Learning a global underwater geolocalization model with sectoral transformer.

Polarization-based underwater geolocalization presents an innovative method for positioning unmanned autonomous devices beneath the water surface, in environments where GPS signals are ineffective. While the state-of-the-art deep neural network (DNN) method achieves high-precision geolocalization based on sun polarization patterns in same-site tasks, its learning-based nature limits its generalizability to unseen sites and subsequently impairs its performance on cross-site tasks, where an unavoidable domain gap between training and test data exists. In this paper, we present an advanced Deep Neural Network (DNN) methodology, which includes a neural network built on a Transformer architecture, similar to the core of large language models such as ChatGPT, and integrates an unscented Kalman filter (UKF) for estimating underwater geolocation using polarization-based images. This combination effectively simulates the sun's daily trajectory, yielding enhanced performance across different locations and quicker inference speeds compared to current benchmarks. Following thorough analysis of over 10 million polarization images from four global locations, we conclude that our proposed technique significantly boosts cross-site geolocalization accuracy by around 28% when contrasted with traditional DNN methods.

Comparative Study of the Short-Term Efficacy and Safety between DEB-TACE and C-TACE in the Treatment of Unresectable Hepatocellular Carcinoma, a Retrospective Study.

Background: This is a retrospective study aimed at comparing the clinical efficacy and safety between drug-eluting bead transcatheter arterial chemoembolization (DEB-TACE) and conventional TACE (C-TACE) in the treatment of unresectable hepatocellular carcinoma. Methods: From July 2019 to April 2021, we enrolled 282 patients with unresectable hepatocellular carcinoma who were admitted to our hospital, of which 179 and 103 were in the DEB-TACE and C-TACE groups, respectively. General information was collected, and treatment effects were evaluated following the modified Response Evaluation Criteria in Solid Tumors. To compare the indexes of liver and kidney function, routine blood and coagulation were collected before treatment, and 1 day, 1 month, 3 months, and 6 months postoperatively. Postoperative adverse reactions (ie, fever, nausea, vomiting, anorexia, abdominal pain) were recorded to evaluate the safety of treatment. The two groups' progression-free survival and overall survival were also calculated to assess the treatment effect. Results: Preoperatively, the bilirubin, transaminase, and absolute neutrophil values between the two groups were not statistically significant (P > .05). At 1 month postoperatively, the absolute neutrophil values were significantly higher in the DEB-TACE group than those in the C-TACE group (P < .05). At 3 months postoperatively, AST, total bilirubin, and direct bilirubin levels were significantly elevated in the DEB-TACE group (P < .05), compared with the C-TACE group. However, at 6 months postoperatively, total and direct bilirubin levels in the C-TACE group were higher than those in the DEB-TACE group, showing a statistically significant difference (P < .05). For patients undergoing DEB-TACE, the survival risk was lower compared to those undergoing C-TACE. The survival risk of patients undergoing DEB-TACE was lower than that of C-TACE within 20 months postoperatively. The survival risk of patients undergoing DEB-TACE was lower than that of patients undergoing C-TACE. Conclusion: DEB-TACE may be superior to C-TACE in terms of safety and efficacy in the treatment of unresectable hepatocellular carcinoma.

Global trends and hotspots of gastrointestinal microbiome and toxicity based on bibliometrics.

Background: Toxicity concerns persist in the fields of public health, environmental science, and pharmacology. The intricate and vital role of the gastrointestinal microbiome in influencing toxicity and overall human health has gained increasing recognition in recent years. This study presents a comprehensive bibliometric analysis to evaluate the global scientific output, emerging trends, and research focal points in the area of gastrointestinal microbiome and toxicity. Methods: The Web of Science Core Collection database was retrieved for publications on the gastrointestinal microbiome and toxicity from 1980 to 2022. Our analysis included scholarly research papers written in English and excluded duplicate publications. We used Biblioshiny and R to summarize the count and citation metrics of included articles, and visualized research trends and keywords. CiteSpace was used to identify reference literature, keywords, and citation bursts. VOSviewer was used to visualize the network of related countries, institutions, authors, co-cited authors, and keywords. Results: A total of 2,140 articles were included, allowing us to identify significant countries, institutions, authors, and research focal points. Our results indicate a growing trend in the field, with China and the United States leading the research. The most productive journal in this area is Science of the Total Environment. Key findings revealed that research hotspots have shifted from drugs to environmental pollutants, emphasizing microplastics. Important mechanisms studied include oxidative stress, metabolism, inflammation, and apoptosis, with target organs being the gastrointestinal tract, liver, and brain. Furthermore, we highlight the rising significance of the gut-brain axis and the usage of zebrafish as a model organism. Conclusion: Despite certain limitations, such as focusing solely on English-language publications and excluding unpublished literature, our findings provide valuable insights into the current state of research on toxicity and the gastrointestinal microbiome. In the future, modifications to the gastrointestinal microbiome could offer new directions for treating and mitigating toxicity. These discoveries provide a comprehensive perspective on the broader scope of this research field.

Angle of polarization calibration for omnidirectional polarization cameras.

Polarization cameras quantify one of the fundamental properties of light and capture intrinsic properties of the imaged environment that are otherwise omitted by color sensors. Many polarization applications, such as underwater geolocalization and sky-based polarization compass, require simultaneous imaging of the entire radial optical field with omnidirectional lenses. However, the reconstructed angle of polarization captured with omnidirectional lenses has a radial offset due to redirection of the light rays within these lenses. In this paper, we describe a calibration method for correcting angle of polarization images captured with omnidirectional lenses. Our calibration method reduces the variance of reconstructed angle of polarization from 76.2 ∘ to 4.1 ∘. Example images collected both on an optical bench and in nature, demonstrate the improved accuracy of the reconstructed angle of polarization with our calibration method. The improved accuracy in the angle of polarization images will aid the development of polarization-based applications with omnidirectional lenses.

Viral metagenomics combined with metabolomics reveals the role of gut viruses in mouse model of depression.

Depression is a heterogeneous mental disorder that has been linked to disturbances in the gut microbiome. As an essential part of the gut microbiome, gut virome may play critical roles in disease progression and development. However, the relationship between the effect of gut virome on neurotransmitter metabolism and depression is unknown. We evaluated the alterations of gut virome and neurotransmitters in chronic restraint stress (CRS)-induced mouse model of depression based on viral metagenomics and LC-MS/MS metabolomics analyses. The results reveal that the gut virome profile of CRS group differed significantly from CON group. Microviridae was the most abundant differential viral family in both groups, followed by Podoviridae, while Siphoviridae was only enriched in CRS group of the top 100 differential viruses. The differential viruses that predicted to Enterobacteriaceae phage, Gammaproteobacteria phage and Campylobacteraceae phage were enriched in CRS group. Furthermore, 12 differential neurotransmitters primarily involved in the tryptophan metabolism pathway were altered in depressive-like mice. Besides, tryptamine and 5-methoxytryptamine hydrochloride were strongly associated with differential viruses belonging to Podoviridae and Microviridae. Our findings provide new insight into understanding the potential role of the gut virome and metabolites in depression.

A male with unilateral microphthalmia reveals a role for TMX3 in eye development.

Anophthalmia and microphthalmia are important birth defects, but their pathogenesis remains incompletely understood. We studied a patient with severe unilateral microphthalmia who had a 2.7 Mb deletion at chromosome 18q22.1 that was inherited from his mother. In-situ hybridization showed that one of the deleted genes, TMX3, was expressed in the retinal neuroepithelium and lens epithelium in the developing murine eye. We re-sequenced TMX3 in 162 patients with anophthalmia or microphthalmia, and found two missense substitutions in unrelated patients: c.116G>A, predicting p.Arg39Gln, in a male with unilateral microphthalmia and retinal coloboma, and c.322G>A, predicting p.Asp108Asn, in a female with unilateral microphthalmia and severe micrognathia. We used two antisense morpholinos targeted against the zebrafish TMX3 orthologue, zgc:110025, to examine the effects of reduced gene expression in eye development. We noted that the morphant larvae resulting from both morpholinos had significantly smaller eye sizes and reduced labeling with islet-1 antibody directed against retinal ganglion cells at 2 days post fertilization. Co-injection of human wild type TMX3 mRNA rescued the small eye phenotype obtained with both morpholinos, whereas co-injection of human TMX3(p.Arg39Gln) mutant mRNA, analogous to the mutation in the patient with microphthalmia and coloboma, did not rescue the small eye phenotype. Our results show that haploinsufficiency for TMX3 results in a small eye phenotype and represents a novel genetic cause of microphthalmia and coloboma. Future experiments to determine if other thioredoxins are important in eye morphogenesis and to clarify the mechanism of function of TMX3 in eye development are warranted.

Abnormal expression of collagen IV in lens activates unfolded protein response resulting in cataract.

Human diseases caused by mutations in extracellular matrix genes are often associated with an increased risk of cataract and lens capsular rupture. However, the underlying mechanisms of cataract pathogenesis in these conditions are still unknown. Using two different mouse models, we show that the accumulation of collagen chains in the secretory pathway activates the stress signaling pathway termed unfolded protein response (UPR). Transgenic mice expressing ectopic Col4a3 and Col4a4 genes in the lens exhibited activation of IRE1, ATF6, and PERK associated with expansion of the endoplasmic reticulum and attenuation of general protein translation. The expression of the transgenes had adverse effects on lens fiber cell differentiation and eventually induced cell death in a group of transgenic fiber cells. In Col4a1(+/Deltaex40) mutant mice, the accumulation of mutant chains also caused low levels of UPR activation. However, cell death was not induced in mutant lenses, suggesting that low levels of UPR activation are not proapoptotic. Collectively, the results provide in vivo evidence for a role of UPR in cataract formation in response to accumulation of terminally unfolded proteins in the endoplasmic reticulum.

Developmental distribution of collagen IV isoforms and relevance to ocular diseases.

Type IV collagens are the most abundant proteins in basement membranes. Distinct genes encode each of six isoforms, alpha1(IV) through alpha6(IV), which assemble into one of three characteristic heterotrimers. Disease-causing mutations in each of the six genes are identified in humans or mice and frequently include diverse ocular pathogenesis that encompass common congenital and progressive blinding diseases, such as optic nerve hypoplasia, glaucoma, and retinal degeneration. Understanding where and when collagen IV molecules are expressed is important because it defines limits for the location and timing of primary pathogenesis. Although localization of collagen IV isoforms in developed human eyes is known, the spatial and temporal distribution of type IV collagens throughout ocular development has not been determined in humans or in mice. Here, we use isoform-specific monoclonal antibodies to systematically reveal the localization of all six collagen IV isoforms in developing mouse eyes. We found that alpha1(IV) and alpha2(IV) always co-localized and were ubiquitously expressed throughout development. alpha3(IV) and alpha4(IV) also always co-localized but in a much more spatially and temporally specific manner than alpha1(IV) and alpha2(IV). alpha5(IV) co-localized both with alpha3(IV)/alpha4(IV), and with alpha6(IV), consistent with alpha5(IV) involvement in two distinct heterotrimers. alpha5(IV) was present in all basement membranes except those of the vasculature. alpha6(IV) was not detected in vasculature or in Bruch's membrane, indicating that alpha5(IV) in Bruch's membrane is part of the alpha3alpha4alpha5 heterotrimer. This comprehensive analysis defines the spatial and temporal distribution of type IV collagen isoforms in the developing eye, and will contribute to understanding the mechanisms underlying collagen IV-related ocular diseases that collectively lead to blindness in millions of people worldwide.

An intramolecular t-SNARE complex functions in vivo without the syntaxin NH2-terminal regulatory domain.

Membrane fusion in the secretory pathway is mediated by SNAREs (located on the vesicle membrane [v-SNARE] and the target membrane [t-SNARE]). In all cases examined, t-SNARE function is provided as a three-helix bundle complex containing three approximately 70-amino acid SNARE motifs. One SNARE motif is provided by a syntaxin family member (the t-SNARE heavy chain), and the other two helices are contributed by additional t-SNARE light chains. The syntaxin family is the most conformationally dynamic group of SNAREs and appears to be the major focus of SNARE regulation. An NH2-terminal region of plasma membrane syntaxins has been assigned as a negative regulatory element in vitro. This region is absolutely required for syntaxin function in vivo. We now show that the required function of the NH2-terminal regulatory domain (NRD) of the yeast plasma membrane syntaxin, Sso1p, can be circumvented when t-SNARE complex formation is made intramolecular. Our results suggest that the NRD is required for efficient t-SNARE complex formation and does not recruit necessary scaffolding factors.

The polybasic juxtamembrane region of Sso1p is required for SNARE function in vivo.

Exocytosis in Saccharomyces cerevisiae requires the specific interaction between the plasma membrane t-SNARE complex (Sso1/2p;Sec9p)and a vesicular v-SNARE (Snc1/2p). While SNARE proteins drive membrane fusion, many aspects of SNARE assembly and regulation are ill defined. Plasma membrane syntaxin homologs (including Sso1p) contain a highly charged juxtamembrane region between the transmembrane helix and the "SNARE domain" or core complex domain. We examined this region in vitro and in vivo by targeted sequence modification, including insertions and replacements. These modified Sso1 proteins were expressed as the sole copy of Sso in S. cerevisiae and examined for viability. We found that mutant Sso1 proteins with insertions or duplications show limited function, whereas replacement of as few as three amino acids preceding the transmembrane domain resulted in a nonfunctional SNARE in vivo. Viability is also maintained when two proline residues are inserted in the juxtamembrane of Sso1p, suggesting that helical continuity between the transmembrane domain and the core coiled-coil domain is not absolutely required. Analysis of these mutations in vitro utilizing a reconstituted fusion assay illustrates that the mutant Sso1 proteins are only moderately impaired in fusion. These results suggest that the sequence of the juxtamembrane region of Sso1p is vital for function in vivo, independent of the ability of these proteins to direct membrane fusion.