bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of zonal advective feedback in depicting the deficiency of ENSO’s diversity in CESM2
Authors: Pang Da , Fang Xianghui , Wang Lei 
Published: May 2024

Abstract

During the mature phases of two types of El Niño, the patterns of sea surface temperature anomalies (SSTA) are obviously different, with the centers near eastern Pacific (EP) for the EP El Niño and near the dateline (180° of longitude) for the central Pacific (CP) El Niño. However, contradicting with the observation, in the Community Earth System Model version 2 (CESM2), the SSTA centers of both types of El Niño are close to the CP area, which makes them difficult to be separated, i.e., the CESM2 shows a relatively poor depiction of the realistic El Niño diversity. To explore the possible reasons for this deficiency, a meticulous comparison of the dominant mechanisms for the equatorial Pacific SSTA evolution, i.e., the thermocline feedback (TH) and the zonal advective feedback (ZA), between the model and observation is conducted in this study. The results suggest that comparing with the observation, the weak intensity of TH and the westward shift of the dominant ZA position in the model are the primary causes that induce such proximity of SSTA centers of the two types of El Niño. The deeper distance between thermocline and sea surface, which induce smaller amplitude of thermocline depth variation, cause the deviation of the TH in CESM2. Furthermore, the deviation of the ZA comes from the pronounced westward bias in simulating the background zonal gradient of sea surface temperature, along with the weak zonal current anomalies in the EP area.
Heat Shock Transcription Factor HSF2b Plays a Critical Role in the Synthesis of Fucoxanthin by Modulating the Expression of ZEP1 in Phaeodactylum tricornutum
Authors: Li Yixuan , Fan Sizhe , Wang Qi , Liu Shixia , Zhang Xin , li xiaohui 
Published: May 2024

Abstract

Fucoxanthin is a pigment with important economic value, however, the transcriptional regulatory mechanism of its synthetic pathway is relatively poorly reported. In this study, we screened a heat-excited transcription factor, HSF2b, which is able to bind to the ZEP1 promoter, using a yeast one-hybrid screen library. Functional studies revealed that overexpression of HSF2b increased the content of fucoxanthin, while gene editing of HSF2b decreased the content of fucoxanthin. Further studies showed that HSF2b was able to further mediate the synthesis of fucoxanthin by regulating the expression of the fucoxanthin synthesis-related genes DXS, PSY1, ZDS, ZEP1, ZEP3 and CRTISO5. In addition, HSF2b was able to bind to the promoters of ZEP1, ZEP3 and CRTISO5 and activate their expression. The results of genetic studies showed that the regulation of fucoxanthin by HSF2b was dependent on ZEP1. Therefore, the present study systematically elucidated the transcriptional regulatory mechanism of fucoxanthin synthesis, which provides a new idea for understanding the mechanism of fucoxanthin synthesis.
Older Fallers and Non-fallers’ Neuromuscular and Kinematic Alterations in Reactive Balance Control: Indicators of Balance Decline or Compensation?
Authors: Zhu Ringo Tang-Long , Hung Timmi Tim Mei , Lam Freddy Man Hin , Li Jun-Zhe , Luo Yu-Yan , Sun Jingting , Wang Shujun , Ma Christina Zong-Hao 
Published: May 2024

Abstract

Background: Falls and fall consequences in older adults are global health issues. Previous studies have compared postural sways or stepping strategies between older adults with and without fall histories, to identify the associated factors of falls. However, more in-depth neuromuscular/kinematic mechanisms have remained unclear. This study therefore aimed to comprehensively investigate and compare the muscle activities and joint kinematics during reactive balance control in older adults with different fall histories.
Methods: This pilot observational study recruited six community-dwelling older fallers (≥1 fall in past one year) and six non-fallers, who received unexpected translational balance perturbations in randomized directions and intensities during natural standing. The whole-body center-of-mass (COM) displacements, eight dominant-leg joint motions and muscle electrical activities were collected, and analyzed using the temporal and amplitude parameters. Four-way ANOVA and post hoc analyses were conducted to examine the effects of fall history, perturbation direction, perturbation intensity, and postural sway/joint/muscle on each parameter.
Results: Post hoc analyses revealed that compared to older non-fallers, fallers had significantly: (a) smaller activation rate in ankle dorsiflexor, delayed activation in hip flexor/extensor, larger activation rate in knee flexor, and smaller agonist-antagonist co-contraction in lower-limb muscles; (b) larger knee/hip flexion angles, longer ankle dorsiflexion duration, and delayed timing of recovery in joint motions; and (c) earlier downward COM displacements and larger anteroposterior overshooting COM displacements following unexpected perturbations (p< 0.05).
Conclusion and Implication: Compared to older non-fallers, fallers tended to use more suspensory strategies to maintain reactive standing balance. Such strategies could enable older fallers to compensate for their inadequate initiation of ankle/hip strategies, but led to prolonged and overacted balance recovery among them. This study’s comprehensive neuromuscular/kinematic analyses and controlled balance perturbation preliminarily uncovered some specific declines and ineffective strategies in fall-prone older adults during reactive balance control, which can potentially enhance the instrumented assessments for early identification of fall-prone older adults and facilitate the targeted training to prevent their falls. Further longitudinal studies are still needed to examine diagnostic accuracies of these identified neuromuscular/kinematic factors in differentiating fall risks of older people.
A Nighttime Driving Detection Model with Adaptive Growth Characteristics
Authors: Ma Hang , Yang Genjian , Chen Wenbai , Hou Junzhuo 
Published: May 2024

Abstract

Nighttime driving scene detection currently trails its daytime counterpart, largely due to challenges such as reduced illumination, glare, and ambiguous datasets. This research introduces an innovative adaptive model crafted to amplify nighttime driving detection precision. The model integrates a specially conceived Confidence Iterative Generative Adversarial Network (CI-GAN) with Adaptive Fine-Tuning, ensuring persistent model enhancement. While safeguarding the foundational features of the initial model, our strategy optimally acclimatizes the model to multifarious nighttime nuances. In daylight conditions, CI-GAN deploys a confidence iterative learning tactic to aptly steer the generative network, subsequently boosting its generative velocity. In tandem, during nocturnal periods, it ceaselessly refines its discriminator, prompting CI-GAN to produce images that bear a closer resemblance to authentic nighttime vistas. Adaptive Fine-Tuning incorporates a differential optimization technique grounded in transfer learning. This obviates the traditionally tedious manual layer selection process, instead harnessing the algorithm's expansive search potential to pinpoint the most effective fine-tuning methodology. Empirical analyses affirm that our refined model progressively elevates nighttime detection capabilities, all while maintaining the original model's inference velocity and dimensions. This advancement diverges from conventional methods that preprocess nighttime imagery prior to detection. Instead, it equips the model to dynamically evolve within nighttime environments, offering fresh insights and techniques for enhancing nighttime driving detection.
Implementation of advanced analytical methods MeD-seq and LC-MS/MS for assessing the epigenetic profile of high-risk myelodysplastic syndrome
Authors: Nikolopoulos Theodoros , Bochalis Eleftherios , Chatzilygeroudi Theodora , Chondrou Vasiliki , Dereki Irene , Athanasopoulou Katerina , Zafeiropoulos John , Bourikas Kyriakos , Patrinos George , Symeonidis Argiris , Sgourou Argyro 
Published: May 2024

Abstract

Treatment decision and response assessment in myelodysplastic syndromes (MDS) can be enhanced by the implementation of advanced diagnostic and prognostic assays for the detection of multiple molecular features. Higher-risk (HR) MDS, ineligible for allogeneic hematopoietic stem cell transplantation (alloHSCT), require prompt therapeutic interventions such as treatment with hypomethylating agents (HMAs) to restore normal DNA methylation levels, mainly of oncosuppressor genes and consequently to delay disease progression and increase overall survival (OS). However, response assessment to HMA treatment relies on conventional methods with limited capacity to uncover a wide spectrum of molecular events. We studied bone marrow aspirates from twenty-one HR MDS patients pre- and post-HMA treatment and seven healthy controls. Genomic DNA was analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) for 5’ methyl-cytosine (5mC), 5’ hydroxy-methyl cytosine (5hmC) levels detection, and global adenosine/thymidine ([dA]/[T]) ratio, to correlate differences during treatment course and at baseline state prior drug therapy. Results from methylation DNA sequencing (MeD-seq) from the same HR MDS cohort were also analyzed to identify targeted differentially methylated regions (DMRs). LC/MS-MS analysis revealed a significant hypomethylation status in responders (Rs) already established at baseline and a trend for further DNA methylation reduction post-HMA treatment. Non-responders (NRs) reached statistical significance for DNA hypomethylation only post-HMA treatment. MeD-seq confirmed results globally for both Rs and NRs and more specifically, identified DMRs associated with HMA treatment. Additionally, within statistically significant selected chromosomal bins, genes encoding for proteins and non-coding RNAs were highlighted with reversed methylation profiles between Rs and NRs. Dynamic DNA methylation changes in HR MDS patients undergoing HMA therapy demonstrated that response to treatment is associated only with few specific hypomethylated DMRs rather than presenting a global effect across genome. The 5hmC epigenetic mark was only rarely detected in Rs and NRs, in contrast to healthy controls. Global [dA]/[T] ratio was lower in both R and NR subgroups compared to controls suggesting high frequences of baseline transitions from 5mC to thymidine. Conclusively, LC-MS/MS methodology provided broad-based but rapid and cost-effective results on the molecular HR MDS background, potentially translatable into responsive phenotypes to HMA treatment.
RNA-seq analysis reveals transcriptome changes associated with the progression of non-alcoholic liver disease in livers from Efcab4b knockout mice
Authors: Cheng Chew W. , Pedicini Lucia , Alcala Cintli Morales , Deligianni Fenia , Smith Jessica , Forde Niamh , McKeown Lynn 
Published: May 2024

Abstract

EFCAB4B is an evolutionarily conserved protein that encodes for the Rab GTPase Rab46, and the CRAC channel modulator, CRACR2A. Previous genome wide association studies have demonstrated the association of EFCAB4B variants in the progression of non-alcoholic liver disease (NAFLD). In this study we show that mice with global depletion of Efcab4b-/-have significantly larger livers than their wild-type (WT) counterparts. We performed RNA-sequencing (RNA-seq) analysis of liver tissues to investigate differential global gene expression among Efcab4b-/-and WT mice. Of the 69 differentially expressed genes (DEGs), analyses of biological processes found significant enrichment in liver and bile development, with 6 genes (Pck1, Aacs, Onecut1, E2f8, Xbp1, and Hes1) involved in both processes. Specific consideration of possible roles of DEGs or their products in NAFLD progression to (NASH) and hepatocarcinoma (HCC), demonstrated DEGs in the livers of Efcab4b-/-mice had roles in molecular pathways including lipid metabolism, inflammation, ER stress and fibrosis. The results in this study provide additional insights into molecular mechanisms responsible for increasing susceptibility of liver injuries associated with EFCAB4B.
Wait times for surgery of cutaneous malignancies following the COVID-19 Pandemic: A retrospective cohort analysis
Authors: Cleland Jane B. , Greenzaid Jonathan D. , Doerfler Laura , Ahn Christine S. 
Published: May 2024

Abstract

There was an increase in undiagnosed skin cancers during the COVID-19 pandemic, resulting in a significant backlog of untreated cases. However, it is unclear how this affected the long-term surgical management of tumors after the recovery from the pandemic. We aimed to determine the impact of the COVID-19 pandemic on the long-term management of cutaneous tumors. We completed a retrospective cohort study of patients diagnosed with cutaneous tumors from June 1, 2018 to August 31, 2018 (pre-COVID cohort) and June 1, 2022 to August 31, 2022 (post-COVID cohort) at Atrium Wake Forest Baptist Medical Center (AWFBMC). For these two cohorts, we compared the number of tumors diagnosed, severity of tumors, tumor duration prior to diagnosis, and time from diagnosis to treatment.
More tumors were diagnosed in the post-COVID cohort compared to the pre-COVID cohort (1045 vs. 850, respectively). There was a larger proportion of patients diagnosed within 6 months of tumor presentation in the pre-COVID cohort compared to the post-COVID cohort (56% vs. 46%, p=0.0005). There was a shorter time from diagnosis to treatment in the post-COVID cohort compared to the pre- COVID cohort (41.7 vs. 48.5 days, p=0.0015). There is still an increased caseload of cutaneous tumors at an academic, tertiary-care medical center in the U.S. However, treatment times have improved, possibly indicating increased productivity of the healthcare system.
Characterization of brain transduction capability of a BBB-penetrant, peptide-displaying AAV vector in mice, rats and non-human primates
Authors: Hernandez-Alcoceba Ruben , Bunuales Maria , Garduno Angeles , Chillon Miguel , Bosch Assumpció , Gonzalez-Aparicio Manuela , Espelosin Maria , Garcia-Gomara Marta , Rico Alberto , Garcia-Osta Ana , Cuadrado-Tejedor Mar , Lanciego Jose Luis 
Published: May 2024

Abstract

Different screening methods are being developed to generate adeno-associated viral vectors (AAV) with the ability to bypass the blood-brain barrier (BBB) upon intravenous administration. Recently, the AAV9P31 stood out as the most efficient version among a library of peptide-displaying capsids selected in C57BL/6 mice using RNA-driven biopanning. In this work we have characterized in detail its biodistribution in different mouse strains (C57BL/6 and Balb/c), as well as in Sprague Dawley rats and non-human primates (Macaca fascicularis). Using GFP and NanoLuc reporter genes, we confirmed homogeneous infection and transgene expression across the CNS of mice injected intravenously with AAV9P31. A more restricted pattern was observed upon either intracerebroventricular or intraparenchymal injection. Following intravenous delivery, region- and cell-specific differential patterns of transduction were observed in the mouse brain, including a preferential transduction of astrocytes and neurons in the cerebral cortex and striatum, whereas neurons were the only transduced cell type in subcortical locations across the hippocampus, thalamus, hypothalamus, mesencephalon, brainstem and cerebellum. Furthermore, transduced microglial cells were never found in any CNS location. Peripheral organs transduced upon intravenous administration included lung, liver, peritoneum, heart and skeletal muscle. However, a comparable performance of AAV9P31 to bypass the BBB in rats and macaques was not observed, although a more limited neuronal transduction was found in the brainstem of rats upon intravenous delivery. Finally, intracerebroventricular delivery in macaques resulted in neuronal transduction in cortical, subcortical structures and cerebellum following a patchy pattern. In conclusion, the widespread CNS transduction obtained in mice upon intravenous delivery of AAV9P31 represents a powerful tool for modeling a wide variety of neurological disorders as well as an appealing choice for the evaluation of gene therapy-based therapeutics.
Power and positionality in the practice of health system responsiveness at sub-national level: insights from the Kenyan Coast
Authors: Kagwanja Nancy , Molyneux Sassy , Whyle Eleanor , Tsofa Benjamin , Leli Hassan , Gilson Lucy 
Published: May 2024

Abstract

Background Health system responsiveness to public priorities and needs is a broad, multi-faceted and complex health system goal thought to be important in promoting inclusivity and reducing system inequity in participation. Power dynamics underlie the complexity of responsiveness but are rarely considered. This paper presents an analysis of various manifestations of power within the responsiveness practices of Health Facility Committees (HFCs) and Sub-county Health Management Teams (SCHMTs) operating at the subnational level in Kenya. Kenyan policy documents identify responsiveness as an important policy goal. Methods Our analysis draws on qualitative data (35 interviews with health managers and local politicians, four focus group discussions with HFC members, observations of SCHMT meetings, and document review) from a study conducted at the Kenyan Coast. We applied a combination of two power frameworks to interpret our findings: Gaventa’s power cube and Long’s actor interface analysis. Results We observed a weakly responsive health system in which system-wide responsiveness and equity were frequently undermined by varied forms and practices of power. The public were commonly dominated in their interactions with other health system actors: invisible and hidden power interacted to limit their sharing of feedback; while the visible power of organisational hierarchy constrained HFCs’ and SCHMTs’ capacity both to support public feedback mechanisms and to respond to concerns raised. These power practices were underpinned by positional power relationships, personal characteristics, and world views. Nonetheless, HFCs, SCHMTs and the public creatively exercised some power to influence responsiveness, for example through collaborations with political actors. However, most resulting responses were unsustainable, and sometimes undermined equity as politicians sought unfair advantage for their constituents. Conclusion Our findings illuminate the structures and mechanisms that contribute to weak health system responsiveness even in contexts where it is prioritised in policy documents. Supporting inclusion and participation of the public in feedback mechanisms can strengthen receipt of public feedback; however, measures to enhance public agency to participate are also needed. In addition, an organisational environment and culture that empowers health managers to respond to public inputs is required.
Pink1/Parkin deficiency alters circulating lymphocyte populations and increases platelet-T cell aggregates in rats
Authors: Manganaro Jane E. , Emanuel Katy , Lamberty Benjamin G. , George Joseph W. , Stauch Kelly L. 
Published: May 2024

Abstract

Parkinson’s disease (PD) is the most common progressive neurodegenerative movement disorder and results from the selective loss of dopaminergic neurons in the substantia nigra pars compacta. Pink1 and Parkin are proteins that function together in mitochondrial quality control, and when they carry loss-of-function mutations lead to familial forms of PD. While much research has focused on central nervous system alterations in PD, peripheral contributions to PD pathogenesis are increasingly appreciated. We report Pink1/Parkin regulate glycolytic and mitochondrial oxidative metabolism in peripheral blood mononuclear cells (PBMCs) from rats. Pink1/Parkin deficiency induces changes in the circulating lymphocyte populations, namely increased CD4 + T cells and decreased CD8 + T cells and B cells. Loss of Pink1/Parkin leads to elevated platelet counts in the blood and increased platelet-T cell aggregation. Platelet-lymphocyte aggregates are associated with increased thrombosis risk, and venous thrombosis is a cause of sudden death in PD, suggesting targeting the Pink1/Parkin pathway in the periphery has therapeutic potential.
Feasibility of all single-qubit gates with four InGaAs Quantum Dots coupled to two silver nanowires
Authors: Kim Chol-Min , Kim Nam-Chol , Ko Myong-Chol , Ryom Ju-Song , Ri Su-Ryon 
Published: May 2024

Abstract

We have proposed all single-qubit logic gates with four InGaAs quantum dots (QDs) coupled to a T-type plasmonic waveguides (PWs) wherein binary qubits are encoded by frequency of photons. Our results reveal that by adjusting distance between QDs, coupling strength and frequency detuning in a proper manner, an arbitrary single-qubit gates can be achieved. We investigated schemes theoretically via the real-space approach and estimated feasibilities of a proposed one by fidelities for a variety of parameters. Under the present technology and high fidelities, our proposed schemes are feasible, opening the promising perspectives for constructing quantum computation and quantum information processing.
Quantification and Clustering of Immune States in Lymphocyte Populations of Hepatitis B Cirrhosis
Authors: Hou Wei , Xing Fangliang , Hu Zhongjie 
Published: May 2024

Abstract

Background: In Hepatitis B Cirrhosis, a severe progression of chronic Hepatitis B infection, understanding the interplay among lymphocyte populations like T cells, NK cells, and B cells is crucial. This insight aids in assessing immune status, diagnosing the condition, and optimizing treatment strategies, offering significant potential benefits.
Methods: Peripheral blood samples were collected from 200 patients diagnosed with Hepatitis B Cirrhosis. Correlation analysis and three-dimensional numerical fitting were performed to establish a mathematical model describing the relationships among lymphocyte subsets. Self-Organizing Feature Maps (SOFM) were employed for unsupervised clustering to identify distinct immune states.
Results: Analysis revealed that the percentages of T cells, NK cells, and B cells are constrained within a three-dimensional plane, as described by the equation: T percentage = -0.9879 ×B percentage - 1.041 ×NK percentage + 97.66, yielding a prediction error (RMSE) of 2.5%. Additionally, another equation was identified: Lymphocytes = 1.2 × T cells + 1.072 × B cells + 18.59, with an RMSE of 3.7%. SOFM clustering further identified four distinct immune states associated with the progression of the disease.
Conclusions: This study provides a quantitative mathematical model describing the states of lymphocyte populations in Hepatitis B Cirrhosis. The identification of distinct immune states associated with disease progression facilitate the assessment of immunological condition and the optimization of treatment strategies.