bluuebunny/crossref_metadata_2025_split huggingface dataset:
Aspergillus Endophthalmitis Secondary to Infectious Scleritis: Utility of Diagnostic PCR
Authors: Elwood Kevin F. , Warner Evan J. , Chang Jonathan S. , Kopplin Laura J. 
Published: July 2024

Purpose:
To describe a case of delayed-onset Aspergillus fumigatus endophthalmitis secondary to infectious fungal scleritis diagnosed with broad range polymerase chain reaction (PCR) from scleral nodular debridement and vitreous sampling during vitrectomy.

Methods:
Retrospective case report with slit lamp photography, optical coherence tomography, and fundus photography.

Results:
A 76-year-old man presented with right eye worsening vision and pain concerning for progressive nodular scleritis and endophthalmitis eight months following a reportedly innocuous tree branch injury. Following the injury, he underwent an MRI, surgical exploration, subconjunctival antibiotic administration, and culturing due to persistent foreign body sensation. Cultures were negative, and the patient was started on oral NSAIDs, oral prednisone, and periocular triamcinolone injections following negative/normal infectious and rheumatologic workup for scleritis. The patient was referred for worsened scleritis with development of endophthalmitis. He underwent lamellar sclerectomy, debridement, and culture of purulent material from scleral nodules in coordination with diagnostic vitrectomy, vitreous sampling, and subconjunctival and intravitreal antibiotic and antifungal treatment. Broad range PCR was positive for Aspergillus fumigatus and targeted antifungal treatment initiated. The eye did not regain visual function and was enucleated for progressive pain six months following diagnosis.

Conclusion:
Fungal scleritis and endophthalmitis results in significant morbidity. Diagnostic vitrectomy and broad range PCR can aid in prompt diagnosis and targeted treatment, and may be useful in refractory cases.
Orbital Oncocytic Carcinoma: A Comprehensive Case Series and Literature Review
Authors: Li Jing , Yang Runzi , Liu Rui , Wang Nan , Zhang Hong , Guo Qihan , Ma Jianmin 
Published: July 2024

Purpose:
This case series and literature review evaluated the baseline variables, clinical symptoms, pathological characteristics, and prognosis of patients with orbital oncocytic carcinoma.

Methods:
This retrospective case series collected the medical histories and other related data from 13 patients pathologically diagnosed with oncocytic carcinoma.

Results:
The average age of patients with orbital oncocytic carcinoma was 64.8 years, with a significantly higher rate of males than females. Furthermore, unilateral disease was more common than bilateral disease. All patients had surrounding tissue invasion, most commonly to extraocular muscles (69.2%) and bones (53.8%). The clinical manifestations were proptosis (30.8%), swelling of the lesion area (23.1%), vision loss (23.1%), diplopia (23.1%), periocular mass (23.1%), tears (15.4%), eye pain (7.7%), ptosis (7.7%), and visual field loss (7.7%). Microscopic examination revealed many large eosinophilic cells. There were obvious nuclei and abundant mitotic figures. The cancer cells expressed cytokeratin, but not P63 or S-100. The follow-up duration was 2–53 months, and the metastasis rate was 16.7%. The patients exhibited a good prognosis. The main treatment methods included surgical resection, surgery combined with radiotherapy, and the enucleation of ocular contents.

Conclusions:
Orbital oncocytic carcinoma has the immunohistochemical characteristics of eosinophilic tumor cells, with expression of cytokeratin but not P63 or S-100. The prognosis is favorable. Surgical resection, surgery combined with radiotherapy, and enucleation of intraocular material are effective treatment options. Nevertheless, long-term follow-up and close observation for metastases are required.
Sst- and Vip-Cre mouse lines without age-related hearing loss
Authors: Foss Calvin T. , Olsen Timothy , Bigelow James , Hasenstaub Andrea R. 
Published: July 2024

AbstractGABAergic interneurons, including somatostatin (SST) and vasoactive intestinal peptide (VIP) positive cells, play a crucial role in cortical circuit processing. Cre recombinase-mediated manipulation of these interneurons is facilitated by commercially available knock-in mouse strains such as Sst-IRES-Cre (Sst-Cre) and Vip-IRES-Cre (Vip-Cre). However, these strains are troublesome for hearing research because they are only available on the C57BL/6 genetic background, which suffer from early onset age-related hearing loss (AHL) due to a mutation of the Cdh23 gene. To overcome this limitation, we backcrossed Sst-Cre and Vip-Cre mice to CBA mice to create normal-hearing offspring with the desired Cre transgenes. We confirmed that in these “CBA Cre” lines, Cre drives appropriate expression of Cre-dependent genes, by crossing CBA Cre mice to Ai14 reporter mice. To assess the hearing capabilities of the CBA Cre mice, we measured auditory brainstem responses (ABRs) using clicks and tones. CBA Cre mice showed significantly lower ABR thresholds compared to C57 control mice at 3, 6, 9, and 12 months. In conclusion, our study successfully generated Sst-Cre and Vip-Cre mouse lines on the CBA background that will be valuable tools for investigating the roles of SST and VIP positive interneurons without the confounding effects of age-related hearing loss.
Claudin-11 regulates immunological barrier formation and spermatogonial proliferation through stem cell factor
Authors: Sugawara Taichi , Sonoda Kayoko , Chompusri Nattapran , Noguchi Kazuhiro , Okada Seiji , Furuse Mikio , Wakayama Tomohiko 
Published: July 2024

AbstractTight junctions (TJs) between adjacent Sertoli cells are believed to form immunological barriers that protect spermatogenic cells expressing autoantigens from autoimmune responses. However, there is no direct evidence that Sertoli cell TJs (SCTJs) do indeed form immunological barriers. Here, we analyzed male mice lacking claudin-11 (Cldn11), which encodes a SCTJ component, and found autoantibodies against antigens of spermatocytes/spermatids in their sera. Defective spermatogenesis was not restored inCldn11-deficient mice on a genetic background mimicking a severely impaired adaptive immune system. This suggests that defective spermatogenesis is not caused by autoimmune responses against spermatogenic cells. Further analyses showed thatCldn11knockout impaired Sertoli cell polarization, localization of stem cell factor (SCF) (a key molecule for maintaining differentiating spermatogonia) to the basal compartment of seminiferous tubules, and also proliferation of differentiating spermatogonia. We propose that CLDN11 creates a microenvironment for SCF-mediated spermatogonial proliferation at the basal compartment via Sertoli cell polarization.
Systematic Targeting of Protein Complexes with Molecular COUPLrs
Authors: Yang Diane , Harry Stefan Andrew , Chong Harrison Byron , Zhang Edwin , Nordenfelt Natalie Shannon , Chen Nicholas , Lee Christine , Kaluziak Stefan , Codd Elizabeth , Trivedi Samay , Gohar Magdy , McKnight Giovan , Mitchell Dawn R. , Ge Maolin , Gao Chengzhuo , Holmes Zavontae , Yang Wenxin , Smith Abigail Elizabeth , Carlin Alexander Daniel , Lazarov Matthew J. , Khandelwal Neha , Hara Mariko , Zhang Siwen , Leong Herman Xin Yang , Martinez Luna Hector , Chearavanont Zander , Emonds Kim , Popoola George , Barakat Idris , Onozato Maristela , Mahamdeh Mohammed , Fujino Toshio , Seo Hyuk-Soo , Dhe-Paganon Sirano , Sun Zhen-Yu Jim , Heffron Gregory J , Hata Aaron , Soberman Roy Jason , Liau Brian B. , Iafrate A. John , Bar-Peled Liron 
Published: July 2024

AbstractMolecular glues that engage protein complexes have transformed the study of cell biology and have had a direct impact on clinical oncology. However, the identification of new glue classes and their corresponding protein complexes has remained largely serendipitous. To overcome this challenge, we report the development of molecular COUPLrs, elaborated small molecules flanked by two cysteine-reactive warheads, as well as CONNECT, an integrated chemical proteomic platform for target deconvolution. By profiling a library of molecular COUPLrs across 13 cancer cell lines, we uncovered hundreds of proteins that can be coupled together, including in some cases in mutant selective fashions. We develop an advanced COUPLr for the oncogene EML4-ALK, which engages the fusion outside of its kinase domain, restricts protein dynamics, and disrupts EML4-ALK signaling. Collectively, molecular COUPLrs substantially expand the scope of proteins that can be chemically connected, providing an unbiased approach to identify small molecules that target protein complexes.
Extensive transcriptional differentiation and specialization of a parasite across its host’s metamorphosis
Authors: DuBose James G. , de Roode Jacobus C. 
Published: July 2024

AbstractFoundational theory on life cycle evolution suggests that given genetic independence, the phenotypes presented by different life stages will diverge more when they occupy more dissimilar niches. When divergence between stages is significant and punctual, we typically consider the life cycle complex. In parasites, the delineation between simple and complex life cycles is usually made between those that occupy single and multiple host species. However, many parasites can experience significant niche shifts in a single host. To explore the potential for a host’s metamorphosis to shape divergence between stages across its parasite’s life cycle, we quantified the transcriptional differentiation and specialization that the protozoan parasiteOphryocystis elektroscirrhaexhibits across the metamorphosis of its host the monarch butterfly. We found evidence thatO. elektroscirrhadifferentiates in concordance with the ecological turnover imposed by monarch transitions to different stages, and that patterns of transcriptional decoupling across theO. elektroscirrhaexceeded even that of its host. However, because of its greater gene content, the monarch exhibited greater total transcriptional turnover than its parasite. These findings highlight that synthesis of evolutionary theory pertaining to free-living and parasitic life cycles could be facilitated by more nuanced and continuous descriptions of life cycle complexity.
Alzheimer’s disease neuropathologic change mediates the relationship between ambient air pollution and dementia severity
Authors: Kim Boram , Blam Kaitlin , Elser Holly , Xie Sharon X. , Van Deerlin Vivianna M. , Penning Trevor M. , Weintraub Daniel , Irwin David J. , Massimo Lauren M. , McMillan Corey T. , Mechanic-Hamilton Dawn , Wolk David A. , Lee Edward B. 
Published: July 2024

AbstractBackgroundExposure to fine particulate matter air pollution (PM2.5increases risk for dementia. However, it is unknown whether this relationship is mediated by dementia-related neuropathologic change found at autopsy. We aimed to examine relationships between PM2.5exposure, dementia severity, and dementia-associated neuropathologic change.MethodsThis cross-sectional study used harmonized demographic, clinical, genetic, and neuropathological data from autopsy cases collected from 1998 to 2022 at the Center for Neurodegenerative Disease Research brain bank, University of Pennsylvania. Cases who had common neuropathologic forms of dementia and complete data on neuropathologic measures,APOEgenotype, and residential address were included in this study cohort. Dementia severity was measured by Clinical Dementia Rating-Sum of Boxes (CDR-SB) scores. Ten dementia-associated neuropathologic measures representing Alzheimer’s disease, Lewy body disease, limbic-predominant age related TDP-encephalopathy, and cerebrovascular disease were graded or staged according to the consensus criteria. One-year average PM2.5exposure prior to death was estimated using a spatiotemporal prediction model based on residential addresses as the primary exposure measure. Linear, logistic and structural equation models were used to examine the relationships between PM2.5, CDR-SB and neuropathologic measures.ResultsA total of 861 autopsy cases were included (mean age at death 76.6 years [SD 10.3]; 481 [56%] male). Each 1 μg/m3increase in one-year average PM2.5concentration prior to death was associated with significantly greater cognitive and functional impairment (increase in CDR-SB score of 0.78; 95% confidence interval [CI], 0.52-1.05), faster cognitive and functional decline (change in CDR-SB scores of 0.13; 95% CI, 0.09-0.16), more severe Alzheimer’s disease neuropathologic change (ADNC; odds ratio [OR] of 1.07; 95% CI, 1.01-1.13), and a higher prevalence of large infarcts (OR, 1.17; 95% CI, 1.05-1.30). The relationship between PM2.5exposure and CDR-SB was mediated by ADNC (change in CDR-SB score due to ADNC level of 0.36; 95% CI, 0.13-0.65).ConclusionsPM2.5exposure may increase dementia risk by increasing ADNC. Measures that improve air quality may represent a population-level intervention for the prevention of dementia.
Structure of yeast RAVE bound to a partial V1complex
Authors: Wang Hanlin , Tarsio Maureen , Kane Patricia M. , Rubinstein John L. 
Published: July 2024

AbstractVacuolar-type ATPases (V-ATPases) are membrane-embedded proton pumps that acidify intracellular compartments in almost all eukaryotic cells. Homologous with ATP synthases, these multi-subunit enzymes consist of a soluble catalytic V1subcomplex and a membrane-embedded proton-translocating VOsubcomplex. The V1and VOsubcomplexes can undergo reversible dissociation to regulate proton pumping, with reassociation of V1and VOrequiring the protein complex known as RAVE (regulator of theATPase ofvacuoles andendosomes). In the yeastSaccharomyces cerevisiae, RAVE consists of subunits Rav1p, Rav2p, and Skp1p. We used electron cryomicroscopy (cryo-EM) to determine a structure of yeast RAVE bound to V1. In the structure, RAVE is a L-shaped complex with Rav2p pointing toward the membrane and Skp1p distant from both the membrane and V1. Only Rav1p interacts with V1, binding to a region of subunit A not found in the corresponding ATP synthase subunit. When bound to RAVE, V1is in a rotational state suitable for binding the free VOcomplex, but it is partially disrupted in the structure, missing five of its 16 subunits. Other than these missing subunits and the conformation of the inhibitory subunit H, the V1complex with RAVE appears poised for reassembly with VO.
Primary bovine white blood cells support dissemination of Lumpy Skin Disease Virus while suppressing viral replication
Authors: Kumar Manoj , Frid Ohad , Sol Asaf , Rouvinski Alexander , Karniely Sharon 
Published: July 2024

AbstractLumpy skin disease (LSD) is a severe infectious, emerging transboundary disease of cattle, caused by a Pox family DNA virus. Lumpy skin disease virus (LSDV) infection is associated with a febrile response followed by emergence of widespread dermal nodules. In addition to the skin, LSDV resides in multiple internal organs and can be isolated from the blood of infected cattle. LSDV is suggested to be mechanically transmitted by biting arthropods. Live attenuated vaccines are commonly used to control disease and its spread. We have characterized the tropism, replication, and dissemination of a LSDV field isolate and of an attenuated vaccine strain usingin vitrosystems. To follow virus infection and dissemination in living cells, we have generated recombinant viruses expressing green fluorescent protein (GFP) under a synthetic viral promoter. Recombinant, GFP-expressing, LSDVs demonstrated similar replication kinetics to their corresponding parental LSDV strains in a bovine kidney cell line (MDBK). We further demonstrated that LSDV-GFP productively replicated in a bovine macrophage cell line and in primary bovine foreskin cells with no apparent differences between the field isolate and the vaccine strain. When bovine peripheral blood mononuclear cells (PBMCs) were infected with either LSDV recombinant strain, we observed specific viral driven GFP fluorescence as well as significant viral gene expression. However, infected PBMCs failed to support substantial viral DNA replication and release of infectious progeny. Subsequent analysis of the anti-viral response revealed that heat treated (HT) LSDV induced the expression of interferon- stimulated genes (ISGs) in PBMCs, but this response was suppressed by infectious viruses. Finally, we show that despite failed replication, LSDV infected PBMCs transmitted the virus to recipient co-cultured MDBK cells and produced infectious foci, suggesting a potential role of PBMCs in LSDV dissemination.HighlightsVirulent and attenuated LSDV productively replicated in bovine kidney and bovine macrophage cell lines as well as in primary fibroblasts.Adherent white blood cells were susceptible to LSDV field and attenuated vaccine infection.LSDV showed active viral transcription in PBMCs yet no significant viral genome replication or production of infectious progeny.PBMCs infected with heat-treated LSDV but not with fully infectious viruses upregulated ISGs’ RNA.PBMCs transmitted and disseminated LSDV to contacting permissive cells.
Brain Structural Correlates of an Impending Initial Major Depressive Episode
Authors: Kraus Anna , Dohm Katharina , Borgers Tiana , Goltermann Janik , Grotegerd Dominik , Winter Alexandra , Thiel Katharina , Flinkenflügel Kira , Schürmeyer Navid , Hahn Tim , Langer Simon , Kircher Tilo , Nenadić Igor , Straube Benjamin , Jamalabadi Hamidreza , Alexander Nina , Jansen Andreas , Stein Frederike , Brosch Katharina , Usemann Paula , Teutenberg Lea , Thomas-Odenthal Florian , Meinert Susanne , Dannlowski Udo 
Published: July 2024

AbstractBackgroundNeuroimaging research has yet to elucidate, whether reported gray matter volume (GMV) alterations in major depressive disorder (MDD) exist already before the onset of the first episode. Recruitment of presently healthy individuals with a known future transition to MDD (converters) is extremely challenging but crucial to gain insights into neurobiological vulnerability. Hence, we compared converters to patients with MDD and sustained healthy controls (HC) to distinguish pre-existing neurobiological markers from those emerging later in the course of depression.MethodsCombining two clinical cohorts (n=1709), voxel-wise GMV ofn=45 converters,n=748 patients with MDD, andn=916 HC were analyzed in regions-of-interest approaches. By contrasting the subgroups and considering both remission state and reported recurrence at a 2-year clinical follow-up, we stepwise disentangled effects of 1) vulnerability, 2) the acute depressive state, and 3) an initial vs. a recurrent episode.ResultsAnalyses revealed higher amygdala GMV in converters relative to HC (pTFCE-FWE=.037,d=0.447) and patients (pTFCE-FWE=.005,d=0.508), remaining significant when compared to remitted patients with imminent recurrence. Lower GMV in the dorsolateral prefrontal cortex (pTFCE-FWE<.001,d=0.188) and insula (pTFCE-FWE=.010,d=0.186) emerged in patients relative to HC but not to converters, driven by patients with acute MDD.ConclusionBy examining one of the largest available converter samples in psychiatric neuroimaging, this study allowed a first determination of neural markers for an impending initial depressive episode. Our findings suggest a temporary vulnerability, which in combination with other common risk factors might facilitate prediction and in turn improve prevention of depression.
Altered Cortical Network Dynamics during Observing and Preparing Action in Patients with Corticobasal Syndrome
Authors: Krösche Marius , Hartmann Christian , Butz Markus , Schnitzler Alfons , Hirschmann Jan 
Published: July 2024

AbstractBesides parkinsonism, higher order cortical dysfunctions such as apraxia are hallmarks of the corticobasal syndrome (CBS). To date, little is known about the electrophysiological underpinnings of these symptoms.To shed more light on the pathophysiology of CBS, we recorded the magnetoencephalogram of 17 CBS patients and 20 age-matched controls engaged in an observe-to-imitate task. The task involved the display of a tool-use video in first person view (action observation), a written instruction to withhold movement until the presentation of a Go cue (movement preparation), and unilateral tool-use imitation. We investigated modulations of spectral power on the source level.Action observation was associated with an event-related desynchronization in the beta-band (13-30Hz), which was weaker in CBS patients than in healthy controls. The group effect localized to superior parietal, primary motor, premotor and inferior frontal cortex bilaterally. While participants awaited the Go cue, beta power was again suppressed in the hemisphere contralateral to movement, and the rate of suppression correlated with reaction time. This modulation, too, was weaker in the CBS group. Immediately before movement onset, however, beta power was similar in both groups.Our results reveal that action observation triggers beta suppression, likely reflecting motor cortical disinhibition, which is reduced in CBS patients. This pathological alteration might be a neural correlate of a selective deficit in the embedding of observed action into a motor representation (visuo-motor mapping). The suboptimal timing of the beta-power suppression to the upcoming Go cue presumably reflects a deficit in learning the trial’s temporal structure rather than a deficit in movement initialization.HighlightsAction observation elicits a suppression of cortical beta power.This suppression is diminished in CBS patients relative to controls.The timing of beta desynchronization to an upcoming Go cue is impaired in CBS patients.No evidence for an alteration of movement initialization in CBS patients.
Banking the unbanked: exploring the impact of internet penetration on accessibility to banking services in developed and developing economies
Authors: Jain Shivani , Sahu Jagadish Prasad 
Published: July 2024

Purpose
The surge in internet usage has generated widespread speculation and optimism regarding its potential impact on the accessibility to financial services. The aim of this study is to investigate the effect of internet penetration on the accessibility of banking services in developed and developing countries.

Design/methodology/approach
Panel data regression methods are used to estimate the impact of internet penetration on accessibility to banking services in a sample of 74 countries from Global Findex survey waves of 2011, 2014, 2017 and 2021. To mitigate potential issues related to heteroscedasticity, autocorrelation and cross-sectional dependence, the study has implemented cluster robust standard errors testing. Furthermore, as a sensitivity check, the sample has been segregated into developed and developing country groups.

Findings
The study finds a significant positive correlation between internet penetration and banking access in full sample. Subsample analysis reveals that this relationship is statistically significant in developed countries, but not in developing ones, despite being positive. The research discusses the implications of these findings for both country groups.

Originality/value
Research to date has largely investigated the link between information and communication technology (ICT) and financial inclusion, often treating internet penetration as one component of ICT, which obscures its individual influence. This study, however, isolates internet penetration to specifically analyze its distinct effects on banking accessibility across developed and developing countries.