Miracle-dz/UniFAR-FTUs huggingface dataset:
Rafting dispersal in a brooding southern sea star (Asteroidea : Anasterias)

Abstract. Marine biogeographers have long speculated that macroalgal rafting presents a dispersal mechanism for brooding marine invertebrates of the Southern Ocean, but few direct observations of rafting by echinoderm taxa have been documented. Here we report rafting of the brooding benthic sea star Anasterias suteri, along with two mollusc taxa (Onithochiton neglectus – also a brooder – and Cantharidus roseus), on detached bull-kelp Durvillaea antarctica in Foveaux Strait, southern New Zealand. The rafting journey, intercepted at sea, likely lasted for 2–3 weeks and may have covered several hundred kilometres. We use DNA sequences, together with meteorological and prevailing oceanographic data, to infer the likely Fiordland (mainland) origins of the raft and its epifauna. This rafting dispersal mechanism provides an explanation for the broad (circum-subantarctic) but disjunct distribution of brooding Anasterias populations, and for the genetic connectivity observed between their populations.
Cyclosporin A and FGF signaling support the proliferation/survival of mouse primordial germ cell-like cells in vitro†

Abstract Primordial germ cells (PGCs) are the founding population of the germ cell lineage that undergo a multistep process to generate spermatozoa or oocytes. Establishing an appropriate culture system for PGCs is a key challenge in reproductive biology. By a chemical screening using mouse PGC-like cells (mPGCLCs), which were induced from mouse embryonic stem cells, we reported previously that forskolin and rolipram synergistically enhanced the proliferation/survival of mPGCLCs with an average expansion rate of ∼20-fold. In the present study, we evaluated other chemicals or cytokines to see whether they would improve the current mPGCLC culture system. Among the chemicals and cytokines examined, in the presence of forskolin and rolipram, cyclosporin A (CsA) and fibroblast growth factors (FGFs: FGF2 and FGF10) effectively enhanced the expansion of mPGCLCs in vitro (∼50-fold on average). During the expansion by CsA or FGFs, mPGCLCs comprehensively erased their DNA methylation to acquire a profile equivalent to that of gonadal germ cells in vivo, while maintaining their highly motile phenotype as well as their transcriptional properties as sexually uncommitted PGCs. Importantly, these mPGCLCs robustly contributed to spermatogenesis and produced fertile offspring. Furthermore, mouse PGCs (mPGCs) cultured with CsA ex vivo showed transcriptomes and DNA methylomes similar to those of cultured mPGCLCs. The improved culture system for mPGCLCs/mPGCs would be instructive for addressing key questions in PGC biology, including the mechanisms for germ cell migration, epigenetic reprogramming, and sex determination of the germline. Summary sentence Cyclosporin A and fibroblast growth factors enhanced the proliferation/survival of mouse primordial germ cell-like cells in vitro with the retention of a capacity to contribute to spermatogenesis.
FRP Confinement of Stone Samples after Real Fire Exposure

The mechanical properties of stone materials can be severely affected by exposure to high temperatures. The effect of fire on stone buildings could cause irreversible damage and make it necessary to retrofit the affected elements. Particularly, the strengthening of columns by confinement with composites has been widely improved during the last decades. Today, fiber reinforced polymer (FRP) confinement represents a very interesting alternative to traditional steel solutions. This work studied the behavior of cylindrical stone specimens subjected to real fire action and confined by means of CFRP or GFRP jackets, with the aim of assessing the effectiveness of these reinforcement systems applied to a material that has previously been seriously damaged by high temperature exposure. In general, the strengthened samples showed notable increases in strength and ductility. The response seemed to depend basically on the FRP properties and not on the degree of damage that the stone core may have suffered. Finally, the results obtained experimentally were compared with the confinement models proposed by the available design guides, in order to evaluate the accuracy that these models can offer under the different situations addressed in this research.
Catch-up Growth in Intrauterine Growth-restricted Piglets Associated with the Return of Pancreatic and Intestinal Functions via Porcine Glucagon-like peptide-2 Microspheres

Background Intrauterine growth restriction (IUGR) results in abnormal morphology and gastrointestinal function. As a gastrointestinal growth factor, the manner by which the porcine glucagon-like peptide-2 (pGLP-2) microsphere administration catches up with the growth of IUGR piglets was investigated. Methods Fourteen newborn IUGR piglets were assigned into the IUGR and pGLP-2 microsphere groups. The piglets in the pGLP-2 microsphere group were intraperitoneally administered with 100 mg of pGLP-2 microspheres on day 1 of birth. Results From days 15 to 26 of trial, the body weight of the IUGR piglets treated with pGLP-2 microspheres was significantly higher than that in the control group. Importantly, the weaning weight in the pGLP-2 group catches up with the body weight of normal birth weight piglets. IUGR piglets treated with pGLP-2 microspheres significantly showed increased pancreas weight, serum insulin content, and activities of digestive enzymes (lipase, trypsin, chymotrypsin, and amylase). Injection of pGLP-2 microspheres returned the intestinal absorptive capacity by significantly increasing the mRNA expression of sodium-glucose cotransporter 1 in the jejunum, glucose transporter type 2 in the duodenum and jejunum, H + -coupled transporter, and peptide transporter 1 in the jejunum and ileum. It also returned the redox balance by increasing the catalase mRNA expression and decreasing the heat shock protein 70 mRNA expression. In addition, this improvement was associated with the significant increase in gut diameter, length, and weight induced by pGLP-2. Conclusions Injection of pGLP-2 microspheres was a suitable therapeutic strategy for compensatory growth in low birth weight IUGR piglet.
Influence of high ambient temperature on reproductive performance and physiology of rabbit does in a commercial rabbitry in Greece

Αντικeίμeνο της παρούσας eργασίας υπήρξe η μeλέτη των αναπαραγωγικών και φυσιολογικών παραμέτρων των κονικλομητέρων υπό τις φυσικές συνθήκeς eκτροφής τους στην Eλλάδα, κατά τη θeρινή (Ιούλιος 2000-Οκτώβριος 2000 και Μάϊος 2001-Ιούνιος 2001) και χeιμeρινή (Νοέμβριος-Απρίλιος 2001) πeρίοδο (μέση θeρμοκρασία θαλάμων eκτροφής 19,5°C και 12,4°C αντίστοιχα). Για τους σκοπούς της μeλέτης χρησιμοποιήθηκαν 809 eνήλικα θηλυκά και 20 eνήλικα αρσeνικά κουνέλια διασταυρωμένα Νέας Ζηλανδίας χ Καλιφόρνιας. Οι φυσιολογικές παράμeτροι που μeλeτήθηκαν ήταν: το σύνολο των γeννηθέντων κονικλιδίων (ζωντανών, νeκρών, θνησιγeνών) ανά κονικλομητέρα, το βάρος της το- κeτοομάδας, το μέσο ατομικό βάρος γέννησης και ο αριθμός απογαλακτισθέντων και το ποσοστό θνησιμότητας των θηλαζόντων κονικλιδίων μe βάση τον αριθμό των ζωντανών γeννηθέντων και των υιοθeτημένων ανά τοκeτοομάδα. Eλήφθη η θeρμοκρασία απeυθυσμένου και ο ρυθμός αναπνοών των κονικλομητέρων. Η δυσμeνής eπίδραση των υψηλών θeρινών θeρμοκρασιών ήταν σημαντική στο μέγeθος της τοκeτοομάδας κατά τη γέννηση (7,38 συνολικά γeννηθέντα τη θeρινή πeρίοδο έναντι 8,05 τη χeιμeρινή Ρ 0,05, και 68g έναντι 65g το χeιμώνα, Ρ>0,05, αντίστοιχα). (Στις κονικλομητέρeς κατά τη θeρινή πeρίοδο παρατηρήθηκe στατιστικά μη σημαντική αύξηση της θeρμοκρασίας απeυθυσμένου (39,09°C έναντι 38,93°C χο χeιμώνα), καθώς και στατιστικά σημαντική αύξηση του αριθμού των αναπνοών/λeπτό (128,08 αναπνοές/λeπτό έναντι 115,37 αναπνοές/ λeπτό το χeιμώνα, Ρ<0,001). Πέρα από την eπίδραση της θeρμοκρασίας του πeριβάλλοντος μeλeτήθηκe τόσο η eπίδραση του αριθμού τοκeτών ανά κονικλομητέρα όσο και η ατομικότητα της κάθe κονικλομητέρας στις αναπαραγωγικές παραμέτρους. Σημαντική ήταν η eπίδραση του αριθμού τοκeτών ανά κονικλομητέρα στο σύνολο των γeννηθέντων κονικλιδίων, στα ζωντανά, νeκρά και απογαλακτισθέντα κονικλίδια, στο βάρος της τοκeτοομάδας κατά τη γέννηση, στο μέσο ατομικό βάρος γέννησης των κονικλιδίων και τέλος στον αριθμό αναπνοών/λeπτό των κονικλομητέρων. Συμπeρασματικά διαπιστώθηκe η αρνητική eπίδραση των υψηλών θeρμοκρασιών του πeριβάλλοντος στις αναπαραγωγικές και φυσιολογικές παραμέτρους των κονικλομητέρων.
Probing metabolic memory in the hepatic response to fasting.

Tissues may respond differently to a particular stimulus if they have been previously exposed to that same stimulus. Here we tested the hypothesis that a strong metabolic stimulus such as fasting may influence the hepatic response to a subsequent fast and thus elicit a memory effect. Overnight fasting in mice significantly increased plasma free fatty acids, glycerol, β-hydroxybutyrate and liver triglycerides, and decreased plasma glucose, plasma triglycerides, and liver glycogen levels. In addition, fasting dramatically changed the liver transcriptome, upregulating genes involved in gluconeogenesis and in uptake, oxidation, storage, and mobilization of fatty acids, and downregulating genes involved in fatty acid synthesis, fatty acid elongation/desaturation, and cholesterol synthesis. Fasting also markedly impacted the liver metabolome, causing a decrease in the levels of numerous amino acids, glycolytic intermediated, TCA cycle intermediates, and nucleotides. However, these fasting-induced changes were unaffected by two previous overnight fasts. Also, no significant effect was observed of prior fasting on glucose tolerance. Finally, analysis of the effect of fasting on the transcriptome in hepatocyte humanized mouse livers indicated modest similarity in gene regulation in mouse and human liver cells. In general, genes involved in metabolic pathways were up- or downregulated to a lesser extent in human liver cells than mouse liver cells. In conclusion, we found that previous exposure to fasting in mice did not influence the hepatic response to a subsequent fast, arguing against the concept of metabolic memory in the liver. Our data provide a useful resource for the study of liver metabolism during fasting.
The role of Smad4 in the regulation of insulin resistance, inflammation and cell proliferation in HTR8‐Svneo cells

Gestational diabetes mellitus (GDM) is a metabolic disorder whose major pathophysiological basis is demonstrated as placental insulin resistance (IR), while Smad4 always functions in the signal transduction of transforming growth factor beta (TGF‐β) pathway. Our study aims to figure out the role of Smad4 in an insulin resistance (IR) cellular model using placental trophoblast cell line. Importantly, HTR8‐Svneo cells, in the status of IR, indicated a significant increase in the expression of Smad4. Subsequently, the HTR8‐Svneo cell line with up‐regulated or depleted Smad4 was respectively achieved by the effective over‐expressed plasmid or siRNA of Smad4. We found out that the deficiency of Smad4 could promote the insulin sensitivity and restrict the inflammatory response in IR group of cells with significant augment in glucose uptake, up‐regulation of insulin signalling‐related molecules and attenuation in inflammatory biomarker expressions. On the contrary, the over‐expression of Smad4 showed a reversal effect on these alterations in IR group of cells. Besides, the positive effect of Smad4 on cell viability was also observed in our study.
Characterization and analysis of genes involved in colorectal and endometrial cancer

Loss o f cellular functions by stepwise mutation of critical regulatory genes can lead to the clonal evolution of cells that metastasize and become pathogenic to their host. These mutations arise by both hereditary and somatic mechanisms. Hereditary cancers account for a minority of cancers but the elucidation of the causative hereditary genes gives insight into how both sporadic and hereditary cancer arises. Colorectal cancer (CRC) is the second deadliest cancer after lung cancer. Hereditary nonpolyposis colorectal cancer (HNPCC) is the most common form of hereditary CRC and is caused by mutation in the mismatch repair genes MSH2, MLHU MSH6 and PMS2. Described herein are direct sequencing methods of mutation detection and an assay for HNPCC carrier determination. Also described is the mapping of a candidate tumor suppressor gene in colorectal cancer to 32.2 cM tiom chromosome Ip-tel. Mutational analysis of the RIZ gene located in this region found frequent truncating frameshift mutations and loss of both RIZ mRNA and protein expression in colorectal tumors. Germline mutations in mismatch repair genes have been implicated in endometrial cancer. Another study was undertaken to determine the mutational frequency of the mismatch repair genes in sporadic endometrial cancer. One pathogenic germline mutation was found in the h4LHl gene, u a rate of at least 1.4% (1/74). This rate is comparable to the hereditary involvement of the mismatch repair genes in colorectal cancer. A hypermutable (A), region was identified in MSH2. Additionally, a nonexpressed pseudogene was found that is highly homologous to the PMS2 gene. The pseudogene is polymorphic for two alterations in an (A), repeat region. Due to the high homology to PMS2, these polymorphisms could be mistaken for mutation in the PMS2 gene and erroneously thought to be a cause of HNPCC. The I1307K polymorphism in the APC gene has been reported to be a low penetrant mutation in individuals o f Ashkenazi Jewish descent. Another study was undertaken to determine its frequency in other ethnic backgrounds. No carriers were found in individuals of Finnish, Italian and Hawaiian-Japanese descent, indicating that the 11307K polymorphism is unique to the Ashkenazi Jewish population.
Clinical characteristics and molecular epidemiology of invasive Streptococcus agalactiae infections between 2007 and 2016 in Nara, Japan

Invasive Streptococcus agalactiae (GBS) infections are increasingly common among neonates and the elderly. Therefore, GBS surveillance for better antibiotic treatment and prophylaxis strategies are needed. We retrospectively evaluated the clinical aspects of invasive infections and the phenotypic and genetic diversity of infectious isolates from Nara, Japan, collected between 2007 and 2016, by using information from hospital records. GBS strains collected from the blood and cerebrospinal fluid cultures were evaluated for capsular types, multi-locus sequence typing (MLST), antibiotic susceptibility, antibiotics resistance gene, and pulsed-field gel electrophoresis. Forty GBS isolates (10 from children and 30 from adults) were analyzed, and the distribution of molecular serotype and allelic profiles varied between children and adults. We found the rates of early-onset disease in neonates with birth complications to be higher than that of previous reports, indicating that there could be relevance between complications at birth and early-onset disease. Standard antibiotic prophylaxis strategies may need to be reconsidered in patients with birth complications. In adults, the mean age of the patients was 68 years (male: 63%). Primary bacteremia was the most common source of infection. In the neonates, six had early-onset diseases and four had late-onset diseases. The most frequently identified strains were molecular serotype Ia ST23 (40%) and molecular serotype Ib ST10 (20%) in children and molecular serotype Ib ST10 (17%), molecular serotype VI ST1 (13%), and molecular serotype V ST1 (13%) in adults. Levofloxacin-resistant molecular serotype Ib strains and molecular serotypes V and VI ST1 were common causes of GBS infection in adults but were rarely found in children. Furthermore, pulsed-field gel electrophoresis in our study showed that specific clone isolates, that tend to have antibiotics resistance were widespread horizontally for a decade. Continuous surveillance and molecular investigation are warranted to identify the transmission route and improve antibiotic treatment strategies.
Periodontal Inflammation Primes the Systemic Innate Immune Response

The presence of periodontal diseases (PDs) often strongly correlates with other severe chronic inflammatory conditions, including cardiovascular disease, diabetes, and arthritis. However, the mechanisms through which these diseases interact are unclear. In PD, tissue and bone destruction in the mouth is driven by elevated recruitment of polymorphonuclear neutrophils (PMNs), which are primed and recruited from the circulation to sites of inflammation. We predicted that systemic effects on PMN mobilization or priming could account for the interaction between PD and other inflammatory conditions. We tested this using a mouse model of ligature-induced PD and found elevated PMN counts specifically in bone marrow, supporting a systemic effect of periodontal tissue inflammation on PMN production. In contrast, mice with induced peritonitis had elevated PMN counts in the blood, peritoneum, and colon. These elevated counts were further significantly increased when acute peritonitis was induced after ligature-induced PD in mice, revealing a synergistic effect of multiple inflammatory events on PMN levels. Flow cytometric analysis of CD marker expression revealed enhanced priming of PMNs from mice with both PD and peritonitis compared to mice with peritonitis alone. Thus, systemic factors associated with PD produce hyperinflammatory PMN responses during a secondary infection. To analyze this systemic effect in humans, we induced gingival inflammation in volunteers and also found significantly increased activation of blood PMNs in response to ex vivo stimulation, which reverted to normal following resolution of gingivitis. Together, these results demonstrate that periodontal tissue inflammation has systemic effects that predispose toward an exacerbated innate immune response. This indicates that peripheral PMNs can respond synergistically to simultaneous and remote inflammatory triggers and therefore contribute to the interaction between PD and other inflammatory conditions. This suggests larger implications of PD beyond oral health and reveals potential new approaches for treating systemic inflammatory diseases that interact with PD.
Substitution of the fish meal by the earthworm and maggot meal in the feed of Nile tilapia Oreochromis niloticus reared in freshwater

The present experiment was conducted to evaluate the efficacy of dietary protein from maggot meal and earthworm meal to replace fish meal protein in Oreochromis niloticus juvenile feed. The fish used for this experiment come from the experience of the larval phase during which fish were fed with the formulated diets [fish diet (FD), maggot diet (MD) and earthworm diet (ED)] content 40% crude protein and the commercial diet (CD) content 34.5% crude protein. At the end of this larval phase, the average weights were 0.75 ± 1.93, 0.71 ± 3.55, 0.55 ± 2.52, 0.62 ± 2.52 g for FD, MD, ED and CD respectively. These different weights constitute the initials weights for this experience. In this experimental, the formulated diets (FD, MD and ED) content 30% crude protein and 29.5% crude protein for CD. Fish were fed four times daily to triplicate groups at 10.7% body weight for consecutive 90 days. After these days, fish fed with FD gave significantly higher average daily gain (ADG, 0.3 ± 0.03 g.day-1) than MD (0.22 ± 0.18 g.day-1). Fish fed with ED had the lowest ADG (0.14 ± 0.12 g.day-1). The specific growth rate (SGR) were higher in fish group fed with FD, MD and CD and shows no significant difference (p > 0.05) compared to ED. Feed conversion ratio (FCR), protein efficiency ratio (PER) and survival rate (SR) show no significant difference (p > 0.05) in the all test. The production cost of 1 kg of fish (PC) and the carcass chemicals composition were evaluated. In conclusion, these results of this study indicate the possibility of completely using maggot meal as a source protein in the diet of O. niloticus juvenile to increase the growth of fish and reduce the cost of 1 kg of fish produced. Key words: Ivory Coast, fish nutrition, replace fishmeal, invertebrates meal, zootechnic, economics parameters.
Stereotactic Body Radiotherapy Versus Delayed Surgery for Early-stage Non-small-cell Lung Cancer

Supplemental Digital Content is available in the text Objective: To evaluate the overall survival of patients with operable stage IA non-small-cell lung cancer (NSCLC) who undergo “early” SBRT (within 0–30 days after diagnosis) versus “delayed” surgery (90–120 days after diagnosis). Summary of Background Data: During the COVID-19 pandemic, national guidelines have recommended patients with operable stage IA NSCLC to consider delaying surgery by at least 3 months or, alternatively, to undergo SBRT without delay. It is unknown which strategy is associated with better short- and long-term outcomes. Methods: Multivariable Cox proportional hazards modeling and propensity score-matched analysis was used to compare the overall survival of patients with stage IA NSCLC in the National Cancer Data Base from 2004 to 2015 who underwent “early” SBRT (0–30 days after diagnosis) versus that of patients who underwent “delayed” wedge resection (90–120 days after diagnosis). Results: During the study period, 570 (55%) patients underwent early SBRT and 475 (45%) underwent delayed wedge resection. In multivariable analysis, delayed resection was associated with improved survival [adjusted hazard ratio 0.61; (95% confidence interval (CI): 0.50–0.76)]. Propensity-score matching was used to create 2 groups of 279 patients each who received early SBRT or delayed resection that were well-matched with regard to baseline characteristics. The 5-year survival associated with delayed resection was 53% (95% CI: 45%–61%) which was better than the 5-year survival associated with early SBRT (31% [95% CI: 24%–37%]). Conclusion: In this national analysis, for patients with stage IA NSCLC, extended delay of surgery was associated with improved survival when compared to early treatment with SBRT.
Use as directed: do standard drink labels on alcohol containers help consumers drink (ir)responsibly? Real-world evidence from a quasi-experimental study in Yukon, Canada.

INTRODUCTION AND AIMS This paper examines the impact of an alcohol labelling intervention on recall of and support for standard drink (SD) labels, estimating the number of SDs in alcohol containers, and intended and unintended use of SD labels. DESIGN AND METHODS A quasi-experimental study was conducted in Canada where labels with a cancer warning, national drinking guidelines and SD information were applied to alcohol containers in the single liquor store in the intervention site, while usual labelling continued in the two liquor stores in the comparison site. Three waves of surveys were conducted in both sites before and at two time-points after the intervention with 2049 cohort participants. Generalised estimating equations were applied to estimate changes in all outcomes. RESULTS Participants in the intervention relative to the comparison site had greater odds of recalling [adjusted odds ratio (AOR) 5.69, 95% confidence interval (CI) 3.02, 10.71] and supporting SD labels (AOR 1.49, 95% CI 1.04, 2.12) and lower odds of reporting using SD labels to purchase high strength, low-cost alcohol (AOR 0.65, 95% CI 0.45, 0.93). Exposure to the labels had negligible effects on accurately estimating the number of SDs (AOR 1.06, 95% CI 0.59, 1.93) and using SD labels to drink within guidelines (AOR 1.04, 95% CI 0.75, 1.46). DISCUSSION AND CONCLUSIONS Evidence-informed labels increased support for and decreased unintended use of SD labels. Such labels can improve accuracy in estimating the number of SDs in alcohol containers and adherence to drinking guidelines.