bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulating immune memory and reversing tumor thermotolerance through a step-by-step starving-photothermal therapy
Authors: Luo Lihua , Qin Bing , Jiang Mengshi , Xie Lin , Luo Zhenyu , Guo Xuemeng , Zhang Junlei , Li Xiang , Zhu Chunqi , Du Yongzhong , Peng Ling , You Jian 
Published: September 2021

Abstract
Background
Photothermal therapy (PTT) is a highly effective treatment for solid tumors and can induce long-term immune memory worked like an in situ vaccine. Nevertheless, PTT inevitably encounters photothermal resistance of tumor cells, which hinders therapeutic effect or even leads to tumor recurrence. Naïve CD8+ T cells are mainly metabolized by oxidative phosphorylation (OXPHOS), followed by aerobic glycolysis after activation. And the differentiate of effector CD8+ T cell (CD8+ Teff) into central memory CD8+ T cell (CD8+ TCM) depends on fatty acid oxidation (FAO) to meet their metabolic requirements, which is regulated by adenosine monophosphate activated protein kinase (AMPK). In addition, the tumor microenvironment (TME) is severely immunosuppressive, conferring additional protection against the host immune response mediated by PTT.

Methods
Metformin (Met) down-regulates NADH/NADPH, promotes the FAO of CD8+ T cells by activating AMPK, increases the number of CD8+ TCM, which boosts the long-term immune memory of tumor-bearing mice treated with PTT. Here, a kind of PLGA microspheres co-encapsulated hollow gold nanoshells and Met (HAuNS-Met@MS) was constructed to inhibit the tumor progress. 2-Deoxyglucose (2DG), a glycolysis inhibitor for cancer starving therapy, can cause energy loss of tumor cells, reduce the heat stress response of tumor cell, and reverse its photothermal resistance. Moreover, 2DG prevents N-glycosylation of proteins that cause endoplasmic reticulum stress (ERS), further synergistically enhance PTT-induced tumor immunogenic cell death (ICD), and improve the effect of immunotherapy. So 2DG was also introduced and optimized here to solve the metabolic competition among tumor cells and immune cells in the TME.

Results
We utilized mild PTT effect of HAuNS to propose an in situ vaccine strategy based on the tumor itself. By targeting the metabolism of TME with different administration strategy of 2DG and perdurable action of Met, the thermotolerance of tumor cells was reversed, more CD8+ TCMs were produced and more effective anti-tumor was presented in this study.

Conclusion
The Step-by-Step starving-photothermal therapy could not only reverse the tumor thermotolerance, but also enhance the ICD and produce more CD8+ TCM during the treatment.

Graphical Abstract
Soft tissue perineurioma involving the kidney: a report of two cases with an emphasis on differential diagnosis
Authors: Ma Tian-shi , Zhou Ling , Zhou Quan , He Xiang-lei , Zhao Ming 
Published: September 2021

Abstract
Background
Soft tissue perineurioma of the kidney is rare, with only a few reported cases. We report two additional cases with histologic, immunohistochemical and genetic analyses.

Case presentation
Both tumors were from adults (1 female aged 49 years and 1 male aged 42 years) and grossly had maximum diameters of 6.5 and 10 cm, respectively. The tumors were overall well circumscribed but unencapsulated, with focally entrapped benign native renal tubules in one case; both tumors seemed to arise in the capsular areas. The tumors had histologic and immunohistochemical profiles consistent with soft tissue perineurioma. Fluorescence in situ hybridization analyses demonstrated that the tumors were negative for amplification of MDM2 and rearrangements of ESWR1, FUS, and KMT2A. Targeted next-generation sequencing revealed a low tumor mutation burden and likely pathogenic mutations (CYP2B6 and FLT1 mutations for 1 each). Follow-up data were available for both patients; neither had tumor recurrence or metastasis.

Conclusions
In conclusion, renal perineurioma is rare, usually arises in the capsular areas, and is cured by resection. Low-grade dedifferentiated liposarcoma and low-grade fibromyxoid sarcoma as well as other spindle cell lesions should be considered in the differential diagnosis.
MicroRNAs as the critical regulators of Cisplatin resistance in ovarian cancer cells
Authors: Moghbeli Meysam 
Published: September 2021

Abstract
Background
Ovarian cancer (OC) is one of the leading causes of cancer related deaths among women. Due to the asymptomatic tumor progression and lack of efficient screening methods, majority of OC patients are diagnosed in advanced tumor stages. A combination of surgical resection and platinum based-therapy is the common treatment option for advanced OC patients. However, tumor relapse is observed in about 70% of cases due to the treatment failure. Cisplatin is widely used as an efficient first-line treatment option for OC; however cisplatin resistance is observed in a noticeable ratio of cases. Regarding, the severe cisplatin side effects, it is required to clarify the molecular biology of cisplatin resistance to improve the clinical outcomes of OC patients. Cisplatin resistance in OC is associated with abnormal drug transportation, increased detoxification, abnormal apoptosis, and abnormal DNA repair ability. MicroRNAs (miRNAs) are critical factors involved in cell proliferation, apoptosis, and chemo resistance. MiRNAs as non-invasive and more stable factors compared with mRNAs, can be introduced as efficient markers of cisplatin response in OC patients.

Main body
In present review, we have summarized all of the miRNAs that have been associated with cisplatin resistance in OC. We also categorized the miRNAs based on their targets to clarify their probable molecular mechanisms during cisplatin resistance in ovarian tumor cells.

Conclusions
It was observed that miRNAs mainly exert their role in cisplatin response through regulation of apoptosis, signaling pathways, and transcription factors in OC cells. This review highlighted the miRNAs as important regulators of cisplatin response in ovarian tumor cells. Moreover, present review paves the way of suggesting a non-invasive panel of prediction markers for cisplatin response among OC patients.
Experimental evidence for opposing effects of high deer density on tick-borne pathogen prevalence and hazard
Authors: Gandy Sara , Kilbride Elizabeth , Biek Roman , Millins Caroline , Gilbert Lucy 
Published: September 2021

AbstractBackgroundIdentifying the mechanisms driving disease risk is challenging for multi-host pathogens, such asBorrelia burgdorferisensu lato (s.l.), the tick-borne bacteria causing Lyme disease. Deer are tick reproduction hosts but do not transmitB. burgdorferis.l., whereas rodents and birds are competent transmission hosts. Here, we use a long-term deer exclosure experiment to test three mechanisms for how high deer density might shapeB. burgdorferis.l. prevalence in ticks: increased prevalence due to higher larval tick densities facilitating high transmission on rodents (M1); alternatively, reducedB. burgdorferis.l. prevalence because more larval ticks feed on deer rather than transmission-competent rodents (dilution effect) (M2), potentially due to ecological cascades, whereby higher deer grazing pressure shortens vegetation which decreases rodent abundance thus reducing transmission (M3).MethodsIn a large enclosure where red deer stags were kept at high density (35.5 deer km−2), we used an experimental design consisting of eight plots of 0.23 ha, four of which were fenced to simulate the absence of deer and four that were accessible to deer. In each plot we measured the density of questing nymphs and nymphal infection prevalence in spring, summer and autumn, and quantified vegetation height and density, and small mammal abundance.ResultsPrevalence tended to be lower, though not conclusively so, in high deer density plots compared to exclosures (predicted prevalence of 1.0% vs 2.2%), suggesting that the dilution and cascade mechanisms might outweigh the increased opportunities for transmission mechanism. Presence of deer at high density led to shorter vegetation and fewer rodents, consistent with an ecological cascade. However, Lyme disease hazard (density of infectedI. ricinusnymphs) was five times higher in high deer density plots due to tick density being 18 times higher.ConclusionsHigh densities of tick reproduction hosts such as deer can drive up vector-borne disease hazard, despite the potential to simultaneously reduce pathogen prevalence. This has implications for environmental pathogen management and for deer management, although the impact of intermediate deer densities now needs testing.Graphical abstract
Association of LRRK2 rs11564258 single nucleotide polymorphisms with type and extent of gastrointestinal mycobiome in ulcerative colitis: a case–control study
Authors: Sharifinejad Niusha , Mozhgani Seyed Hamidreza , Bakhtiyari Mahmood , Mahmoudi Elaheh 
Published: September 2021

Abstract
Background
Recently, the role of endogenous microbiota and the genotype-microbiota correlation in inflammatory bowel disease (IBD) pathogenesis have been highlighted. However, fungi, as the second most prevalent residents of the intestine, and their primary receptor, Dectin-1, are underrated. Thus, we conducted the first human study investigating the association of Leucine-rich repeat kinase 2 (LRRK2) polymorphism (rs11564258) with type and the extent of intestinal fungi in IBD patients.

Material and methods
A case–control study was performed on 79 ulcerative colitis (UC)-patients (case group) and 58 healthy subjects (HS group). DNA was extracted from blood samples of both groups and amplified with the primers designed for the specific locus containing the LRRK2 polymorphism (rs11564258) and then sequenced. Dectin-1 and LRRK2 mRNA expression levels were also determined. Furthermore, the type and prevalence of fecal yeast species were surveyed in case and control groups.

Results
A positive correlation was observed between rs11564258 polymorphism and UC susceptibility (p = 0.008 vs. HS). Patients with active UC had the highest rate of isolated fungal colonies (50.41%), followed by patients with non-active UC (24.6%) and HS (25%). These results showed a relationship between UC severity with the increased fungal load. Candida albicans had the highest prevalence in both UC (78.7%) and HS groups (55.8%). Whereas Saccharomyces cerevisiae was the second most common species detected in HS (15.23%), it was significantly reduced in the UC patient group (1.68%) (P = 0.0001). On the other hand, single nucleotide polymorphism (SNP, rs11564258) was not correlated with the increased fungal flora in the UC patients. The expression of LRRK2 and Dectin-1 mRNA detected in blood samples was notably higher in the UC patients (P < 0.01) than in the HS group, without being affected by rs11564258 polymorphism.

Conclusions
Here, we disclosed that LRRK2 mediates Dectin-1 signaling pathway activation and subsequent inflammation in the UC patients without being affected by the presence of SNP rs11564258. Our data showed an increased global fungal load in the UC patients along with elevated UC susceptibility in cases carrying rs11564258 polymorphism. However, more clinical investigations, particularly in larger populations with different ethnic groups, are required to support this conclusion.
On generalized Bessel–Maitland function
Authors: Zayed Hanaa M. 
Published: September 2021

AbstractAn approach to the generalized Bessel–Maitland function is proposed in the present paper. It is denoted by$\mathcal{J}_{\nu , \lambda }^{\mu }$Jν,λμ, where$\mu >0$μ>0and$\lambda ,\nu \in \mathbb{C\ }$λ,ν∈Cget increasing interest from both theoretical mathematicians and applied scientists. The main objective is to establish the integral representation of$\mathcal{J}_{\nu ,\lambda }^{\mu }$Jν,λμby applying Gauss’s multiplication theorem and the representation for the beta function as well as Mellin–Barnes representation using the residue theorem. Moreover, themth derivative of$\mathcal{J}_{\nu ,\lambda }^{\mu }$Jν,λμis considered, and it turns out that it is expressed as the Fox–Wright function. In addition, the recurrence formulae and other identities involving the derivatives are derived. Finally, the monotonicity of the ratio between two modified Bessel–Maitland functions$\mathcal{I}_{\nu ,\lambda }^{\mu }$Iν,λμdefined by$\mathcal{I}_{\nu ,\lambda }^{\mu }(z)=i^{-2\lambda -\nu }\mathcal{J}_{ \nu ,\lambda }^{\mu }(iz)$Iν,λμ(z)=i−2λ−νJν,λμ(iz)of a different order, the ratio between modified Bessel–Maitland and hyperbolic functions, and some monotonicity results for$\mathcal{I}_{\nu ,\lambda }^{\mu }(z)$Iν,λμ(z)are obtained where the main idea of the proofs comes from the monotonicity of the quotient of two Maclaurin series. As an application, some inequalities (like Turán-type inequalities and their reverse) are proved. Further investigations on this function are underway and will be reported in a forthcoming paper.
Estimating thigh skeletal muscle volume using multi-frequency segmental-bioelectrical impedance analysis
Authors: Taniguchi Masashi , Yamada Yosuke , Yagi Masahide , Nakai Ryusuke , Tateuchi Hiroshige , Ichihashi Noriaki 
Published: September 2021

Abstract
Background
The primary aim of this study was to investigate whether using the extracellular water/intracellular water (ECW/ICW) index and phase angle combined with segmental-bioimpedance analysis (BIA) improved the model fitting of skeletal muscle volume (SMV) estimation. The secondary aim was to compare the accuracy of segmental-BIA with that of ultrasound for estimating the quadriceps SMV measured with MRI.

Methods
Seventeen young men (mean age, 23.8 ± 3.3 years) participated in the study. The T-1 weighted images of thigh muscles were obtained using a 1.5 T magnetic resonance imaging (MRI) scanner. Thigh and quadriceps SMVs were calculated as the sum of the products of anatomical cross-sectional area and slice thickness of 6 mm across all slices. Segmental-BIA was applied to the thigh region, and data on the 50-kHz bioelectrical impedance (BI) index, ICW index, ECW/ICW index, and phase angle were obtained. The muscle thickness index was calculated as the product of the mid-thigh muscle thickness, determined using ultrasound, and thigh length. The standard error of estimate (SEE) of the regression equation was calculated to determine the model fitting of SMV estimation and converted to %SEE by dividing the SEE values by the mean SMV.

Results
Multiple regression analysis indicated that the combination of 50-kHz BI and the ECW/ICW index or phase angle was a significant predictor when estimating thigh SMV (SEE = 7.9 and 8.1%, respectively), but were lower than the simple linear regression (SEE = 9.4%). The ICW index alone improved the model fitting for the estimation equation (SEE = 7.6%). The model fitting of the quadriceps SMV with the 50-kHz BI or ICW index was similar to that with the skeletal muscle thickness index measured using ultrasound (SEE = 10.8, 9.6 and 9.7%, respectively).

Conclusions
Combining the traditionally used 50-kHz BI index with the ECW/ICW index and phase angle can improve the model fitting of estimated SMV measured with MRI. We also showed that the model suitability of SMV estimation using segmental-BIA was equivalent to that on using ultrasound. These data indicate that segmental-BIA may be a useful and cost-effective alternative to the gold standard MRI for estimating SMV.
Bacterial mutagenicity test data: collection by the task force of the Japan pharmaceutical manufacturers association
Authors: Hakura Atsushi , Awogi Takumi , Shiragiku Toshiyuki , Ohigashi Atsushi , Yamamoto Mika , Kanasaki Kayoko , Oka Hiroaki , Dewa Yasuaki , Ozawa Shunsuke , Sakamoto Kouji , Kato Tatsuya , Yamamura Eiji 
Published: September 2021

Abstract
Background
Ames test is used worldwide for detecting the bacterial mutagenicity of chemicals. In silico analyses of bacterial mutagenicity have recently gained acceptance by regulatory agencies; however, current in silico models for prediction remain to be improved. The Japan Pharmaceutical Manufacturers Association (JPMA) organized a task force in 2017 in which eight Japanese pharmaceutical companies had participated. The purpose of this task force was to disclose a piece of pharmaceutical companies’ proprietary Ames test data.

Results
Ames test data for 99 chemicals of various chemical classes were collected for disclosure in this study. These chemicals are related to the manufacturing process of pharmaceutical drugs, including reagents, synthetic intermediates, and drug substances. The structure-activity (mutagenicity) relationships are discussed in relation to structural alerts for each chemical class. In addition, in silico analyses of these chemicals were conducted using a knowledge-based model of Derek Nexus (Derek) and a statistics-based model (GT1_BMUT module) of CASE Ultra. To calculate the effectiveness of these models, 89 chemicals for Derek and 54 chemicals for CASE Ultra were selected; major exclusions were the salt form of four chemicals that were tested both in the salt and free forms for both models, and 35 chemicals called “known” positives or negatives for CASE Ultra. For Derek, the sensitivity, specificity, and accuracy were 65% (15/23), 71% (47/66), and 70% (62/89), respectively. The sensitivity, specificity, and accuracy were 50% (6/12), 60% (25/42), and 57% (31/54) for CASE Ultra, respectively. The ratio of overall disagreement between the CASE Ultra “known” positives/negatives and the actual test results was 11% (4/35). In this study, 19 out of 28 mutagens (68%) were detected with TA100 and/or TA98, and 9 out of 28 mutagens (32%) were detected with either TA1535, TA1537, WP2uvrA, or their combination.

Conclusion
The Ames test data presented here will help avoid duplicated Ames testing in some cases, support duplicate testing in other cases, improve in silico models, and enhance our understanding of the mechanisms of mutagenesis.
Brain White Matter Microstructure as a Risk Factor for Cognitive Decline After Chemotherapy for Breast Cancer
Authors: de Ruiter Michiel B. , Reneman Liesbeth , Kieffer Jacobien M. , Oldenburg Hester S. A. , Schagen Sanne B. 
Published: September 2021

PURPOSE Cognitive decline is frequently observed after chemotherapy. As chemotherapy is associated with changes in brain white matter microstructure, we investigated whether white matter microstructure before chemotherapy is a risk factor for cognitive decline after chemotherapy. METHODS Neuropsychologic tests were administered before and 6 months (n = 49), 2 years (n = 32), and 3 years (n = 32) after chemotherapy in patients with breast cancer receiving anthracycline-based chemotherapy (BC + CT group), at matched intervals to patients with BC who did not receive systemic therapy (BC – CT group: n = 39, 23, and 19, respectively) and to no-cancer controls (NC group: n = 37, 29, and 28, respectively). Using multivariate normative comparison, we evaluated to what extent the cognitive profiles of patients deviated from those of controls. Fractional anisotropy (FA), derived from magnetic resonance diffusion tensor imaging, was used to measure white matter microstructure before treatment. FA was evaluated as a risk factor for cognitive decline, in addition to baseline age, fatigue, cognitive complaints, and premorbid intelligence quotient. We subsequently ran voxel-wise diffusion tensor imaging analyses to investigate white matter microstructure in specific nerve tracts. RESULTS Low FA independently predicted cognitive decline early (6 months, P = .013) and late (3 years, P < .001) after chemotherapy. FA did not predict cognitive decline in the BC – CT and NC groups. Voxel-wise analysis indicated involvement of white matter tracts essential for cognitive functioning. CONCLUSION Low FA may reflect low white matter reserve. This may be a risk factor for cognitive decline after chemotherapy for BC. If validated in future trials, identification of patients with low white matter reserve could improve patient care, for example, by facilitating targeted, early interventions or even by influencing choices of patients and doctors for receiving chemotherapy.
Genomic Profiling of Lung Adenocarcinoma in Never-Smokers
Authors: Devarakonda Siddhartha , Li Yize , Martins Rodrigues Fernanda , Sankararaman Sumithra , Kadara Humam , Goparaju Chandra , Lanc Irena , Pepin Kymberlie , Waqar Saiama N. , Morgensztern Daniel , Ward Jeffrey , Masood Ashiq , Fulton Robert , Fulton Lucinda , Gillette Michael A. , Satpathy Shankha , Carr Steven A. , Wistuba Ignacio , Pass Harvey , Wilson Richard K. , Ding Li , Govindan Ramaswamy 
Published: September 2021

PURPOSE Approximately 10%-40% of patients with lung cancer report no history of tobacco smoking (never-smokers). We analyzed whole-exome and RNA-sequencing data of 160 tumor and normal lung adenocarcinoma (LUAD) samples from never-smokers to identify clinically actionable alterations and gain insight into the environmental and hereditary risk factors for LUAD among never-smokers. METHODS We performed whole-exome and RNA-sequencing of 88 and 69 never-smoker LUADs. We analyzed these data in conjunction with data from 76 never-smoker and 299 smoker LUAD samples sequenced by The Cancer Genome Atlas and Clinical Proteomic Tumor Analysis Consortium. RESULTS We observed a high prevalence of clinically actionable driver alterations in never-smoker LUADs compared with smoker LUADs (78%-92% v 49.5%; P < .0001). Although a subset of never-smoker samples demonstrated germline alterations in DNA repair genes, the frequency of samples showing germline variants in cancer predisposing genes was comparable between smokers and never-smokers (6.4% v 6.9%; P = .82). A subset of never-smoker samples (5.9%) showed mutation signatures that were suggestive of passive exposure to cigarette smoke. Finally, analysis of RNA-sequencing data showed distinct immune transcriptional subtypes of never-smoker LUADs that varied in their expression of clinically relevant immune checkpoint molecules and immune cell composition. CONCLUSION In this comprehensive genomic and transcriptome analysis of never-smoker LUADs, we observed a potential role for germline variants in DNA repair genes and passive exposure to cigarette smoke in the pathogenesis of a subset of never-smoker LUADs. Our findings also show that clinically actionable driver alterations are highly prevalent in never-smoker LUADs, highlighting the need for obtaining biopsies with adequate cellularity for clinical genomic testing in these patients.
How to Design and Analyze Persistent Phosphors?
Authors: Ueda Jumpei 
Published: September 2021

Abstract
Persistent phosphors show contentious luminescence even after ceasing excitation light. This unique phenomenon is caused by several processes such as carrier generation, trapping and detrapping. Based on the mechanism, persistent luminescence can be designed by controlling the carrier transportation. By utilizing the vacuum referred binding energy diagram of lanthanoid and transition metal ions for the prediction of the trap levels in host compounds, new persistent phosphors have been developed successfully. This design guides for persistent phosphors are introduced, and the analyzing methods for persistent phosphors are also explained.
Assortative Matching or Exclusionary Hiring? The Impact of Employment and Pay Policies on Racial Wage Differences in Brazil
Authors: Gerard François , Lagos Lorenzo , Severnini Edson , Card David 
Published: September 2021

We measure the effects of firm policies on racial pay differences in Brazil. Non-Whites are less likely to be hired by high-wage firms, explaining about 20 percent of the racial wage gap for both genders. Firm-specific pay premiums for non-Whites are also compressed relative to Whites, contributing another 5 percent for that gap. A counterfactual analysis reveals that about two-thirds of the underrepresentation of non-Whites at higher-wage firms is explained by race-neutral skill-based sorting. Non-skill-based sorting and differential wage setting are largest for college-educated workers, suggesting that the allocative costs of discriminatory hiring and pay policies may be relatively large in Brazil. (JEL J15, J24, J31, J41, J46, J71, O15)