Instance Segmentation and Berry Counting of Table Grape before Thinning Based on AS-SwinT.

Berry thinning is one of the most important tasks in the management of high-quality table grapes. Farmers often thin the berries per cluster to a standard number by counting. With an aging population, it is hard to find adequate skilled farmers to work during thinning season. It is urgent to design an intelligent berry-thinning machine to avoid exhaustive repetitive labor. A machine vision system that can determine the number of berries removed and locate the berries removed is a challenge for the thinning machine. A method for instance segmentation of berries and berry counting in a single bunch is proposed based on AS-SwinT. In AS-SwinT, Swin Transformer is performed as the backbone to extract the rich characteristics of grape berries. An adaptive feature fusion is introduced to the neck network to sufficiently preserve the underlying features and enhance the detection of small berries. The size of berries in the dataset is statistically analyzed to optimize the anchor scale, and Soft-NMS is used to filter the candidate frames to reduce the missed detection of densely shaded berries. Finally, the proposed method could achieve 65.7 APbox, 95.0 AP0.5box, 57 APsbox, 62.8 APmask, 94.3 AP0.5mask, 48 APsmask, which is markedly superior to Mask R-CNN, Mask Scoring R-CNN, and Cascade Mask R-CNN. Linear regressions between predicted numbers and actual numbers are also developed to verify the precision of the proposed model. RMSE and R2 values are 7.13 and 0.95, respectively, which are substantially higher than other models, showing the advantage of the AS-SwinT model in berry counting estimation.

The Recent Progress of Pitch Nanoengineering to Obtain the Carbon Anode for High-Performance Sodium Ion Batteries.

As an anode material for sodium ion batteries (SIBs), carbon materials have attracted people's interest because of their abundant resources, good structural stability and low cost. Among most carbon precursors, pitch is viewed as a promising one because of a higher carbon content, good oxidation reversibility and low cost. However, the pitch-based carbon obtained with direct pyrolysis of pitch displays a high degree of graphitization and small layer spacing, which is unfavorable for the storage of sodium ions. In recent years, with the aid of the development of the nanoengineering process, the storage of sodium ions with pitch-based carbon has been drastically improved. This review article summarizes the recent progress of pitch nanoengineering to obtain the carbon anode for high-performance SIBs, including porous structure adjustment, heteroatom doping, co-carbonization and pre-oxidation. In addition, the merits and demerits of a variety of nanoengineering processes are discussed, and future research directions of pitch-based carbon are prospected.

Influenza vaccination-induced H3 stalk-reactive memory B-cell clone expansion.

Current vaccine formulations elicit a recall immune response against viruses by targeting epitopes on the globular head of hemagglutinin (HA), and stalk-reactive antibodies are rarely found. However, stalk-specific memory B-cell expansion after influenza vaccination is poorly understood. In this study, B cells were isolated from individuals immunized with seasonal tetravalent influenza vaccines at days 0 and 28 for H7N9 stimulation in vitro. Plasma and supernatants were collected for the analysis of anti-HA IgG using ELISA and a Luminex assay. Memory B cells were positively enriched, and total RNA was extracted for B cell receptor (BCR) H-CDR3 sequencing. All subjects displayed increased anti-H3 antibody secretion after vaccination, whereas no increase in cH5/3-reactive IgG levels was detected. The number of shared memory B-cell clones among individuals dropped dramatically from 593 to 37. Four out of 5 subjects displayed enhanced frequencies of the VH3-23 and VH3-30 genes, and one exhibited an increase in the frequency of VH1-18, which are associated with the stalk of HA. An increase in H3 stalk-specific antibodies produced by B cells stimulated with H7N9 viruses was detected after vaccination. These results demonstrated that H3 stalk-specific memory B cells can expand and secrete antibodies that bind to the stalk in vitro, although no increase in serum H3 stalk-reactive antibodies was found after vaccination, indicating potential for developing a universal vaccine strategy.

Overexpression of SHARPIN promotes tumor progression in ovarian cancer.

SHARPIN (Shank-associated RH domain interacting protein) plays an important role in tumorigenesis. However, its role in ovarian cancer remains largely unknown. To investigate this issue, we systematically analyzed the amplification and expression of the SHARPIN in the TCGA database. From the database, we found that SHARPIN was amplified in ovarian cancer compared to normal ovarian tissue, and the mRNA level of SHARPIN was significantly elevated in ovarian cancer compared to non-tumorigenic ovarian tissue. In addition, we observed similar results from ovarian cancer cell lines and clinical samples from ovarian cancer patients, which indicated that increased SHARPIN expression is associated with tumorigenesis in ovarian cancer. SHARPIN knockdown inhibited the migration and invasion of ovarian cancer cells, also inhibited cell cycle and promoted apoptosis, thereby suppressing cell proliferation. RNA-seq results showed that SHARPIN significantly increased the expression of P53 and P21 and decreased the expression of Cyclin D1 and c-Myc, all of which are involved in the regulation of cell proliferation. Subsequent mechanistic exploration revealed that SHARPIN knockdown increased the expression of caspases 3 and 9, leading to apoptosis of ovarian cancer cells. We also found that high expression of SHARPIN was associated with poor prognosis of ovarian cancer patients. Collectively, we demonstrated a positive correlation between SHARPIN and ovarian cancer progression and provide a basis for combined targeted therapy strategies for future ovarian cancer treatment.

Proteo-Transcriptomic Characterization of Sirex nitobei (Hymenoptera: Siricidae) Venom.

The wood-boring woodwasp Sirex nitobei is a native pest in Asia, infecting and weakening the host trees in numerous ecological and commercial coniferous forest plantations. In China, hosts of S. nitobei are diverse, so the pest has spread to several provinces of China, resulting in considerable economic and ecological damage. During female oviposition, S. nitobei venom along with arthrospores of the symbiotic fungus Amylostereum areolatum or A. chaetica is injected into host trees, and the combination of these two biological factors causes the death of xylem host trees. The presence of venom alone causes only the yellowing and wilting of needles. In this study, we constructed the venom gland transcriptome of S. nitobei for the first time and a total of 15,036 unigenes were acquired. From the unigenes, 11,560 ORFs were identified and 537 encoding protein sequences with signal peptides at the N-terminus. Then, we used the venomics approach to characterize the venom composition of female S. nitobei and predicted 1095 proteins by liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. We focused on seven proteins that were both highly expressed in the venom gland transcriptome and predicted in the crude venom proteome. These seven proteins are laccase-2, laccase-3, a protein belonging to the Kazal family, chitooligosaccharidolytic ß-N-acetylglucosaminidase, beta-galactosidase, icarapin-like protein, and waprin-Thr1-like protein. Using quantitative real-time PCR (qRT-PCR), we also proved that the genes related to these seven proteins are specifically expressed in the venom glands. Finally, we revealed the functional role of S. nitobei venom in the physiological response of host trees. It can not only promote the colonization of symbiotic fungus but contribute to the development of eggs and larvae. This study provides a deeper understanding of the molecular mechanism of the woodwasp-pine interaction.

LncRNA LINC00858 enhances cervical cancer cell growth through miR-3064-5p/ VMA21 axis.

BACKGROUND: Cervical cancer (CC) is the most common form of gynecological malignancy. Long intergenic non-protein coding RNA 858 (LINC00858) has been identified to participate in multiple cancers. However, the role and mechanism of LINC00858 in CC cells are still elusive. AIM: The aim of this study is to explore the biological functions and mechanisms of LINC00858 in CC cells. METHODS: RT-qPCR analysis was used to examine the expression of LINC00858 in CC cells. EdU and colony formation assay were utilized to assess cell proliferation. TUNEL assay and flow cytometry assay were conducted to assess cell apoptosis. The mechanism regarding LINC00858 was certified through RNA pull down, RIP and luciferase reporter assays. RESULTS: The up-regulated LINC00858 was detected in CC cells. Reduction of LINC00858 effectively subdued CC cells proliferation and stimulated cell apoptosis. LINC00858 was determined to bind with miR-3064-5p and up-regulate VMA21 in CC cells. In rescue assays, miR-3064-5p down-regulation and VMA21 up-regulation were able to counteract the effect caused by LINC00858 decrease on CC cell proliferation and apoptosis. CONCLUSION: LINC00858 enhances cell proliferation, while restraining cell apoptosis in CC through targeting miR-3064-5p/VMA21 axis, implying that LINC00858 may serve as a promising therapeutic target for CC.

MicroRNA-140-5p regulates the proliferation, apoptosis and inflammation of RA FLSs by repressing STAT3.

Ectopic expression of microRNA (miRNA) in rheumatoid arthritis (RA) fibroblast-like synoviocyte (RA FLS) is associated with the development of rheumatoid arthritis. The present study aimed to evaluate the effects of miRNA-140-5p (miR-140) on the properties of RA FLSs. It was found that miR-140 expression was decreased in 33 RA patients and extracted RA FLS samples, when compared to the corresponding healthy controls. Abnormally increased miR-140 expression in RA FLSs attenuated cell proliferation and increased cell apoptosis. Additionally, reduced pro-inflammatory cytokine production was observed in RA FLSs transfected with a miR-140 precursor. Furthermore, the 3'-UTR of the signal transducer and activator of transcription (STAT) 3 gene was identified as a target of miR-140. Notably, restoration of STAT3 expression rescued the regulatory effect of miR-140 on the proliferation, apoptosis and inflammatory cytokine production of RA FLSs. Therefore, the current findings indicated that miR-140 is a crucial modulator of both proliferation and apoptosis, shedding light on the etiology behind RA FLS viability, which is modulated by an interplay between miR-140 and STAT3 in the context of RA.

Association of pregnancy-associated plasma protein A and vascular endothelial growth factor with pregnancy-induced hypertension.

The present study aimed to evaluate changes of pregnancy-associated plasma protein A (PAPP-A) and vascular endothelial growth factor (VEGF) in pregnancy-induced hypertension (PIH). A total of 105 cases (observation group) with complete data that underwent delivery and suffered from PIH in The Affiliated Hospital of Xuzhou Medical University from February 2015 to February 2017 were retrospectively analyzed. The observation group was further divided into the mild observation and severe observation groups according to severity degree of the disease. Another 65 asymptomatic pregnant women were recruited as the healthy control group. Basic data, obstetric data, PAPP-A and VEGF and data of perinatal infants were compared and analyzed. The Logistic regression model was adopted to screen out risk factors for PIH. In the observation group, the rate of periodic antenatal care was lower, and there were more primigravidas and housewives, with lower education level and economic income (P<0.05). In the observation group, the occurrence rates of placental abruption as well as turbid and bloody amniotic fluid were higher than those in the healthy control group (P<0.05). The neonatal birth weight was lower in the observation group than that in the healthy control group, while the occurrence rates of neonatal department transfer, small for gestational age (SGA), neonatal asphyxia and survival rates of perinatal infants were higher (P<0.05). PAPP-A levels at 34-40 gestational weeks in the observation group were significantly higher than those in the healthy control group (P<0.05). VEGF levels were lower than those in the healthy control group (P<0.05). Multivariate analysis revealed that high PAPP-A value [odds ratio (OR)=3.736] and identity of housewife (OR=2.514) were risk factors for PIH, while high VEGF value (OR=5.258), non-primigravid (OR=2.173), higher economic income (OR=4.162) and periodic antenatal care (OR=1.201) were regarded as protective factors. Therefore, enhancement of gestational management, early discovery and early treatment are critical for improving the prognosis of pregnant women and infants.

LINC01170 promotes the progression of endometrial carcinoma by activating the AKT pathway.

PURPOSE: To investigate the function of LINC01170 in the progression of endometrial carcinoma and its underlying mechanism. METHODS: The expression profiles and prognostic data of endometrial carcinoma were downloaded by GDC (genomic data commons) analysis tools. Differentially expressed long noncoding (lnc)RNAs were analyzed by the edgeR (empirical analysis of digital gene expression data in R) package. LncRNAs that were related to prognosis of endometrial carcinoma were calculated by the survival function. Moreover, the PHEAT map package was introduced to edit heatmaps of differentially expressed lncRNAs. Human endometrial carcinoma cell lines (Ishikawa, ECC and HEC-IA) were cultured. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of lncRNAs and related genes. Cell proliferation was detected by MTT, and cell cycle and apoptosis were detected by flow cytometry. Additionally, Western blot was used to detect protein expressions of relative genes. RESULTS: Results showed that LINC01170 was a non-coding RNA. LINC01170 was overexpressed in endometrial carcinoma, which was a risk factor for prognosis of this disease. LINC01170 expressions in carcinoma and para-cancerous tissues of 50 patients with endometrial carcinoma were detected by qRT-PCR and found that the expression level of LINC01170 in endometrial carcinoma was remarkably increased than that of para-cancerous tissues. Moreover, the expression level of LINC01170 in advanced endometrial carcinoma was remarkably higher than that of early-stage disease. After interfering with LINC01170, the proliferation of both the Ishikawa and HEC-1A cells were remarkably decreased, and cell cycle was arrested at the G0/G1 phase. Meanwhile, apoptosis results showed a remarkable apoptosis rate after interfering with LINC01170. Western blot results also demonstrated the decreased activity of AKT pathway and phosphorylated expression of AKT protein after LINC01170 knockdown. In addition, expressions of CDK2, CDK4 and Bcl-2 were decreased after LINC01170 knockdown. CONCLUSIONS: LINC01170 promotes the progression of endometrial carcinoma through stimulating proliferation, cell cycle transition and inhibiting apoptosis of endometrial carcinoma cells via AKT pathway.

Reaction of 1-amino-2-methylenecyclopropane-1-carboxylate with 1-aminocyclopropane-1-carboxylate deaminase: analysis and mechanistic implications.

1-aminocyclopropane-1-carboxylate (ACC) deaminase is a pyridoxal 5'-phosphate (PLP) dependent enzyme which catalyzes the opening of the cyclopropane ring of ACC to give alpha-ketobutyric acid and ammonia. In an early study of this unusual C(alpha)-C(beta) ring cleavage reaction, 1-amino-2-methylenecyclopropane-1-carboxylic acid (2-methylene-ACC) was shown to be an irreversible inhibitor of ACC deaminase. The sole turnover product was identified as 3-methyl-2-oxobutenoic acid. These results provided strong evidence supporting the ring cleavage of ACC via a nucleophilic addition initiated process, thus establishing an unprecedented mechanism of coenzyme B(6) dependent catalysis. To gain further insight into this inactivation, tritiated 2-methylene-ACC was prepared and used to trap the critical enzyme nucleophiles. Our results revealed that inactivation resulted in the modification of an active site residue, Ser-78. However, an additional 5 equiv of inhibitor was also found to be incorporated into the inactivated enzyme after prolonged incubation. In addition to Ser-78, other nucleophilic residues modified include Lys-26, Cys-41, Cys-162, and Lys-245. The location of the remaining unidentified nucleophile has been narrowed down to be one of the residues between 150 and 180. Labeling at sites outside of the active site is not enzyme catalyzed and may be a consequence of the inherent reactivity of 2-methylene-ACC. Further experiments showed that Ser-78 is responsible for abstracting the alpha-H from d-vinylglycine and may serve as the base to remove the beta-H in the catalysis of ACC. However, it is also likely that Ser-78 serves as the active site nucleophile that attacks the cyclopropane ring and initiates the fragmentation of ACC, while the conserved Lys-51 is the base required for beta-H abstraction. Clearly, the cleavage of ACC to alpha-ketobutyrate by ACC deaminase represents an intriguing conversion beyond the common scope entailed by coenzyme B(6) dependent catalysts.