Towards humanlike grasp in robotic hands: mechanical implementation of force synergies.

In the field of robotic hands, finger force coordination is usually achieved by complex mechanical structures and control systems. This study presents the design of a novel transmission system inspired from the physiological concept of force synergies, aiming to simplify the control of multifingered robotic hands. To this end, we collected human finger force data during six isometric grasping tasks, and force synergies (i.e. the synergy weightings and the corresponding activation coefficients) were extracted from the concatenated force data to explore their potential for force modulation. We then implemented two force synergies with a cable-driven transmission mechanism consisting of two spring-loaded sliders and five V-shaped bars. Specifically, we used fixed synergy weightings to determine the stiffness of the compression springs, and the displacements of sliders were determined by time-varying activation coefficients. The derived transmission system was then used to drive a five-finger robotic hand named SYN hand. We also designed a motion encoder to selectively activate desired fingers, making it possible for two motors to empower a variety of hand postures. Experiments on the prototype demonstrate successful grasp of a wide range of objects in everyday life, and the finger force distribution of SYN hand can approximate that of human hand during six typical tasks. To our best knowledge, this study shows the first attempt to mechanically implement force synergies for finger force modulation in a robotic hand. In comparison to state-of-the-art robotic hands with similar functionality, the proposed hand can distribute humanlike force ratios on the fingers by simple position control, rather than resorting to additional force sensors or complex control strategies. The outcome of this study may provide alternatives for the design of novel anthropomorphic robotic hands, and thus show application prospects in the field of hand prostheses and exoskeletons.

[Retracted] Actin­binding protein anillin promotes the progression of hepatocellular carcinoma in vitro and in mice.

[This retracts the article DOI: 10.3892/etm.2021.9885.].

[Retracted] KIF2C promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo.

[This retracts the article DOI: 10.3892/etm.2021.10528.].

Synthesis, Antifungal Activity, 3D-QSAR and Controlled Release on Hydrotalcite Study of Longifolene-Derived Diphenyl Ether Carboxylic Acid Compounds.

Twenty-two novel longifolene-derived diphenyl ether-carboxylic acid compounds 7a-7v were synthesized from renewable biomass resources longifolene, and their structures were confirmed by FT-IR, 1H NMR, 13C NMR, and HRMS. The preliminary evaluation of in vitro antifungal activity displayed that compound 7b presented inhibition rates of 85.9%, 82.7%, 82.7%, and 81.4% against Alternaria solani, Cercospora arachidicola, Rhizoctonia solani, and Physalospora piricola, respectively, and compound 7l possessed inhibition rates of 80.7%, 80.4%, and 80.3% against R. solani, C. arachidicola, P. piricola, respectively, exhibiting excellent and broad-spectrum antifungal activities. Besides, compounds 7f and 7a showed significant antifungal activities with inhibition rates of 81.2% and 80.7% against A.solani, respectively. Meanwhile, a reasonable and effective 3D-QSAR mode (r2 = 0.996, q2 = 0.572) has been established by the CoMFA method. Furthermore, the drug-loading complexes 7b/MgAl-LDH were prepared and characterized. Their pH-responsive controlled-release behavior was investigated as well. As a result, complex 7b/MgAl-LDH-2 exhibited excellent controlled-releasing performance in the water/ethanol (10:1, v:v) and under a pH of 5.7.

KIF2C promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo.

Hepatocellular carcinoma (HCC) is one of the most common malignancies with high mortality and morbidity rates. In recent years, HCC targeted therapy has gained increasing attention. Due to the heterogeneity and high metastasis of HCC, more effective therapeutic targets are needed. Kinesin family member 2C (KIF2C), also known as mitotic centromere-associated kinesin, is a microtubule-based motor protein which is involved in a variety of important cellular processes, such as mitosis. The effects of KIF2C on cancer progression and development have been widely studied; however, its potential effects on HCC remains unclear. In the present study, high expression of KIF2C in human HCC tissues was demonstrated using The Cancer Genome Atlas database and immunohistochemistry assays. KIF2C expression was associated with HCC prognosis, including overall survival and disease-free survival. KIF2C expression was also associated with clinical pathological characteristics including the number of tumor nodes (P=0.015) and tumor size (P=0.009). KIF2C knockdown inhibited the proliferation of HCC cells in vitro, confirmed by MTT and colony formation assays, and suppressed tumor growth in mice which was confirmed by a xenograft mouse model. Together, the results suggested that KIF2C may serve as a promising therapeutic target for the treatment of HCC.

Actin-binding protein anillin promotes the progression of hepatocellular carcinoma in vitro and in mice.

Hepatocellular carcinoma (HCC) is a common type of tumor with high mortality worldwide. Investigations associated with the molecular etiology of HCC and screening novel therapeutic targets are still urgently in need. Anillin (ANLN), as a type of evolutionarily conserved actin-binding protein, is involved in multiple cellular processes. ANLN widely affected the progression and metastasis of several types of cancer, and its overexpression was frequently demonstrated in previous studies. The present study demonstrated high expression of ANLN in human HCC tissues, which was also associated the prognosis of patients with HCC. The associations between ANLN expression and the clinicopathological features were determined, including the number of tumor nodes (P=0.011) and tumor size (P=0.003) of patients with HCC. It was found that ANLN promoted cell proliferation, invasion and migration of HCC cells in vitro, and affected tumor growth in vivo. Therefore, ANLN is suggested as a promising therapeutic target for the treatment of HCC.

Actin-binding protein Anillin promotes the progression of gastric cancer in vitro and in mice.

BACKGROUND: To detect the expression levels of actin-binding protein anillin (ANLN) in human gastric cancer (GC) tissues and explore the possible involvement of ANLN in GC cell proliferation, migration, and invasion. METHODS: The bioinformation analysis was performed in TCGA database to explore the expression of ANLN in human GC tissues and the difference of ANLN expression between multiple types of cancers. IHC assays and clinical pathological analysis were performed to confirm ANLN expression and its correlation with clinical features of GC patients. Colony formation, CCK-8, wound closure, and transwell assays were performed to detect its effects on GC cell proliferation, migration, and invasion in vitro. Tumor growth was also measured using a xenograft animal model. RESULTS: We found the high expression of ANLN in human GC tissues based on the results from TCGA database and IHC staining. We further noticed ANLN depletion resulted in the inhibition of GC cell proliferation, migration, and invasion. Our data further confirmed that ANLN contributed to tumor growth of GC cells in vivo. CONCLUSIONS: We confirmed the involvement of ANLN in GC progression and thought ANLN could serve as a promising therapeutic target for GC.

KIF18B promotes the proliferation of pancreatic ductal adenocarcinoma via activating the expression of CDCA8.

Pancreatic cancer is one of the malignant tumors with the worst prognosis, and the 5-year survival rate of this disease is less than 1%. About 90% of pancreatic cancer is pancreatic ductal adenocarcinoma (PDAC), and targeting therapy has become a promising treatment for PDAC in recent years. To improve the survival rate, novel therapeutic targets for PDAC are still urgently needed. KIF18B was initially identified as a member of the kinesin family and involved in multiple cellular processes, such as separation of chromosomes in mitosis. Recently, it was found that KIF18B was involved in the growth and development of multiple cancers. However, the potential link between KIF18B and PDAC is still unclear. In this study, we demonstrated that KIF18B was highly expressed in human PDAC tissues, and related with the poor prognosis and clinical features, such as tumor size (*p = .013) and pTNM stage (*p = .025), of patients with PDAC. We further found that KIF18B knockdown blocked the cell proliferation of PDAC in vitro and in vivo, and the cell cycle was arrested caused by KIF18B depletion. Additionally, we also found that KIF18B bound to the promoter region of the cell division cycle associated 8 and thus activated its transcription. Taken together, this study explored the molecular mechanism underlying KIF18B promoting PDAC and provided a novel therapeutic target of this disease.

Development of a multiplex RT-PCR for the detection of major diarrhoeal viruses in pig herds in China.

The major enteric RNA viruses in pigs include porcine epidemic diarrhoea virus (PEDV), transmissible gastroenteritis virus (TGEV), porcine rotavirus A (PRV-A), porcine kobuvirus (PKV), porcine sapovirus (PSaV) and porcine deltacoronavirus (PDCoV). For differential diagnosis, a multiplex RT-PCR method was established on the basis of the N genes of TGEV, PEDV and PDCoV, the VP7 gene of PRV-A, and the polyprotein genes of PKV and PSaV. This multiplex RT-PCR could specifically detect TGEV, PEDV, PDCoV, PRV-A, PKV and PSaV without cross-reaction to any other major viruses circulating in Chinese pig farms. The limit of detection of this method was as low as 100 -101  ng cDNA of each virus. A total of 398 swine faecal samples collected from nine provinces of China between October 2015 and April 2017 were analysed by this established multiplex RT-PCR. The results demonstrated that PDCoV (144/398), PSaV (114/398), PEDV (78/398) and PRV-A (70/398) were the main pathogens, but TGEV was not found in the pig herds in China. In addition, dual infections, for example, PDCoV + PSaV, PDCoV + PRV-A, PRA-V + PSaV and PEDV + PDCoV, and triple infections, for example, PDCoV + PRV-A + PSaV and PEDV + PDCoV + PKV, were found among the collected samples. The multiplex RT-PCR provided a valuable tool for the differential diagnosis of swine enteric viruses circulating in Chinese pig farms and will facilitate the prevention and control of swine diarrhoea in China.

Suppression of KIF22 Inhibits Cell Proliferation and Xenograft Tumor Growth in Colon Cancer.

Background: Kinesin family member 22 (KIF22) is known as a regulator of cell mitosis and cellular vesicle transport. The alterations of KIF22 are associated with a series of tumors; however, its possible role in the progression of colon cancer is still unclear. Materials and Methods: This retrospective research collected 82 paired tissues with colon cancer. KIF22 protein and mRNA expression levels were detected by immunohistochemistry assays and Immunoblot assays, respectively. Short hairpin RNA (shRNA) plasmids were used to suppress the expression of KIF22 in HCT116 and HT29 cells, and the silencing efficiencies of shRNA plasmids targeted KIF22 were detected by quantitative PCR assays and immunoblot assays. In addition, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assays and xenograft tumor growth assays were performed to observe cell proliferation in vitro and in vivo. Results: In human colon cancer tissues, the expression level of KIF22 was increased and correlated with clinical pathological features, including tumor stage and clinical stage (p = 0.034, and p = 0.015, respectively). Suppression of KIF22 inhibited cell proliferation and xenograft tumor growth. Conclusion: KIF22 might play an important role in the regulation of cell proliferation in colon cancer and might therefore serve as a promising therapeutic target.

A study on the mechanism of rapamycin mediating the sensitivity of pancreatic cancer cells to cisplatin through PI3K/AKT/mTOR signaling pathway.

PURPOSE: To study the mechanism of rapamycin mediating the sensitivity of pancreatic cancer cells to cisplatin through phosphatidylinositol 3-kinase (PI3K)/serine-threonine kinase (AKT)/mammalian target of rapamycin (mTOR) signaling pathway in vitro. METHODS: SW1990 cells were cultured in vitro and treated with rapamycin, cisplatin, and rapamycin combined with cisplatin, respectively, with dimethyl sulphoxide (DMSO) as the control. Cell Counting Kit-8 (CCK-8) and flow cytometry were adopted for determination of cell proliferation and apoptosis levels, respectively. The changes in PI3K/AKT/mTOR signal transmission were detected via Western blotting and reverse transcription polymerase chain reaction (RT-PCR), respectively. RESULTS: 1: Compared with those in DMSO blank control group, the proliferation level of pancreatic cancer cells was markedly decreased and the cell apoptosis rate was remarkably increased in simple drug group (p<0.05). 2: The combined administration group had markedly decreased proliferation level and remarkably increased cell apoptosis rate of human pancreatic cancer cells, compared with those in the rapamycin alone group or cisplatin alone group (p<0.05). 3: Rapamycin combined with cisplatin could inhibit the expressions of PI3K, AKT and phosphorylated mTOR (p-mTOR) in pancreatic cancer cells (p<0.05). CONCLUSION: Rapamycin combined with cisplatin can alter the PI3K/AKT/mTOR signal transduction pathway which leads to markedly increased cell apoptosis rate, indicating that rapamycin can mediate the sensitivity of pancreatic cancer cells to cisplatin.

Development of a live vector vaccine against infectious hematopoietic necrosis virus in rainbow trout.

Infectious hematopoietic necrosis virus (IHNV) leads to serious disease and economic losses in the salmonid aquaculture industry. The present study aimed to develop an effective and efficient vaccine to protect rainbow trout (Oncorhynchus mykiss) against IHNV infection. Administered via the immersion route, a live vector vaccine containing the regions of the IHNV glycoprotein (G) induced immune responses in rainbow trout. Use of the immersion route induced more-efficient mucosal immunity than intramuscular injection vaccination. IHNV G gene expression was detected in the spleens of rainbow trout at 3, 7 and 15 days post-vaccination (dpv). The G gene expression continuously decreased between 3 and 15 dpv. In addition, the expression of TLR-3, TLR-7 and TLR-8 was upregulated after vaccination, and the highest expression levels of IFN-1, Mx-1, Mx-3, Vig-1 and Vig-2 were observed at 3 dpv. Four markers of the adaptive immune response (CD4, CD8, IgM and IgT) gradually increased. When experimental fish were challenged with IHNV by immersion, significant differences in cumulative percentage mortality were observed in the vaccinated fish and the unvaccinated (empty-plasmid-vaccinated) fish. The relative survival rate was 92% and 6% in the vaccinated group and empty-plasmid group, respectively. Serum antibody levels gradually increased in the vaccinated fish, unlike in the unvaccinated fish, after 7 dpv. Our results suggest there was a significant increase in fish immune responses and resistance to infection with IHNV following administration of the live vector vaccine. Therefore, this live vector vaccine is a promising vaccine that may be utilized to protect rainbow trout against IHNV.

High expression of RAB38 promotes malignant progression of pancreatic cancer.

Ras­Related Protein Rab­38 (RAB38), which belongs to the RAB family, is involved in the biogenesis of lysosome­related organelles and defense against certain microbial infections. However, the clinical significance and potential function of RAB38 in pancreatic adenocarcinoma remain unclear. In the present study, an immunohistochemical assay was performed to analyze the expression of RAB38 in pancreatic adenocarcinoma tumor specimens from 82 patients, and the clinicopathological characteristics and survival rate of these patients were further examined. To validate the role of RAB38 in tumors, the effect of RAB38 on tumor cell proliferation, migration and invasion was assessed by establishing RAB38 knockdown cell lines. Reverse transcription­quantitative polymerase chain reaction and western blotting were used to examine the expression levels of proteins associated with the cancer cell behavior. In addition, the inhibitory effect of RAB38 silencing on pancreatic cancer was examined in mice. The immunohistochemistry results revealed that RAB38 was upregulated and positively correlated with the grade of progression in pancreatic adenocarcinoma patients. Further investigation indicated that RAB38 downregulation significantly suppressed the proliferation, migration and invasive capacity of pancreatic cancer cells, as well as decreased the expression levels of Ki67, proliferating cell nuclear antigen, and matrix metalloproteinases 2 and 9. RAB38 silencing also inhibited the development of pancreatic cancer in vivo. Taken together, a high level of RAB38 was significantly associated with the malignant phenotypes of pancreatic cancer, suggesting that RAB38 may serve as a novel biomarker and a potential therapeutic target for pancreatic cancer.

MiR-195 suppresses colon cancer proliferation and metastasis by targeting WNT3A.

MicroRNAs (miRNAs) are a novel class of diagnostic and therapeutic target in cancer. Here, we aimed to explore the effects and mechanism of miR-195 regulation in colon cancer. The expressions of several putative miRNAs in colon tumors, compared to those in normal tissues, were investigated by bioinformatical analysis of a Gene Expression Omnibus database. Quantitative real-time PCR analysis (qRT-PCR) was used to validate the identified changes in normal tissues, primary tumors, and metastatic tumors. MTT, soft agar colony formation, and transwell assays were used to evaluate the effects of miR-195 overexpression or inhibition on cell viability, proliferation, migration, and invasion. Targets of miR-195 were identified by TargetScan, and subsequently verified by qRT-PCR and Western blot. The role of miR-195 in the ß-catenin pathway was also studied using RT-PCR and Western blot. MiR-195 expression was downregulated in colon carcinoma tissues and negatively correlated with the metastatic potential. While transfecting miR-195 mimics decreased the proliferation, migration, and invasion of colon cancer cells, miR-195 inhibition exerted opposing effects. WNT3A was identified as a direct target of miR-195. ß-catenin was also downregulated by miR-195 in colon cancers. MiR-195 downregulation is associated with the enhanced proliferation, migration, and invasion of colon cancer. MiR-195 directly downregulates WNT3A. Our results indicate that miR-195 is a potential diagnostic marker and therapeutic target for improving the clinical management of colon cancer.

Down-regulation of LINC00341 predicts a poor prognosis and acts as a tumor suppressor in gastric cancer.

Accumulating evidence has suggested that long noncoding RNAs (lncRNAs) play critical roles in tumor cell development and in the progression of human cancer. However, the significance and role of most lncRNAs, especially long intergenic ncRNAs (lincRNAs, the main type of lncRNAs), in gastric cancer is unclear. This study aimed to identify the clinical significance and potential biological function of LINC00341 in gastric cancer. Here, a qRT-PCR assay indicated that the relative expression level of LINC00341 were significantly down-regulated in gastric cancer tissues compared to matched adjacent normal tissues. Levels of LINC00341 in gastric cancer cell lines (MGC-803, BGC-823 and SGC-7901) were also significantly lower than in human normal gastric epithelial cell (GES-1). Patient with low LINC00341 expression were found to be negatively correlated with the TNM stage and lymph node metastasis. A Kaplan-Meier analysis showed that low expression of LINC00341 was significantly correlated with shorter overall survival (OS) of gastric cancer patients. Furthermore, an in vitro assay indicated that the over-expression of LINC00341 inhibited cell growth and migration and induced cell apoptosis in gastric cancer. In summary, this study provides the first evidence that the down-regulation of LINC00341 predicts a poor prognosis and acts as a tumor suppressor in the carcinogenesis of gastric cancer, indicating that LINC00341 may serve as a potential therapeutic target for gastric cancer.

EGCG in Green Tea Induces Aggregation of HMGB1 Protein through Large Conformational Changes with Polarized Charge Redistribution.

As a major effective component in green tea, (-)-epigallocatechin-3-gallate (EGCG)'s potential benefits to human health have been widely investigated. Recent experimental evidences indicate that EGCG can induce the aggregation of HMGB1 protein, a late mediator of inflammation, which subsequently stimulates the autophagic degradation and thus provides protection from lethal endotoxemia and sepsis. In this study, we use molecular dynamics (MD) simulations to explore the underlying molecular mechanism of this aggregation of HMGB1 facilitated by EGCG. Our simulation results reveal that EGCG firmly binds to HMGB1 near Cys106, which supports previous preliminary experimental evidence. A large HMGB1 conformational change is observed, where Box A and Box B, two homogenous domains of HMGB1, are repositioned and packed together by EGCG. This new HMGB1 conformation has large molecular polarity and distinctive electrostatic potential surface. We suggest that the highly polarized charge distribution leads to the aggregation of HMGB1, which differs from the previous hypothesis that two HMGB1 monomers are linked by the dimer of EGCG. Possible aggregating modes have also been investigated with potential of mean force (PMF) calculations. Finally, we conclude that the conformation induced by EGCG is more aggregation-prone with higher binding free energies as compared to those without EGCG.

[Analysis of spectral characteristics of oil film on water based on wavelet transform].

The diagnostic features are the basis to detect and characterize the oil film on water through optical remote sensing. This work shows the results of lab spectral measurements of light diesel oil with thickness ranged 1.0 - 127 microm. A wavelet transform were performed to the reflectance, and the singularity (388-393 nm) was explored as the indicators of oil film thickness. The results indicate that the reflectance of light diesel oil film is higher than that of water in the range from 350-2 500 nm. There is a reflectance peak near 388 nm when the thickness of oil film is larger than 6 microm, however, no distinguished features could be recognized when oil films were thinner than 6 microm. The wavelet coefficients of the fifth decomposition level by applying Daubechies 4 (db4) mother wavelets proved successful for identifying the singularity of oil film's reflectance spectra and its accurate position. With the thickness lager than 6 microm, the detail coefficients performed an abrupt change within the range of 388-393 nm, and became more violent while oil films' thickness increased. This research demonstrated that oil films on water with different thickness could be distinguished based on wavelet detail coefficients, with important implications for detection of oils on water using UV and short wave optical remote sensing.