Search

Here, the taxonomy of the genus Rhagastis Rothschild & Jordan, 1903 (Lepidoptera, Sphingidae, Macroglossinae, Macroglossini) from China is revised based on differences in wing morphology, male and female genitalia, and the phylogenetic relationship of the DNA barcodes. Subspecies of Rhagastis albomarginatus (Rothschild, 1894) and R. castor (Walker, 1856) are treated as “good” species, namely Rhagastis dichroae Mell, 1922 stat. nov.; R. everetti Rothschild & Jordan, 1903 stat. nov.; R. aurifera (Butler, 1875) stat. rev.; R. chinensis Mell, 1922 stat. nov.; R. formosana Clark, 1925 stat. nov.; and R. jordani Oberthür, 1904 stat. rev. The distribution maps, biological notes, and ecological records of the genus Rhagastis Rothschild & Jordan, 1903 from China are given, and a species inventory of genus Rhagastis in the world is also included.

Water is one of the limiting factors that impact the agricultural production in the black soil region in Northeast China. The seasonal drought caused by the uneven distribution of precipitation threatens crop yield in this region. The objective of this study was to examine if different fertilization treatments would affect soil water supply, then mitigate the impact of seasonal drought on crop yield. A long-term experiment was conducted at the National Field Research Station of Agro-ecosystem in the Chinese Academy of Science in Hailun County in Heilongjiang province in Northeast China from 2005 to 2008. Three fertilizer treatments including no fertilizer (CK), chemical fertilizer (NP) and chemical fertilizer plus pig manure (NPM) were tested. The results showed that crop received chemical fertilizer plus pig manure had the largest evapo-transpiration (ET) in observed four-years followed by NP and CK, which resulted in soil water storage (0-170 cm) showed a decreasing trend of CK > NP > NPM during the growing seasons. Water stored in the soil profile was one of the most important sources for crop water consumption. Crops in NPM and NP treatments could utilize more water stored in soil profile, by 41.52% and 24.94%, respectively, compared with CK. The yield and water use efficiency of maize and soybean in NPM were higher than that in NP and CK, suggesting that utilized soil water could mitigate the effect of seasonal drought on crop yield. Therefore, NPM was a viable management practice in the black soil zone in Northeast China for improving soil water supply and crop yields. [ABSTRACT FROM AUTHOR]

Pancreatic ductal adenocarcinoma (PDAC) cells can utilise the tumour microenvironment to metastasise to the liver. Here the authors show that hepatoctyes overexpress SLIT2 to enable premetastatic niche formation for ROBO1-positive PDAC cells to support the survival of these tumour cells in the liver.

Background Known for its rich history and culture, Qingdao is a typical symbol of Chinese maritime culture. Its unique genetic landscape has aroused interest among geneticists and forensic scientists. However, the genetic landscape of Qingdao has never been uncovered. Aim This investigation intends to provide light on Qingdao’s paternal genetic diversity and its evolutionary connections to other Han subgroups. Subjects and methods The genetic polymorphisms of 41 Y-chromosomal short tandem repeat (STR) loci in the Qingdao Han were investigated using SureID® PathFinder Plus Kit. Phylogenetic studies were performed using genotype data from 52 East Asian groups at 23 common Y-STR loci. A multidimensional scaling plot and cladogram were constructed. Linear Discriminant Analysis (LDA) was carried out for predicting categories among the Han people. The k-nearest neighbour (kNN) algorithm was utilised to designate Y-SNP haplogroups for each haplotype. Results The Qingdao Han were genetically far from the Tibeto-Burman populations and close with the Han people from northern China. LDA indicated a deep integration among the present-day Han people. By the kNN model, the predicted O2a2 and O2a1 were shown to be the predominant Y-SNP haplogroups. Conclusions This study would be helpful for reconstructing the patrilineal history in China and establishing a more comprehensive Y-STR database.

Abstract Background Proteostasis unbalance and mitochondrial dysfunction are two hallmarks of aging. While the chaperone folds and activates its clients, it is the cochaperone that determines the specificity of the clients. Ids2 is an HSP90’s cochaperone controlling mitochondrial functions, but no in vivo clients of Ids2 have been reported yet. Results We performed a screen of the databases of HSP90 physical interactors, mitochondrial components, and mutants with respiratory defect, and identified Atp3, a subunit of the complex V ATP synthase, as a client of Ids2. Deletion of IDS2 destabilizes Atp3, and an α-helix at the middle region of Ids2 recruits Atp3 to the folding system. Shortage of Ids2 or Atp3 leads to the loss of mitochondrial DNA. The intermembrane space protease Yme1 is critical to maintaining the Atp3 protein level. Moreover, Ids2 is highly induced when cells carry out oxidative respiration. Conclusions These findings discover a cochaperone essentially for maintaining the stability of mitochondrial DNA and the proteostasis of the electron transport chain—crosstalk between two hallmarks of aging.

Abstract Hypoxic microenvironment is common in solid tumors, particularly in pancreatic ductal adenocarcinoma (PDAC). The Warburg effect is known to facilitate cancer aggressiveness and has long been linked to hypoxia, yet the underlying mechanism remains largely unknown. In this study, we identify that lysyl oxidase-like 2 (LOXL2) is a hypoxia-responsive gene and is essential for the Warburg effect in PDAC. LOXL2 stabilizes hypoxia-inducible factor 1α (HIF1α) from prolyl hydroxylase (PHD)-dependent hydroxylation via hydrogen peroxide generation, thereby facilitating the transcription of multiple glycolytic genes. Therefore, a positive feedback loop exists between LOXL2 and HIF1α that facilitates glycolytic metabolism under hypoxia. Moreover, LOXL2 couples the Warburg effect to tumor growth and metastasis in PDAC. Hijacking glycolysis largely compromises LOXL2-induced oncogenic activities. Collectively, our results identify a hitherto unknown hypoxia-LOXL2-HIF1α axis in regulating the Warburg effect and provide an intriguing drug target for PDAC therapy.

Hot spot gene mutations in splicing factor 3b subunit 1 (SF3B1) are observed in many types of cancer and create abundant aberrant mRNA splicing, which is profoundly implicated in tumorigenesis. Here, we identified that the SF3B1 K700E (SF3B1K700E) mutation is strongly associated with tumor growth in pancreatic ductal adenocarcinoma (PDAC). Knockdown of SF3B1 significantly retarded cell proliferation and tumor growth in a cell line (Panc05.04) with the SF3B1K700E mutation. However, SF3B1 knockdown had no notable effect on cell proliferation in two cell lines (BxPC3 and AsPC1) carrying wild‐type SF3B1. Ectopic expression of SF3B1K700E but not SF3B1WT in SF3B1‐knockout Panc05.04 cells largely restored the inhibitory role induced by SF3B1 knockdown. Introduction of the SF3B1K700E mutation in BxPC3 and AsPC1 cells also boosted cell proliferation. Gene set enrichment analysis demonstrated a close correlation between SF3B1 mutation and aerobic glycolysis. Functional analyses showed that the SF3B1K700E mutation promoted tumor glycolysis, as evidenced by glucose consumption, lactate release, and extracellular acidification rate. Mechanistically, the SF3B1 mutation promoted the aberrant splicing of PPP2R5A and led to the activation of the glycolytic regulator c‐Myc via post‐translational regulation. Pharmacological activation of PP2A with FTY‐720 markedly compromised the growth advantage induced by the SF3B1K700E mutation in vitro and in vivo. Taken together, our data suggest a novel function for SF3B1 mutation in the Warburg effect, and this finding may offer a potential therapeutic strategy against PDAC with the SF3B1K700E mutation.

The nonunion following a fracture is associated with severe patient morbidity and economic consequences. Currently, accumulating studies are focusing on the importance of macrophages during fracture repair. However, details regarding the process by which macrophages facilitate endochondral ossification (EO) are largely unknown. In this study, we present evidence that apoptotic chondrocytes (ACs) are not inert corpses awaiting removal, but positively modulate the osteoinductive ability of macrophages. In vivo experiments revealed that fatty acid (FA) metabolic processes up-regulated following EO. In vitro studies further uncovered that FAs derived from ACs are taken up by macrophages mainly through macrophage scavenger receptor 1 (MSR1). Then, our functional experiments confirmed that these exogenous FAs subsequently activate peroxisome proliferator-activated receptor α (PPARα), which further facilitates lipid droplets generation and fatty acid oxidation (FAO). Mechanistically, elevated FAO is involved in up-regulating the osteoinductive effect by generating BMP7 and NAD+/SIRT1/EZH2 axis epigenetically controls BMP7 expression in macrophages cultured with ACs culture medium. Our findings advanced the concept that ACs could promote bone regeneration by regulating metabolic and function reprogram in macrophages and identified macrophage MSR1 represents a valuable target for fracture treatments.

Summary: Background: Cancer elicits a complex adaptive response in an organism. Limited information is available for the body-wide effects induced by cancer. Here, we evaluated multiorgan changes in mouse models of pancreatic ductal adenocarcinoma (PDAC) and its precursor lesions (pancreatic intraepithelial neoplasia, PanIN) to decipher changes that occur during PDAC development. Methods: RNA-sequencing was employed in the brain, colon, stomach, kidney, heart, liver, and lung tissues of mice with PanIN and PDAC. A combination of differential expression analysis and functional-category enrichment was applied for an in-depth understanding of the multiorgan transcriptome. Differentially expressed genes were verified by quantitative real-time polymerase chain reaction. Neutrophil and macrophage infiltration in multiple organs was analyzed by immunohistochemical staining. Leukotriene B4 (LTB4) levels in mouse and human serum samples were determined by enzyme-linked immunosorbent assay. Findings: Transcriptional changes within diverse organs during PanIN and PDAC stages were identified. Using Gene Ontology enrichment analysis, increased neutrophil infiltration was discovered as a central and prominent affected feature, which occurred in the liver, lung, and stomach at the PanIN stage. The brain appeared to be well protected from the sequels of PanIN or PDAC. Importantly, serum LTB4 was able to discriminate PDAC from normal controls, chronic pancreatitis, and intraductal papillary mucinous neoplasms with high performance. Interpretation: Our study provides a high-resolution cartographic view of the dynamic multiorgan transcriptomic landscape of mice with PDAC and its precursor lesions. Our findings suggest that LTB4 could serve as a biomarker for the early detection of PDAC. Funding: The complete list of funders can be found in the Acknowledgement section.

Abstract Background Reprogrammed glucose metabolism, also known as the Warburg effect, which is essential for tumor progression, is regarded as a hallmark of cancer. MAP17, a small 17-kDa non-glycosylated membrane protein, is frequently dysregulated in human cancers. However, its role in hepatocellular carcinoma (HCC) remains largely unknown. Methods Immunohistochemistry was used to analyze the expression pattern of MAP17 in HCC. Loss-of-function and gain-of-function studies were performed to investigate the oncogenic roles of MAP17 in vitro and in vivo. RNA sequencing, co-immunoprecipitation, immunofluorescence and western blotting were used to study the molecular mechanism of MAP17 affecting the tumor growth and glycolytic phenotype of HCC. Results An integrative analysis showed that MAP17, a small 17-kDa non-glycosylated membrane protein, is significantly related to the glycolytic phenotype of hepatocellular carcinoma (HCC). Firstly, we found that MAP17 expression is hypoxia-dependent and predicts a poor prognosis in HCC. Genetic silencing of MAP17 reduced the rate of glucose uptake, lactate release, extracellular acidification rate, and expression of glycolytic genes. Ectopic expression of wild type MAP17 but not its PDZ binding domain mutant MAP17-PDZm increased tumor glycolysis. Further research showed that MAP17 knockdown markedly retarded in vivo tumor growth in HCC. Importantly, attenuation of tumor glycolysis by galactose largely hijacked the growth-promoting role of MAP17 in HCC cells. RNA sequencing analysis revealed that MAP17 knockdown leads to transcriptional changes in the ROS metabolic process, cell surface receptor signaling, cell communication, mitotic cell cycle progression, and regulation of cell differentiation. Mechanistically, MAP17 exerted an increased tumoral phenotype associated with an increase in reactive oxygen species (ROS), which activates downstream effectors AKT and HIF1α to enhance the Warburg effect. In HCC clinical samples, there is a close correlation between MAP17 expression and HIF1α or phosphorated level of AKT. Conclusions Our results show that MAP17 is a novel glycolytic regulator, and targeting MAP17/ROS pathway may be an alternative approach for the prevention and treatment of HCC.

Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, which lacks effective treatment strategies. There is an urgent need for the development of new strategies for PDAC therapy. The genetic and phenotypic heterogeneity of PDAC cancer cell populations poses further challenges in the clinical management of PDAC. In this study, we performed single-cell RNA sequencing to characterize PDAC tumors from KPC mice. Functional studies and clinical analysis showed that PDAC cluster 2 cells with highly Hsp90 expression is much more aggressive than the other clusters. Genetic and pharmacologic inhibition of Hsp90 impaired tumor cell growth both in vitro and in vivo. Further mechanistic study revealed that HSP90 inhibition disrupted the interaction between HSP90 and OPA1, leading to a reduction in mitochondrial cristae amount and mitochondrial energy production. Collectively, our study reveals that HSP90 might be a potential therapeutic target for PDAC.

Objective To compare the learning outcomes of “interactive anatomical teaching” combined with “peer education” with traditional teaching in shoulder joint ultrasound training. Methods Two groups of refresher doctors were given shoulder joint ultrasound training, using “interactive anatomical teaching” combined with “peer education” (combined teaching group) and traditional teaching (traditional teaching group)respectively. Before and after the training, selected-response examination, practical operation and film reading ability were evaluated. After the training, a questionnaire survey was conducted to refresher doctors, including comprehensive course evaluation and satisfaction with personal capacity building. Results After the training, there was no statistically significant difference in Objective examination questions between the two groups. The score of combined teaching group was significantly higher than that of traditional teaching group on practical operation and film reading ability (P＜0.05). The comprehensive course evaluation and satisfaction with personal ability improvement in combined teaching group was significantly higher than that of traditional teaching group(P＜0.05). Conclusions The“interactive anatomical teaching” combined with “peer education” enable the refresher doctors to master the theoretical knowledge, operation skills and diagnosis of shoulder joint ultrasound tecnhology, which is believed to be a better teaching and training method than traditional approaches.

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive metastatic disease characterized by an immunosuppressive microenvironment. Here the authors show that a subset of P2RX1-negative neutrophils with immunosuppressive properties accumulate in PDAC metastatic liver tissues and promote tumor growth.

Background. The cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS) plays critical functions in innate immune responses via the production of the second messenger cyclic guanosine monophosphate-adenosine monophosphate (cGAMP), which stimulates the adaptor stimulator of interferon genes (STING). However, the clinical relevance and prognostic value of the cGAS-STING pathway in human cancers remains largely unexplored. Methods. A gene signature related to the cGAS-STING score was identified. The pan-cancer landscape of cGAS-STING expression was calculated using the RNAseq data acquired from the TCGA cohort. Tumor-infiltrating immune cells (TIICs) were determined by the ssGSEA method. Kaplan–Meier curves, Cox regression analyses, and the area under the curve (AUC) were employed to decipher the predictive value of cGAS-STING risk score and TIICs across several human cancers. Results. Most tumor tissues displayed a higher cGAS-STING score compared with their corresponding nontumor tissues, except for prostate adenocarcinoma (PRAD) and uterine corpus endometrial carcinoma (UCEC). Higher cGAS-STING score was closely associated with poor clinical outcome of kidney renal clear cell carcinoma (KIRC) and kidney renal papillary cell carcinoma (KIRP), whereas the cGAS-STING score predicted a better prognosis in pheochromocytoma and paraganglioma (PCPG). Enrichment analysis showed that cGAS-STING was profoundly implicated in diverse immune-related pathways in KIRC, KIRP, and PCPG. Significant positive correlations were noticed between cGAS-STING score and TIICs, including activated CD8+ T cells, activated CD4+ T cells, monocytes, and mast cells. Finally, the cGAS-STING score was revealed to be an independent prognostic factor for KIRC patients and possessed a strong predictive power for the prognostic evaluation of KIRC and KIRP patients. Conclusions. We constructed a cGAS-STING gene signature to predict survival and tumor immunity across human cancers, which can serve as a novel prognostic indicator and therapeutic target, especially in KIRC and KIRP.

Background: Liver is one of the most preferred destinations of distant metastasis in gastric cancer (GC). As effective treatment is still limited, the prognosis of GC patients bearing liver metastasis is poor. We filter out lysyl oxidase (LOX) to study its function in the tumor microenvironment (TME) and seek for potential therapeutic targets. Methods: Transcription analysis on 6 cases of liver metastasis of GC patients with respective paired primary tumors and adjacent normal livers was performed. The filtration out of LOX was done using 5 datasets. 69 GC liver metastasis tissues were utilized to perform immunohistochemistry (IHC) and analyze prognosis. Computed Tomography (CT) combined 3D organ reconstruction bioluminescence imaging was performed to precisely evaluate the metastatic tumor burden on liver of intrasplenic injection mouse model. Human and mouse cancer associated fibroblasts (CAFs) in liver metastasis were separated to culture to study the interaction of LOX and TGF-β1. Patients-derived xenograft (PDX) model was established using liver metastasis of patients to evaluate the therapeutic value of LOX inhibitor β‐aminopropionitrile (BAPN). Results: CAFs-derived LOX at liver metastatic niche of GC promotes niche formation and outgrowth thus predicts poor prognosis. Meanwhile tumor cells in niche secrete TGF-β1 to nourish CAFs and stimulate them to produce more LOX in turn. The mechanism involved in LOX-mediated proliferation facilitation is enhancement of Warburg effect. The inhibitor of LOX, BPAN could hamper the effect brought by LOX in vivo and in vitro. Interpretation: Our study has unveiled a positive feedback loop between CAFs and tumor cells in liver metastasis niche of GC. The core molecule is LOX which facilitates Warburg effect. Targeting LOX with its inhibitor BAPN might serve as a potential therapeutic strategy. Fund: This research was supported by the National Natural Science Foundation of China (31872740), the 100-member plan of the Shanghai Municipal Commission of Health and Family Planning (2017BR043), Shanghai Science and Technology Commission Project(17ZR1416800), Renji Hospital Training Fund (PYMDT-003, PYIII-17–015), National Natural Science Foundation of China (81672358), the Shanghai Municipal Education Commission—Gao feng Clinical MedicineGrant Support (20181708), Program of Shanghai Academic/Technology Research Leader(19XD1403400), Science and Technology Commission of Shanghai Municipality (18410721000), Shanghai Municipal Health Bureau (2018BR32), China Postdoctoral Science Foundation (2018M640403), National Natural Science Foundation of China (81701945) and Youth project of Shanghai Municipal Health Commission(20164Y0045). Keywords: Gastric cancer, Liver metastasis, LOX, CAFs, Warburg effect

Abstract Background Gastric cancer is one of the deadliest malignant tumours, with a high incidence in China, and is regulated by aberrantly overexpressed oncogenes. However, existing therapies are insufficient to meet patients’ needs; thus, the identification of additional therapeutic targets and exploration of the underlying mechanism are urgently needed. GPAA1 is the subunit of the GPI transamidase that transfers the GPI anchor to proteins within the ER. The functional impacts of increased expression levels of GPAA1 in human cancers are not well understood. Methods Data mining was performed to determine the pattern of GPAA1 expression and the reason for its overexpression in tumour and adjacent normal tissues. In vitro and in vivo experiments evaluating proliferation and metastasis were performed using cells with stable deletion or overexpression of GPAA1. A tissue microarray established by the Ren Ji Hospital was utilized to analyse the expression profile of GPAA1 and its correlation with prognosis. Western blotting, an in situ proximity ligation assay, and co-immunoprecipitation (co-IP) were performed to reveal the mechanism of GPAA1 in gastric cancer. Results GPAA1 was a markedly upregulated oncogene in gastric cancer due to chromosomal amplification. GPAA1 overexpression was confirmed in specimens from the Ren Ji cohort and was associated with ERBB2 expression, predicting unsatisfactory patient outcomes. Aberrantly upregulated GPAA1 dramatically contributed to cancer growth and metastasis in in vitro and in vivo studies. Mechanistically, GPAA1 enhanced the levels of metastasis-associated GPI-anchored proteins to increase tumour metastasis and intensified lipid raft formation, which consequently promoted the interaction between EGFR and ERBB2 as well as downstream pro-proliferative signalling. Conclusions GPAA1 facilitates the expression of cancer-related GPI-anchored proteins and supplies a more robust platform—the lipid raft—to promote EGFR-ERBB2 dimerization, which further contributes to tumour growth and metastasis and to cancer progression. GPAA1 could be a promising diagnostic biomarker and therapeutic target for gastric cancer.

BackgroundHypoxia is an important environmental factor and has been correlated with tumor progression, treatment resistance and poor prognosis in many solid tumors, including triple-negative breast cancer (TNBC). Emerging evidence suggests that long noncoding RNA (lncRNA) functions as a critical regulator in tumor biology. However, little is known about the link between hypoxia and lncRNAs in TNBC.MethodsTNBC molecular profiles from The Cancer Genome Atlas (TCGA) were leveraged to identify hypoxia-related molecular alterations. Loss-of-function studies were performed to determine the regulatory role of MIR210HG in tumor glycolysis. The potential functions and mechanisms of hypoxia-MIR210HG axis were explored using qPCR, Western blotting, luciferase reporter assay, and polysome profiling.ResultsWe found that MIR210HG is a hypoxia-induced lncRNA in TNBC. Loss-of-function studies revealed that MIR210HG promoted the Warburg effect as demonstrated by glucose uptake, lactate production and expression of glycolytic components. Mechanistically, MIR210HG potentiated the metabolic transcription factor hypoxia-inducible factor 1α (HIF-1α) translation via directly binding to the 5’-UTR of HIF-1α mRNA, leading to increased HIF-1a protein level, thereby upregulating expression of glycolytic enzymes. MIR210HG knockdown in TNBC cells reduced their glycolytic metabolism and abolished their tumorigenic potential, indicating the glycolysis-dependent oncogenic activity of MIR210HG in TNBC. Moreover, MIR210HG was highly expressed in breast cancer and predicted poor clinical outcome.ConclusionOur results decipher a positive feedback loop between hypoxia and MIR210HG that drive the Warburg effect and suggest that MIR210HG may be a good prognostic marker and therapeutic target for TNBC patients.

The overarching view of current tumor therapies simplifies cancer to a cell-biology problem in which neoplasms are caused solely by malignant cells and the exploration of carcinogenesis and tumor progression largely focuses on somatic mutations and other genetic abnormalities of cancer cells. The limited therapeutic response indicates that cancer is driven not only by endogenous oncogenic factors and reciprocal interactions within the tumor microenvironment, but also by complex systemic processes. Homeostasis is the fundamental premise of health, and is maintained by systemic regulation of neuro-endocrine-immune axis. Cancer is also a systemic disease that manifested by dysfunction of the nervous, endocrine, and immune systems. Multiple axes of regulation exist in cancer, including central-, organ-, and microenvironment-level manipulation. At each specific regulatory level, the tridirectional communication among the nervous, endocrine, and immune factors transmit flexible signaling to induce proliferation, invasion, reprogrammed metabolism, therapeutic resistance, and other malignant phenotypes of cancer cells, resulting in the extremely poor prognosis of this lethal disease. Understanding this coordinated signaling network will enable the development of new approaches for cancer treatment via behavioral and pharmacological interventions.

The scenario that multiple cell-edge mobile stations (MS) all without direct-links to the base station (BS) but have confidential messages in the uplink in the presence of untrusted relay (UR) cooperation was considered.In order to implement the secure communication between BS and multiple MS，destination-based jamming (DBJ) scheme was adopted.With the assumption that all MS had fixed transmit power，the joint UR and BS power control which aims at maximizing system sum secrecy rate was discussed.For this problem，analysis indicated that it was equivalent to joint access control and power allocation problem thus its NP-hard.Through problem relaxation，a suboptimal MS access control and alternatively power allocation algorithm was provided.This algorithm is proved to have polynomial complexity and can converge to at least a suboptimal solution for original problem.Simulation results show that compared with the benchmark algorithms，the proposed suboptimal algorithm is better in the achievable secrecy rate performance.

This study aimed to investigate the anatomical factors affecting iatrogenic injury of the deep branch of radial nerve during the Thompson approach and to propose corresponding countermeasures. Thompson approach was used to measure the horizontal/longitudinal distance from the position where the deep branch of radial nerve leaves the supinator to the ulnar margin of extensor carpi radialis brevis/humeroradial joint line. Measurements were obtained by using 48 adult cadaver specimens, which were used in teaching. We observed the lentor situation of the extensor digitorum and extensor carpi radialis brevis in proximal forearm segments and measured the distance from the deep branch of radial nerve to the humeroradial joint line at the lateral side of the radius in the neutral position of forearm rotation. The horizontal distance from the point where the deep branch of radial nerve leaves the inferior margin of supinator to the ulnar margin of extensor carpi radialis brevis was 1.3 ± 0.3 cm. The distance to the humeroradial joint line was 61.3 ± 17.6 mm. The distance to the lentor extent of extensor digitorum and extensor carpi radialis brevis at the distal part of humeroradial joint was 7.1 ± 2.1 cm. The distance from the deep branch of radial nerve to the humeroradial joint line at the lateral side of the radius is 3.2 ± 0.6 mm. Anatomical factors are observed in iatrogenic injury of the deep branch of radial nerve during the Thompson approach. Stretching the extensor digitorum before the dissection of the supinator is hazardous. [ABSTRACT FROM AUTHOR]

We report on mechanisms for suppressing diamond secondary nucleation in microwave plasma self-bias-enhanced growth (SBEG) of diamond films in methane diluted by argon. High-density plasma at a small distance from the substrate induces a floating potential which promotes high-flux, low-energy ion bombardment on diamond growing surfaces along with an equal flux of electrons. Increased atomic hydrogen generated by electron impact dissociation of methane and low-energy ion bombardment help remove hydrocarbon coatings on diamond grains in favor of continuous grain growth and, therefore, the suppression of secondary diamond nucleation. Energetic meta-stable excited argon, abundant C2 dimers, and enhanced effective surface temperature due to low-energy ion bombardment further promote the diamond grain growth resulting in the deposition of a diamond film with columnar diamond grains of much larger grain sizes and a much lower density of grain boundaries than ultrananocrystalline diamond (UNCD) films grown under similar conditions without optimized plasma-substrate interactions. SEM, XRD, PL, and Raman scattering help confirm the deposition of diamond films with columnar grains.

The pyroptosis of renal tubular epithelial cells leads to tubular loss and inflammation and then promotes renal fibrosis. The transcription factor Krüppel-like factor 4 (KLF4) can bidirectionally regulate the transcription of target genes. Our previous study revealed that sustained elevation of KLF4 is responsible for the transition of acute kidney injury (AKI) into chronic kidney disease (CKD) and renal fibrosis. In this study, we explored the upstream mechanisms of renal tubular epithelial cell pyroptosis from the perspective of posttranslational regulation and focused on the transcription factor KLF4. Mice were subjected to unilateral ureteral obstruction (UUO) surgery and euthanized on D7 or D14 for renal tissue harvesting. We showed that the pyroptosis of renal tubular epithelial cells mediated by both the Caspase-1/GSDMD and Caspase-3/GSDME pathways was time-dependently increased in UUO mouse kidneys. Furthermore, we found that the expression of the transcription factor KLF4 was also upregulated in a time-dependent manner in UUO mouse kidneys. Tubular epithelial cell-specific Klf4 knockout alleviated UUO-induced pyroptosis and renal fibrosis. In Ang II-treated mouse renal proximal tubular epithelial cells (MTECs), we demonstrated that KLF4 bound to the promoter regions of Caspase-3 and Caspase-1 and directly increased their transcription. In addition, we found that ubiquitin-specific protease 11 (USP11) was increased in UUO mouse kidneys. USP11 deubiquitinated KLF4. Knockout of Usp11 or pretreatment with the USP11 inhibitor mitoxantrone (3 mg/kg, i.p., twice a week for two weeks before UUO surgery) significantly alleviated the increases in KLF4 expression, pyroptosis and renal fibrosis. These results demonstrated that the increased expression of USP11 in renal tubular cells prevents the ubiquitin degradation of KLF4 and that elevated KLF4 promotes inflammation and renal fibrosis by initiating tubular cell pyroptosis., (© 2024. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.)

Acute kidney injury (AKI) is a worldwide public health problem characterized by the massive loss of tubular cells. However, the precise mechanism for initiating tubular cell death has not been fully elucidated. Here, we reported that phosphoglycerate mutase 5 (PGAM5) was upregulated in renal tubular epithelial cells during ischaemia/reperfusion or cisplatin-induced AKI in mice. PGAM5 knockout significantly alleviated the activation of the mitochondria-dependent apoptosis pathway and tubular apoptosis. Apoptosis inhibitors alleviated the activation of the mitochondria-dependent apoptosis pathway. Mechanistically, as a protein phosphatase, PGAM5 could dephosphorylate Bax and facilitate Bax translocation to the mitochondrial membrane. The translocation of Bax to mitochondria increased membrane permeability, decreased mitochondrial membrane potential and facilitated the release of mitochondrial cytochrome c (Cyt c) into the cytoplasm. Knockdown of Bax attenuated PGAM5 overexpression-induced Cyt c release and tubular cell apoptosis. Our results demonstrated that the increase in PGAM5-mediated Bax dephosphorylation and mitochondrial translocation was implicated in the development of AKI by initiating mitochondrial Cyt c release and activating the mitochondria-dependent apoptosis pathway. Targeting this axis might be beneficial for alleviating AKI., (© 2023. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.)

Transforming growth factor-β1 (TGF-β1) is regarded as a key factor in promoting renal fibrosis during chronic kidney disease (CKD). Signaling transduction of TGF-β1 starts with binding to TGF-β type II receptor (Tgfbr2), a constitutively activated kinase that phosphorylates TGF-β type I receptor (Tgfbr1), and then activates downstream Smad2/3 or noncanonical pathways. Previous studies show that cellular senescence is associated with the progression of CKD, and accelerated tubular cell senescence is implicated in promoting renal fibrosis. In the present study we investigated the renal parenchymal cell senescence in fibrosis from the sight of posttranslational regulation and focused on Tgfbr2, the important gatekeeper for TGF-β1 downstream signaling. In mice with unilateral ureteral obstruction (UUO) and folic acid (FA)-induced fibrotic kidneys, we found that Tgfbr2 was markedly elevated without obvious change in its mRNA levels. As an important member of deubiquitinating enzymes, ubiquitin-specific protease 11 (Usp11) was also significantly increased in fibrotic kidneys, and co-distributed with Tgfbr2 in tubular epithelial cells. Pretreatment with Usp11 inhibitor mitoxantrone (MTX, 30 mg · kg -1  · d -1 , i.p.) twice a week, for 2 weeks significantly attenuated the elevation of Tgfbr2, activation in downstream senescence-related signaling pathway, as well as renal senescence and fibrosis. In cultured mouse tubular epithelial cells (MTECs), treatment with angiotensin II (Ang-II, 10 -7 , 10 -6  M) dose-dependently elevated both Tgfbr2 and Usp11 levels. Inhibition or knockdown on Usp11 attenuated Ang-II-induced elevation in Tgfbr2 level, and attenuated the activation of downstream senescent-related signaling pathway and as well as cell senescence. We conducted Co-IP experiments, which revealed that Usp11 was able to interact with Tgfbr2, and inhibition of Usp11 increased the ubiquitination of Tgfbr2. Taken together, these results demonstrate that the elevation of Usp11 under pathological condition is implicated in promoting renal fibrosis. Usp11 promotes the development of renal fibrosis by deubiquitinating Tgfbr2, reducing Tgfbr2 ubiquitination degradation, and then facilitating the activation of downstream senescent signaling pathway., (© 2022. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.)

Objectives: To assess the prevalence and factors associated with physical and nonphysical violence in a sample of general practitioners (GPs)., Methods: We used a cross-sectional design to collect data from December 2014 to March 2015 with a structured self-administered questionnaire from 1015 GPs in Hubei Province, Central China (response rate, 85.6%). We used a multivariable logistic regression model to identify the predictors associated with workplace violence toward GPs., Results: Of the respondents, 62.2% of respondents reported exposure to workplace violence in the preceding year, including 18.9% and 61.4% who encountered physical and nonphysical violence, respectively. Multivariable logistic regression analysis suggested that GPs who were male, at a higher professional level, and who had a lower average monthly income were more likely to experience physical violence. Male GPs, less-experienced GPs, and those with administrative responsibility were more likely than their counterparts to encounter nonphysical violence., Conclusions: This study shows that the prevalence of workplace violence against GPs is high in Hubei, China. Creating a prevention strategy and providing safer workplace environments for GPs should be urgently prioritized.

The precursor powders of LuAG : Ce3+ transparent ceramics were synthesized by solvo-thermal method. The crystal structure and morphology of powders were analyzed by means of Fourier transform infra-red spectroscopy, X-ray diffraction and scanning electron microscopy. The precursor powders were sintered into transparent ceramics in vacuum and then in nitrogen without any additive. The surface morphology of the transparent unpolished ceramics was characterized using scanning electron microscopy. Some factors that affect the transparency of ceramics were discussed. The UV-Vis fluorescence excitation and emission spectra of LuAG : Ce3+ transparent ceramics were measured. The vacuum ultraviolet spectra of transparent ceramics were investigated using the synchrotron radiation as the excitation source. The excitation mechanism of Ce3+ was discussed at different excitation wavelength.

In this paper, life-table method was used to study the effects of different concentration Alexandrium tamarense on the durations of different development stages of Brachionus plicatilis and the characters of its population growth. The results showed that A. tamarense had significant effects on the growth and development of B. plicatilis via prolonging the durations of the rotifer' s pre-reproduction and generation succession, shortening the durations of its reproduction and post-reproduction and its mean lifespan, and reducing its laying eggs and fecundity. The net reproduction rate and intrinsic increasing rate of B. plicatilis decreased significantly, in comparison with those of the control. B. plicatilis could maintain definite population increase at the presence of different concentration A. tamarense.

Objective: To comparatively study the effects and mechanisms of burn-blast combined injury and burn-firearm combined injury complicated with seawater immersion on vascular endothelial cells., Methods: A total of 40 healthy adult hybrid dogs of both sexes, weighing 12-15 kg, were used in this study. Randomly-selected 20 dogs were established as models of burn-blast combined injury (the burn-blast injury group) and the other 20 dogs as models of burn-firearm combined injury (the burn-firearm injury group). Then the wounds of all the dogs were immediately immersed in seawater for 4 hours, and then they were taken out from the seawater. Blood samples were withdrawn from the central vein of the dogs before injury, and at 4, 7, 10, 20, and 28 hours after injury to measure the circulating endothelial cells and the von Willebrand factor., Results: Circulating endothelial cells increased significantly at 4 hours after injury in all the dogs. But they reached peak at 7 hours after injury in the burn-blast injury group and at 28 hours after injury in the burn-firearm injury group. The changes of circulating endothelial cells in the burn-blast injury group were significantly different from those in the burn-firearm injury group at 4, 7, 20, and 28 hours after injury (P < 0.01). The von Willebrand factor reached peak at 4 hours after injury in the burn-blast injury group and at 28 hours in the burn-firearm injury group. The changes of von Willebrand factor in the burn-blast injury group were significantly different from those in the burn-firearm injury group at 4, 20, and 28 hours after injury (P < 0.01)., Conclusions: In burn-blast injury combined with seawater immersion, the vascular endothelial cells changed most significantly at 4 hours or 7 hours after injury, while burn-firearm injury combined with seawater immersion have the same at 20 hours or 28 hours after injury.

Objective: To compare hemodynamic effects of resuscitation with Parkland formula or with the improved protocol on projectile-burn combined wound in dogs with seawater immersion., Methods: A model of projectile-burn combined wound in dogs with seawater immersion was reproduced, and 20 dogs were randomized into three groups: projectile-burn combined wound with seawater immersion (immersion group, n=8), Parkland formula resuscitation (lactated Ringer's solution 4 ml/kg per 1%total body surface area for 24 hours, standard resuscitation group, n=6), and improved protocol groups (lactated Ringer's solution 2.5 ml/kg per 1% total body surface area colloid solution 6% hetastarch 0.5 ml/kg per 1% total body surface area for 24 hours, improved group, n=6). Changes of hemodynamics and central temperature (CT) before injury, and 4, 7, 10, 20 and 28 hours after injury were observed. The mortality was observed., Results: After resuscitation with Parkland formula, CT as well as hemodynamic indexes and amount of urine were improved, but central venous pressure (CVP) and the amount of urine were higher in early period of resuscitation. CVP was (14.7+/-3.1)cm H2O and the amount of urine was (2.38+/-0.18)ml.h(-1).kg(-1) at 7 hours after injury. Hemodynamics was not stable during later period of experiment. After resuscitation with the improved protocol, the hemodynamics ameliorated better than resuscitation with Parkland formula. No animals died in improved group, but 4 and 1 died respectively in immersion group and standard resuscitation group., Conclusion: Fluid resuscitation according to the improved protocol is more suitable for projectile-burn combined wound in dogs with seawater immersion than resuscitation with Parkland formula.

Enhanced UV-B (280 - 320 nm) radiation resulting from ozone depletion is one of global environmental problems. Not only marine organisms but also marine ecosystems can be affected by enhanced UV-B radiation. The effects of UV-B radiation on interaction of macro-algae and micro-algae were investigated using Ulva pertusa Kjellman and Alexandrium tamarense as the materials in this study. The results demonstrated that UV-B radiation could inhibit the growth of Ulva pertusa and Alexandrium tamarense when they were both mono-cultured, and the growth inhibition of algae was more significant with increasing doses of UV-B radiation. Alexandrium tamarense could inhibit the growth of Ulva pertusa in mixed culture, and the growth inhibition was more significant when increasing the initial cell density. However, Ulva pertusa could inhibit the growth of Alexandrium tamarense in early phase and stimulate the growth in latter phase when they were grown in mixed culture. Lower initial cell density (10(2) cell/ml) of Alexandrium tamarense could inhibit the growth of Ulva pertusa under UV-B radiation treatment, however, with the initial cell density increasing (10(3) and 10(4) cell/ml), the growth of Ulva pertusa was stimulated under lower dose of UV-B radiation and inhibited under higher dose of UV-B radiation by Alexandrium tamarense. Compared with that in mixed culture, Ulva pertusa showed more positive inhibition to the growth of Alexandrium tamarense under UV-B radiation treatment.