Miracle-dz/UniFAR-FTUs huggingface dataset:
Effects of Stepwise Microwave Synergistic Process Water Recirculation During Hydrothermal Carbonization on Properties of Wheat Straw

In this study, wheat straw (WS) was treated using two-step synergistic techniques, which were process water recirculation (PWR) during hydrothermal carbonization (HTC) and microwave energy activation (MEA). The physicochemical properties of solid and liquid products during the process of HTC PWR were characterized. The temperature-rising properties, yields, and fuel properties of hydrochar after MEA were explored. Then the optimal technique conditions were explored. When HTC PWR was twice, the carbon content (55.59%) and higher heating value (21.72 MJ/kg) were the highest, and the ash content (1.93%) and the O/C and H/C ratios were the lowest. When HTC PWR was three times, the fixed carbon content, mass yield, and energy yield were the highest: 18.53%, 58.25%, and 71.84%, respectively. Many more carbon microspheres and pores appeared on the surface of hydrochar after PWR, which could improve the fuel characteristics and mass yield. After HTC PWR, the concentration of organic acids and HMF in liquid by-products increased, which was conducive to the increase of carbon content and mass yield. The best effect was HTC PWR twice or three times. With the increase of microwave power or the extension of microwave activation duration, the temperature-rising properties of hydrochar significantly increased, and the mass and energy yields decreased. The volatile contents of hydrochar decreased and their fixed carbon contents and HHV increased with the increase of microwave power. The properties of hydrochar could be improved when MEA was 900 W or 1000 W for 4 min. Therefore, MEA had significant effects on the properties of hydrochar after different PWR conditions.
Intergenerational Educational Inequality and Its Transmission in China’s Elite Universities

China is experiencing high social inequality accompanying influential education reforms. The Independent Freshmen Admission (IFA) policy was one of the multiple strategies in higher education reforms in China against the social context of high social inequality and the expansion of higher education. By comparing students admitted through IFA with those admitted by the National College Entrance Examination (NCEE), we examined how family advantages contributed to higher education inequality in terms of educational opportunity, process, and results. Using data from an elite university in Beijing, we found that: (1) Family advantages improved a student’s likelihood of being admitted through IFA, exhibiting opportunity inequality. (2) No significant difference in academic grades existed between the students admitted through IFA and NCEE. In comprehensive quality, however, those recruited through IFA performed significantly better than those admitted through NCEE. (3) Family social capital not only increased the likelihood of students being admitted through IFA but also, through direct and indirect effects, increased their comprehensive quality performance in terms of receiving student association and social practice awards.
Unsteady Motion of Shock Wave for a Supersonic Compression Ramp Flow Based on Large Eddy Simulation

A large eddy simulation (LES) is conducted to investigate shock wave/turbulent boundary layer interaction in a 24° compression ramp at a high inlet Mach number of M a = 2.9 . The recycling/rescaling Method is used as the inflow turbulence generation technique. The shock wave structure and boundary layer flow in the interaction region are studied by flow visualization methods, such as vortex recognition and numerical schlieren. The distributions of turbulent kinetic energy and Reynolds normal stresses at different streamwise locations are analyzed. The results show that a strong anisotropy turbulent flow appears in the reattached boundary layer after the interaction of the shock wave. The large-scale unsteady motion of the separation shock wave is analyzed by using the intermittent factor and power spectrum. It is found that the shock moves around the averaged separation position, and the length scale is equal to 72% of the inlet boundary layer thickness. The power spectrum analysis reveals the existence of low-frequency instability in the separation region.
Suppressive Effect of Autocrine FGF21 on Autophagy-Deficient Hepatic Tumorigenesis

Mice with hepatocyte-specific deletion of autophagy-related 7 (Atg7ΔHep mice) develop hepatoma, suggesting that autophagy deficiency could be a factor in the initiation of tumorigenesis. We have shown that FGF21 is induced as a ‘mitokine’ when Atg7 is disrupted in insulin target tissues such as the liver, which could affect systemic metabolism through endocrine activity. Since FGF21 or other endocrine FGF such as FGF19 can affect tumor growth, we hypothesized that FGF21 produced by Atg7-knockout (KO) hepatocytes may affect the behavior of Atg7-KO hepatoma in an autocrine manner. We, thus, crossed Atg7ΔHep mice with systemic Fgf21-KO (Fgf21−/−) mice to generate Atg7ΔHepFgf21−/− mice. The number and size of hepatoma of Atg7ΔHep mice were significantly increased by additional Fgf21 KO. The proliferation of Atg7-KO hepatocyte was significantly increased by Fgf21 KO. pYAP1/YAP1 representing YAP1 degradation was significantly decreased in the liver of Atg7ΔHepFgf21−/− mice compared to Atg7ΔHepFgf21+/+ mice. Consistently, expression of YAP1/TAZ downstream genes was significantly increased in the liver of Atg7ΔHepFgf21−/− mice compared to Atg7ΔHepFgf21+/+ mice, which could explain the increased size of hepatoma in Atg7ΔHepFgf21−/− mice. Accumulation of ROS and ROS-mediated DNA damage were increased in the liver of Atg7ΔHepFgf21+/+ mice, which was further aggravated by additional Fgf21 KO probably due to the absence of positive effect of FGF21 on mitochondrial function, explaining the increased number of hepatoma in Atg7ΔHepFgf21−/− mice compared to Atg7ΔHepFgf21+/+ mice. These results show that FGF21 produced by autophagy-deficient hepatocytes could have autocrine or paracrine effects on the number and proliferation of autophagy-deficient hepatoma, suggesting that hormones or factors released from autophagy-deficient tumors can influence the behavior or prognosis of the tumor in addition to the effects on host metabolism.
Self-Compassion and Its Association With Ruminative Tendencies and Vagally Mediated Heart Rate Variability in Recurrent Major Depression

Background Recurrent Major Depressive Disorder (MDD) is one of the most disabling mental disorders in modern society. Prior research has shown that self-compassion protects against ruminative tendencies, a key feature of recurrent MDD. In addition, self-compassion has been found to be positively related to higher psychophysiological flexibility (indexed by a higher vagally mediated heart rate variability; vmHRV) in young, healthy adults. To our knowledge, there is a lack of studies on how self-compassion relates to vmHRV in patients with recurrent MDD. The aim of the current study was to investigate whether higher self-compassion would associate with (1) lower ruminative tendencies and (2) higher vmHRV in a sample of adults with recurrent MDD. Methods We included a sample of 63 patients (46 females) between 20 and 71 years old (M = 40.24, SD = 12.8) with a history of three or more depressive episodes. They filled out the Self-Compassion Scale (SCS), Beck Depression Inventory (BDI), and Rumination Rating Scale (RRS). ECG (used to derive vmHRV) was acquired while resting and the square root of the mean squared differences of successive RR interval values (RMSSD) was calculated as measure of vmHRV. Results As hypothesized, self-compassion was associated with lower ruminative tendencies. However, self-compassion was not associated with level of vmHRV. Several confounding variables were controlled for in the statistical analyses, and higher age predicted lower vmHRV across all statistical analyses. Conclusion The results confirmed our hypothesis that higher self-compassion would be associated with lower ruminative tendencies in recurrent MDD. Contrary to our expectation, we did not find that the tendency to be more self-compassionate was associated with higher vmHRV. As such, higher self-compassion seems to relate with a lower tendency to ruminate about past mistakes and events but does not seem to relate to a flexible autonomic stress response (as indexed by higher vmHRV). Other potential explanatory factors for lower vmHRV in recurrent MDD is suggested as focus for exploration in future studies.
Different Roles of Resident and Non-resident Macrophages in Cardiac Fibrosis

Cardiac fibrosis is a key pathological link of various cardiovascular diseases to heart failure. It is of great significance to deeply understand the development process of cardiac fibrosis and the cellular and molecular mechanisms involved. Macrophages play a special role in promoting heart development, maintaining myocardial cell homeostasis and heart function. They are involved in the whole process from inflammatory to cardiac fibrosis. This article summarizes the relationship between inflammation and fibrosis, discusses the bidirectional regulation of cardiac fibrosis by macrophages and analyses the functional heterogeneity of macrophages from different sources. It is believed that CCR2– cardiac resident macrophages can promote cardiac function, but the recruitment and infiltration of CCR2+ cardiac non-resident macrophages aggravate cardiac dysfunction and heart remodeling. After heart injury, damage associated molecular patterns (DAMPs) are released in large quantities, and the inflammatory signal mediated by macrophage chemoattractant protein-1 (MCP-1) promotes the infiltration of CCR2+ monocytes and transforms into macrophages in the heart. These CCR2+ non-resident macrophages not only replace part of the CCR2– resident macrophage subpopulation in the heart, but also cause cardiac homeostasis and hypofunction, and release a large number of mediators that promote fibroblast activation to cause cardiac fibrosis. This article reveals the cell biology mechanism of resident and non-resident macrophages in regulating cardiac fibrosis. It is believed that inhibiting the infiltration of cardiac non-resident macrophages and promoting the proliferation and activation of cardiac resident macrophages are the key to improving cardiac fibrosis and improving cardiac function.
Analysis of HLA Variants and Graves’ Disease and Its Comorbidities Using a High Resolution Imputation System to Examine Electronic Medical Health Records

Hyperthyroidism is a prevalent endocrine disorder, and genetics play a major role in the development of thyroid-associated diseases. In particular, the inheritance of HLA has been demonstrated to induce the highest susceptibility to Graves’ disease (GD). However, thus far, no studies have reported the contribution of HLA to the development of GD and the complications that follow. Thus, in the present study, to the best of our knowledge, for the first time, a powerful imputation method, HIBAG, was used to predict the HLA subtypes among populations with available genome-wide SNP array data from the China Medical University Hospital (CMUH). The disease status was extracted from the CMUH electronic medical records; a total of 2,998 subjects with GD were identified as the cases to be tested and 29,083 subjects without any diagnosis of thyroid disorders were randomly selected as the controls. A total of 12 HLA class I genotypes (HLA-A*02:07-*11:01, HLA-B*40:01-*46:01 and *46:01-*46:01, and HLA-C*01:02-*01:02, *01:02-*03:04, and *01:02-*07:02) and 17 HLA class II genotypes (HLA-DPA1*02:02-*02:02, HLA-DPB1*02:01-*05:01, *02:02-*05:01, and *04:01-*05:01, HLA-DQA1*03:02, HLA-DRB1*09:01-*15:01, and *09:01-*09:01) were found to be associated with GD in the Taiwanese population. Moreover, the HLA subtypes HLA-A*11:01, HLA-B*46:01, HLA-DPA1*01:03, and HLA-DPB1*05:01 were found to be associated with heart disease, stroke, diabetes, and hypertension among subjects with GD. Our data suggest that several HLA alleles are markedly associated with GD and its comorbidities, including heart disease, hypertension, and diabetes.
Treatment of Focal-Onset Seizures in Children: Should This Be More Etiology-Driven?

To accelerate the process of licensing antiseizure medication (ASM) in children, extrapolation of efficacy data for focal-onset seizures from adults to children ≥2 or ≥4 years of age is now accepted. We summarized the efficacy evidence from randomized, controlled trials that was used to grant approval for the pediatric indication of focal-onset seizures for the different ASMs available in Europe. Data from high-quality randomized, controlled trials in young children are limited, especially on the use of ASMs in monotherapy. Licensure trials are typically focused on seizure type irrespective of etiology or epilepsy syndrome. We elaborate on the importance of etiology- or syndrome-driven research and treatment, illustrating this with examples of childhood epilepsy syndromes characterized by predominantly focal-onset seizures. Some of these syndromes respond well to standard ASMs used for focal-onset seizures, but others would benefit from a more etiology- or syndrome-driven approach. Advances in molecular genetics and neuroimaging have made it possible to reveal the underlying cause of a child's epilepsy and tailor research and treatment. More high-quality randomized, controlled trials based on etiology or syndrome type are needed, including those assessing effects on cognition and behavior. In addition, study designs such as “N-of-1 trials” could elucidate possible new treatment options in rare epilepsies. Broadening incentives currently in place to stimulate the development and marketing of drugs for rare diseases (applicable to some epilepsy syndromes) to more common pediatric epilepsy types and syndromes might be a means to enable high-quality trials, and ultimately allow more evidence-based treatment in children.
Yamanaka Factors in the Budding Tunicate Botryllus schlosseri Show a Shared Spatio-Temporal Expression Pattern in Chordates

In vertebrates, the four transcription factors Sox2, c-Myc, Pou5f1 and Klf4 are involved in the differentiation of several tissues during vertebrate embryogenesis; moreover, they are normally co-expressed in embryonic stem cells and play roles in pluripotency, self-renewal, and maintenance of the undifferentiated state in adult cells. The in vitro forced co-expression of these factors, named Yamanaka factors (YFs), induces pluripotency in human or mouse fibroblasts. Botryllus schlosseri is a colonial tunicate undergoing continuous stem cell-mediated asexual development, providing a valuable model system for the study of pluripotency in the closest living relatives of vertebrates. In this study, we identified B. schlosseri orthologs of human Sox2 and c-Myc genes, as well as the closest homologs of the vertebrate-specific Pou5f1 gene, through an in-depth evolutionary analysis of the YF gene families in tunicates and other deuterostomes. Then, we studied the expression of these genes during the asexual cycle of B. schlosseri using in situ hybridization in order to investigate their possible involvement in tissue differentiation and in pluripotency maintenance. Our results show a shared spatio-temporal expression pattern consistent with the reported functions of these genes in invertebrate and vertebrate embryogenesis. Moreover, Myc, SoxB1 and Pou3 were expressed in candidate stem cells residing in their niches, while Pou2 was found expressed exclusively in the immature previtellogenic oocytes, both in gonads and circulating in the colonial vascular system. Our data suggest that Myc, SoxB1 and Pou3 may be individually involved in the differentiation of the same territories seen in other chordates, and that, together, they may play a role in stemness even in this colonial ascidian.
The Impact of Lateral Gene Transfer in Chlamydia

Lateral gene transfer (LGT) facilitates many processes in bacterial ecology and pathogenesis, especially regarding pathogen evolution and the spread of antibiotic resistance across species. The obligate intracellular chlamydiae, which cause a range of diseases in humans and animals, were historically thought to be highly deficient in this process. However, research over the past few decades has demonstrated that this was not the case. The first reports of homologous recombination in the Chlamydiaceae family were published in the early 1990s. Later, the advent of whole-genome sequencing uncovered clear evidence for LGT in the evolution of the Chlamydiaceae, although the acquisition of tetracycline resistance in Chlamydia (C.) suis is the only recent instance of interphylum LGT. In contrast, genome and in vitro studies have shown that intraspecies DNA exchange occurs frequently and can even cross species barriers between closely related chlamydiae, such as between C. trachomatis, C. muridarum, and C. suis. Additionally, whole-genome analysis led to the identification of various DNA repair and recombination systems in C. trachomatis, but the exact machinery of DNA uptake and homologous recombination in the chlamydiae has yet to be fully elucidated. Here, we reviewed the current state of knowledge concerning LGT in Chlamydia by focusing on the effect of homologous recombination on the chlamydial genome, the recombination machinery, and its potential as a genetic tool for Chlamydia.
Functional Remodeling Associated With Language Recovery After Repetitive Transcranial Magnetic Stimulation in Chronic Aphasic Stroke

Background Repetitive transcranial magnetic stimulation (rTMS) has shown promising efficacy in improving the language functions in poststroke aphasia. However, randomized controlled trials were lacking to investigate the rTMS-related neuroimaging changes underlying the therapeutic effects on language improvement in chronic aphasia. Objective In this study, we aimed to evaluate the effects of low-frequency rTMS (LF-rTMS) on chronic poststroke aphasia. We hypothesized that the deactivation of the right pars triangularis could restore the balance of interhemispheric inhibition and, hence, facilitated the functional remodeling of language networks in both the hemispheres. Furthermore, the rTMS-induced functional reorganization should underpin the language recovery after rTMS. Methods A total of 33 patients (22 males; age: 58.70 ± 13.77 years) with chronic stroke in the left hemisphere and nonfluent aphasia were recruited in this randomized double-blinded study. The ratio of randomization between the rTMS and sham groups is 17:16. All the patients received real 1-Hz rTMS or sham stimulation (placebo coil delivered < 5% of magnetic output with similar audible click-on discharge) at the right posterior pars triangularis for 10 consecutive weekdays (stroke onset to the first stimulation: 10.97 ± 10.35 months). Functional connectivity of language networks measured by resting-state fMRI was calculated and correlated to the scores of the Concise Chinese Aphasia Test by using the stepwise regression analysis. Results After LF-rTMS intervention, significant improvement in language functions in terms of comprehension and expression abilities was observed compared with the sham group. The rTMS group showed a significant decrease of coupling strength between right pars triangularis and pars opercularis with a strengthened connection between right pars orbitalis and angular gyrus. Furthermore, the LF-rTMS significantly enhanced the coupling strength associated with left Wernicke area. Results of regression analysis showed that the identified functional remodeling involving both the hemispheres could support and predict the language recovery after LF-rTMS treatment. Conclusion We reported the therapeutic effects of LF-rTMS and corresponding functional remodeling in chronic poststroke aphasia. Our results provided neuroimage evidence reflecting the rebalance of interhemispheric inhibition induced by LF-rTMS, which could facilitate future research in the refinement of rTMS protocol to optimize the neuromodulation efficacy and benefit the clinical management of patients with stroke.
High Levels of Cerebrospinal Fluid Kappa Free Light Chains Relate to IgM Intrathecal Synthesis and Might Have Prognostic Implications in Relapsing Multiple Sclerosis

Cerebrospinal kappa free light chain (KFLC)-index is a marker of intrathecal immunoglobulin synthesis that aids in the diagnosis of multiple sclerosis (MS). However, little evidence exists on its prognostic role. Our aim is to analyze the relationship between KFLC-index and other MS biomarkers and to explore its prognostic role. This is a monocentric observational study in a cohort of 52 people with relapsing MS (pwRMS) performed on prospectively acquired clinical data and with retrospective evaluation of biomarkers. We measured KFLC-index, immunoglobulin intrathecal synthesis, cerebrospinal fluid (CSF) chitinase 3-like 1 (CHI3L1), and neurofilament light protein (NFL) and reviewed MRI to detect leptomeningeal contrast enhancement (LMCE). We compared time to Expanded Disability Status Scale (EDSS) 3 and to initiation of high-efficacy disease-modifying therapies (heDMTs) by multivariate Cox regression analysis. Median KFLC-index correlated with IgG/IgM indexes (p < 0.0001/p < 0.05) and IgG-oligoclonal bands (OCGBs) (p < 0.001). Patients with IgM-oligoclonal bands (OCMBs) had a higher KFLC-index (p = 0.049). KFLC-index was higher in patients with LMCE (p = 0.008) and correlated with CHI3L1 (p = 0.007), but disease activity had no effect on its value. Bivariate and multivariate analyses confirmed KFLC-index > 58 as an independent risk factor for reaching an EDSS of 3 (hazard ratio (HR) = 12.4; 95% CI = 1.1–147; p = 0.047) and for the need of treatment with heDMTs (HR = 3.0; 95% CI = 1.2–7.1; p = 0.0013). To conclude, our data suggest a potential prognostic role of the KFLC-index during the MS course.
Omicron Variant of SARS-CoV-2 Virus: In Silico Evaluation of the Possible Impact on People Affected by Diabetes Mellitus

The Omicron variant of SARS-CoV-2 (Spike mutant B.1.1.529) carrying more than 30-point mutations in its structure, of which 15 are localized in the receptor-binding domain (RBD), allows to hypothesize a relevant change in interactivity with ACE2. In previous reports we hypothesized that the worse outcome of the COVID-19 disease in diabetes mellitus condition could be related to the non-enzymatic glycation of ACE2 receptor and an in silico evaluation led to the demonstration that the number of interactions is decreased in comparison to the unmodified model, possibly shifting the virus attack through different, multiple alternative entry routes. Given the evidenced features of this variant, we aimed to investigate with a computational approach the characteristics of Omicron SARS-CoV-2 with respect to its binding to human ACE-2 receptor, in a particular population, namely people affected by diabetes mellitus, at risk for unfavorable outcomes of the COVID-19. The computational analysis, considering the case in which all the lysine residues in the system are subjected to non-enzymatic glycation, confirmed that lysine glycation causes a general loss of interactivity between wild-type (WT)-Spike-RBD and ACE2. In the Omicron variant, Lys417 mutates into an asparagine, preventing the possible non-enzymatic glycation of this residue. Therefore, if non-enzymatic glycation seemed to cause a shift in the way in which the virus enters the cell from the ACE2-mediated mechanism to other pathways, in the case of the Omicron variant the ACE2-mediated approach of the virus seems to remain an important event to take into account. Indeed, interaction profile analysis, together with molecular mechanics–generalized Born surface area (MM-GBSA) calculations, suggests that the Omicron-Spike-RBD maintains a higher affinity for ACE2 subsequently to non-enzymatic glycation with respect to WT-Spike-RBD. The finding of the present computational study may suggest a different clinical relevance of the Omicron variant for the diabetes mellitus field, also in the possible direction of a lower severity of the disease.