Ligustrazine Attenuates Liver Fibrosis by Targeting miR-145 Mediated Transforming Growth Factor-ß/Smad Signaling in an Animal Model of Biliary Atresia.

To investigate therapeutic target for ligustrazine during liver fibrosis in an ethanol-induced biliary atresia rat model and transforming growth factor-ß (TGF-ß) induced hepatic stellate cell activation cell model, and the underlying mechanism, a total of 30 rats were randomly assigned into five groups (n = 6 per group): control, sham, ethanol-induced biliary atresia model, model plus pirfenidone, and model plus ligustrazine groups. The liver changes were assessed using H&E and Masson staining and transmission electron microscopy. Expression of miR-145 and mRNA and protein levels of TGF-ß/smads pathway-related proteins were detected. HSC-T6 cells were infected with LV-miR or rLV-miR-145 in the presence or absence of SMAD3 inhibitor SIS3 and treated with 2.5 ng/ml TGF-ß1 and then with ligustrazine. Collected cells were subjected to detect the expression of miR-145 and mRNA and protein expression levels of TGF-ß/smads pathway-related proteins. Ligustrazine rescued liver fibrogenesis and pathology for ethanol-caused bile duct injury, revealed by decreased α-smooth muscle actin and collagen I expression and liver tissue and cell morphology integrity. Further experiments showed that ligustrazine inhibited intrinsic and phosphorylated Smad2/3 protein expression and modification. Similar results were obtained in cells. In addition, ligustrazine altered miR-145 expression in both animal and cell models. Lentivirus mediated miR-145 overexpression and knockdown recombinant virus showed that miR-145 enhanced the TGF-ß/Smad pathway, which led to hepatic stellate cell activation, and ligustrazine blocked this activation. This work validated that ligustrazine-regulated miR-145 mediated TGF-ß/Smad signaling to inhibit the progression of liver fibrosis in a biliary atresia rat model and provided a new therapeutic strategy for liver fibrosis. SIGNIFICANCE STATEMENT: With an ethanol-induced biliary atresia rat model, ligustrazine was found to rescue liver fibrogenesis and pathology for ethanol caused bile duct injury, revealed by decreased α-smooth muscle actin and collagen I expression and liver tissue and cell morphology integrity. Furthermore, we found ligustrazine upregulated miR-145 expression and inhibited TGF-ß/SMAD signaling pathway both in vivo and in vitro. In addition, overexpression and knockdown of miR-145 confirmed that miR-145 is involved in the ligustrazine inhibition of liver fibrosis through the TGF-ß/SMAD signaling pathway.

Weighted gene co-expression network analysis identifies specific modules and hub genes related to Parkinson's disease.

OBJECTIVE: Parkinson's disease (PD) is one of the most common neurodegenerative diseases. This study aims to screen specific modules and key genes related to PD. METHODS: Gene expression profile data GSE6613 and GSE22491 were downloaded from the Gene Expression Omnibus database. The significantly differentially expressed genes (DEGs) in different datasets were screened, followed by gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The Weighted Gene Co-expression Network Analysis (WGCNA) was used to screen disease-related modules that are significantly stable across datasets. The protein-protein interaction network was constructed using the DEGs in the stable module obtained and preservation modules. Finally, the hub genes directly related to PD were screened. RESULTS: A total of 179 DEGs with the same significant difference direction were screened. The enrichment analysis of GO and KEGG pathways showed that 20 significantly related GO biological processes and 9 KEGG signaling pathways were screened. A total of three highly conservative modules were detected in the WGCNA network. Finally, three significant PD-related KEGG pathways screened from the Comparative Toxicogenomics Database were identified, including neuroactive ligand-receptor interaction (CRHR2, CTSG, GRIN1, GRIN2D, LPAR4 and P2RX3), amyotrophic lateral sclerosis (BCL2, GRIN1 and GRIN2D) and alcoholism (CAMKK2, GRIN1, GRIN2D and SLC18A2). Key genes, such as SLC18A2, GRIN1 and GRIN2D, may be potential candidate genes for PD progression. CONCLUSIONS: Our findings indicate that SLC18A2, GRIN1 and GRIN2D may play an important role in the pathogenesis of PD.

LINC01278 is Highly Expressed in Osteosarcoma and Participates in the Development of Tumors by Mediating the miR-134-5p/KRAS Axis.

PURPOSE: There is increasing evidence that non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), produce a critical regulatory effect on osteosarcoma (OS). LINC01278, as a newly discovered lncRNA, is found to be highly expressed in OS, but its related mechanism remains unclear. This research, therefore, is designed to study the mechanism of LINC01278 in OS and to find potential targets for clinical use. METHODS: qRT-PCR was applied to determine the relative expression of LINC01278 and analyze its diagnostic value in OS. CCK-8, Transwell and flow cytometry were utilized for the determination of cell proliferation, migration/invasion, and apoptosis. RIP and RNA pull-down experiments were used to verify the targeted binding effect of miR-134-5p and LINC01278. The relationship between miR-134-5p and LINC01278 or KRAS was analyzed using dual luciferase reporter gene. The effects of LINC01278 on tumor growth in nude mice was analyzed by in vivo experiment. RESULTS: qRT-PCR showed that LINC01278 increased in OS tissues and serum, indicating poor prognosis. In addition, LINC01278 was also of high value for OS diagnosis. Functional experiments showed that LINC01278 inhibited KRAS-mediated OS cell proliferation and metastasis through miR-134-5p. Finally, the results of an in vivo animal model indicated that LINC01278 promoted OS growth. CONCLUSION: LINC01278 is expressed highly in OS, and patients with high LINC01278 expression have poor prognosis. Moreover, LINC01278 can suppress the proliferation and apoptosis of OS cells through mediating miR-134-5p/KRAS axis, which is expected to become a potential therapeutic target for OS.

Enhancing the performance of an open quantum battery via environment engineering.

We investigate the charging process of open quantum battery in the weak system-environment coupling regime. A method to improve the performance of open quantum battery in a reservoir environment, which described by a band-gap environment model or a two-Lorentzian environment model, is proposed by manipulating the spectral density of environment. We find that the optimal quantum battery, characterized by fast charging time and large ergotropy, in the band-gap environment can be obtained by increasing the weights of two Lorentzians and the spectral width of the second Lorentzian, which is in sharp contrast to the quantum battery in two-Lorentzian environment. Then we extend our discussion to multiple coupled reservoir environments, which are composed of N coupled dissipative cavities. We show that, the performance of quantum battery can be enhanced by increasing the coupling strength between the nearest-neighbor environments and decreasing the size of the environments. In particular, to fully charge and extract the total stored energy as work for quantum battery can be achieved by manipulating the coupling strength between the nearest-neighbor environments. Our results provide a practical approach for the realization of the optimal quantum batteries in future experiments.

Overexpression of microRNA-205-5p exerts suppressive effects on stem cell drug resistance in gallbladder cancer by down-regulating PRKCE.

Some microRNAs (miRs or miRNAs) have been reported to function as tumor suppressors in gallbladder cancer (GBC). However, the specific effect of miR-205-5p on GBC remains unclear. The objective of the present study was to unravel the effects of miR-205-5p on the drug resistance in GBC. For this purpose, the expression of miR-205-5p and protein kinase C ϵ (PRKCE) was quantified in the peripheral blood sample harvested from GBC patients and healthy volunteers. Then the relationship between miR-205-5p and PRKCE was validated. After isolating the GBC stem cells, ectopic expression and depletion experiments were conducted to analyze the effect of miR-205-5p and PRKCE on cell proliferation, drug resistance, apoptosis, and colony formation rate as well as the expression of apoptotic factors (Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), and cleaved caspase 3). Finally, the mouse xenograft model of GBC was established to verify the function of miR-205-5p in vivo. Intriguingly, our results manifested that miR-205-5p was down-regulated, while PRKCE was up-regulated in peripheral blood samples and stem cells of patients with GBC. Moreover, miR-205-5p targeted PRKCE and negatively regulated its expression. The overexpression of miR-205-5p or silencing of PRKCE inhibited the drug resistance, proliferation, and colony formation rate while promoting apoptosis of GBC stem cells. Additionally, the overexpression of miR-205-5p attenuated drug resistance to gemcitabine but promoted the gemcitabine-induced cell apoptosis by inhibiting the PRKCE in vivo. Overall, an intimate correlation between miR-205-5p and PRKCE is a key determinant of drug resistance of GBC stem cells, thus, suggesting a novel miR-205-5p-based clinical intervention target for GBC patients.

Finite-Component Multicriticality at the Superradiant Quantum Phase Transition.

We demonstrate the existence of finite-component multicriticality in a qubit-boson model where biased qubits collectively coupled to a single-mode bosonic field. The interplay between biases and boson-qubit coupling produces a rich phase diagram which shows multiple superradiant phases and phase boundaries of different orders. In particular, multiple phases become indistinguishable in appropriate bias configurations, which is the signature of multicriticality. A series of universality classes characterizing these multicritical points are identified. Moreover, we present a trapped-ion realization with the potential to explore multicritical phenomena experimentally using a small number of ions. The results open a novel way to probe multicritical universality classes in experiments.

Outbreak of Human Parainfluenza Virus Type 1 in a Kindergarten from China, 2018.

Objective We reported an outbreak of human parainfluenza virus type 1 (HPIV1) in a kindergarten and explored the genetic characteristics of HPIV1 hemagglutinin-neuraminidase (HN) and fusion (F) genes to provide more evidence about HPIV1 outbreaks. Methods Suspected cases were the children with an influenza-like illness during June 20 to 26, 2018. Nasopharyngeal swabs were collected and screened to determine the presence of respiratory pathogens by real-time fluorescent quantitative polymerase chain reaction. The HN and F gene sequences of HPIV-positive samples were further amplified and sequenced to confirm the HPIV genotype and identify genetic characteristics. A phylogenetic tree, based on the HN and F genes, was reconstructed by maximum likelihood method. Results Fourteen children in the outbreak were diagnosed as upper respiratory tract infection. The most common symptom was cough (10/14), followed by rhinorrhea (5/14), sore throat (4/14), headache (1/14), and abdominal pain (1/14). Eight patients were positive for HPIV1 and negative for other pathogens. Phylogenetic tree demonstrated that the eight strains from the year 2018 in our study located in the clade 2.3. Two specific substitutions (N333S and I509M) in the amino acids of the F protein and two substitutions (V19A and L436I) in the HN protein were different from other strains in the clade 2. Conclusion HPIV1 was attributed to the outbreak, which may be related to the genetic variations of HPIV1.

Wnt/ß-catenin signaling as an emerging potential key pharmacological target in cholangiocarcinoma.

Cholangiocarcinoma (CCA) is a fatal malignant tumor of biliary epithelial cells involving intra- or extra-hepatic bile ducts. The prognosis of CCA is generally poor due to its diagnosis at the late stages. The currently employed chemotherapeutic agents do not increase the survival rate in patients with unresectable CCA. Accordingly, there is a need to identify new therapeutic agents for the effective management of intra- and extra-hepatic CCA. Clinical as well as preclinical studies have suggested the key role of the activation of Wnt/ß-catenin signaling pathway in the induction and progression of CCA. There is an up-regulation of different Wnt ligands including Wnt2, Wnt3, Wnt5, Wnt7 and Wnt10 along with redistribution of ß-catenin (more expression in the nucleus and lesser on the cell surface due to nuclear translocation of ß-catenin) in different types of malignant biliary tumors. Apart from the role of this pathway in the induction and progression of CCA, this pathway is also involved in inducing multidrug resistance by inducing the expression of P-glycoprotein efflux pump on the cancer cells. These deleterious effects of Wnt/ß-catenin signaling are mediated in association with other signaling pathways involving microRNAs (miRNAs), PI3K/AKT/PTEN/GSK-3ß, retinoic acid receptors (RARs), dickkopf-1 (DKK1), protein kinase A regulatory subunit 1 α (PRKAR1A/PKAI), (SLAP), liver kinase B1 (LKB1) and CXCR4. The selective inhibitors of Wnt/ß-catenin signaling may be potentially employed to overcome multidrug-resistant, fatal CCA. The present review discusses the role of Wnt/ß-catenin along with its relation with other signaling pathways in the induction and progression of CCA.

Unified and Exact Framework for Variance-Based Uncertainty Relations.

We provide a unified and exact framework for the variance-based uncertainty relations. This unified framework not only recovers some well-known previous uncertainty relations, but also fixes the deficiencies of them. Utilizing the unified framework, we can construct the new uncertainty relations in both product and sum form for two and more incompatible observables with any tightness we require. Moreover, one can even construct uncertainty equalities to exactly express the uncertainty relation by the unified framework, and the framework is therefore exact in describing the uncertainty relation. Some applications have been provided to illustrate the importance of this unified and exact framework. Also, we show that the contradiction between uncertainty relation and non-Hermitian operator, i.e., most of uncertainty relations will be violated when applied to non-Hermitian operators, can be fixed by this unified and exact framework.

Efficacy of Emamectin Benzoate Trunk Injection Against the Asian Long-Horned Beetle [Anoplophora glabripennis (Coleoptera: Cerambycidae)].

The efficacy of tree injected with emamectin benzoate (EB) against the Asian long-horned beetle (ALB) was tested in a heavily infested willow forest in Beijing, China. In a 1.7-ha plot, 240 out of 310 trees were treated with two EB formulations at various rates. After fall application, the larval population decreased by 89% in the following spring and by >99% during the second year detected by monitoring new frass emission from marked holes. Consequently, the number of exit holes of emerging adults decreased to 0 in the second year. Re-infestation occurred in the third year after application. This high efficacy and lasting activity might be contributed to: a) a favorable translocation of EB in trees when injected into the sapwood; b) the high intrinsic activity against ALB larvae with LC50 of 20-30 ppb; and c) a reduced lifespan of ALB adults by over 60% when feeding on twigs of EB-treated trees. On untreated control trees, the larval population decreased during the first winter. In the second year after application, the larval population was wiped out during winter and a re-infestation started from border trees by adults flying in from outside the trial plot. This pattern indicates an eradication of the ALB population in the 1.7-ha plot can be expected 2 yr after EB treatment. The benefit of treating with EB on the surrounding population was observed in both the untreated trees and imidacloprid-treated trees, suggesting that treatment of EB benefits both the treated trees and the surrounding trees in the area.

Spatiotemporal expression of NDRG2 in the human fetal brain.

N-myc downstream-regulated gene 2 (NDRG2) has been implicated in the development of central nervous system and brain diseases such as brain tumors, ischemic stroke and neurodegenerative disorders. However, it remains unclear that the spatiotemporal distribution of NDRG2 in the human fetal brain. In this study, we examined the expression pattern of NDRG2 in different regions of human fetal brain at 16-28 gestational weeks (GWs) by using RT-PCR, western blot and immunohistochemistry. Firstly, RT-PCR revealed that mRNA of NDRG2 was detected in the human brain regions of fetuses at 16-28 GWs such as medulla oblongata (MdO), mesencephalon (MeE), cerebellum (Cbl), frontal lobe (Fr), ventricular (VZ)/subventricular zone (SVZ) and hippocampus (hip), and the expressions of NDRG2 mRNA in these human fetal brain regions were increased with gestational maturation. Furthermore, western blot and immunohistochemistry results revealed that at 28 GWs, the expression of NDRG2 protein was restricted to the MdO's olivary nucleus, MeE's aqueduct, cerebellar internal granular layers, cerebral cortex of the Fr, VZ/SVZ of lateral ventricle, and hippocampal dentate gyrus, and highest expression in the VZ/SVZ, and lowest in the MeE. Finally, double immunohistochemistry results showed that NDRG2 in the MdO, Cbl and VZ/SV at 28 GWS was mainly expressed in neurons (NeuN positive cells), and in some astrocytes (GFAP positive cells). Taken together, these results suggest that NDRG2 is mainly expressed in human fetal neurons of various brain regions during development, which may be involved in neuronal growth and maturation.

Universal Dissipationless Dynamics in Gaussian Continuous-Variable Open Systems.

We investigate the universal dissipationless dynamics of Gaussian continuous-variable systems in the presence of a band-gapped bosonic environment. Our results show that environmental band gaps can induce localized modes, which give rise to the dissipationless dynamics where the system behaves as free oscillators instead of experiencing a full decay in the long-time limit. We present a complete characterization of localized modes and show the existence of the critical system-environment coupling. Beyond the critical values, localized modes can be produced, and the system dynamics become dissipationless. This novel dynamics can be utilized to overcome the environmental noises and protect the quantum resources in the continuous-variable quantum information.

Novel oncogenic and chemoresistance-inducing functions of resistin in ovarian cancer cells require miRNAs-mediated induction of epithelial-to-mesenchymal transition.

Resistin plays a role in the growth, proliferation, angiogenesis, metastasis and therapeutic resistance in different cancers. However, such effects of resistin have never been evaluated in ovarian cancer, a deadly gynecological malignancy. We observed a significant induction of ovarian cancer cells' growth, invasion and cisplatin resistance, and established a mechanism of resistin action that included induction of EMT and stemness, as evidenced by down-regulated epithelial marker e-cadherin and up-regulated mesenchymal markers vimentin/ ZEB1 and stemness markers sox2, oct4 and nanog. The mechanism also included suppression of tumor suppressor miRNAs, let-7a, miR-200c and miR-186. Over-expression of these miRNAs significantly reversed the resistin-mediated effects on invasion and chemoresistance. We further validated our results in vivo where resistin administration significantly enhanced tumor growth in mice. Our results provide first evidence for such oncogenic effects of resistin in ovarian cancer models and a rationale for future studies to further understand the mechanistic role of resistin in ovarian cancer invasiveness, metastasis and therapy resistance.

Mefloquine targets ß-catenin pathway and thus can play a role in the treatment of liver cancer.

The current study was designed and performed to investigate the effect of mefloquine on the proliferation and tumor formation potential of liver cancer stem cells. CD133 + HepG2 cells were identified using MACS and showed markedly higher tumor formation potential compared to the parental cells. The secondary tumors formed by CD133 + cells were markedly large in size and more in number compared to the parental cells. Mefloquine treatment of CD133 + HepG2 cells inhibited the proliferation selectively in concentration based manner. The rate of proliferation was inhibited to 82 and 12% in parental and CD133 + sphere forming cells, respectively on treatment with 10 µM concentration of mefloquine. The number of secondary tumors formed by primary tumors was decreased significantly on treatment with 10 µM mefloquine concentration. Treatment of the liver cancer stem cells with mefloquine markedly decreased the potential to undergo self-renewal at 10 µM concentration after 48 h. The results from western blot analysis showed significantly higher expression of cancer stem cell molecules ß-catenin and cyclin D1 in LCSCs. Treatment of the LCSCs with various concentrations of mefloquine reduced the expression levels of ß-catenin and cyclin D1. Administration of the CD133 + cell tumor xenografts in the mice led to the formation of large sized tumors in the control group. However, the tumor growth was inhibited significantly in the mice on treatment with 10 mg/kg doses of mefloquine after day 21. The tumor weight was significantly lower in the animals of mefloquine treatment group compared to the control group. Thus, mefloquine treatment inhibits self-renewal and proliferation potential of cells through targeting ß-catenin pathway.

Correlations of insulin-like growth factor I and insulin-like growth factor I receptor with the clinicopathological features and prognosis of patients with colon cancer.

OBJECTIVE: This study is designed to evaluate the correlations of insulin-like growth factor I (IGF-I) and insulin-like growth factor I receptor (IGF-IR) expressions with the clinicopathological features and prognosis of patients with colon cancer. METHODS: From January 2010 to January 2009, tissue samples were collected from 121 colon cancer patients, 147 with colon adenoma and 63 patients with chronic diarrhea. Real-time quantitative polymerase chain reaction was used to analyze the mRNA expressions of IGF-I and IGF-IR. Immunohistochemistry was utilized to detect the protein expressions of IGF-I and IGF-IR. RESULTS: The IGF-I and IGF-IR mRNA expressions in colon cancer tissues were higher than those in colon adenoma tissues and normal tissues. The positive protein expressions of IGF-I and IGF-IR in colon cancer tissues were also higher than those in colon adenoma tissues and normal tissues. The mRNA expressions of IGF-I and IGF-IR were associated with the degree of differentiation, tumor node metastasis stage and lymphatic metastasis of colon cancer. Tumor node metastasis stage, lymphatic metastasis, postoperative chemotherapy and IGF-IR protein expression were independent factors for the prognosis of colon cancer. CONCLUSIONS: This study has demonstrated that overexpression of IGF-I and IGF-IR contributes to the development and progression of colon cancer.

Study on the influence of curcumin on chemosensitivity of nephroblastoma cells.

OBJECTIVE: To study the influence of curcumin on chemosensitivity of nephroblastoma cells. METHODS: Human nephroblastoma cells line SK-NEP-1 was transplanted to the nude mice subcutaneously to establish the implantation tumor model of human nephroblastoma cells. A total of 30 tumor-bearing mice were divided into three groups of ten randomly. The routine chemotherapy group was given vincristine (0.05 mg/mL·0.2 mL/d) and actinomycin D (15 ng/mL·0.2 mL/d) combined chemotherapy regime. The curcumin chemotherapy group was given the same combined chemotherapy regimens and curcumin (30 mg/kg/d) by intraperitoneal injection. The control group was given normal saline (NS) of the same volume by intraperitoneal injection. Continuous administration would be kept for 4 weeks and 3 days a week. The volumetric changes of every group were recorded. The serum of every group in different time was collected and the VEGF content was detected by ELISA. All mice were cercrificed and the tumor tissues were stripped and weighed after 4 weeks' treatment. The tumor inhibition rate was calculated. The cell proliferation activity and apoptosis rate were detected by MTT and flow cytometry method. All data were statistically analyzed by SPSS 19.0. RESULTS: The tumor volume, serum VEGF content, tumor inhibition rate, cell proliferation activity and apoptosis rate of routine chemotherapy group and curcumin chemotherapy group had significant differences comparing with the control group (P < 0.05) after 4-week's treatment. The cancer growth of curcumin chemotherapy group was obviously decreased and even tended to shrink comparing with routine chemotherapy group (χ(2) = 15.732, P = 0.007). The cell proliferation activity was significantly reduced and the apoptosis rate was significantly higher, (χ(2) = 9.427, P = 0.012) which showing the effect of chemotherapy was enhanced. CONCLUSIONS: The chemosensitivity of nephroblastoma cells could be improved by curcumin, then the effect of preoperative adjuvant chemotherapy scheme would be enhanced, the growth of nephroblastoma cells would be inhibited and the surgical risk of nephroblastoma would be reduced.

Monodisperse AIE-Active Conjugated Polymer Nanoparticles via Dispersion Polymerization Using Geminal Cross-Coupling of 1,1-Dibromoolefins.

Monodisperse AIE (aggregation-induced emission)-active conjugated polymer nanoparticles are synthesized by dispersion polymerization using geminal Suzuki cross-coupling of 1,1-dibromoolefins. The size of the nanoparticles can be adjusted by varying the concentration of the initial monomer.

Influence of intrinsic decoherence on tripartite entanglement and bipartite fidelity of polar molecules in pendular states.

An array of ultracold polar molecules trapped in an external electric field is regarded as a promising carrier of quantum information. Under the action of this field, molecules are compelled to undergo pendular oscillations by the Stark effect. Particular attention has been paid to the influence of intrinsic decoherence on the model of linear polar molecular pendular states, thereby we evaluate the tripartite entanglement with negativity, as well as fidelity of bipartite quantum systems for input and output signals using electric dipole moments of polar molecules as qubits. According to this study, we consider three typical initial states for both systems, respectively, and investigate the temporal evolution with variable values of the external field intensity, the intrinsic decoherence factor, and the dipole-dipole interaction. Thus, we demonstrate the sound selection of these three main parameters to obtain the best entanglement degree and fidelity.

[Interpolation of daily mean temperature by using geographically weighted regression-Kriging].

Air temperature is the input variable of numerous models in agriculture, hydrology, climate, and ecology. Currently, in study areas where the terrain is complex, methods taking into account correlation between temperature and environment variables and autocorrelation of regression residual (e.g., regression Kriging, RK) are mainly adopted to interpolate the temperature. However, such methods are based on the global ordinary least squares (OLS) regression technique, without taking into account the spatial nonstationary relationship of environment variables. Geographically weighted regression-Kriging (GWRK) is a kind of method that takes into account spatial nonstationarity relationship of environment variables and spatial autocorrelation of regression residuals of environment variables. In this study, according to the results of correlation and stepwise regression analysis, RK1 (covariates only included altitude), GWRK1 (covariates only included altitude), RK2 (covariates included latitude, altitude and closest distance to the seaside) and GWRK2 (co-variates included altitude and closest distance to the seaside) were compared to predict the spatial distribution of mean daily air temperature on Hainan Island on December 18, 2013. The prediction accuracy was assessed using the maximum positive error, maximum negative error, mean absolute error and root mean squared error based on the 80 validation sites. The results showed that GWRK1's four assessment indices were all closest to 0. The fact that RK2 and GWRK2 were worse than RK1 and GWRK1 implied that correlation among covariates reduced model performance.