bluuebunny/crossref_metadata_2025_split huggingface dataset:
Vitamin D insufficiency is associated with inflammation and deregulation of adipokines in patients with metabolic syndrome
Authors: Khademi Zeinab , Hamedi-Shahraki Soudabeh , Amirkhizi Farshad 
Published: September 2022

Abstract
Background
Previous studies have been reported that vitamin D deficiency increased the risk of metabolic syndrome (MetS). Nonetheless, the exact mechanisms underlying this association is unclear. Besides, inflammation and deregulation of adipokines secretion have been recognized as pivotal factors that contribute to the pathogenesis of these conditions. Therefore, we assessed whether serum vitamin D status is associated with serum levels of adipokines and inflammatory markers in these patients.

Methods
This case-control study was carried out among 65 patients with MetS who had vitamin D insufficiency (cases) and 130 MetS patients who had vitamin D sufficiency (controls). Cases and controls were recruited from among those referred to health centers in Zabol County, Iran. Vitamin D insufficiency was regarded as a serum 25-hydroxyvitamin D [25(OH)D] concentration below 30 ng/ml. Serum concentrations of leptin, adiponectin, visfatin, and resistin and also adiponectin/leptin ratio along with serum levels of interleukin 6 (IL-6), IL-10 and tumor necrosis factor-alpha (TNF-α), were evaluated.

Results
Serum levels of leptin, resistin, and TNF-α were significantly higher, whereas, serum adiponectin and adiponectin/leptin ratio were significantly lower in cases than the controls. There was no significant difference in serum visfatin, IL-6, and IL-10 between the groups. Serum levels of 25(OH)D were inversely correlated with leptin, resistin, and TNF-α in both unadjusted models and after adjustment for potential confounders.

Conclusion
Our findings indicated that vitamin D insufficiency in MetS patients is associated with increased inflammation and serum adipokine abnormalities which may be associated with developing metabolic complications in these patients.
Next-generation sequencing-assisted diagnosis of a case of leprosy misdiagnosed as erythema multiforme
Authors: Zhang Yanfang , Lei Xuezhong , Lu Jiajie 
Published: September 2022

Abstract
Background
Leprosy is a chronic infectious disease caused by Mycobacterium leprae or Mycobacterium lepromatosis that is mainly transmitted through droplets from the nose and mouth of untreated patients. Owing to the lack of specific serological markers and clinical manifestations, leprosy can be easily confused with other skin lesion-related diseases and is difficult to distinguish.

Case presentation
This study introduces and summarises the diagnosis and treatment process of a case of leprosy misdiagnosed as erythema multiforme for a long time. A 43-year-old female was admitted to our hospital because of “repeated fever with superficial lymphadenopathy and systemic rash in May”. The diagnosis of the patient was based on the two main clinical characteristics of superficial lymphadenopathy and systemic pleomorphic erythema by using a combination of multiple samples of lymph nodes and skin, routine pathological examination, immunohistochemistry, acid-fast, silver hexamine, periodic acid-Schiff (PAS) staining, and second-generation gene sequencing of fresh biopsy tissue. The patient was treated with dapsone, rifampicin, and clofazimine at the Institute of Dermatology and Venereal Diseases. After treatment for 1 year, her temperature returned to normal, the area of facial erythema decreased, and the volume of axillary lymph nodes had gradually reduced.

Conclusions
In conclusion, special pathological staining and second-generation gene sequencing show promising advantages in distinguishing leprosy from other skin lesion-related diseases.
Abnormal molecular signatures of inflammation, energy metabolism, and vesicle biology in human Huntington disease peripheral tissues
Authors: Neueder Andreas , Kojer Kerstin , Hering Tanja , Lavery Daniel J. , Chen Jian , Birth Nathalie , Hallitsch Jaqueline , Trautmann Sonja , Parker Jennifer , Flower Michael , Sethi Huma , Haider Salman , Lee Jong-Min , Tabrizi Sarah J. , Orth Michael 
Published: September 2022

Abstract
Background
A major challenge in neurodegenerative diseases concerns identifying biological disease signatures that track with disease progression or respond to an intervention. Several clinical trials in Huntington disease (HD), an inherited, progressive neurodegenerative disease, are currently ongoing. Therefore, we examine whether peripheral tissues can serve as a source of readily accessible biological signatures at the RNA and protein level in HD patients.

Results
We generate large, high-quality human datasets from skeletal muscle, skin and adipose tissue to probe molecular changes in human premanifest and early manifest HD patients—those most likely involved in clinical trials. The analysis of the transcriptomics and proteomics data shows robust, stage-dependent dysregulation. Gene ontology analysis confirms the involvement of inflammation and energy metabolism in peripheral HD pathogenesis. Furthermore, we observe changes in the homeostasis of extracellular vesicles, where we find consistent changes of genes and proteins involved in this process. In-depth single nucleotide polymorphism data across the HTT gene are derived from the generated primary cell lines.

Conclusions
Our ‘omics data document the involvement of inflammation, energy metabolism, and extracellular vesicle homeostasis. This demonstrates the potential to identify biological signatures from peripheral tissues in HD suitable as biomarkers in clinical trials. The generated data, complemented by the primary cell lines established from peripheral tissues, and a large panel of iPSC lines that can serve as human models of HD are a valuable and unique resource to advance the current understanding of molecular mechanisms driving HD pathogenesis.
Genomic insights into the evolutionary history and diversification of bulb traits in garlic
Authors: Li Ningyang , Zhang Xueyu , Sun Xiudong , Zhu Siyuan , Cheng Yi , Liu Meng , Gao Song , Zhang Jiangjiang , Wang Yanzhou , Yang Xiai , Chen Jianrong , Li Fu , He Qiaoyun , Zeng Zheng , Yuan Xiaoge , Zhou Zhiman , Ma Longchuan , Wang Taotao , Li Xiang , Liu Hanqiang , Pan Yupeng , Zhou Mengyan , Gao Chunsheng , Zhou Gang , Han Zhenlin , Liu Shiqi , Su Jianguang , Cheng Zhihui , Tian Shilin , Liu Touming 
Published: September 2022

Abstract
Background
Garlic is an entirely sterile crop with important value as a vegetable, condiment, and medicine. However, the evolutionary history of garlic remains largely unknown.

Results
Here we report a comprehensive map of garlic genomic variation, consisting of amazingly 129.4 million variations. Evolutionary analysis indicates that the garlic population diverged at least 100,000 years ago, and the two groups cultivated in China were domesticated from two independent routes. Consequently, 15.0 and 17.5% of genes underwent an expression change in two cultivated groups, causing a reshaping of their transcriptomic architecture. Furthermore, we find independent domestication leads to few overlaps of deleterious substitutions in these two groups due to separate accumulation and selection-based removal. By analysis of selective sweeps, genome-wide trait associations and associated transcriptomic analysis, we uncover differential selections for the bulb traits in these two garlic groups during their domestication.

Conclusions
This study provides valuable resources for garlic genomics-based breeding, and comprehensive insights into the evolutionary history of this clonal-propagated crop.
AQP4-dependent glioma cell features affect the phenotype of surrounding cells via extracellular vesicles
Authors: Simone Laura , Pisani Francesco , Binda Elena , Frigeri Antonio , Vescovi Angelo L. , Svelto Maria , Nicchia Grazia P. 
Published: September 2022

AbstractBackgroundExtracellular vesicles (EVs) are membrane-enclosed particles released systemically by all cells, including tumours. Tumour EVs have been shown to manipulate their local environments as well as distal targets to sustain the tumour in a variety of tumours, including glioblastoma (GBM).We have previously demonstrated the dual role of the glial water channel aquaporin-4 (AQP4) protein in glioma progression or suppression depending on its aggregation state. However, its possible role in communication mechanisms in the microenvironment of malignant gliomas remains to be unveiled.ResultsHere we show that in GBM cells AQP4 is released via EVs that are able to affect the GBM microenvironment. To explore this role, EVs derived from invasive GBM cells expressing AQP4-tetramers or apoptotic GBM cells expressing orthogonal arrays of particles (AQP4-OAPs) were isolated, using a differential ultracentrifugation method, and were added to pre-seeded GBM cells. Confocal microscopy analysis was used to visualize the interaction and uptake of AQP4-containing EVs by recipient cells. Chemoinvasion and Caspase3/7 activation assay, performed on recipient cells after EVs uptake, revealed that EVs produced by AQP4-tetramers expressing cells were able to drive surrounding tumour cells toward the migratory phenotype, whereas EVs produced by AQP4-OAPs expressing cells drive them toward the apoptosis pathway.ConclusionThis study demonstrates that the different GBM cell phenotypes can be transferred by AQP4-containing EVs able to influence tumour cell fate toward invasiveness or apoptosis.This study opens a new perspective on the role of AQP4 in the brain tumour microenvironment associated with the EV-dependent communication mechanism.Graphical Abstract
Increasing the intensity of regeneration treatments decreased beta diversity of temperate hardwood forest understory 20 years after disturbance
Authors: Jaeger Romain , Delagrange Sylvain , Aubin Isabelle , Joanisse Gilles , Raymond Patricia , Rivest David 
Published: September 2022

Abstract
Context
In temperate hardwood forests, increased intensity of soil and canopy disturbances tends to increase species richness due to the establishment of numerous early-successional plant species. However, while competitive pioneer species from early stages of succession can become recalcitrant and alter patterns of natural regeneration, very few studies have examined longer-term effects of these treatments on plant biodiversity.

Aims
In this study, we investigated mid-term (ca. 20 years) effects of different regeneration treatments with varying soil and canopy disturbance intensities. We compared understory plant communities in temperate hardwood forests from all the South of Quebec (Canada).

Methods
Using circular experimental plots of 1962.5 m2 (radius = 25 m), we measured taxonomic and functional diversity indices and soil properties using four levels of disturbance intensity in six temperate hardwood forests of Quebec distributed along a longitudinal gradient. Reference forests, i.e. control forests with no silvicultural treatment known for ≥ 80 years, were compared to 20-year-old single-tree selection cuts, group-selection cuts and group-selection cuts with soil scarification.

Results
Species richness in both group-selection treatments was higher than that in reference forests. Plant equitability and beta diversity among sites in both group-selection treatments were lower than in single-tree selection cuts and control forests. More intense treatments contributed to the mid-term persistence of recalcitrant competitor species (e.g. Rubus idaeus L., Prunus pensylvanica L.f.) whereas soil scarification appears to have negative sustained effects on species known to be sensitive to regeneration treatments (e.g. Monotropa uniflora L., Dryopteris spinulosa Kuhn).

Conclusions
In temperate hardwood forests of Southern Quebec, silvicultural treatments of higher intensities resulted in detrimental effects on soil properties, especially in the surface horizon, 20 years after disturbance. This legacy, in turn, affected the composition and diversity of understory plant communities. The more intense silvicultural treatments contributed to the persistence of pioneer species better adapted to a wider range of environmental conditions and resulted in a decrease in understory plant community heterogeneity among sites. Conversely, single-tree selection cutting appeared to be the most appropriate silvicultural treatment for maintaining soil functions and heterogeneity of understory plant communities after 20 years; composition and structure being similar to long-undisturbed forests.
The putative mechanistic insights on how SARS-CoV-2 might influence the outcomes in cancer patients
Authors: Deng Jingwen , Cai Xiaopeng , Chen Zhi 
Published: September 2022

AbstractEarly evidence indicated that cancer patients are at increased risk of adverse outcomes and mortality after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. To determine the putative mechanism by which SARS-CoV-2 affects patients with cancers, we conducted a preliminary exploration at the molecular level. We collected differentially expressed proteins (DEPs) in the lung, liver, kidney, and thyroid of postmortem coronavirus disease 2019 (COVID-19) and non-COVID-19 patients from iProX database. Furthermore, we collected differentially expressed genes (DEGs) related to overall survival (OS) in lung cancer, liver cancer, kidney cancer and thyroid cancer based on the Cancer Genome Atlas (TCGA) database. We obtained the intersection of DEPs and DEGs and identified the roles of shared and remaining DEPs in corresponding cancers based on published research. Finally, we found 192, 179, 154 and 147 DEPs in lung, liver, kidney and thyroid tissues and 486, 1140, 2245 and 31 DEGs related to OS in lung cancer, liver cancer, kidney cancer and thyroid cancer, respectively. 4, 8, 6 and 0 shared genes/proteins and 48, 42, 14 and 10 remaining proteins were verified to play a role in lung cancer, liver cancer, kidney cancer and thyroid cancer, respectively. Changes in 85% (44/52), 78% (39/50), 80% (16/20) and 90% (9/10) of the verified genes/proteins, including shared and remaining genes, showed poor effects on patients with the 4 cancer types with COVID-19. In conclusion, the changes in genes/proteins caused by SARS-CoV-2 might dictate the different degrees of adverse outcomes in patients with different tumors.
Tsunami deposits associated with the 1983 Nihonkai-Chubu earthquake tsunami in coastal forests near Happo Town, Akita Prefecture, Japan
Authors: Chiba Takashi , Nishimura Yuichi 
Published: September 2022

AbstractOn 26 May 1983 the Nihonkai-Chubu earthquake occurred off the western coast of Noshiro City, Akita Prefecture, Japan. The tsunami associated with this earthquake caused widespread damage to the northeastern coastal region of the Sea of Japan, including Akita Prefecture, and left behind sand and mud deposits. These deposits were first described in the 1990s, but have not been studied further. During December 2019 and January 2020, we conducted geological surveys to investigate post-1948 soil thinning in the pine-based coastal protective forests planted near Happo Town. A sand layer that thinned inland was observed in the soil at depths greater than 10 cm. Because the sand layer contained well-preserved fossil brackish–marine diatoms and exhibited a high bulk density, it is likely that the sand was transported inland from the coast. The sand layer was distributed from the coast to 150–270 m inland, but only within the coastal protective forest. By reference to historical records, we concluded that this sand layer was deposited by the 1983 tsunami, because this region could not have been reached by any event other than the tsunami produced by the Nihonkai-Chubu earthquake. We also observed another sand layer above the tsunami deposits, which may have been formed by Typhoon 9119 on 28 September 1991.
Graphical Abstract
Safety, Immunogenicity, and 1-Year Efficacy of Universal Cancer Peptide–Based Vaccine in Patients With Refractory Advanced Non–Small-Cell Lung Cancer: A Phase Ib/Phase IIa De-Escalation Study
Authors: Adotévi Olivier , Vernerey Dewi , Jacoulet Pascale , Meurisse Aurélia , Laheurte Caroline , Almotlak Hamadi , Jacquin Marion , Kaulek Vincent , Boullerot Laura , Malfroy Marine , Orillard Emeline , Eberst Guillaume , Lagrange Aurélie , Favier Laure , Gainet-Brun Marie , Doucet Ludovic , Teixeira Luis , Ghrieb Zineb , Clairet Anne-Laure , Guillaume Yves , Kroemer Marie , Hocquet Didier , Moltenis Mélanie , Limat Samuel , Quoix Elisabeth , Mascaux Céline , Debieuvre Didier , Fagnoni-Legat Christine , Borg Christophe , Westeel Virginie 
Published: September 2022

PURPOSE Universal cancer peptide–based vaccine (UCPVax) is a therapeutic vaccine composed of two highly selected helper peptides to induce CD4+ T helper-1 response directed against telomerase. This phase Ib/IIa trial was designed to test the safety, immunogenicity, and efficacy of a three-dose schedule in patients with metastatic non–small-cell lung cancer (NSCLC). PATIENTS AND METHODS Patients with refractory NSCLC were assigned to receive three vaccination doses of UCPVax (0.25 mg, 0.5 mg, and 1 mg) using a Bayesian-based phase Ib followed by phase IIa de-escalating design. The primary end points were dose-limiting toxicity and immune response after three first doses of vaccine. Secondary end points were overall survival (OS) and progression-free survival at 1 year. RESULTS A total of 59 patients received UCPVax; 95% had three prior lines of systemic therapy. No dose-limiting toxicity was observed in 15 patients treated in phase Ib. The maximum tolerated dose was 1 mg. Fifty-one patients were eligible for phase IIa. The third and sixth dose of UCPVax induced specific CD4+ T helper 1 response in 56% and 87.2% of patients, respectively, with no difference between three dose levels. Twenty-one (39%) patients achieved disease control (stable disease, n = 20; complete response, n = 1). The 1-year OS was 34.1% (95% CI, 23.1 to 50.4), and the median OS was 9.7 months, with no significant difference between dose levels. The 1-year progression-free survival and the median OS were 17.2% (95% CI, 7.8 to 38.3) and 11.6 months (95% CI, 9.7 to 16.7) in immune responders ( P = .015) and 4.5% (95% CI, 0.7 to 30.8) and 5.6 months (95% CI, 2.5 to 10) in nonresponders ( P = .005), respectively. CONCLUSION UCPVax was highly immunogenic and safe and provide interesting 1-year OS rate in heavily pretreated advanced NSCLC.
Quantitative proteomic analysis of SARS-CoV-2 infection of primary human airway ciliated cells and lung epithelial cells demonstrates the effectiveness of SARS-CoV-2 innate immune evasion
Authors: Crozier Thomas W.M. , Greenwood Edward J.D. , Williamson James C. , Guo Wenrui , Porter Linsey M. , Gabaev Ildar , Teixeira-Silva Ana , Grice Guinevere L. , Wickenhagen Arthur , Stanton Richard J. , Wang Eddie C. Y. , Wilson Sam J. , Matheson Nicholas J. , Nathan James A. , McCaughan Frank , Lehner Paul J. 
Published: September 2022

Background: Quantitative proteomics is able to provide a comprehensive, unbiased description of changes to cells caused by viral infection, but interpretation may be complicated by differential changes in infected and uninfected ‘bystander’ cells, or the use of non-physiological cellular models. Methods: In this paper, we use fluorescence-activated cell sorting (FACS) and quantitative proteomics to analyse cell-autonomous changes caused by authentic SARS-CoV-2 infection of respiratory epithelial cells, the main target of viral infection in vivo. First, we determine the relative abundance of proteins in primary human airway epithelial cells differentiated at the air-liquid interface (basal, secretory and ciliated cells). Next, we specifically characterise changes caused by SARS-CoV-2 infection of ciliated cells. Finally, we compare temporal proteomic changes in infected and uninfected ‘bystander’ Calu-3 lung epithelial cells and compare infection with B.29 and B.1.1.7 (Alpha) variants. Results: Amongst 5,709 quantified proteins in primary human airway ciliated cells, the abundance of 226 changed significantly in the presence of SARS-CoV-2 infection (q <0.05 and >1.5-fold). Notably, viral replication proceeded without inducing a type-I interferon response. Amongst 6,996 quantified proteins in Calu-3 cells, the abundance of 645 proteins changed significantly in the presence of SARS-CoV-2 infection (q < 0.05 and > 1.5-fold). In contrast to the primary cell model, a clear type I interferon (IFN) response was observed. Nonetheless, induction of IFN-inducible proteins was markedly attenuated in infected cells, compared with uninfected ‘bystander’ cells. Infection with B.29 and B.1.1.7 (Alpha) variants gave similar results. Conclusions: Taken together, our data provide a detailed proteomic map of changes in SARS-CoV-2-infected respiratory epithelial cells in two widely used, physiologically relevant models of infection. As well as identifying dysregulated cellular proteins and processes, the effectiveness of strategies employed by SARS-CoV-2 to avoid the type I IFN response is illustrated in both models.
Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis, A Review of Pathogenesis, Clinical Features, Diagnosis and Treatment
Authors: Rozenbajgier Martyna , Wójcik-Grudzień Justyna , Pawłowska Paulina , Ozga-Stachurska Alicja 
Published: September 2022

Stevens Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare, acute conditions, potentially life-threatening, immune-mediated and often unpredictable.
Characteristic for SJS and TEN is acute necrosis of the epidermis and mucous membranes, caused by the extensive death of keratinocytes. These syndromes are considered hypersensitivity reactions. They are most often caused by drugs. There have also been reports of SJS / TEN being caused by infection,
SJS/TEN disease is very rare and due to its rarity there is no specific pharmaceutical algorythm. Supportive care and treatment of symptoms are very important. The most crucial part of non-pharmacologic treatment of SJS/TEN is the detection and cessation of the pharmaceutical that caused the disease.
The aim of this literature review was to summarize current knowledge about the pathogenesis, clinical features, diagnosis and treatment of Stevens- Johnson Syndrom and Toxic Epidermal Necrolysis.
Standard criteria were used to review the literature data. The search of articles in the PubMed and Google Scholar database was carried out using the following keywords: Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, cutaneous adverse drug reactions