bluuebunny/crossref_metadata_2025_split huggingface dataset:
A rapid and simple MALDI-TOF MS lipid profiling method for differentiating
Mycobacterium ulcerans
from
Mycobacterium marinum
Authors: Komine Takeshi , Fukano Hanako , Yoshida Mitsunori , Miyamoto Yuji , Nakaya Makoto , Fujinaga Azumi , Doke Kohei , Hoshino Yoshihiko 
Published: January 2025

ABSTRACT

Mycobacterium ulcerans
, a slow-growing nontuberculous mycobacterium, causes Buruli ulcer, a neglected tropical disease. Distinguishing
M. ulcerans
from related species, including
Mycobacterium marinum
, poses challenges with respect to making accurate identifications. In this study, we developed a rapid and simple identification method based on mycobacterial lipid profiles and used matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) to analyze the lipid profiles of
M. ulcerans
(
n
= 35) and
M. marinum
(
n
= 19) isolates. Bacterial colonies pre-cultured on 2% Ogawa egg slants for 2 months were collected, and total lipids were extracted using an MBT Lipid Xtract kit. Spectra were obtained in negative ion mode using a MALDI Biotyper Sirius system, with ClinProTools v3.0 being used to analyze the spectra based on the application of three algorithms (genetic algorithm [GA], supervised neural network [SNN], and quick classifier [QC)]). Cross-validation was performed using a 20% leave-out set randomly selected from the samples. Models generated using GA, SNN, and QC showed cross-validation values of 100%, 100%, and 97.9%, respectively, and all algorithms achieved 100% recognition capability values. Our findings indicate that MALDI-TOF analysis of lipid profiles can accurately differentiate two mycobacterial species (
M. ulcerans
and
M. marinum
) that are difficult to distinguish using conventional protein-targeting methods.

IMPORTANCE

Buruli ulcer, caused by
Mycobacterium ulcerans
, is a neglected tropical disease. However, distinguishing
M. ulcerans
from related species, including
Mycobacterium marinum
, presents certain challenges. In this study, we demonstrate the utility of a rapid yet simple method for differentiating isolates of these mycobacteria based on their lipid profiles using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. This new approach can accurately identify species that are otherwise difficult to distinguish using conventional techniques. This represents a significant diagnostic advance for clinical laboratories, in that it enables a more rapid and precise identification, thereby leading to earlier treatment initiation and more appropriate treatment regimens for infections caused by these bacteria.
Duplexed direct RNA sequencing protocol using polyadenylation and polyuridylation
Authors: Watson Kaylee J. , Bromley Robin E. , Dunning Hotopp Julie C. 
Published: January 2025

ABSTRACT

Oxford Nanopore Technologies provides multiplexing options for DNA and cDNA sequencing, but not for direct RNA sequencing. Here we describe a duplexing approach and validate it by simultaneously sequencing the
Saccharomyces cerevisiae
rRNA from wild type and knockout that have differential rRNA modifications, successfully demultiplexing the data using bioinformatics approaches.
Complete genome sequence of
Enterobacter cloacae
ST462 harboring the
mcr-9
gene on the chromosome, isolated from a pediatric diarrhea patient in Southern Vietnam
Authors: Le Nga Thi , Hoang Phuong Hoai , Dang Chinh Van , Ho Tinh Huu , Hoang Phuc Le , Truong Dinh Quang , Nguyen Ha Thi Thanh , Le Chuong Van , Truong Minh Nhat Ha , Truong Tuom Thi Tinh , Phan Trang Thi Phuong 
Published: January 2025

ABSTRACT

Colistin resistance threatens global health as it compromises the effectiveness of a last-resort antibiotic. We present the complete genome sequence of
Enterobacter cloacae
ST462, which carries the
mcr-9.1
gene, isolated from a pediatric diarrhea case in southern Vietnam. The 5,049,362 bp genome contains 24 resistance genes distributed across 107 contigs.
Interspecies interactions mediated by arginine metabolism enhance the stress tolerance of
Fusobacterium nucleatum
against
Bifidobacterium animalis
Authors: Zhou Zhongkun , Yang Mengyue , Fang Hong , Niu Yuqing , Lu Juan , Ma Yunhao , Zhang Baizhuo , Zhu Hongmei , Chen Peng 
Published: January 2025

ABSTRACT

Colorectal cancer (CRC) is a common cancer accompanied by microbiome dysbiosis. Exploration of probiotics against oncogenic microorganisms is promising for CRC treatment. Here, differential microorganisms between CRC and healthy control were analyzed. Antibacterial experiments, whole-genome sequencing, and metabolic network reconstruction were combined to reveal the anti-
Fusobacterium nucleatum
mechanism, which was verified by co-culture assay and mendelian randomization analysis. Sequencing results showed that
F. nucleatum
was enriched in CRC, yet
Bifidobacterium animalis
decreased gradually from healthy to CRC. Additionally,
F. nucleatum
could be inhibited by
B. animalis
. Whole-genome sequencing of
B. animalis
showed high phylogenetic similarity with known probiotic strains and highlighted its functions for amino acid and carbohydrate metabolism. Metabolic network reconstruction demonstrated that cross-feeding and specific metabolites (acidic molecules, arginine) had a great influence on the coexistence relationship. Finally, the arginine supplement enhanced the competitive ability of
F. nucleatum
against
B. animalis
, and the mendelian randomization and metagenomic sequencing analysis confirmed the positive relationship among
F. nucleatum
, arginine metabolism, and CRC. Thus, whole-genome sequencing and metabolic network reconstruction are valuable for probiotic mining and patient dietary guidance.

IMPORTANCE

Using probiotics to inhibit oncogenic microorganisms (
Fusobacterium nucleatum
) is promising for colorectal cancer (CRC) treatment. In this study, whole-genome sequencing and metabolic network reconstruction were combined to reveal the anti-
F. nucleatum
mechanism of
Bifidobacterium animalis
, which was verified by co-culture assay and mendelian randomization analysis. The result indicated that the arginine supplement enhanced the competitive ability of
F. nucleatum
, which may be harmful to
F. nucleatum
-infected CRC patients.
B. animalis
is a potential probiotic to relieve this dilemma. Thus, using in silico simulation methods based on flux balance analysis, such as genome-scale metabolic reconstruction, provides valuable insights for probiotic mining and dietary guidance for cancer patients.
HIV-1 and BLV are insensitive to SERINC5 restriction under the cell-cell infection
Authors: Yu Changqing , Jiang Faming , Li Yujing , Li Qiushui , Tokunaga Kenzo , Yang Dan , Xu Chao , Li Nan , Li Sunan , Khan Ilyas , Xian Yuanhua , Xia Changyou , Zhang He 
Published: January 2025

ABSTRACT

Ser
ine
inc
orporator 5 (
SER
INC5, SER5) suppresses viral cell-free infection. However, its antiviral potency under viral cell-cell infection is not examined yet. Here, we established the
in vitro
cell-cell infection systems to assess SER5’s antiviral activity on HIV-1 and bovine leukemia virus (BLV). Our results showed SER5 from different mammalian species, including
Homo sapiens
,
Bos taurus
, and
Felis catus
, was capable of significantly inhibiting HIV-1 cell-free infection. However, these SER5s were unable to restrict HIV-1 cell-cell infection. Intriguingly, Ebola virus glycoprotein-mediated pseudoviral cell-free infection was greatly enhanced by
Homo sapiens
and
Bos taurus
SER5. Notably, BLV was also insensitive to SER5-mediated restriction under the cell-cell infection. In addition, BLV envelope glycoproteins, which contained one glycosylation variation, were not restricted by SER5 in the model of cell-cell infection. Overall, our results indicated SER5 was ineffective against HIV-1 and BLV under the cell-cell infection, which was utilized by them to circumvent SER5-imposed restriction
in vitro
and may aid their transmission
in vivo
.

IMPORTANCE
SER5 potently inhibits virus infection under the cell-free mode. However, few studies check whether SER5 keeps its restriction under the virus cell-cell transmission. In this work, we uncover SER5 loses its restriction to HIV-1 and BLV under the mode of cell-cell infection, demonstrating the viruses could employ this mode to overcome SER5 restriction and thus facilitate their transmission.
Cerebral injury and long-term neurodevelopment impairment in children following severe fetomaternal transfusion: a retrospective cohort study
Authors: El Emrani Salma , van der Hoorn Marie-Louise , Tan Ratna N G B , Steggerda Sylke J , de Vries Linda S , Haak Monique C , van Klink Jeanine M M , de Haas Masja , van der Meeren Lotte E , Lopriore Enrico 
Published: January 2025

ObjectiveFetomaternal transfusion (FMT) is associated with increased perinatal mortality and morbidity, but data on postnatal outcomes are scarce. Our aim was to determine the incidence of adverse short-termand long-term sequelae of severe FMT.DesignRetrospective cohort study.SettingDutch tertiary neonatal intensive care unit.PatientsLiveborn neonates with FMT admitted in 2017–2022.Main outcome measuresSevere FMT was defined as ≥30 mL of fetal red blood cells in the maternal circulation diagnosed with positive Kleihauer-Betke/flow cytometry test. Adverse outcomes were compared between severe and mild FMT (10–30 mL blood loss) to highlight the impact of FMT severity. Primary outcome was an adverse composite outcome consisting of neonatal mortality or severe neurological morbidity (ie, severe cerebral injury and/or neurodevelopmental impairment (NDI) at 2 years). Secondary outcome was perinatal asphyxia.Results109 neonates with FMT were included, 16 with severe FMT and 93 with mild FMT. Neonatal mortality occurred in 19% (3/16) of neonates with severe FMT and in 4% (4/93) with mild FMT (p=0.063). Perinatal asphyxia was diagnosed in 25% (4/16) of neonates with severe FMT compared with 6% (6/93) with mild FMT (p=0.038). Long-term outcome was assessed in 60 neonates. NDI occurred in 22% (2/9) of children with severe FMT compared with 16% (8/51) with mild FMT (p=0.637). Adverse outcome occurred in 43% (95% CI 38 to 50%) of neonates with severe FMT compared with 18% (95% CI 17% to 24%) with mild FMT (p=0.074).ConclusionNeonatal mortality or long-term neurological morbidity occurred in 38%–50% of children with fetal blood loss and anaemia due to severe FMT.
Risk factors for pancreatic cancer in individuals with intraductal papillary mucinous neoplasms and no high-risk stigmata during up to 5 years of surveillance: a prospective longitudinal cohort study
Authors: Hamada Tsuyoshi , Oyama Hiroki , Nevo Daniel , Tange Shuichi , Takaoka Shinya , Kawaguchi Yoshikuni , Ishigaki Kazunaga , Noguchi Kensaku , Saito Tomotaka , Sato Tatsuya , Suzuki Tatsunori , Takahara Naminatsu , Tanaka Mariko , Hasegawa Kiyoshi , Ushiku Tetsuo , Nakai Yousuke , Petrov Maxim S , Fujishiro Mitsuhiro 
Published: January 2025

BackgroundCyst size, its growth rate, and diameter of the main pancreatic duct (MPD) are all associated with pancreatic carcinoma prevalence in intraductal papillary mucinous neoplasms (IPMNs).ObjectiveTo examine the above factors in relation to future risk of incident pancreatic carcinoma in individuals with IPMNs harbouring no high-risk stigmata.DesignIn a prospective longitudinal cohort, we analysed 2549 patients with IPMNs. A multivariable cause-specific Cox proportional hazards regression model was built to estimate HRs for incident pancreatic carcinoma.ResultsIPMN size at baseline and its annual growth rate over 2 years of follow-up were associated with incident pancreatic carcinoma (ptrend<0.001). The multivariable cause-specific HR per 10 mm increase in IPMN size was 1.28 (95% CI 1.10 to 1.50). The annual growth rates of 1.5–2.4 mm/year and ≥2.5 mm/year over 2 years were associated with multivariable cause-specific HRs of 1.91 (95% CI 0.78 to 4.67) and 4.52 (95% CI 2.28 to 8.98), respectively (vs <1.5 mm/year). Neither IPMN size at 5 years nor its maximum growth rate during 5 years was associated with incident pancreatic carcinoma (ptrend>0.07). MPD diameter at 5 years was associated with incident pancreatic carcinoma (multivariable cause-specific HR per 2 mm increase, 2.12; 95% CI 1.72 to 2.63). A predictive nomogram was generated for calculating the risk of incident pancreatic carcinoma.ConclusionIPMN size and its growth rate predict future pancreatic carcinoma risk only during first 5 years of follow-up. MPD diameter at 5 years may identify patients who still harbour a high risk for pancreatic carcinoma.
In vitromicrobiota model recapitulates and predicts individualised sensitivity to dietary emulsifier
Authors: Rytter Héloïse , Naimi Sabrine , Wu Gary , Lewis Jim , Duquesnoy Maeva , Vigué Lucile , Tenaillon Olivier , Belda Eugeni , Vazquez-Gomez Marta , Touly Nina , Arnone Djésia , Hao Fuhua , Ley Ruth E , Clément Karine , Peyrin-Biroulet Laurent , Patterson Andrew D , Gewirtz Andrew T , Chassaing Benoit 
Published: January 2025

BackgroundNon-absorbed dietary emulsifiers, including carboxymethylcellulose (CMC), directly disturb intestinal microbiota, thereby promoting chronic intestinal inflammation in mice. A randomised controlled-feeding study (Functional Research on Emulsifiers in Humans, FRESH) found that CMC also detrimentally impacts intestinal microbiota in some, but not all, healthy individuals.ObjectivesThis study aimed to establish an approach for predicting an individual’s sensitivity to dietary emulsifiers via their baseline microbiota.DesignWe evaluated the ability of anin vitromicrobiota model (MiniBioReactor Arrray, MBRA) to reproduce and predict an individual donor’s sensitivity to emulsifiers. Metagenomes were analysed to identify signatures of emulsifier sensitivity.ResultsExposure of human microbiotas, maintained in the MBRA, to CMC recapitulated the differential CMC sensitivity previously observed in FRESH subjects. Furthermore, select FRESH control subjects (ie, not fed CMC) had microbiotas that were highly perturbed by CMC exposure in the MBRA model. CMC-induced microbiota perturbability was associated with a baseline metagenomic signature, suggesting the possibility of using one’s metagenome to predict sensitivity to dietary emulsifiers. Transplant of human microbiotas that the MBRA model deemed CMC-sensitive, but not those deemed insensitive, into IL-10−/−germfree mice resulted in overt colitis following CMC feeding.ConclusionThese results suggest that an individual’s sensitivity to emulsifier is a consequence of, and can thus be predicted by, examining their baseline microbiota, paving the way to microbiota-based personalised nutrition.
The $$(1+3)$$-dimensional ‘quantum principle of relativity’ is Einstein’s principle of relativity
Authors: Lake Matthew J. 
Published: January 2025

Abstract
We show that the

$$(1+3)$$

(
1
+
3
)

-dimensional ‘superboost’ operators, proposed in Dragan and Ekert’s most recent work on superluminal reference frames (Dragan et al. in Class Quantum Gravity 40(2): 025013, 2023), are simply the canonical Lorentz boosts, expressed in nonstandard notation. Their

$$(1+3)$$

(
1
+
3
)

-dimensional ‘superflip’, which is claimed to interchange time and space dimensions for a superluminal observer, travelling with infinite speed, is equivalent to applying the identity operator together with an arbitrary relabeling. Physically, it corresponds to staying put within the canonical rest frame, then renaming space as ‘time’ and time as ‘space’. We conclude that their extension of the ‘quantum principle of relativity’, proposed in earlier work on

$$(1+1)$$

(
1
+
1
)

-dimensional spacetimes (Dragan and Ekert in New J Phys 22(3): 033038, 2020), to ordinary Minkowski space, is simply Einstein’s principle of relativity, proposed in 1905.
The Changing Pathogenesis of Liver Cancer in Hawaii over Three Decades
Authors: Wong Linda L. , Hromalik Larry R. , Hernandez Brenda Y. , Acoba Jared D. , Kwee Sandi A. 
Published: January 2025

Abstract

Background:
Worldwide trends support the increasing contribution of hepatic steatosis to the incidence of hepatocellular carcinoma (HCC). This study investigates if similar changes are seen in Hawaii, where the incidence of HCC is higher than in most of the United States.

Methods:
This is a retrospective study of 1,651 patients diagnosed with HCC (1991–2023) that includes 60% to 70% of HCC cases in Hawaii. We evaluated changes in patient demographics, risk factors, and disease etiology over the past three decades.

Results:
From 1991 to 2023, there were significant increases in the proportion of HCC cases attributable to metabolic dysfunction–associated steatotic liver disease (MASLD), coinciding with an increase in the prevalence of metabolic risk factors including obesity, diabetes, hyperlipidemia, and hypertension. Cases with a history of smoking also increased through 2020. Conversely, HCC cases presenting with cirrhosis alone decreased. Hepatitis C virus (HCV)-associated cases increased through 2015 and then tapered, whereas Hepatitis B virus (HBV)-associated cases decreased through 2020. There was no significant change in the proportion of alcohol-associated cases.

Conclusions:
Although HBV continues to be a major contributor to HCC in Hawaii, HCV-related HCC cases have tapered, whereas metabolic risk factors for HCC and cases attributable to MASLD have increased over time, paralleling overall trends observed in the United States. Efforts are needed to manage these metabolic factors to address the burden of HCC.

Impact:
Although Hawaii continues to have a large burden of viral hepatitis–related HCC, metabolic factors and MASLD have affected the pathogenesis of liver cancer in Hawaii over the past three decades.
Receptor CDCP1 is a potential target for personalized imaging and treatment of poor outcome HER2+, triple negative and metastatic ER+/HER2- breast cancers
Authors: Gough Madeline , Kwah Kayden KX. , Khan Tashbib , Ghosh Saikat , Sun Biao , Lee Catherine YJ. , Sokolowski Kamil A. , Tse Brian WC. , Wickramasuriya Lashith , Ferguson Kaltin , Rogers Rebecca , Goh Justin B. , Fletcher Nicholas L. , Houston Zachary H. , Thurecht Kristofer J. , Bray Laura J. , Liu Cheng , Pyke Christopher , Lim Elgene , Snell Cameron E. , He Yaowu , Hooper John D. , Kryza Thomas 
Published: January 2025

Abstract
Purpose: Receptor CUB-domain containing- protein 1 (CDCP1) was evaluated as a target for detection and treatment of breast cancer. Experimental Design: CDCP1 expression was assessed immunohistochemically in tumors from 423 patients (119 triple-negative breast cancer (TNBC); 75 HER2+; 229 ER+/HER2- including 228 primary tumors, 229 lymph node and 47 distant metastases). Cell cytotoxicity induced in vitro by a CDCP1-targeting antibody-drug conjugate (ADC), consisting of the human/mouse chimeric antibody ch10D7 and the microtubule disruptor monomethyl auristatin E (MMAE), was quantified, including in combination with HER2-targeting ADC T-DM1. Detection of CDCP1-expressing primary and metastatic xenografts in mice was examined by PET-CT imaging using 89zirconium-labelled ch10D7 (89Zr-ch10D7). The impact of ch10D7-MMAE on tumor burden and survival in vivo, including in combination with T-DM1, was quantified in cell line and patient-derived xenograft mouse models. Results: CDCP1 is expressed predominantly on the surface of malignant cells of 70% of TNBCs, 80% of HER2+ tumors, and increases in ER+/HER2- tumors from 44.9% in primary tumors to 56.4% in lymph node metastases and 74.3% in distant metastases. PET-CT imaging with 89Zr-ch10D7 is effective for the detection of primary and metastatic CDCP1-expressing TNBCs in mice. ADC ch10D7-MMAE kills CDCP1-expressing cells in vitro and controls primary and metastatic TNBC xenografts in mice, conferring significant survival advantages over chemotherapy. It compares favorably to T-DM1 in vivo, and ch10D7-MMAE combined with T-DM1 showed the most potent efficacy, markedly reducing tumor burden of CDCP1+/HER2+ xenografts and prolonging mouse survival, compared with T-DM1 or ch10D7. Conclusions: CDCP1-directed molecular imaging has potential to identify aggressive breast cancers for CDCP1-targeted treatment.
Myocardial Inflammation in Cardiac Transthyretin Amyloidosis: Prevalence and Potential Prognostic Implications
Authors: Müller Maximilian Leo , Brand Anna , Mattig Isabel , Spethmann Sebastian , Messroghli Daniel , Hahn Katrin , Violano Michele , Mitchell Joshua D. , Hare Joshua M. , Frustaci Andrea , Klingel Karin , Lüscher Thomas F. , Landmesser Ulf , Heidecker Bettina 
Published: January 2025

BACKGROUND:
Despite previous histopathologic evidence for its presence, the role of myocardial inflammation in the development and progression of cardiac transthyretin amyloidosis (ATTR-CA) remains insufficiently understood. Thus, this study sought to characterize the prevalence and potential prognostic implications of myocardial inflammation in ATTR-CA.

METHODS:

A retrospective observational study including patients with ATTR-CA diagnosed by endomyocardial biopsy was conducted. Myocardial inflammation was diagnosed through a review of routine endomyocardial biopsy reports. Baseline characteristics were compared using the Mann-Whitney
U
test and the Pearson χ
2
test. Clinical outcomes were monitored via follow-up visits or telephone calls. Primary outcomes were all-cause death and a composite end point of all-cause death or heart failure hospitalization. Kaplan-Meier analyses, as well as univariable and age- and sex-adjusted multivariable Cox regression analyses, were used to assess differences in overall and composite end point-free survival between patients with ATTR-CA with and without myocardial inflammation.

RESULTS:

A total of 103 patients with ATTR-CA (100 wild type; 3 variant) were enrolled. Median follow-up was 18.2 (8.0–31.1) months. Myocardial inflammation was prevalent in 32% (n=33/103) of patients with ATTR-CA. Among evaluable patients with myocardial inflammation, 96% (n=26/27) and 31% (n=9/29) had elevated CD68 (clusters of differentiation 68)–positive macrophage and CD3 (clusters of differentiation 3)–positive T-cell counts, respectively. Overall survival (
P
=0.017) and composite end point-free survival (
P
=0.014) were significantly impaired in patients with ATTR-CA with myocardial inflammation (n=33) compared with those without (n=70). Statistical significance for both associations was sustained after adjustment for age and sex, yielding adjusted hazard ratios of 4.72 (95% CI, 1.33–16.71;
P
=0.016) and 2.30 (95% CI, 1.04–5.11;
P
=0.041) for all-cause death and the composite end point, respectively.

CONCLUSIONS:
Our findings affirm previous evidence that myocardial inflammation is present in approximately one-third of all patients with ATTR-CA. Moreover, we provide first data indicating that myocardial inflammation may be associated with a higher risk of death and heart failure hospitalizations in ATTR-CA.