Miracle-dz/UniFAR-FTUs huggingface dataset:
The Rate of Infectious Complications After Intrathecal Drug Delivery System Implant for Cancer-Related Pain Is Low Despite Frequent Concurrent Anticancer Treatment or Leukopenia

BACKGROUND: The efficacy of intrathecal drug delivery (IDD) for cancer-related pain is well established. Cancer therapies are often associated with immunosuppression and increased risk of infection, and the rate of infection after intrathecal drug delivery system (IDDS) implant in cancer patients has been reported as 2.4%–6.3%. Our objective is to report on the rate of surgical site infections (SSI) in patients implanted with IDDS for cancer-related pain and to provide a data-driven discussion on the relationship between antineoplastic treatment, leukopenia, and other clinical or demographic characteristics and SSI. METHODS: Following local institutional review board approval, we conducted a retrospective chart review of IDDS implants from May 2014 through December 2018. Data collected included demographic data, health status, prophylactic antibiotic administration, surgery duration, presence of leukopenia (white blood cell [WBC] count of <4.0 K/µL) or moderate neutropenia (absolute neutrophil count [ANC] of <1000/μL) within the 30 days before IDDS implant, and details of antineoplastic treatment or systemic corticosteroid use in the perioperative period. This information was assessed in relation to SSI incidence up to 6 months following implant. RESULTS: Two hundred seventeen IDDS implants were identified. A majority of patients (79.3%) received ≥1 form of antineoplastic therapy within 30 days before or after implant, and 42.4% received multiple forms of antineoplastic therapy. Therapies included chemotherapy in 46.5%, immunotherapy in 28.6%, systemic steroids in 32.3%, and radiation therapy in 28.1%. One-quarter of patients (25.8%) were leukopenic within 30 days before implant, with 3.2% having moderate neutropenia. There were 2 infectious complications representing an infection rate of 0.9% (95% CI, 0.1%–3.3%), with limited shared characteristics between those experiencing SSI. CONCLUSIONS: SSI risk after IDDS placement for cancer pain is low, despite frequent concurrent antineoplastic therapy and leukopenia in the perioperative period. Concomitant cancer therapies should not be a barrier to the implementation of IDD for cancer pain.
Increased capture of Aedes aegypti (Linnaeus, 1762) (Diptera: Culicidae) by removing one ADULTRAP component

Abstract INTRODUCTION: Aedes aegypti is the main vector responsible for the transmission of numerous arboviruses. Adultrap® has been developed to catch these insects. METHODS: We tested the effectiveness of capturing adults with and without one of the components of Adultrap®. RESULTS: The mean number of insects caught by the original trap was 1.25 (standard deviation = 1.28), while the average obtained with the modified trap was 8.88 (standard deviation = 3.44). The medians were statistically different (p = 0.001) according to the Mann-Whitney test. CONCLUSIONS: The modification of Adultrap® increased the average catch of Ae. aegypti by up to seven times.
Expression and Cellular Distribution of P-Glycoprotein and Breast Cancer Resistance Protein in Amyotrophic Lateral Sclerosis Patients

Abstract For amyotrophic lateral sclerosis (ALS), achieving and maintaining effective drug levels in the brain is challenging due to the activity of ATP-binding cassette (ABC) transporters which efflux drugs that affect drug exposure and response in the brain. We investigated the expression and cellular distribution of the ABC transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) using immunohistochemistry in spinal cord (SC), motor cortex, and cerebellum from a large cohort of genetically well characterized ALS patients (n = 25) and controls (n = 14). The ALS group included 17 sporadic (sALS) and 8 familial (fALS) patients. Strong P-gp expression was observed in endothelial cells in both control and ALS specimens. Immunohistochemical analysis showed higher P-gp expression in reactive astroglial cells in both gray (ventral horn) and white matter of the SC, as well as in the motor cortex of all ALS patients, as compared with controls. BCRP expression was higher in glia in the SC and in blood vessels and glia in the motor cortex of ALS patients, as compared with controls. P-gp and BCRP immunoreactivity did not differ between sALS and fALS cases. The upregulation of both ABC transporters in the brain may explain multidrug resistance in ALS patients and has implications for the use of both approved and experimental therapeutics.
Association of FTO rs9939609 polymorphism with serum leptin, insulin, adiponectin, and lipid profile in overweight adults

ABSTRACT FTO gene polymorphisms are associated with obesity and food intake. This study aimed to investigate the association of FTO rs9939609 polymorphism genotypes with serum glucose, lipid profile and serum hormones level. This cross-sectional study was carried out on 196 randomly selected overweight adults. Anthropometric measurements including weight, height, body mass index (BMI), fat mass, and fat-free mass were assessed. Serum TGs, total cholesterol, HDL cholesterol, LDL cholesterol, glucose and insulin levels were measured. The FTO gene was Genotyped for rs9939609 polymorphism. Dietary intake was assessed by avalid 168-item semi-quantitative food frequency questionnaire (FFQ). The homozygotes for the FTO rs9939609 risk allele (A) had higher serum leptin (p = 0.005, F: 5.131) and lower HDL (p = 0.001, F: 7.687) level than TT genotype. The differences between TT and AT genotypes were not significant. The association remained significant for HDL level after adjustments for age and sex, calorie intake, physical activity, and BMI. The association between rs9939609 polymorphism genotypes and leptin was disappeared after adjustments for calorie intake and physical activity. In conclusion, rs9939609 risk allele was associated with higher serum leptin and lower HDL levels in overweight people. Further studies are warranted.
Diminished social attention in pediatric brain tumor survivors: Using eye tracking technology during naturalistic social perception.

OBJECTIVE The etiology of pediatric brain tumor survivor (PBTSs) social difficulties is not well understood. A model of social competence for youth with brain disorder and evidence from youth with autism spectrum disorder (ASD) suggests that diminished social attention may underlie social deficits in PBTSs. This study used eye tracking technology to compare visual social attention in PBTSs, youth with ASD, and typically developing (TD) youth. METHODS Participants included 90 age-, gender-, and IQ-matched youth (N = 30 per group). PBTSs were at least 5 years from diagnosis and 2 years from the completion of tumor-directed therapy. Participants' eye gaze patterns were recorded while watching an established social play paradigm that presented videos of children engaging in either interactive or parallel play. Group differences in proportional gaze duration toward social versus nonsocial areas of interest were compared. Medical correlates of social attention in PBTSs were evaluated. RESULTS Groups significantly differed in gaze preference across conditions, with PBTSs looking less at social areas of interest than TD youth and in a manner comparable to youth with ASD. Among PBTSs, multimodal tumor-directed therapy was associated with reduced gaze preference for faces. CONCLUSIONS This study provides the first evidence of disrupted social attention in PBTSs, with parallels to the social attention deficits observed in ASD. Findings offer a new way to conceptualize the social difficulties of PBTSs and could guide interventions aimed at improving PBTS social adjustment by increasing visual attention to socially relevant information during social interactions. (PsycINFO Database Record (c) 2020 APA, all rights reserved).
Comparative proteomic analyses of Duchenne muscular dystrophy and Becker muscular dystrophy muscles: changes contributing to preserve muscle function in Becker muscular dystrophy patients

Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are characterized by muscle wasting leading to loss of ambulation in the first or third decade, respectively. In DMD, the lack of dystrophin hampers connections between intracellular cytoskeleton and cell membrane leading to repeated cycles of necrosis and regeneration associated with inflammation and loss of muscle ordered structure. BMD has a similar muscle phenotype but milder. Here, we address the question whether proteins at variance in BMD compared with DMD contribute to the milder phenotype in BMD, thus identifying a specific signature to be targeted for DMD treatment.
Robust Rate-Place Coding of Resolved Components in Harmonic and Inharmonic Complex Tones in Auditory Midbrain

Harmonic complex tones (HCTs) commonly occurring in speech and music evoke a strong pitch at their fundamental frequency (F0), especially when they contain harmonics individually resolved by the cochlea. When all frequency components of an HCT are shifted by the same amount, the pitch of the resulting inharmonic tone (IHCT) can also shift, although the envelope repetition rate is unchanged. Harmonic complex tones (HCTs) commonly occurring in speech and music evoke a strong pitch at their fundamental frequency (F0), especially when they contain harmonics individually resolved by the cochlea. When all frequency components of an HCT are shifted by the same amount, the pitch of the resulting inharmonic tone (IHCT) can also shift, although the envelope repetition rate is unchanged. A rate-place code, whereby resolved harmonics are represented by local maxima in firing rates along the tonotopic axis, has been characterized in the auditory nerve and primary auditory cortex, but little is known about intermediate processing stages. We recorded single-neuron responses to HCT and IHCT with varying F0 and sound level in the inferior colliculus (IC) of unanesthetized rabbits of both sexes. Many neurons showed peaks in firing rate when a low-numbered harmonic aligned with the neuron's characteristic frequency, demonstrating “rate-place” coding. The IC rate-place code was most prevalent for F0 > 800 Hz, was only moderately dependent on sound level over a 40 dB range, and was not sensitive to stimulus harmonicity. A spectral receptive-field model incorporating broadband inhibition better predicted the neural responses than a purely excitatory model, suggesting an enhancement of the rate-place representation by inhibition. Some IC neurons showed facilitation in response to HCT relative to pure tones, similar to cortical “harmonic template neurons” (Feng and Wang, 2017), but to a lesser degree. Our findings shed light on the transformation of rate-place coding of resolved harmonics along the auditory pathway. SIGNIFICANCE STATEMENT Harmonic complex tones are ubiquitous in speech and music and produce strong pitch percepts when they contain frequency components that are individually resolved by the cochlea. Here, we characterize a “rate-place” code for resolved harmonics in the auditory midbrain that is more robust across sound levels than the peripheral rate-place code and insensitive to the harmonic relationships among frequency components. We use a computational model to show that inhibition may play an important role in shaping the rate-place code. Our study fills a major gap in understanding the transformations in neural representations of resolved harmonics along the auditory pathway.
Predictors of Emergency Room Admission in Patients With Liver Cirrhosis

This study aimed to identify the predictors of emergency room (ER) admission in patients with liver cirrhosis. The data of 215 patients with liver cirrhosis who visited the ER were collected from January 1 to March 15, 2017, at Yeungnam hospital in Daegu city, South Korea. Measurement scales were designed on the basis of the liver function test and evaluation of anxiety and depression, self-care, and family support. Diseases that cause liver cirrhosis, their associated characteristics, and respective hematologic examination results were reviewed from the hospital's electronic medical records. Among the 215 patients with liver cirrhosis who visited the ER, 47 (21.9%) had previous ER admissions, whereas 168 (78.1%) had none. Fifteen predictive factors that were significantly different between the ER admission and non-ER admission groups were included as variables in logistic regression analysis. This analysis revealed that the 3 significant predictors of ER admission in patients with liver cirrhosis were number of prior complications, serum bilirubin level, and self-care compliance. An increased number of prior complications, increased bilirubin level, and low self-care compliance increased the ER admission rates in patients with liver cirrhosis. Thus, further studies are necessary to measure the effects of nursing intervention strategies based on these findings.
The Japanese Encephalitis Virus NS1′ Protein Inhibits Type I IFN Production by Targeting MAVS

Key Points JEV NS1′, not NS1, inhibits IFN-I production by targeting MAVS. NS1′ antagonizes host MAVS through regulating miR-22. NS1′ upregulates miR-22 by enhancing the binding of TFs to its promoter. Japanese encephalitis virus (JEV) is a mosquito-borne Flavivirus that causes severe neurologic disease in humans. NS1′ is a NS1-related protein only reported in the Japanese encephalitis serogroup members of Flavivirus. It is produced through programmed −1 ribosomal frameshift in NS2A. Our previous study demonstrated that JEV NS1′ could antagonize type I IFN (IFN-I) production, but the mechanism is still unclear. In the current study, we found that JEV NS1′ inhibits the expression of MAVS, and knockdown of MAVS hampers inhibition of IFN-β induction by NS1′, suggesting that JEV NS1′ inhibits IFN-I production by targeting MAVS. This finding is further supported by the result of the in vivo assay that showed the similar mortality caused by NS1′-deficient virus and its wild type virus in MAVS-deficient mice. Based on our previous sequencing results of noncoding RNA in JEV-infected cells, microRNA-22 (miR-22) was identified to be a key regulator for MAVS expression during JEV infection. Furthermore, we demonstrated that JEV NS1′ could induce the expression of miR-22 by increasing the binding of transcriptional factors, CREB and c-Rel, to the promoter elements of miR-22. Taken together, our results reveal a novel mechanism by which JEV NS1′ antagonizes host MAVS by regulating miR-22, thereby inhibiting the IFN-I production and facilitating viral replication.
Mechanisms of new blood vessel formation and proliferative heterogeneity of endothelial cells.

The vast blood vessel network of the circulatory system is crucial for maintaining bodily homeostasis, delivering essential molecules and blood cells, and removing waste products. Blood vessel dysfunction and dysregulation of new blood-vessel formation are related to the onset and progression of many diseases including cancer, ischemic disease, inflammation and immune disorders. Endothelial cells (ECs) are fundamental components of blood vessels and their proliferation is essential for new vessel formation, making them good therapeutic targets for regulating the latter. New blood-vessel formation occurs by vasculogenesis and angiogenesis during development. Induction of ECs termed tip, stalk and phalanx cells by interactions between vascular endothelial growth factor A (VEGF-A) and its receptors (VEGFR1-3) and between Notch and Delta-like Notch ligands (DLLs) is crucial for regulation of angiogenesis. Although the importance of angiogenesis is unequivocal in the adult, vasculogenesis effected by endothelial progenitor cells (EPCs) may also contribute to post-natal vessel formation. However, the definition of these cells is ambiguous and they include several distinct cell types under the simple classification of "EPC". Furthermore, recent evidence indicates that ECs within the intima show clonal expansion in some situations and that they may harbor vascular-resident endothelial stem cells. In this article, we summarize recent knowledge on vascular development and new blood vessel formation in the adult. We also introduce concepts of EC heterogeneity and EC clonal expansion, referring to our own recent findings.
Water insecurity potentially undermines dietary diversity of children aged 6–23 months: Evidence from India

Abstract Dietary diversity is a crucial pathway to child nutrition; lack of diversity may deprive children of critical macro and micronutrients. Though water along with hygiene and sanitation is a known driver of child undernutrition, a more direct role of household water in shaping dietary diversity remains unexplored. Existing literature provides a sound theoretical basis to expect that water could affect dietary diversity among young children. Here, we test the proposition that suboptimal household access to water and low regional water availability associate with lower dietary diversity among young children. Using the nationally representative 2015–2016 India Demographic and Health Survey data, we conducted a probit analysis on the sample of 69,841 children aged 6–23 months to predict the probability that a child achieves minimum standards of dietary diversity (MDD). After controlling for relevant socioeconomic and gender‐related covariates, we found that children in household with suboptimal household water access were two percentage points less likely to achieve MDD, when compared with those from households with optimal water access. Children in high water availability regions had nine percentage points greater probability of achieving MDD compared with children from low water availability regions, accounting for household water access. As dietary diversity is central to nutrition, establishing the role of water access in shaping early childhood dietary diversity broadens the framework on how household material poverty shapes child malnutrition—independent of sanitation and hygiene pathways. This provides additional window for nutrition planning and intervention wherein water‐based strategies can be leveraged in multiple ways.
Piezoresistive Carbon Nanofiber-Based Cilia-Inspired Flow Sensor

Evolving over millions of years, hair-like natural flow sensors called cilia, which are found in fish, crickets, spiders, and inner ear cochlea, have achieved high resolution and sensitivity in flow sensing. In the pursuit of achieving such exceptional flow sensing performance in artificial sensors, researchers in the past have attempted to mimic the material, morphological, and functional properties of biological cilia sensors, to develop MEMS-based artificial cilia flow sensors. However, the fabrication of bio-inspired artificial cilia sensors involves complex and cumbersome micromachining techniques that lay constraints on the choice of materials, and prolongs the time taken to research, design, and fabricate new and novel designs, subsequently increasing the time-to-market. In this work, we establish a novel process flow for fabricating inexpensive, yet highly sensitive, cilia-inspired flow sensors. The artificial cilia flow sensor presented here, features a cilia-inspired high-aspect-ratio titanium pillar on an electrospun carbon nanofiber (CNF) sensing membrane. Tip displacement response calibration experiments conducted on the artificial cilia flow sensor demonstrated a lower detection threshold of 50 µm. Furthermore, flow calibration experiments conducted on the sensor revealed a steady-state airflow sensitivity of 6.16 mV/(m s−1) and an oscillatory flow sensitivity of 26 mV/(m s−1), with a lower detection threshold limit of 12.1 mm/s in the case of oscillatory flows. The flow sensing calibration experiments establish the feasibility of the proposed method for developing inexpensive, yet sensitive, flow sensors; which will be useful for applications involving precise flow monitoring in microfluidic devices, precise air/oxygen intake monitoring for hypoxic patients, and other biomedical devices tailored for intravenous drip/urine flow monitoring. In addition, this work also establishes the applicability of CNFs as novel sensing elements in MEMS devices and flexible sensors.
Alpha-1 Adrenergic Receptors Modulate Glutamate and GABA Neurotransmission onto Ventral Tegmental Dopamine Neurons during Cocaine Sensitization

The ventral tegmental area (VTA) plays an important role in the reward and motivational processes that facilitate the development of drug addiction. Presynaptic α1-AR activation modulates glutamate and Gamma-aminobutyric acid (GABA) release. This work elucidates the role of VTA presynaptic α1-ARs and their modulation on glutamatergic and GABAergic neurotransmission during cocaine sensitization. Excitatory and inhibitory currents (EPSCs and IPSCs) measured by a whole cell voltage clamp show that α1-ARs activation increases EPSCs amplitude after 1 day of cocaine treatment but not after 5 days of cocaine injections. The absence of a pharmacological response to an α1-ARs agonist highlights the desensitization of the receptor after repeated cocaine administration. The desensitization of α1-ARs persists after a 7-day withdrawal period. In contrast, the modulation of α1-ARs on GABA neurotransmission, shown by decreases in IPSCs’ amplitude, is not affected by acute or chronic cocaine injections. Taken together, these data suggest that α1-ARs may enhance DA neuronal excitability after repeated cocaine administration through the reduction of GABA inhibition onto VTA dopamine (DA) neurons even in the absence of α1-ARs’ function on glutamate release and protein kinase C (PKC) activation. α1-AR modulatory changes in cocaine sensitization increase our knowledge of the role of the noradrenergic system in cocaine addiction and may provide possible avenues for therapeutics.
Antibacterial composite membranes of polycaprolactone/gelatin loaded with zinc oxide nanoparticles for guided tissue regeneration

The bacterial colonization of absorbable membranes used for guided tissue regeneration (GTR), as well as their rapid degradation that can cause their rupture, are considered the major reasons for clinical failure. To address this, composite membranes of polycaprolactone (PCL) and gelatin (Gel) loaded with zinc oxide nanoparticles (ZnO-NPs; 1, 3 and 6 wt% relative to PCL content) were fabricated by electrospinning. To fabricate homogeneous fibrillar membranes, acetic acid was used as a sole common solvent to enhance the miscibility of PCL and Gel in the electrospinning solutions. The effects of ZnO-NPs in the physico-chemical, mechanical and in vitro biological properties of composite membranes were studied. The composite membranes showed adequate mechanical properties to offer a satisfactory clinical manipulation and an excellent conformability to the defect site while their degradation rate seemed to be appropriate to allow successful regeneration of periodontal defects. The presence of ZnO-NPs in the composite membranes significantly decreased the planktonic and the biofilm growth of the Staphylococcus aureus over time. Finally, the viability of human osteoblasts and human gingival fibroblasts exposed to the composite membranes with 1 and 3 wt% of ZnO-NPs indicated that those membranes are not expected to negatively influence the ability of periodontal cells to repopulate the defect site during GTR treatments. The results here obtained suggest that composite membranes of PCL and Gel loaded with ZnO-NPs have the potential to be used as structurally stable GTR membranes with local antibacterial properties intended for enhancing clinical treatments.