrocyte progenitor cultures. Activation of AMPA receptors, in the presence of cyclothiazide to selectively block desensitization, produced a massive Ca2+ influx and cytotoxicity which were blocked by the antagonists CNQX and GYKI 52466. A role for free radical generation in oligodendrocyte progenitor cell death was deduced from three observations: (i) treatment with AMPA agonists decreased intracellular glutathione; (ii) depletion of intracellular glutathione with buthionine sulfoximine potentiated cell death; and (iii) the antioxidant N‐acetylcysteine replenished intracellular glutathione and protected cultures from AMPA receptor‐mediated toxicity. Cell death displayed some characteristics of apoptosis, including DNA fragmentation, chromatin condensation and activation of caspase‐3 and c‐Jun N‐terminal kinase (JNK). A substrate of calpain and caspase‐3, α‐spectrin, was cleaved into characteristic products following treatment with AMPA agonists. In contrast, inhibition of either caspase‐3 by DEVD‐CHO or calpain by PD 150606 protected cells from excitotoxicity. Our results indicate that overactivation of AMPA receptors causes apoptosis in oligodendrocyte progenitors through mechanisms involving Ca2+ influx, depletion of glutathione, and activation of JNK, calpain, and caspase‐3.
TLR activation and ionizing radiation induce strong immune responses against multiple tumor entities

Toll-like receptor (TLR) 7/8 ligands act together with radiotherapy and induce profound systemic antitumor immune reactions coordinated by dendritic cells and executed by natural killer (NK) and cytotoxic T cells. Combining TLR ligands and radiation improves both local and distant tumor control and has been shown to be effective against multiple tumor entities.
Expression of HLA‐ABC and ‐DR Locus Antigens on Human Kidney, Endothelial, Tubular and Glomerular Cells

The distribution of the major histocompatibility complex antigens on the various cellular structures of the human kidney was analysed by using a modified Staphalococcus aureus Cowan I method Conventional alloantisera and heterologous antisera raised against Isolated molecules were used for the HLA‐ABC antisera were expressed on all types of kidney passenger leucocytes, on vascular endothelial cells, and on kidney tubular cells, but not substantially on the glomerular podocytes, The DR antigens were strongly expressed on (a fraction of) the passenger lymphocytes and on the kidney vascular endothelial cells, weakly on the passenger monocytes, but not measurably on the urine‐producing apparatus of the kidney—that is, on the glomerular and tubular cells.
Is Favorable Outcome Possible After Prolonged Refractory Status Epilepticus?

Summary: When status epilepticus (SE) remains refractory to appropriate therapy, it is associated with high mortality and with substantial morbidity in survivors. Many outcome predictors such as age, seizure type, level of consciousness before treatment, and mostly, etiology, are well-established. A longer duration of SE is often associated with worse outcome, but duration may lose its prognostic value after several hours. Several terms and definitions have been used to describe prolonged, refractory SE, including “malignant SE,” “prolonged” SE, and more recently, “super refractory” SE, defined as “SE that has continued or recurred despite 24 hours of general anesthesia (or coma-inducing anticonvulsants). ” There are few data available regarding the outcome of prolonged refractory SE, and even fewer for SE remaining refractory to anesthetic drugs. This article reviews reports of outcome after prolonged, refractory, and “super refractory” SE. Most information detailing the clinical outcome of patients surviving these severe illnesses, in which seizures can persist for days or weeks (and especially those concerning “super-refractory” SE) come from case reports and retrospective cohort studies. In many series, prolonged, refractory SE has a mortality of 30% to 50%, and several studies indicate that most survivors have a substantial decline in functional status. Nevertheless, several reports demonstrate that good functional outcome is possible even after several days of SE and coma induction. Treatment of refractory SE should not be withdrawn from younger patients without structural brain damage at presentation solely because of the duration of SE.
Species richness of crustacean zooplankton and trophic structure of brackish lagoons in contrasting climate zones: north temperate Denmark and Mediterranean Catalonia (Spain)

We sought to identify environmental factors influencing crustacean zooplankton species richness in brackish lagoons and to elucidate whether crustacean zooplankton species richness and trophic structure of brackish lagoons differ among two regions with contrasting temperatures. We sampled 35 and 42 brackish lagoons (salinity ranging from 0.3 to 55‰) in Mediterranean Catalonia (NE Spain) and northern-temperate Denmark, respectively. No significant differences were found in total crustacean zooplankton species richness or cladoceran richness between the climatic regions. Calanoid richness was higher in Denmark than in Catalonia, while cyclopoid richness was higher in Catalonia. Salinity was the most important variable associated with zooplankton species richness in both regions, richness of total zooplankton species, cladocerans and cyclopoids being negatively related with salinity. In both regions, a shift occurred from dominance of large filter feeding cladoceran species at low salinities to copepods and small cladoceran species at higher salinities. Cladoceran richness increased with increasing total phosphorus, but was not influenced by total nitrogen or chlorophyll-a. Trophic structure in Mediterranean brackish lagoons showed a more pronounced seasonal variation than in north temperate brackish lagoons. Our results imply that the indirect effects of climate warming, such as changes in salinity and hydrology, will have a larger impact on brackish lagoon ecosystems than the increase in temperature per se.
Perihepatic packing of major liver injuries: complications and mortality.

HYPOTHESIS Perihepatic packs used to control hemorrhage after liver injury increase the risk of complications and this risk increases the longer packs are left in place. DESIGN Retrospective case series. SETTING University level I trauma center. PATIENTS Consecutive patients with hepatic injury. MAIN OUTCOME MEASURES Liver-related complications (biliary leak and abscess), rebleeding, and mortality. RESULTS One hundred twenty-nine of 804 patients with liver injuries were treated with perihepatic packing. Of the 69 who survived more than 24 hours, 75% lived to hospital discharge. Mortality rates were 14% and 30% in patients with and without liver complications, respectively (P = .23). Liver complication rates were similar (P = .83) when packs were removed within 36 hours (early [33%]) or between 36 and 72 hours (late [29%]) after they were placed; the rebleeding rate was greater in the early group (21% vs 4%; P<.001). CONCLUSIONS Liver complications associated with perihepatic packing did not affect survival. Removing liver packs 36 to 72 hours after placement reduced the risk of rebleeding without increasing the risk of liver-related complications.
Skewing to the LFA‐3 adhesion pathway by influenza infection of antigen‐presenting cells

The effect of influenza (FLU) infection on heterotypic conjugate formation between antigen‐presenting cells and T lymphocytes has been studied with FLU‐specific T cell clones and FLU‐infected B‐lymphoblastoid cells (B‐LCL). Conjugate formation between FLU‐infected B‐LCL (FLU+ B‐LCL) and T cells was found to be consistently enhanced in comparison with peptide‐sensitized or uninfected B‐LCL. Treatment of B‐LCL with exogenous neuraminidase (NA‐NAse) similarly enhanced conjugate formation indicating that increased conjugate formation may be mediated by the viral neuraminidase. Monoclonal antibody blocking experiments revealed that the contribution by CD2/LFA‐3 is increased relative to that of LFA‐l/ICAM‐1 in conjugates between FLU+ B‐LCL or NANAse‐treated B‐LCL and T cell clones. In contrast, both pathways of adhesion contributed equally to conjugate formation between peptide‐sensitized B‐LCL or control B‐LCL and T cell clones. Thus, FLU infection causes increased conjugate formation between antigen‐presenting cells and T cells and skews towards CD2/LFA‐3‐dependent adhesion, independent of T cell receptor signalling.
Molecular analysis of the Haemophilus influenzae type b pilin gene

A Haemophilus influenzae DNA library was prepared in the vector lambda EMBL3, and recombinant phage were screened for the pilin gene (pil) using a synthetic oligonucleotide. Southern blot analysis of the positive clones revealed a 2.5kb Pstl/Pvul fragment that hybridized with the oligonucleotide probe. This fragment was subcloned into pBR322 and sequenced. The nucleotide sequence disclosed an open reading frame of 653 bases. The deduced amino acid sequence corresponded with the known amino acid sequence of the purified pilin protein. Primer extension analysis using total RNA from piliated H. influenzae cells delineated a start site for the gene, ‐10 and ‐35 promoter regions, and a ribosome‐binding site. No transcripts were seen with the RNA derived from a non‐piliated strain. Southern blots of DNA from a number of H. influenzae strains revealed homology with the pil structural gene. DNA from a non‐piliated strain of H. influenzae also hybridized with the pil probe. Transcriptional and translational studies were performed in Escherichia coli with plasmids containing: (i) the pil gene on the 2.5kb Pstl/Pvul fragment, (ii) the pil gene fused to the phoA gene, and (iii) the pil gene present on a 12.2 kb insert containing extensive H. influenzae DNA flanking the pil gene. The results suggest that the H. influenzae pil gene is expressed in Escherichia coli, but from a promoter other than the one used in H. influenzae.
Ustekinumab for the treatment of acrodermatitis continua of Hallopeau refractory to anti‐TNF agents

Acrodermatitis continua of Hallopeau (ACH) is a variant of pustular psoriasis that is often very difficult to treat. Almost all anti‐psoriatic agents have been used in the treatment of ACH. Ustekinumab, a fully human monoclonal antibody of the IgG1 class, is directed to the shared p40 subunit of cytokines IL‐12 and IL‐23. Herein, we present our experience of ustekinumab use in a 50‐year‐old man who was resistant to anti‐tumor necrosis factor‐α agents. Though initial therapy with ustekinumab achieved a sustained response in our patient, after a seven months of interruption, retreatment resulted in a slower and poorer response than the initial regimen. Both responses of our patient reflects: (i) the recalcitrant chronic nature of ACH in some patients, (ii) the value of ustekinumab in ACH treatment, (iii) the fact that, as with other biologics, a loss of response may also occur with ustekinumab when the treatment is interrupted. All these data provides evidence for the fact that the course of ACH is unpredictable and possibly indicate that concerning current biologics used in the treatment of ACH, we have still failed to hit the target we aimed for.
Differences in auditory and physiological properties of HVc neurons between reproductively active male and female canaries (Serinus canaria)

Based on neuronal recordings in the HVc, this study investigated differences between reproductively active male and sexually receptive female canaries. It is the first study to describe auditory responses and cell characteristics of HVc neurons in female songbirds and to compare them with the responses and characteristics obtained in males. Extracellular single unit recordings showed that in males HVc cells exhibited two types of auditory responses to conspecific and heterospecific song playbacks: tonic and phasic responses. The major finding of the present study is the absence of tonic responses in females. Neurons in the HVc of females only responded phasically to song playbacks. In both sexes, neurons exhibiting auditory responses had thinner action potentials than the others. As all the tonic cells recorded in males were thin spike cells (action potential = 0.6 ms) and had high firing rates (6 Hz in average), they are potentially interneurons. In both sexes, two categories of nonresponsive cells were found: neurons that did not fire at song onset and had the lowest spontaneous firing rate; and neurons that did not exhibit changes in activity in response to song playbacks. Analyses of physiological characteristics of HVc neurons revealed that the rate of spontaneous activity was higher in males than in females. This study is a first step towards in dentifying the cellular bases of the sexual dimorphism in HVc function and highlights the pivotal role of interneurons in HVc auditory processing.
A complex classification approach of partial discharges from covered conductors in real environment

Partial discharges are known as indicators of degradation of insulation systems. In case of medium voltage overhead lines with covered conductors, the internal partial discharges indicate the degradation of insulation system, rupture or downfall of the line. The reliability and selectivity of methods to detect internal partial discharges in the covered conductors are mainly given by the level of background noise. The background noise distorts the pattern of partial discharges (PD-pattern) and decreases the capability of detection methods to recognize the features of PD-pattern corresponding to the degradation of an insulation system. This paper presents the results from the testing of a developed and optimized model for detection of covered conductor faults. The ability to identify covered conductor faults was verified in the real environment.
Local Anesthetics: Importance of Mode of Application, Concentration and Adrenaline for the Appearance of Nerve Lesions: An Experimental Study of Axonal Degeneration and Barrier Damage after Intrafascicular Injection or Topical Application of Bupivacaine (Marcah®)

Local anesthetics are designed for application in or close to nerve tissue. In spite of their wide clinical use, surprisingly few investigations deal with the neural toxicity of modern local anesthetics. In this experimental study, the effects were investigated of intrafascicular or topical application of the long‐acting local anesthetic bupivacaine on the rabbit sciatic nerve. Axonal degeneration was histologically evaluated and a fluorescence‐microscopic technique used to detect lesions in the blood‐nerve barrier. Topical application of bupivacaine in clinically recommended concentrations around the nerve caused no detectable nerve injury, while intrafascicular injections caused considerable axonal degeneration and damaged the blood‐nerve barrier. Axonal degeneration was the same after injection of physiologic saline solution and bupivacaine 0.5%, but it increased with increasing bupivacaine concentration and especially with the addition of adrenaline. On the other hand, the acute effects of intrafascicular injection, as visualized in the barrier experiments, changed little with the addition of adrenaline, indicating that it is the injection trauma itself which is deleterious. It is concluded that intraneural injections should be avoided and that plain bupivacaine solutions should be routinely used.
Pituitary function in paediatric survivors of severe traumatic brain injury

Background: Traumatic brain injury (TBI)-mediated hypopituitarism is an increasingly recognised problem. Paediatric survivors of TBI may be vulnerable to the possible effects of pituitary deficits as pituitary hormones control normal growth and development. Research concerning pituitary dysfunction following childhood TBI is limited. Aim: To identify pituitary dysfunction in paediatric survivors of severe TBI. Methods: Of 1020 children who sustained a TBI and were admitted to the Royal Children’s Hospital, Melbourne, Australia over 10 years, 117 were identified as survivors of severe TBI. 54 patients (31 males) were enrolled and administered questionnaires regarding quality of life and possible endocrine dysfunction. Where indicated, hormone testing was performed. Results: 29 of the 54 patients underwent hormonal investigations, while 21 who had satisfactory questionnaires did not (four patients had already been diagnosed with pituitary deficiencies). In those 29 patients, TBI occurred at ages ranging from 0.25 to 16.80 years (median 9.7 years). Time from TBI to study ranged from 0.9 to 8.5 years (median 4.5 years). Of the 54 patients, nine had pituitary dysfunction, of whom four had multiple pituitary hormone deficiencies. Conclusions: Our study that confirms that paediatric survivors of severe TBI may develop pituitary dysfunction. Pituitary function should therefore be determined in these patients.
Albumin, Hemoglobin, and the Trajectory of Cognitive Function in Community-Dwelling Older Japanese: A 13-Year Longitudinal Study.

BACKGROUND Cognitive function can substantially decline over a long period, and understanding the trajectory of cognitive function is important. However, little is known about the linkage between nutritional biomarkers and long-term cognitive change. OBJECTIVES We analyzed 13-year longitudinal data for older Japanese to examine the associations of serum albumin and hemoglobin levels with the trajectory of cognitive function. DESIGN Longitudinal study. SETTING Community-based. PARTICIPANTS A total of 1,744 community-dwelling adults aged 65 years or older who participated in annual health examinations in Kusatsu town, Gunma Prefecture, Japan, from 2002-2014. MEASUREMENTS Cognitive function was assessed annually by the Mini-Mental State Examination (MMSE). Albumin and hemoglobin levels at baseline (the year when a respondent first participated in the health examination) were divided into quartiles. Hierarchical linear modeling was used to analyze intrapersonal and interpersonal differences in cognitive function. RESULTS Participants' MMSE scores decreased at an accelerated rate over the 13-year period. Participants with the lowest baseline albumin level (below the first quartile line) showed a greater accelerated decline in MMSE scores over time, compared with those with the highest level (above the third quartile line). Moreover, MMSE scores in participants with a lower hemoglobin level and lower MMSE score at baseline tended to decline faster over time at an accelerated rate. CONCLUSIONS These findings yield new insights about the complex and diverse roles of these nutritional biomarkers on the trajectory of cognitive function in old age.