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Journals instruct authors to proofread their accepted manuscripts before signing them off for publication and expect them to submit errata to correct any mistakes identified thereafter. Herein, I examine papers with obvious errors in the author name list. I queried PubMed for papers under common Greek forenames looking for citations where author surnames and forenames are swapped. I identified 113 such papers from 101 journals. Author names are corrected with errata only in 20, after a median of 6.5 mo. Time to name correction is shorter for journals with impact factor above the median (P=0.015). To further explore this suggested association of apparent author sloppiness with journal impact, I use as controls all errata published between 1996 and 2008 in 5 top-cited general medical journals (New England Journal of Medicine, JAMA, The Lancet, Annals of Internal Medicine, and British Medical Journal); 3.4% of the latter contain name corrections (vs. 18.1% of all errata in the 101 journals during the same period, P<10(-6)). Egregious errors may be markers of cursory if any proofreading and, therefore, markers for additional unidentified inaccuracies. In addition, I wonder whether authors may be as reluctant to rectify other, nonobvious (yet potentially consequential) mistakes after a paper's publication.

Background: We studied the type and frequency of differences between data presented in conference abstracts and subsequent published papers in the fields of infectious diseases and microbiology., Methods: We reviewed all abstracts from the first session of 7 of 15 major research categories presented in the 1999 and 2000 Interscience Conference on Antimicrobial Agents and Chemotherapy. For each selected pair of abstract and related published paper, two independent investigators performed a detailed data comparison., Results: From 190 abstracts reviewed, 68 (36%) were subsequently published as full papers by March 2004. Fifty-two pairs referred to the same study population and period. Differences were found in 30 of 51 pairs, which were further analyzed (point estimate=59%, 95% C.I.: 45-73%). The identified differences were related to both the aims and conclusions of the study (3/30), the study conclusions only (2/30), numbers and/or rates of the studied patients (10/30), numbers or rates of microbiological isolates (9/30), MIC values or K(i) values (5/30), other pharmacological properties of antibiotics (2/30), odds ratio (1/30), and duration of observation (1/30). Some differences were considered major. In bivariable associations, time to publication (from presentation in the conference to publication of the full paper) was associated with identifiable differences between the conference abstract and the full paper (OR=1.76, 95% CI 0.95-3.24/year of delay, P=0.07)., Conclusions: It is reassuring that although we identified several reportable differences, only a very small proportion of studies exhibited differences in their aims and/or conclusions. Researchers may benefit from the above findings in improving the accuracy of presented data.

Cardiac remodeling is the major pathological change of heart failure. And let-7 family has been implicated in the development and pathogenesis of cardiovascular diseases. However, the mechanisms underlying let-7b-5p-mediated cellular pathogenesis of cardiac remodeling are not well understood. The present study aimed to explore the effects of let-7b-5p on cardiac remodeling and the corresponding regulatory mechanism. In vivo results indicated that cardiac let-7b-5p was upregulated in the mouse model of Angiotensin II (Ang II)-induced cardiac remodeling. Additionally, let-7b-5p knockdown ameliorated the effects of Ang II-induced cardiac remodeling, whereas let-7b-5p overexpression facilitated cardiac remodeling. In vitro, let-7b-5p mimics induced cardiomyocyte hypertrophy, fibroblast transdifferentiation, and the expression of inflammatory factors in neonatal mouse cardiomyocytes (NMCMs), neonatal mouse cardiac fibroblasts (NMCFs), and bone marrow-derived macrophages (BMDMs), respectively. Furthermore, let-7b-5p exerted its cardiac pro-remodeling effects at least partially through a small extracellular vesicle (SEV)-based delivery strategy. We found that let-7b-5p was enriched in SEVs derived from Ang II-treated NMCMs (NMCM-SEV) but not from Ang II-treated NMCFs (NMCF-SEV). Mechanistic analyses revealed that NMCM-SEV promoted TLR7 and MyD88 expression, which increased NF-κB phosphorylation levels. Knockdown of let-7b-5p, TLR7 or MyD88 in NMCMs, NMCFs, and BMDMs abolished the cardiac pro-remodeling effects of NMCM-SEV. These results uncover that let-7b-5p-containing NMCM-SEVs promote cardiac remodeling via the TLR7/MyD88/NF-κB pathway, implicating let-7b-5p as a potential therapeutic target for heart failure., (© 2024 Federation of American Societies for Experimental Biology.)

Intestinal failure-associated liver disease (IFALD) is a serious complication of long-term parenteral nutrition in patients with short bowel syndrome (SBS), and is the main cause of death in SBS patients. Prevention of IFALD is one of the major challenges in the treatment of SBS. Impairment of intestinal barrier function is a key factor in triggering IFALD, therefore promoting intestinal repair is particularly important. Intestinal repair mainly relies on the function of intestinal stem cells (ISC), which require robust mitochondrial fatty acid oxidation (FAO) for self-renewal. Herein, we report that aberrant LGR5+ ISC function in IFALD may be attributed to impaired farnesoid X receptor (FXR) signaling, a transcriptional factor activated by steroids and bile acids. In both surgical biopsies and patient-derived organoids (PDOs), SBS patients with IFALD represented lower population of LGR5+ cells and decreased FXR expression. Moreover, treatment with T-βMCA in PDOs (an antagonist for FXR) dose-dependently reduced the population of LGR5+ cells and the proliferation rate of enterocytes, concomitant with decreased key genes involved in FAO including CPT1a. Interestingly, however, treatment with Tropifexor in PDOs (an agonist for FXR) only enhanced FAO capacity, without improvement in ISC function and enterocyte proliferation. In conclusion, these findings suggested that impaired FXR may accelerate the depletion of LGR5 + ISC population through disrupted FAO processes, which may serve as a new potential target of preventive interventions against IFALD for SBS patients., (© 2024 Federation of American Societies for Experimental Biology.)

Metacestodiasis is an infectious disease caused by the larval stage of cestode parasites. This disease poses a serious health hazard to wildlife, livestock, and humans, and it incurs substantial economic losses by impacting the safety of the livestock industry, the quality of meat production, and public health security. Unfortunately, there is currently no available molecular diagnostic method capable of distinguishing cysticercus- and Echinococcus-derived microRNAs (miRNAs) from other helminthes and hosts in the plasma of metacestode-infected animals. This study aims to develop a specific, sensitive, and cost-efficient molecular diagnostic method for cysticercosis and echinococcosis, particularly for early detection. The study developed a rolling circular amplification (RCA)-assisted CRISPR/Cas9 detection method based on parasite-derived miRNA let-7-5p. Using a series of dilutions of the let-7 standard, the limit of detection (LOD) of the qPCR, RCA, and RCA-assisted CRISPR/Cas9 methods was compared. The specificity of qPCR and CRISPR/Cas9 was evaluated using four artificially synthesized let-7 standards from different species. A total of 151 plasma samples were used to evaluate the diagnostic performance. Additionally, the study also assessed the correlation between plasma levels of let-7-5p, the number of Taenia pisiformis cysticerci, and the weight of Echinococcus multilocularis cysts. The results demonstrated that the RCA-assisted CRISPR/Cas9 assay could significantly distinguish let-7 from cestodes and other species, achieving a LOD of 10 aM; the diagnostic sensitivity and specificity for rabbit cysticercosis and mouse E. multilocularis were 100% and 97.67%, and 100% and 100%, respectively. Notably, let-7-5p gradually increased in the plasma of T. pisiformis-infected rabbits from 15 days post infection (dpi), peaked at 60 dpi, and persisted until 120 dpi. In E. multilocularis-infected mice, let-7-5p gradually increased from 15 dpi and persisted until 90 dpi. Furthermore, the expression of let-7-5p positively correlated with the number of cysticerci and cyst weight. These results indicated that the let-7-5p-based RCA-assisted CRISPR/Cas9 assay is a sensitive and specific detection method that can be used as a universal diagnostic method for metacestodiasis, particularly for early diagnosis (15 dpi)., (© 2024 The Author(s). The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.)