Change pattern and stability of oasisization land in Mu Us Sandy Land.

Understanding land structure change and stability in the process of oasisization is particularly important for the desertification control in sandy land. Based on land use data of eight periods from 1980 to 2020, we extracted the spatial distribution information of oasis land in Mu Us Sandy Land, and analyzed the spatio-temporal variations of land transformation patterns and stability of oasis land with overlay analysis and grid analysis. The results showed that desertification in the Mu Us Sandy Land had reversed, with a significant process of oasis. The area of forest and grassland increased from 10.2% in 1980 to 73.7% in 2020, while the area of oasisization land increased from 32500 km2 in 1980 to 33900 km2 in 2020. The area of extremely severe, severe, and moderate desertification significantly decreased, while the area of non-desertification and mild desertification obviously increased. The four patterns of oasisization land transformation, including stability, fluctuation, expansion, and retreat, which accounted for 78.7%, 12.2%, 6.2%, and 2.9% of the oasisization land area in 2020, respectively. The oasisization land with low change intensity (the cumulative change intensity less than 0.12) in the Mu Us Sandy Land accounted for 82.7% of the total oasisization area, and the oasisization land in the sandy land was generally stable. Zoning management strategies should be applied according to the stability of sand belt and transformation pattern of oasisization land to achieve the goal of efficient system management and improvement, including eliminating sand hazards at desertification expansion areas with strong wind and sand activities, consolidating sand resources at oasisization areas where ecologically fragile desertification was frequent, and sustainably managing and utilizing sand resources at stable expansion of oases in forest- and grass-rich oasisization areas.

A new mammal from the Lower Cretaceous Jehol Biota and implications for eutherian evolution.

Here we report on a new Early Cretaceous eutherian represented by a partial skeleton from the Jiufotang Formation at Sihedang site, Lingyuan City, Liaoning Province that fills a crucial gap between the earliest eutherians from the Yixian Formation and later Cretaceous eutherians. The new specimen reveals, to our knowledge for the first time in eutherians, that the Meckelian cartilage was ossified but reduced in size, confirming a complete detachment of the middle ear from the lower jaw. Seven hyoid elements, including paired stylohyals, epihyals and thyrohyals and the single basihyal are preserved. For the inner ear the ossified primary lamina, base of the secondary lamina, ossified cochlear ganglion and secondary crus commune are present and the cochlear canal is coiled through 360°. In addition, plesiomorphic features of the dentition include weak conules, lack of pre- and post-cingula and less expanded protocones on the upper molars and height differential between the trigonid and talonid, a large protoconid and a small paraconid on the lower molars. The new taxon displays an alternating pattern of tooth replacement with P3 being the last upper premolar to erupt similar to the basal eutherian Juramaia. Parsimony analysis places the new taxon with Montanalestes, Sinodelphys and Ambolestes as a sister group to other eutherians. This article is part of the theme issue 'The impact of Chinese palaeontology on evolutionary research'.

Crystal structure of catena-poly[[di-aqua-cobalt(II)]-bis-[µ-5-(4-carb-oxy-ylato-phenyl)picolinato]-κ(3) N,O (2):O (5);κ(3) O (5):N,O (2)-[di-aqua-cobalt(II)]-µ-1-[4-(1H-imidazol-1-yl)phen-yl]-1H-imidazole-κ(2) N (3):N (3')].

The asymmetric unit of the title polymeric Co(II) complex, [Co2(C13H7NO4)2(C12H10N4)(H2O)4] n , contains a Co(II) cation, a 5-(4-carboxyl-atophen-yl)picolinate dianion, two coordination water mol-ecules and half of 1-[4-(1H-imidazol-1-yl)phen-yl]-1H-imidazole ligand. The Co(II) cation is coordinated by two picolinate dianions, two water mol-ecules and one 1-[4-(1H-imidazol-1-yl)phen-yl]-1H-imidazole mol-ecule in a distorted N2O4 octa-hedral coordination geometry. The two picolinate dianions are related by an inversion centre and link two Co(II) cations, forming a binuclear unit, which is further bridged by the imidazole mol-ecules, located about an inversion centre, into the polymeric chain propagating along the [-1-11] direction. In the crystal, the three-dimensional supra-molecular architecture is constructed by O-H⋯O hydrogen bonds between the coordinating water mol-ecules and the non-coordinating carboxyl-ate O atoms of adjacent polymeric chains.

ß, ß-Dimethylacrylshikonin induces mitochondria-dependent apoptosis of human lung adenocarcinoma cells in vitro via p38 pathway activation.

AIM: ß, ß-Dimethylacrylshikonin (DMAS) is an anticancer compound extracted from the roots of Lithospermum erythrorhizon. In the present study, we investigated the effects of DMAS on human lung adenocarcinoma cells in vitro and explored the mechanisms of its anti-cancer action. METHODS: Human lung adenocarcinoma A549 cells were tested. Cell viability was assessed using an MTT assay, and cell apoptosis was evaluated with flow cytometry and DAPI staining. The expression of the related proteins was detected using Western blotting. The mitochondrial membrane potential was measured using a JC-1 kit, and subcellular distribution of cytochrome c was analyzed using immunofluorescence staining. RESULTS: Treatment of A549 cells with DMAS suppressed the cell viability in dose- and time-dependent manners (the IC50 value was 14.22 and 10.61 µmol/L, respectively, at 24 and 48 h). DMAS (7.5, 10, and 15 µmol/L) dose-dependently induced apoptosis, down-regulated cIAP-2 and XIAP expression, and up-regulated Bax and Bak expression in the cells. Furthermore, DMAS resulted in loss of mitochondrial membrane potential and release of cytochrome c in the cells, and activated caspase-9, caspase-8, and caspase-3, and subsequently cleaved PARP, which was abolished by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor. DMAS induced sustained p38 phosphorylation in the cells, while pretreatment with SB203580, a specific p38 inhibitor, blocked DMAS-induced p38 activation and apoptosis. CONCLUSION: DMAS inhibits the growth of human lung adenocarcinoma A549 cells in vitro via activation of p38 signaling pathway.

Activation of JNK/p38 pathway is responsible for α-methyl-n-butylshikonin induced mitochondria-dependent apoptosis in SW620 human colorectal cancer cells.

α-Methyl-n-butylshikonin (MBS), one of the active components in the root extracts of Lithospermum erythrorhizon, posses antitumor activity. In this study, we assess the molecular mechanisms of MBS in causing apoptosis of SW620 cells. MBS reduced the cell viability of SW620 cells in a dose-and time-dependent manner and induced cell apoptosis. Treatment of SW620 cells with MBS down-regulated the expression of Bcl-2 and up-regulated the expression of Bak and caused the loss of mitochondrial membrane potential. Additionally, MBS treatment led to activation of caspase-9, caspase-8 and caspase-3, and cleavage of PARP, which was abolished by pretreatment with the pan-caspase inhibitor Z-VAD-FMK. MBS also induced significant elevation in the phosphorylation of JNK and p38. Pretreatment of SW620 cells with specific inhibitors of JNK (SP600125) and p38 (SB203580) abrogated MBS-induced apoptosis. Our results demonstrated that MBS inhibited growth of colorectal cancer SW620 cells by inducing JNK and p38 signaling pathway, and provided a clue for preclinical and clinical evaluation of MBS for colorectal cancer therapy.

Inhibitory effect of cryptotanshinone on angiogenesis and Wnt/ß-catenin signaling pathway in human umbilical vein endothelial cells.

OBJECTIVE: To investigate the anti-angiogenic effect of cryptotanshinone (CPT) on human umbilical vein endothelial cells (HUVECs) and the effect of CPT on Wnt/ß-catenin signaling pathway. METHODS: HUVECs were incubated with 0, 2.5, 5, 10, and 20 µ mol/L CPT for detecting cell viability with dimethyl thiazolyl-2,5-diphenyltetrazolium bromide (MTT) assay. Then, HUVECs were incubated with 0, 2.5, 5, and 10 µ mol/L CPT for detecting endothelial cell migration, invasion, and tubular-like structure formation with wound healing, transwell invasion and matrigel tube formation assays, respectively. To gain insight into CPT-mediated signaling, the effects of CPT on T-cell factor/lymphocyte enhancer factor (TCF/LEF) transcription factors were detected by the Dual-luciferase reporter assay. Next, the nuclear expression of ß-catenin was evaluated using Western blot and immunochemistry. Finally, vascular endothelial growth factor (VEGF) and cyclin D1, downstream proteins of the Wnt pathway were examined with Western blot. RESULTS: CPT dose-dependently suppressed endothelial cell viability, migration, invasion, and tubular-like structure formation. In particular, CPT blocked ß-catenindependent transcription in HUVECs in a dose-dependent manner. In Western bolt, 10 µ mol/L CPT decreased expression of ß-catenin in nucleus of HUVECs (P<0.01). In immunohistochemistry, ß-catenin was more potent in response to LiCl (an activator of the pathway) treatment. However, the signals were weaker in the nucleus of the CPT (10 µ mol/L) group, compared to the positive control. Also, VEGF and cyclin D1 were both eliminated by CPT in 5 and 10 µ mol/L doses (P<0.05). CONCLUSION: Our study supported the role of CPT as an angiogenic inhibitor, which may impact on the Wnt/ß-catenin signaling pathway.

[Vacuum sealing drainage and free coupling chain-link posterior tibial artery flap in the reconstruction of degloving injury of propodium].

OBJECTIVE: To present the methods of vacuum sealing drainage and free coupling chain-link flap of posterior tibial artery flap and medial plantar flap in the reconstruction of degloving injury of propodium. METHODS: From Oct. 2008 to Dec. 2011 five cases with degloving injury of propodium underwent debridement and vacuum sealing drainage on the first stage. Free chain-link flap of posterior tibial artery flap and medial plantar flap were applied to close the wound at the secondary stage. The nerve was included in the coupling flaps. The size of posterior tibial artery flap ranged from 14 cm x 10 cm to 11 cm x 8 cm,and the size of medial plantar flap ranged from 12 cm x 8 cm to 8 cm x 6 cm. RESULTS: All flaps were survived with no vascular crisis. The flap sensation recovered to S3-S3 during the follow-up period of 6-21 months. The texture and appearance of flaps were satisfied. The plantar had not ulcer and corpus callosum. CONCLUSION: Vacuum sealing drainage and free chain-link flap of posterior tibial artery flap and medial plantar flap with nerve are the ideal methods for the reconstruction of degloving injury of propodium.

[Fingertip replantation with anastomosis of palm vein and retaining the nail].

OBJECTIVE: To study the replantation methods and clinical results of amputated fingertip. METHODS: From October 2007 to June 2011, 18 fingers of 13 cases were replanted with anastomosis of palm vein and retaining the nail, including 9 males and 4 females,with an average age of 26 years old ranging from 17 to 45 years old. The time from injury to therapy was from 30 min to 5 h, time of broken finger ischemia was from 1.5 to 7 h. All broken fingers were preservation under normal temperature. RESULTS: All fingers were survived, no vascular crisis happened. All cases were followed up from 3 to 24 months with an average of 14 months. The length and shape of replanted fingers were similar to that of the healthy side. The new nails were smooth, the function was perfect,the sense of pain and touched sensation had been recovered. Their two-piont discriminations ranged from 3 to 6 mm with an average of 5 mm. According to the assessment standard of Chinese Medical Association of Hand Surgery, the results were excellent in 14 cases, good in 3 cases, poor in 1 case. CONCLUSION: Fingertip replantation with anastomosis of palm vein and retaining the nail is regained satisfactory appearance and function of the digits with a high survival rate.

[Mechanism of platycodin D-induced apoptosis in A549 human lung cancer cells].

OBJECTIVE: To investigate the molecular mechanism of platycodin D showing the inhibitory effect on proliferation and induced apoptosis of humane long cancer cells A549. METHOD: Humane long cancer cells A549 were cultured in vitro, with the final PD concentration of 5-20 micromol x L(-1). PD's inhibitory effect on cell proliferation was examined by MTT assay. Morphological changes in cells were observed with microscope. The cell apoptosis rate was detected by Annexin V-FITC/PI double staining. The change of mitochondrial membrane potential was detected by JC-1. The protein expressing of leaved Caspase-3, cleaved Caspase-9, cleaved PARP, Bcl-2, Bcl-xl, Bak and Bax were detected by Western blot analysis. RESULT: PD could inhibit the proliferation of A549 cells and show stronger effect with the increase of concentration and over time. Compared with the control group, PDs of different concentration showed significant increase in the cell apoptosis rate, decrease in mitochondrial membrane potential after 24 h. Protein electrophoresis inspection showed cut segments in both protein Caspase-3 and Caspase-9 and notable fractures with time. Further study found that PD decreased Bcl-2, Bcl-xl proteins and increased Bax, Bak proteins after processing A549 cells. CONCLUSION: PD shows notable effect on cytotoxicity and can induce A549 cell apoptosis. It causes decrease in mitochondrial membrane potential by regulating Bax, Bak, Bcl-2 and Bcl-xl expressions, and thus activating caspase and finally causing long cancer cell apoptosis.

ß,ß-Dimethylacrylshikonin induces mitochondria dependent apoptosis through ERK pathway in human gastric cancer SGC-7901 cells.

ß,ß-Dimethylacrylshikonin, one of the active components in the root extracts of Lithospermum erythrorhizon, posses antitumor activity. In this study, we discussed the molecular mechanisms of ß,ß-dimethylacrylshikonin in the apoptosis of SGC-7901 cells. ß,ß-Dimethylacrylshikonin reduced the cell viability of SGC-7901 cells in a dose- and time-dependent manner and induced cell apoptosis. ß,ß-Dimethylacrylshikonin treatment in SGC-7901 cells down-regulated the expression of XIAP, cIAP-2, and Bcl-2 and up-regulated the expression of Bak and Bax and caused the loss of mitochondrial membrane potential and release of cytochrome c. Additionally, ß,ß-dimethylacrylshikonin treatment led to activation of caspases-9, 8 and 3, and cleavage of poly (ADP-ribose) polymerase (PARP), which was abolished by pretreatment with the pan-caspase inhibitor Z-VAD-FMK. ß,ß-Dimethylacrylshikonin induced phosphorylation of extracellular signal-regulated kinase (ERK) in SGC-7901 cells. U0126, a specific MEK inhibitor, blocked the ERK activation by ß,ß-dimethylacrylshikonin and abrogated ß,ß-dimethylacrylshikonin -induced apoptosis. Our results demonstrated that ß,ß-dimethylacrylshikonin inhibited growth of gastric cancer SGC-7901 cells by inducing ERK signaling pathway, and provided a clue for preclinical and clinical evaluation of ß,ß-dimethylacrylshikonin for gastric cancer therapy.

[Mechanisms of (2-methyl-n-butyl) shikonin induced apoptosis of gastric cancer SGC-7901 cells].

This study is to investigate the effect of (2-methyl-n-butyl) shikonin (MBS) on inducing apoptosis of human gastric cancer cell line SGC-7901 and the role of ERK1/2 signal pathway in the apoptosis. MTT assay was used to detect SGC-7901 cell proliferation. DNA condensation was measured by DAPI stain. Cell apoptosis was analyzed by flow cytometry. Mitochondrial membrane potential (MMP) was analyzed by JC-1 staining. The protein expressions of Bcl-2, Bax, Survivin, cleaved caspase-9, cleaved caspase-3, cleaved PARP, p-ERK1/2, ERK1/2, p-JNK, JNK, p-p38 and p38 were detected by Western blotting. The results showed that MBS reduced the cell viability of SGC-7901 cells in a dose- and time-dependent manner. The IC50 at 24 h and 48 h for SGC-7901 cells was 10.113 and 4.196 micromolL(-1), respectively. After being treated with MBS, the typical nuclear condensation was observed in SGC-7901 cells by DAPI stain. Apoptosis in SGC-7901 cells was induced by MBS in a dose dependent manner. The protein expression of Bcl-2 was down-regulated, while the protein expressions of cleaved caspase-9, cleaved caspase-3, cleaved PARP, p-ERK1/2 and p-JNK were up-regulated after MBS treatment. U0126, a specific MAP kinase (MEK1/2) inhibitor, blocked the ERK1/2 activation by MBS. MMP was decreased by MBS treatment. It can be concluded that MBS could inhibit SGC-7901 cell proliferation and induce apoptosis. Mitochondrial apoptosis pathway, ERK1/2 signal pathway and JNK signal pathway might be involved in this process.

Transforming growth factor-ß1 induces epithelial-to-mesenchymal transition in human lung cancer cells via PI3K/Akt and MEK/Erk1/2 signaling pathways.

Metastasis of tumor cells is associated with epithelial-to-mesenchymal transition (EMT), which is a process whereby epithelial cells lose their polarity and acquire new features of mesenchyme. EMT has been reported to be induced by transforming growth factor-ß1 (TGF-ß1), but its mechanism remains elusive. In this study, we performed a study to investigate whether PI3K/Akt and MAPK/Erk1/2 signaling pathways involved in EMT in the human lung cancer A549 cells. The results showed that after treated with TGF-ß1 for 48 h, A549 cells displayed more fibroblast-like shape, lost epithelial marker E-cadherin and increased mesenchymal markers Vimentin and Fibronectin. Moreover, TGF-ß1-induced EMT after 48 h was accompanied by increased of cell migration and change of Akt and Erk1/2 phosphorylation. In addition, EMT was reversed by PI3K inhibitor LY294002 and MEK1/2 inhibitor U0126, which suggested that A549 cells under stimulation of TGF-ß1 undergo a switch into mesenchymal cells and PI3K/Akt and MAPK/Erk1/2 signaling pathways serve to regulate TGF-ß1-induced EMT of A549 cells.

[Video-assisted thoracic surgery lobectomy versus open lobectomy for mini pathologic N2 non-small cell lung cancer].

OBJECTIVE: To assess early and late outcomes of patients with minimal mediastinal lymph nodes metastasis N2 non-small cell lung cancer disease unexpectedly detected during the operation, who underwent video-assisted thoracic surgery lobectomy for clinical stage I. METHODS: This study retrospectively reviewed and analyzed the medical records of 263 patients underwent surgery between January 2004 and December 2007, who were diagnosed as having early-stage non-small cell lung cancer (clinical stage was cT1-2N0M0, stage I) before the surgery, but were found to have mini mediastinal lymph nodes metastasis disease (clinical stage was pT1-2N2M0, stage IIIa) unexpectedly detected during the operation and after the operation. All patients underwent lobectomy and systematic lymph nodes dissection as radical treatments. Among them, 63 patients underwent video-assisted thoracic surgery (VATS) lobectomy, including 37 male patients (58.7%) with a mean age of (58 ± 11) years old. Two hundred patients underwent open thoracotomy lobectomy, including 132 male patients (66%) with a mean age of (59 ± 11) years old. To compare and analyze clinical features, early and late outcomes of patients in these two groups. RESULTS: A total of 263 patients with an average survival time (34.9 ± 1.2) months (median 31 months), 63 cases in VATS lobectomy group with an average survival time (40.3 ± 2.2) months (median 37 months), 200 cases in open pulmonary lobectomy group with an average survival time (33.1 ± 1.3) months (median 29 months). The 1-, 2-, 3-year over survival rate of all the patients was 92.0%, 57.4%, 29.3%. The 1-, 2-, 3-year survival rate of patients in VATS lobectomy group was 92.1%, 82.5%, 41.3%. The 1, 2, 3 year survival rate of patients in thoracotomy lobectomy group was 92.0%, 49.5%, 25.5%. There was significant difference between the two groups in this factor (χ(2) = 5.58, P = 0.018). CONCLUSIONS: VATS lobectomy is feasibility and safety for unexpected mini N2 disease. Even if lymph node metastasis is unexpectedly detected during video-assisted thoracic surgery lobectomy for clinical stage I disease after rigorous evaluation of preoperative, it is no need to convert to conventional thoracotomy.

Genetic variants in MARCO are associated with the susceptibility to pulmonary tuberculosis in Chinese Han population.

BACKGROUND: Susceptibility to tuberculosis is not only determined by Mycobacterium tuberculosis infection, but also by the genetic component of the host. Macrophage receptor with a collagenous structure (MARCO) is essential components required for toll like receptor-signaling in macrophage response to Mycobacterium tuberculosis, which may contribute to tuberculosis risk. PRINCIPAL FINDINGS: To specifically investigated whether single nucleotide polymorphisms (SNPs) in MARCO gene are associated with pulmonary tuberculosis in Chinese Han population. By selecting tagging SNPs in MARCO gene, 17 tag SNPs were identified and genotyped in 923 pulmonary tuberculosis patients and 1033 healthy control subjects using a hospital based case-control association study. Single-point and haplotype analysis revealed an association in intron and exon region of MARCO gene. One SNP (rs17009726) was associated with susceptibility to pulmonary tuberculosis, where the carriers of the G allele had a 1.65 fold (95% CI = 1.32-2.05, p(corrected) = 9.27E-5) increased risk of pulmonary tuberculosis. Haplotype analysis revealed that haplotype GC containing G allele of 17009726 and haplotype TGCC (rs17795618T/A, rs1371562G/T, rs6761637T/C, rs2011839C/T) were also associated with susceptibility to pulmonary tuberculosis (p(corrected) = 0.0001 and 0.029, respectively). CONCLUSIONS: Our study suggested that genetic variants in MARCO gene were associated with pulmonary tuberculosis susceptibility in Chinese Han population, and the findings emphasize the importance of MARCO mediated immune responses in the pathogenesis of tuberculosis.

Transforming growth factor-ß1 promotes lung adenocarcinoma invasion and metastasis by epithelial-to-mesenchymal transition.

Lung cancer is a highly malignant carcinoma, and most deaths of lung cancer are caused by metastasis. The alterations associated with epithelial-to-mesenchymal transition (EMT) may be related to the cancer cell metastasis. Nevertheless, the mechanism of lung cancer metastasis remains unclear. We conducted a study in vitro to investigate whether transforming growth factor-ß1 (TGF-ß1) could induce changes of, such as cell morphology, expression of relative protein markers, and cellular motile and invasive activities. In this research, the changes of cell morphology were first investigated under a phase contrast microscope, then western blotting was employed to detect the expression of E-cadherin, vimentin, and fibronectin, and finally cell motility and invasion were evaluated by cell wound-healing as well as invasion assays. The data indicated that human lung adenocarcinoma cell lines, A-549 and PC-9 cells of epithelial cell characteristics, were induced to undergo EMT by TGF-ß1. Following TGF-ß1 treatment, cells showed dramatic morphological changes assessed by phase contrast microscopy, accompanied by decreased epithelial marker E-cadherin and increased mesenchymal markers vimentin and fibronectin. More importantly, cell motility and invasion were also enhanced in the EMT process. These results indicated that TGF-ß1 may promote lung adenocarcinoma invasion and metastasis via the mechanism of EMT.

[Epithelial-mesenchymal transition (EMT) and its effect on microRNA expression in lung cancer].

OBJECTIVE: To investigate the effect of epithelial-mesenchymal transition (EMT) on the expression of microRNAs (miRNAs) in lung cancer A549 cells. METHODS: Transforming growth factor beta-1 (TGF-beta 1) in different concentrations was used to induce EMT in lung cancer A549 cells. The morphological changes were observed under phase-contrast microscope. The changes of EMT-related proteins were analyzed by Western blot. The changes of miRNAs expression after EMT were detected by microRNA (miRNA) array. Real time quantitative RT-PCR was applied to verify the reliability of miRNA array results. RESULTS: The lung cancer A549 cells became elongated and the cell-cell junction became loose after EMT. The epithelial protein marker E-cadherin was down-regulated and the mesenchymal protein markers vimentin and fibronectin up-regulated. There were 51 miRNAs showing statistically significant changes of expression more than double (P<0.05) after EMT. Among them 18 were up-regulated and 33 down-regulated. Of them, mir-33a was down-regulated by 92.8% and mir-193a-3p by 86.5%. Real time quantitative RT-PCR showed that mir-33a was down-regulated by 73.1% and mir-193a-3p by 56.6%. CONCLUSION: Epithelial-mesenchymal transition has effects on the expression of miRNAs, and miRNAs may regulate the invasion and metastasis of lung cancer cells via EMT.