CrossZoom: Simultaneous Motion Deblurring and Event Super-Resolving.

Even though the collaboration between traditional and neuromorphic event cameras brings prosperity to frame-event based vision applications, the performance is still confined by the resolution gap crossing two modalities in both spatial and temporal domains. This paper is devoted to bridging the gap by increasing the temporal resolution for images, i.e., motion deblurring, and the spatial resolution for events, i.e., event super-resolving, respectively. To this end, we introduce CrossZoom, a novel unified neural Network (CZ-Net) to jointly recover sharp latent sequences within the exposure period of a blurry input and the corresponding High-Resolution (HR) events. Specifically, we present a multi-scale blur-event fusion architecture that leverages the scale-variant properties and effectively fuses cross-modal information to achieve cross-enhancement. Attention-based adaptive enhancement and cross-interaction prediction modules are devised to alleviate the distortions inherent in Low-Resolution (LR) events and enhance the final results through the prior blur-event complementary information. Furthermore, we propose a new dataset containing HR sharp-blurry images and the corresponding HR-LR event streams to facilitate future research. Extensive qualitative and quantitative experiments on synthetic and real-world datasets demonstrate the effectiveness and robustness of the proposed method. Codes and datasets are released at https://bestrivenzc.github.io/CZ-Net/.

Differential oral and gut microbial structure related to systemic metabolism in kidney stone patients.

OBJECTIVES: To investigate the role of the oral and gut microbiome related to systemic metabolism and clinical parameters in various types of kidney stone disease. PATIENTS AND METHODS: We conducted a case-control study by analyzing 16S rRNA and untargeted metabolomics profiling of 76 fecal, 68 saliva, 73 urine, and 43 serum samples from 76 participants aged 18-75 years old. The participants included 15 patients with uric acid stones, 41 patients with calcium oxalate stones, and 20 healthy controls. Correlations among microbiome, metabolism, and clinical parameters were identified through Spearman's correlation analysis. (Clinical trial No. ChiCTR2200055316). RESULTS: Patients with uric acid stones exhibited reduced richness and diversity in their microbiome, as well as altered composition in both oral and gut microbiome. Furthermore, their fecal samples showed lower relative abundances of Bacteroides and Lachnospiraceae, while their saliva samples showed higher relative abundances of Porphyromonas and Neisseria. Predicted KEGG metabolism pathways, including amino acid and fatty acid metabolisms, were significantly altered in subjects with uric acid stones. Oral, gut microbiota, and metabolism were also associated with low water intake and urine pH. The area under the curve (AUC) of the specific microbiota and metabolite prediction models was over 0.85. CONCLUSION: The structure and composition of the oral and gut microbiome in different types of kidney stone disease, the correlations between oral and gut microbiome, and the associations among oral and gut microbiota, systemic metabolism and clinical parameters imply an important role that the oral and gut microbiome may play in kidney stone disease.

Production of MSTN knockout porcine cells using adenine base-editing-mediated exon skipping.

Gene-knockout pigs have important applications in agriculture and medicine. Compared with CRISPR/Cas9 and cytosine base editing (CBE) technologies, adenine base editing (ABE) shows better safety and accuracy in gene modification. However, because of the characteristics of gene sequences, the ABE system cannot be widely used in gene knockout. Alternative splicing of mRNA is an important biological mechanism in eukaryotes for the formation of proteins with different functional activities. The splicing apparatus recognizes conserved sequences of the 5' end splice donor and 3' end splice acceptor motifs of introns in pre-mRNA that can trigger exon skipping, leading to the production of new functional proteins, or causing gene inactivation through frameshift mutations. This study aimed to construct a MSTN knockout pig by inducing exon skipping with the aid of the ABE system to expand the application of the ABE system for the preparation of knockout pigs. In this study, first, we constructed ABEmaxAW and ABE8eV106W plasmid vectors and found that their editing efficiencies at the targets were at least sixfold and even 260-fold higher than that of ABEmaxAW by contrasting the editing efficiencies at the gene targets of endogenous CD163, IGF2, and MSTN in pigs. Subsequently, we used the ABE8eV106W system to realize adenine base (the base of the antisense strand is thymine) editing of the conserved splice donor sequence (5'-GT) of intron 2 of the porcine MSTN gene. A porcine single-cell clone carrying a homozygous mutation (5'-GC) in the conserved sequence (5'-GT) of the intron 2 splice donor of the MSTN gene was successfully generated after drug selection. Unfortunately, the MSTN gene was not expressed and, therefore, could not be characterized at this level. No detectable genomic off-target edits were identified by Sanger sequencing. In this study, we verified that the ABE8eV106W vector had higher editing efficiency and could expand the editing scope of ABE. Additionally, we successfully achieved the precise modification of the alternative splice acceptor of intron 2 of the porcine MSTN gene, which may provide a new strategy for gene knockout in pigs.

The Threshold Effects of Low-Dose-Rate Radiation on miRNA-Mediated Neurodevelopment of Zebrafish.

The biological effects and regulatory mechanisms of low-dose and low-dose-rate radiation are still rather controversial. Therefore, in this study we investigated the effects of low-dose-rate radiation on zebrafish neurodevelopment and the role of miRNAs in radiation-induced neurodevelopment. Zebrafish embryos received prolonged gamma-ray irradiation (0 mGy/h, 0.1 mGy/h, 0.2 mGy/h, 0.4 mGy/h) during development. Neurodevelopmental indicators included mortality, malformation rate, swimming speed, as well as the morphology changes of the lateral line system and brain tissue. Additionally, spatiotemporal expression of development-related miRNAs (dre-miR-196a-5p, dre-miR-210-3p, dre-miR-338) and miRNA processing enzymes genes (Dicer and Drosha) were assessed by qRT-PCR and whole mount in situ hybridization (WISH). The results revealed a decline in mortality, malformation and swimming speed, with normal histological and morphological appearance, in zebrafish that received 0.1 mGy/h; however, increased mortality, malformation and swimming speed were observed, with pathological changes, in zebrafish that received 0.2 mGy/h and 0.4 mGy/h. The expression of miRNA processing enzyme genes was altered after irradiation, and miRNAs expression was downregulated in the 0.1 mGy/h group, and upregulated in the 0.2 mGy/h and 0.4 mGy/h groups. Furthermore, ectopic expression of dre-miR-210-3p, Dicer and Drosha was also observed in the 0.4 mGy/h group. In conclusion, the effect of low-dose and low-dose-rate radiation on neurodevelopment follows the threshold model, under the regulation of miRNAs, excitatory effects occurred at a dose rate of 0.1 mGy/h and toxic effects occurred at a dose rate of 0.2 mGy/h and 0.4 mGy/h.

Full length sequencing reveals novel transcripts of detoxification genes along with related alternative splicing events and lncRNAs in Phyllotreta striolata.

The striped flea beetle, Phyllotreta striolata (Fabricius), damages crops in the Brassicaceae. The genetic data for this pest are insufficient to reveal its insecticide resistance mechanisms or to develop molecular markers for resistance monitoring. We used PacBio Iso-Seq technology to sequence the full-length transcriptome of P. striolata. After isoform sequence clustering and removal of redundant transcripts, a total of 41,293 transcripts were obtained, and 35,640 of these were annotated in the database of gene products. Structure analysis uncovered 4,307 alternative splicing events, and 3,836 sequences were recognized as lncRNAs. Transcripts with the complete coding region of important detoxification enzymes were further classified. There were 57 transcripts of P450s distributed in CYP2, CYP3, CYP4, and Mito CYP clades, 29 transcripts of ESTs from 4 functional groups, 17 transcripts of GSTs classified into 5 families, 51 transcripts of ABCs distributed in 6 families, and 19 transcripts of UGTs. Twenty-five lncRNAs were predicted to be regulators of these detoxification genes. Full-length transcriptome sequencing is an efficient method for molecular study of P. striolata and it is also useful for gene function analysis.

The role of protein kinase C alpha in tri-ortho-cresyl phosphate-induced autophagy in human neuroblastoma SK-N-SH cells.

As an organophosphorus ester, tri-ortho-cresyl phosphate (TOCP) has been widely used in agriculture and industry. It is reported that TOCP can induce organophosphate-induced delayed neuropathy (OPIDN) in sensitive animal and human species. However, the exact molecular mechanisms underlying TOCP-induced neurotoxicity are still unknown. In this study, we found that TOCP could induce autophagy by activating protein kinase C alpha (PKCα) signaling in neuroblastoma SK-N-SH cells. PKCα activators could positively regulate TOCP-induced autophagy by increasing the expression levels of neighbor BRCA1 gene protein 1 (NBR1), LC3 and P62 autophagic receptor protein. Furthermore, PKCα activation impaired the ubiquitin-proteasome system (UPS), resulting in inhibition of proteasome activity and accumulation of ubiquitinated proteins. UPS dysfunction could stimulate autophagy to serve as a compensatory pathway, which contributed to the accumulation of the abnormally hyperphosphorylated tau proteins and degradation of impaired proteins of the MAP 2 and NF-H families in neurodegenerative disorders.

The Efficacy of New Chinese Diabetes Risk Score in Screening Undiagnosed Type 2 Diabetes and Prediabetes: A Community-Based Cross-Sectional Study in Eastern China.

The New Chinese Diabetes Risk Score (NCDRS) is one of the recommended tools for screening undiagnosed type 2 diabetes in China. However, its performance in detecting undiagnosed diabetes needs to be verified in different community populations. Also, it is unknown whether NCDRS can be used in detecting prediabetes. In the present study, we aimed to evaluate the performance of NCDRS in detecting undiagnosed diabetes and prediabetes among the community residents in eastern China. We applied NCDRS in 7675 community residents aged 18-65 years old in Jiangsu Province. The results showed that the participants with undiagnosed diabetes reported the highest NCDRS value, followed by those with prediabetes (P < 0.001). The best cut-off points of NCDRS for detecting undiagnosed diabetes and prediabetes were 27 (with a sensitivity of 78.0% and a specificity of 57.7%) and 27 (with a sensitivity of 66.0% and a specificity of 62.9%). The AUCs of NCDRS for identifying undiagnosed diabetes and prediabetes were 0.749 (95% CI: 0.739~0.759) and 0.694 (95% CI: 0.683~0.705). These results demonstrate the excellent performance of NCDRS in screening undiagnosed diabetes in the community population in eastern China and further provide evidence for using NCDRS in detecting prediabetes.

Parallel Connected Generative Adversarial Network with Quadratic Operation for SAR Image Generation and Application for Classification.

Thanks to the availability of large-scale data, deep Convolutional Neural Networks (CNNs) have witnessed success in various applications of computer vision. However, the performance of CNNs on Synthetic Aperture Radar (SAR) image classification is unsatisfactory due to the lack of well-labeled SAR data, as well as the differences in imaging mechanisms between SAR images and optical images. Therefore, this paper addresses the problem of SAR image classification by employing the Generative Adversarial Network (GAN) to produce more labeled SAR data. We propose special GANs for generating SAR images to be used in the training process. First, we incorporate the quadratic operation into the GAN, extending the convolution to make the discriminator better represent the SAR data; second, the statistical characteristics of SAR images are integrated into the GAN to make its value function more reasonable; finally, two types of parallel connected GANs are designed, one of which we call PWGAN, combining the Deep Convolutional GAN (DCGAN) and Wasserstein GAN with Gradient Penalty (WGAN-GP) together in the structure, and the other, which we call CNN-PGAN, applying a pre-trained CNN as a discriminator to the parallel GAN. Both PWGAN and CNN-PGAN consist of a number of discriminators and generators according to the number of target categories. Experimental results on the TerraSAR-X single polarization dataset demonstrate the effectiveness of the proposed method.

Wnt signaling pathway involvement in genotypic and phenotypic variations in Waardenburg syndrome type 2 with MITF mutations.

Mutation in the gene encoding microphthalmia-associated transcription factor (MITF) lead to Waardenburg syndrome 2 (WS2), an autosomal dominantly inherited syndrome with auditory-pigmentary abnormalities, which is clinically and genetically heterogeneous. Haploinsufficiency may be the underlying mechanism for WS2. However, the mechanisms explaining the genotypic and phenotypic variations in WS2 caused by MITF mutations are unclear. A previous study revealed that MITF interacts with LEF-1, an important factor in the Wnt signaling pathway, to regulate its own transcription through LEF-1-binding sites on the MITF promoter. In this study, four different WS2-associated MITF mutations (p.R217I, p.R217G, p.R255X, p.R217del) that are associated with highly variable clinical features were chosen. According to the results, LEF-1 can activate the expression of MITF on its own, but MITF proteins inhibited the activation. This inhibition weakens when the dosage of MITF is reduced. Except for p.R217I, p.R255X, p.R217G, and p.R217del lose the ability to activate TYR completely and do not inhibit the LEF-1-mediated activation of the MITF-M promoter, and the haploinsufficiency created by mutant MITF can be overcome; correspondingly, the mutants' associated phenotypes are less severe than that of p.R217I. The dominant negative of p.R217del made it have a second-most severe phenotype. This study's data imply that MITF has a negative feedback loop of regulation to stabilize MITF gene dosage that involves the Wnt signaling pathway and that the interaction of MITF mutants with this pathway drives the genotypic and phenotypic differences observed in Waardenburg syndrome type 2 associated with MITF mutations.

Functional analysis of a SOX10 gene mutation associated with Waardenburg syndrome II.

Waardenburg syndrome (WS) is an autosomal dominant inherited non-syndromic type of hereditary hearing loss characterized by varying combinations of sensorineural hearing loss and abnormal pigmentation of the hair, skin, and inner ear. WS is classified into four subtypes (WS1-WS4) based on additional symptoms. WS2 is characterized by the absence of additional symptoms. Recently, we identified a SOX10 missense mutation c.422T > C (p.L141P) associated with WS2. We performed functional assays and found the mutant loses DNA-binding capacity, shows aberrant cytoplasmic and nuclear localization, and fails to interact with PAX3. Therefore, the mutant cannot transactivate the MITF promoter effectively, inhibiting melanin synthesis and leading to WS2. Our study confirmed haploinsufficiency as the underlying pathogenesis for WS2.

[Effect of Thrombocytopenia on Migration and Homing Pattern of Dendritic Cells].

OBJECTIVE: To investigate the effect of thrombocytopenia on the migration patterns of adoptive dendritic cell(DC) in vivo. METHODS: The mouse model of thrombocytopenia was established by intraperitoneal administration of anti-CD41 mAb MWReg30. Mouse bone marrow(BM)-derived DC were injected into thrombocytopenia mouse by footpad infusion and intravenous infusion. The DC migration and distribution pattern were detected by bioluminescence imaging. RESULTS: More than 80% platelets were cleared in the experimental group which was infused with anti-CD41 antibody. At 72 h after injection, the percentage of injected DC that migrated from footpad to popliteal lymph nodes(PLNs) and inguinal lymph nodes(ILNs) were (0.32±0.02)% and (0.02±0.01)% in experimental group, and (0.27±0.15)% and (0.02±0.02)% in control group, respectively. Statistic data showed that there was no statistical difference between these 2 groups (P>0.05). The issue distribution pattern of intravenously injected DC between experimental group and control group were not distinctly different, and large amounts of injected DC accumulated in the spleen, liver draining lymph-nodes lungs and liver. CONCLUSION: Thrombocytopenia has not a distinct effect on the migratory capacity and tissue distribution of DC by either footpad or intravenous injection.

Exome sequencing identifies POU4F3 as the causative gene for a large Chinese family with non-syndromic hearing loss.

Hearing impairment, or deafness (in its most severe form), is one of the most common human sensory disorders. There have been several reports of autosomal dominant mutations in the POU4F3 gene, which is associated with non-syndromic hearing loss. In this study, we identified a novel heterozygous mutation (c.602delT, p.L201fs) in the gene POU4F3 by taking advantage of whole-exome sequencing, which was validated by Sanger sequencing and completely co-segregated within a large hearing impaired Chinese family. We have focused on this pedigree since 2002, and we have mapped a deafness locus named DFNA42 (which has been renamed DFNA52, OMIM entry 607683) via a genome-wide scan. Furthermore, we analyzed this mutational variant and found that it was located at the beginning of the first functional domain of POU4F3, which could theoretically impair the function of POU4F3. We have identified a novel frameshift mutation in the POU4F3 gene. Further functional studies of variants of this specific gene are needed to illustrate the pathogenic mechanism(s) that underlie hearing impairment.

Digenic mutations involving both the BSND and GJB2 genes detected in Bartter syndrome type IV.

Bartter syndrome type IV, characterized by salt-losing nephropathies and sensorineural deafness, is caused by mutations of BSND or simultaneous mutations of both CLCNKA and CLCNKB. GJB2 is the primary causative gene for non-syndromic sensorineural deafness and associated with several syndromic sensorineural deafness. Owing to the rarity of Bartter syndrome, only a few mutations have been reported in the abovementioned causative genes. To investigate the underlying mutations in a Chinese patient with Bartter syndrome type IV, genetic analysis of BSND, CLCNKA, CLCNKB and GJB2 were performed by polymerase chain reaction and direct sequencing. Finally, double homozygous mutations c.22C > T (p.Arg8Trp) and c.127G > A (Val43Ile) were detected in exon 1 of BSND. Intriguingly, compound heterozygous mutations c.235delC (p.Leu79CysfsX3) and c.109G > A (p.Val37Ile) were also revealed in exon 2 of GJB2 in the same patient. No pathogenic mutations were found in CLCNKA and CLCNKB. Our results indicated that the homozygous mutation c.22C > T was the key genetic reason for the proband, and a digenic effect of BSND and GJB2 might contributed to sensorineural deafness. To our knowledge, it was the first report showing that the GJB2 gene mutations were detected in Bartter syndrome.

Identification and functional analysis of a novel mutation in the SOX10 gene associated with Waardenburg syndrome type IV.

Waardenburg syndrome type IV (WS4) is a rare genetic disorder, characterized by auditory-pigmentary abnormalities and Hirschsprung disease. Mutations of the EDNRB gene, EDN3 gene, or SOX10 gene are responsible for WS4. In the present study, we reported a case of a Chinese patient with clinical features of WS4. In addition, the three genes mentioned above were sequenced in order to identify whether mutations are responsible for the case. We revealed a novel nonsense mutation, c.1063C>T (p.Q355*), in the last coding exon of SOX10. The same mutation was not found in three unaffected family members or 100 unrelated controls. Then, the function and mechanism of the mutation were investigated in vitro. We found both wild-type (WT) and mutant SOX10 p.Q355* were detected at the expected size and their expression levels are equivalent. The mutant protein also localized in the nucleus and retained the DNA-binding activity as WT counterpart; however, it lost its transactivation capability on the MITF promoter and acted as a dominant-negative repressor impairing function of the WT SOX10.

WLD: a robust local image descriptor.

Inspired by Weber's Law, this paper proposes a simple, yet very powerful and robust local descriptor, called the Weber Local Descriptor (WLD). It is based on the fact that human perception of a pattern depends not only on the change of a stimulus (such as sound, lighting) but also on the original intensity of the stimulus. Specifically, WLD consists of two components: differential excitation and orientation. The differential excitation component is a function of the ratio between two terms: One is the relative intensity differences of a current pixel against its neighbors, the other is the intensity of the current pixel. The orientation component is the gradient orientation of the current pixel. For a given image, we use the two components to construct a concatenated WLD histogram. Experimental results on the Brodatz and KTH-TIPS2-a texture databases show that WLD impressively outperforms the other widely used descriptors (e.g., Gabor and SIFT). In addition, experimental results on human face detection also show a promising performance comparable to the best known results on the MIT+CMU frontal face test set, the AR face data set, and the CMU profile test set.

[Screening and identification interaction proteins of connexin 30].

OBJECTIVE: To explore interaction proteins affect functions of connexin 30 (Cx30) by screening and identification interaction proteins of Cx30. METHODS: The fusion expression vecto of CX30-C-terminal functional domain-pGEX-4T-2-GST was constructed, and then, fusion protein and GST were purified. They were incubated with the proteins of the foetus brain tissue disruption to pull down interaction proteins. The interaction proteins were separated by SDS-PAGE. Differential straps were cut to enzymolysis to prepare for mass chromatographic analysis, and then to index and screen interaction proteins in NCBInr database. The interaction proteins were identified by immunolocalization. RESULTS: The four interaction proteins of Cx30 were screened in the foetus brain tissue, as follow, Keratin 16, Camk2b, Tubulin beta-3 and alpha-tubulin. Cx30 was proved to coexist with Keratin 16 and Tubulin beta-3. CONCLUSIONS: Keratin 16, Camk2b, Tubulin beta-3 and alpha-tubulin are the interaction proteins of Cx30. The interaction proteins affect the assembly, intracellular transport, and channel switch of Cx30.

[Transplantation of free latissimus dorsi myocutaneous flaps for craniomaxillofacial reconstruction].

OBJECTIVE: This clinical study was to improve the surgical treatment to craniomaxillofacial tissue defects. METHODS: Since 1997, eight cases with severe craniomaxillofacial defects were treated using free latissimus dorsi myocutaneous flaps. In the operation, nerve anastomosis was performed. Of the 8 cases, 7 were treated in one stage, 1 was treated in 3 steps. The craniomaxillofacial defects ranged from 10 cm x 8 cm to 30 cm x 12 cm. The flaps was 12 cm x 10 cm to 32 cm x 16 cm in size. RESULTS: Postoperative follow-up for 6 months to 4 years demonstrated satisfactory results in all the cases. There was neither necrosis nor ulcer after the operation. The sensation recovery of the flap was also satisfactory. CONCLUSION: Free transfer of the latissimus dorsi myocutaneous flap is an ideal treatment to severe craniomaxillofacial defects as it possesses the advantages of reliable blood supply, ability against infections, large size, concealed donor site, and functional restoration of sensation and movement.

[An analysis of a large hereditary postlingually deaf families and detecting mutation of the deafness genes].

OBJECTIVE: To make a further exploration of the mutation frequence of Chinese genetic deafness and make clear if the genetic deafness genealogy that we collected recently was resulted from the mutation of the deafness genes which had been cloned. METHOD: We made regular otologic examination, hearing test and physical examination among the members of this genealogy, and also inspected the mutation of seven autosomal domiant deafness genes, HDIAI,GJB2, GJB3, DFNA5, a-tectorin(resulting in two types of genetic deafness, DFNA8 and DFNA12), MYO7A,POU4F3, with PCR-Sequencing method in this genealogy. RESULT: 1. The analysis of hereditary mode: There were forty-seven persons collected in five generations of this genealogy, and eighteen persons of them were deafness. It accorded with autosomal dominant inheritance from the pedigree. 2. The clinic feature: All patients with deafness were postlingual deafness. Their hearing decreased onset between sixteen to thirty years old, and the deafness was binaural symmetrical, progressive sensorineural and without other systems abnormity. 3. Analysis of mutation detection: We found two nucleotides changes in CX26 genes, A341G and GC257-258CG, and one changed nucleotide in POU4F3 gene,T90C. But we didn't think the changed nucleotides caused deafness after we analysed them. No mutation was found in other five genes. CONCLUSION: The possibility that the deafness of this genealogy was resulted from the cloned gene is relatively small. Now, We are scanning the whole gene groups and making linkage analysis on this pedigree, it is most probably to orientate a new deafness gene position.