Reproductive biology of blue marlin (Makaira nigricans) in the western Pacific Ocean

The reproductive biology of blue marlin (Makaira nigricans) was assessed from 1001 fish (ranging from 121 to 275 cm in eye-to-fork length; EFL) caught by Taiwanese offshore longliners in the western Pacific Ocean from September 2000 to December 2001 and from 843 gonad samples from these fish, The overall sex ratio of the catch was approximately 1:1 dur ing the sampling period, but blue marlin are sexually dimorphic; females are larger than males. Reproductive activity (assessed by histology), a gonadosomatic index, and the distribution of oocyte diameters, indicated that spawning occurred predominantly from May to September. The estimated sizes-at-maturity (EFL50) were 179.76 ±1.01 cm (mean ±standard error) for females and 130 ±1 cm EFL for males. Blue marlin are multiple spawners and oocytes develop asynchronously. The proportion of mature females with ovaries containing postovulatory follicles (0.41) and hydrated oocytes (0.34) indicated that the blue marlin spawned once every 2–3 days on average. Batch fecundity (BF) for 26 females with the most advanced oocytes (≥1000 μm), but without postovulatory follicles, ranged from 2.11 to 13.50 million eggs (6.94 ± 0.54 million eggs). The relationships between batch fecundity (BF, in millions of eggs) and EFL and round weight (RW, kg) were BF = 3.29 × 10 –12 EFL5.31 (r2 = 0.70) and BF = 1.59 × 10–3 RW 1.73 (r2= 0.67), respectively. The parameters estimated in this study are key information for stock assessments of blue marlin in the western Pacific Ocean and will contribute to the conservation and sustainable yield o

Inferring the ecology of north-Pacific albacore tuna from catch-and-effort data

Catch-and-effort data are among the primary sources of information for assessing the status of terrestrial wildlife and fish. In fishery science, elaborate stock-assessment models are fitted to such data in order to estimate fish-population sizes and guide management decisions. Given the importance of catch-and-effort data, we scoured a comprehensive dataset pertaining to albacore tuna (Thunnus alalunga) in the north Pacific ocean for novel ecological information content about this commercially valuable species. Specifically, we used unsupervised learning based on finite mixture modelling to reveal that the north Pacific albacore-tuna stock can be divided into four pseudo-cohorts ranging in age from approximately 3 to 12 years old. We discovered that smaller size pseudo-cohorts inhabit relatively high -- subtropical to temperate -- latitudes, with hotspots off the coast of Japan. Larger size pseudo-cohorts inhabit lower -- tropical to subtropical -- latitudes, with hotspots in the western and central north Pacific. These results offer evidence that albacore tuna prefer different habitats depending on their size and age, and point to long-term migratory routes for the species that the current tagging technology is unlikely to capture in full. We discuss the implications of the results for data-driven modelling of albacore tuna in the north Pacific, as well as the management of the north Pacific albacore-tuna fishery.Comment: 9 pages, 4 figure

Increased IgG4-Positive Plasma Cells in Granulomatosis with Polyangiitis: A Diagnostic Pitfall of IgG4-Related Disease

Granulomatosis with polyangiitis (Wegener's) (GPA) may mimic IgG4-related disease (IgG4-RD) on histologic examination of some biopsies, especially those from head and neck sites. IgG4 immunostain is often performed in this context for differential diagnosis with IgG4-RD. However, the prevalence of IgG4+ cells in GPA has not been explored. We examined the IgG4+ cells in 26 cases confirmed as GPA by a thorough clinical and pathologic assessment. Twenty-six biopsies consisted of 14 sinonasal/oral cavity/nasopharynx, 7 orbit/periorbital, 3 lung/pleura, 1 iliac fossa/kidney, and 1 dura specimens. Eight of 26 (31%) biopsies revealed increased IgG4+ cells (>30/HPF and >40% in IgG4+/IgG+ ratio). The IgG4+ cells and IgG4+/IgG+ ratio ranged 37–137/hpf and 44–83%, respectively. Eight biopsies with increased IgG4+ cells were from sinonasal (n = 4) or orbital/periorbital (n = 4) sites. In conclusion, increased IgG4+ cells are not uncommonly seen in sinonasal or orbital/periorbital biopsies of GPA, which could pose as a diagnostic pitfall

Can diagnostic tests help identify model misspecification in integrated stock assessments?

AbstractA variety of data types can be included in contemporary integrated stock assessments to simultaneously provide information on all estimated parameters. Conflicts between data, which are often a symptom of model misspecification and evident as model misfit, can affect the estimates of important parameters and derived quantities. Unfortunately, there are few standard diagnostic tools available for integrated stock assessment models that can provide the analyst with all the information needed to determine if there is substantial model misspecification. In this study, we use simulation methods to evaluate the ability of commonly-used and recently-proposed diagnostic tests to detect model misspecification in the observation model process (i.e., the incorrect form for survey selectivity), systems dynamics (i.e., incorrect assumed values for steepness of the stock-recruitment relationship and natural mortality), and incorrect data weighting. The diagnostic tests evaluated here were: i) residuals analysis (SDNR and runs test); ii) retrospective analysis; iii) the R0 likelihood component profile; iv) the age-structured production model (ASPM); and v) catch-curve analysis (CCA). The efficacy of the diagnostic tests depended on whether the misspecification was in the observation or systems dynamics model. Residual analyses were easily the best detector of misspecification of the observation model while the ASPM test was the only good diagnostic for detecting misspecification of system dynamics model. Retrospective analysis and the R0 likelihood component profile infrequently detected misspecified models, and CCA had a high probability of rejecting correctly-specified models. Finally, applying multiple carefully selected diagnostics can increase the power to detect misspecification without substantially increasing the probability of falsely concluding there is misspecification when the model is correctly specified

Enhancing Mechanical Properties of a Lightweight TiAlCrNbVZr Medium-Entropy Alloy: Fine-Tuning Alloy Composition and Thermomechanical Treatment

Abstract: The quest to reduce fuel consumption and environmental pollution in the transportation sector has heightened the demand for developing lightweight alloys with enhanced mechanical properties. Accordingly, this study focused on optimizing the mechanical properties of a lightweight Ti65(AlCrNbV)28Zr7 medium entropy alloy (MEA) by strategically adjusting its Al, Cr, Nb, and V elemental contents. Hardness testing indicated a strengthening ability hierarchy of Cr > Al > V > Nb. Furthermore, tensile tests revealed that although a high Cr content significantly enhances strength, it also reduces the ductility of an MEA. Drawing on mechanical insights gained from a previously studied Ti60Al10Cr10Nb10V10 MEA and the present findings, a novel Ti60Al10Cr4Nb10V9Zr7 (Ti60Zr7) MEA was developed. This new alloy retains a single body-centered cubic structure and demonstrated exceptional mechanical performance in tensile testing, with a yield strength of 1066 MPa and 22% ductility. The Ti60Zr7 MEA underwent a series of thermomechanical treatments, including 50% hot rolling, 80% cold rolling, and rapid annealing up to 800 °C at a rate of 25 °C/s. After thermal processing, the Ti60Zr7 MEA not only preserved its single body-centered cubic structure but also achieved a remarkable combination of yield strength (>1200 MPa) and ductility (measured as >15% elongation). These advancements underscore the alloy’s considerable potential for application in sports equipment and transportation vehicles

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment

An Unexpected Function of the Prader-Willi Syndrome Imprinting Center in Maternal Imprinting in Mice

Genomic imprinting is a phenomenon that some genes are expressed differentially according to the parent of origin. Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are neurobehavioral disorders caused by deficiency of imprinted gene expression from paternal and maternal chromosome 15q11–q13, respectively. Imprinted genes at the PWS/AS domain are regulated through a bipartite imprinting center, the PWS-IC and AS-IC. The PWS-IC activates paternal-specific gene expression and is responsible for the paternal imprint, whereas the AS-IC functions in the maternal imprint by allele-specific repression of the PWS-IC to prevent the paternal imprinting program. Although mouse chromosome 7C has a conserved PWS/AS imprinted domain, the mouse equivalent of the human AS-IC element has not yet been identified. Here, we suggest another dimension that the PWS-IC also functions in maternal imprinting by negatively regulating the paternally expressed imprinted genes in mice, in contrast to its known function as a positive regulator for paternal-specific gene expression. Using a mouse model carrying a 4.8-kb deletion at the PWS-IC, we demonstrated that maternal transmission of the PWS-IC deletion resulted in a maternal imprinting defect with activation of the paternally expressed imprinted genes and decreased expression of the maternally expressed imprinted gene on the maternal chromosome, accompanied by alteration of the maternal epigenotype toward a paternal state spread over the PWS/AS domain. The functional significance of this acquired paternal pattern of gene expression was demonstrated by the ability to complement PWS phenotypes by maternal inheritance of the PWS-IC deletion, which is in stark contrast to paternal inheritance of the PWS-IC deletion that resulted in the PWS phenotypes. Importantly, low levels of expression of the paternally expressed imprinted genes are sufficient to rescue postnatal lethality and growth retardation in two PWS mouse models. These findings open the opportunity for a novel approach to the treatment of PWS