Monocots and eudicots have more conservative flower water use strategies than basal angiosperms.

Water balance is crucial for the growth and flowering of plants. However, the mechanisms by which flowers maintain water balance are poorly understood across different angiosperm branches. Here, we investigated 29 floral hydraulic and economic traits in 24 species from ANA grade, magnoliids, monocots, and eudicots. Our main objective was to compare differences in flower water use strategies between basal angiosperms (ANA grade and magnoliids) and derived group (monocots and eudicots). We found that basal angiosperms had richer petal stomatal density, higher pedicel hydraulic diameter, and flower mass per area, but lower pedicel vessel wall reinforcement and epidermal cell thickness compared to monocots and eudicots. We also observed significant trade-offs and coordination among different floral traits. Floral traits associated with reproduction, such as floral longevity and size, were strongly linked with physiological and anatomical traits. Our results systematically reveal the variation in flower economic and hydraulic traits from different angiosperm branches, deepening understanding of flower water use strategies among these plant taxa. We conclude that basal angiosperms maintain water balance with high water supply, whereas monocots and eudicots maintain a more conservative water balance.

Does the use of tranexamic acid increase the risk of VTE in patients with hemoptysis?

OBJECTIVE: The aim of this study was to create a predictive nomogram that can accurately identify the risk factors of venous thromboembolism (VTE) in hospitalized patients exhibiting hemoptysis. PATIENTS AND METHODS: The present study gathered clinical and demographic data of 1,052 hospitalized patients with hemoptysis at Dongyang Hospital between January 2016 and January 2021 through the Lejiu database. The patients were categorized into two groups: the thrombotic event group (n=123) and the non-thrombotic event group (n=929), based on the presence of VTE before discharge. The study utilized univariable and multivariable logistic regression analyses to identify the independent risk factors for VTE, with the occurrence of thrombotic events serving as the dependent variable. Furthermore, a nomogram prediction model was formulated to verify the findings. RESULTS: In hospitalized patients with hemoptysis, the risk of VTE was found to be independently associated with the administration of tranexamic acid (TXA), the presence of D-dimer, and the Charlson Comorbidity Index (CCI) score (p<0.05). CONCLUSIONS: A nomogram model was constructed to evaluate the probability of VTE in patients hospitalized with hemoptysis. This model allows for the timely detection of early VTE warning signs, which may ultimately reduce its occurrence.

A case of drug-induced myopathy in alcoholic cirrhosis caused by voriconazole.

BACKGROUND: Voriconazole is a new generation of broad-spectrum antifungal agents commonly used in the treatment of invasive aspergillus infections. CASE REPORT: We reported a rare case of myopathy induced by voriconazole, which showed severe muscle pain and significantly elevated myocardial enzymes. Enzymes eventually achieved good efficacy by switching voriconazole to micafungin and the use of L-carnitine. CONCLUSIONS: This reminded us it was necessary to be vigilant for rare adverse reactions of voriconazole in the population with liver dysfunction, the elderly population, and people with multiple underlying diseases in clinical practice. During medication of voriconazole, close attention should be paid to the occurrence of adverse reactions to avoid life-threatening complications.

Comparison of long non-coding RNAs in adipose and muscle tissues between seven indigenous Chinese and the Yorkshire pig breeds.

lncRNAs play crucial roles in fat metabolism in animals. Previously, we have compared the mRNA transcriptome profiles between seven fat-type Chinese pig breeds and one lean-type Western breed (Yorkshire, YY). The associations between differentially expressed (DE) genes and phenotypical traits were investigated. In the present study, to further explore the underlying regulatory mechanisms, lncRNAs were sequenced and compared between YY and Chinese indigenous breeds. The results showed 9114 and 7538 DE lncRNAs between at least one Chinese breed and the YY breed in the adipose and muscle tissue respectively. KEGG enrichment analysis revealed that the target genes of these DE lncRNAs mainly influenced the glucolipid metabolism, which is an important process affecting meat quality. Correlation analyses between the DE lncRNA and DE mRNA genes related to meat quality and growth traits were performed. The results showed that LTCONS_00073280 was associated with intramuscular fat content. Four lncRNAs (LTCONS_00101781, LTCONS_00037879, LTCONS_00088260 and LTCONS-00128343) might mediate backfat thickness. Overall, this study provides candidate lncRNAs that potentially affect meat quality, which might be useful for molecular breeding of pig breeds in future.

Leaf morphology, photosynthesis and pigments change with age and light regime in savin juniper.

Savin juniper is an excellent species for desertification control in arid and semi-arid areas, where it typically establishes under the protection of nurse plants. Ultimately, established plants emerge into full light as they grow, and this transition is accompanied by an increase in the preponderance of scale-like versus needle-like leaf forms. To test how age and variable light environments affect shade tolerance in savin juniper, we established a pot study under field conditions, with two age cohorts (1- and 4-year-old rooted scions) and three light regimes (10%, 50% and 100% light transmittance). We measured growth, leaf parameters, photosynthesis, chlorophyll fluorescence and foliar pigments on a monthly basis (seven growing months per year, from 2015 to 2017). Overall, there was little interaction among all variables, and both cohort and light regime had significant effects. Leaf form and spacing varied continuously, tending towards shorter, more closely spaced and more appressed scale leaves with higher dry leaf mass per area in older plants or under higher light. There were no clear age-related patterns in carotenoids but both cohort and light had significant effects on gas exchange and chlorophyll fluorescence variables. We conclude that savin juniper shows an intermediate tolerance to shade that changes with growth in that younger plants were less tolerant of full sun than older plants, consistent with its reliance on nurse plants for ultimate establishment in the open.

LINC00261 regulates EBF1 to suppress malignant progression of thyroid cancer.

OBJECTIVE: We aimed to explore the role of LINC00261 in thyroid cancer (TC) and the potential regulatory mechanism. PATIENTS AND METHODS: 40 cases of tumor tissues and adjacent tissues of TC patients were collected, and the expressions of LINC00261 and EBF1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and the relationship between LINC00261 and the clinical pathological indicators and prognosis of TC patients were analyzed. Next, LINC00261 overexpression and knockdown cell models were constructed in TC cell lines BPH5-16 and K1, respectively. Cell counting kit-8 (CCK-8) and transwell migration were used to detect the impact of LINC00261 overexpression or silencing on cell proliferative and migration ability. The bioinformatics website was used to screen the possible target gene of LINC00261. RESULTS: qRT-PCR analysis showed that LINC00261 level was markedly reduced in TC tumor tissues, as well as corresponding cell lines. Retrospective analysis showed that low expression of LINC00261 was in positive correlation with the pathological stage, lymphatic and distant metastasis in patients with TC, meanwhile, the expression of LINC00261 was also in positive correlation with overall survival rate of TC patients. Bioinformatics analysis suggested that LINC00261 could target EBF1. Luciferase reporter gene experiment and qRT-PCR analysis suggested that LINC00261 could target EBF1 and that their expressions showed a negative correlation in TC tumor tissues and cells. Cell functional experiments confirmed that LINC00261 can inhibit the proliferative and migration ability of TC cells. Subsequently, the recovery experiment also suggested that silencing EBF1 could reverse the promotion effect of LINC00261 knockdown on the proliferative and migration ability of TC cells; while EBF1 overexpression could reverse the inhibition of LINC00261 on the proliferative and migration ability of TC cells. CONCLUSIONS: LINC00261 was markedly downregulated in TC tissues and cells. In addition, the level of LINC00261 was closely related to lymph node and distant metastasis, as well as the prognosis in TC patients. Moreover, LINC00261 could negatively regulate EBF1, thereby promoting the malignant progression of TC.

Peanut (Arachis hypogaea L.) S-adenosylmethionine decarboxylase confers transgenic tobacco with elevated tolerance to salt stress.

Polyamines play an important role in stress response. In the pathway of polyamines synthesis, S-adenosylmethionine decarboxylase (SAMDC) is one of the key enzymes. In this study, a full length cDNA of SAMDC (AhSAMDC) was isolated from peanut (Arachis hypogaea L.). Phylogenetic analysis revealed high sequence similarity between AhSAMDC and SAMDC from other plants. In peanut seedlings exposed to sodium chloride (NaCl), the transcript level of AhSAMDC in roots was the highest at 24 h that decreased sharply at 72 and 96 h after 150 mM NaCl treatment. However, the expression of AhSAMDC in peanut leaves was significantly inhibited, and the transcript levels in leaves were not different compared with control These results implied the tissue-specific and time-specific expression of AhSAMDC. The physiological effects and functional mechanism of AhSAMDC were further evaluated by overexpressing AhSAMDC in tobaccos. The transgenic tobacco lines exhibited higher germination rate and longer root length under salt stress. Reduced membrane damage, higher antioxidant enzyme activity, and higher proline content were also observed in the transgenic tobacco seedlings. What's more, AhSAMDC also led to higher contents of spermidine and spermine, which can help to scavenge reactive oxygen species. Together, this study suggests that AhSAMDC enhances plant resistance to salt stress by improving polyamine content and alleviating membrane damage.

NAA10 promotes proliferation of renal cell carcinoma by upregulating UPK1B.

OBJECTIVE: The purpose of this study was to illustrate the role of NAA10 in aggravating the malignant progression of renal cell carcinoma (RCC) by upregulating UPK1B. PATIENTS AND METHODS: NAA10 levels in RCC tissues and paracancerous tissues were detected. Thereafter, the potential relationship between NAA10 level and clinical parameters of RCC patients was analyzed. After knockdown of NAA10, changes in proliferative potential of 786-O and Caki-1 cells were examined by cell counting kit-8 (CCK-8), colony formation and 5-Ethynyl-2'-deoxyuridine (EdU) assay. Finally, the regulatory role of NAA10 in the downstream gene UPK1B and the involvement of UPK1B in the development of RCC were determined via rescue experiments. RESULTS: NAA10 was upregulated in RCC tissues than paracancerous tissues. Tumor staging was much worse in RCC patients expressing a higher level of NAA10. Knockdown of NAA10 inhibited proliferative potential and downregulated UPK1B in RCC cells. Besides, NAA10 level was identified to be positively linked to UPK1B level in RCC tissues. At last, overexpression of UPK1B was able to abolish the inhibitory effect of silenced NAA10 on RCC proliferation. CONCLUSIONS: NAA10 level is closely linked to tumor staging and poor prognosis in RCC patients. NAA10 aggravates the malignant progression of RCC by upregulating UPK1B and may be a specific biomarker in RCC.

Inactivation of lncRNA HOTAIRM1 caused by histone methyltransferase RIZ1 accelerated the proliferation and invasion of liver cancer.

OBJECTIVE: Liver cancer is the second most common cause of cancer death, causing more than 700,000 deaths every year. It has been demonstrated that Long non-coding RNA (LncRNA) plays an important regulatory role in a series of diseases. However, the regulatory mechanism of LncRNAs in liver cancer has not been fully elucidated. The purpose of this study was to explore the interaction of lncRNA HOTAIRM1 and aberrant histone modification in liver cancer. MATERIALS AND METHODS: qRT-PCR was used to detect the expression levels of RIZ1 and miR-125b in liver cancer cells. Cell proliferation was measured using the CCK8 assay. ChIP-Real-time PCR confirmed the binding site of the promoter of HOTAIRM1 by H3K9me1. The direct target of HOTAIRM1 and miR-125b in liver cancer cells was measured by a luciferase reporter assay. Cell proliferation was detected by Cell Counting Kit-8 (CCK8). Cell invasion was measured by transwell assays and cell migration was detected by wound healing assay. RESULTS: The expression level of RIZ1 and miR-125b was upregulated, and HOTAIRM1 was downregulated in liver cancer cells. Transwell and CCK-8 assay showed that RIZ1 expression is associated with the proliferation, invasion and migration of liver cancer cells, silencing of RIZ1 inhibited cell proliferation, migration, and invasion in HEPG2 and HCC-LM3 cells. RIZ1 interference could significantly inhibit H3K9me1 expression. H3K9me1 protein can bind to HOTAIRM1 promoter directly. Furthermore, the bioinformatics prediction and luciferase assay demonstrated that miR-125b can interact with HOTAIRM1 by direct binding. HOTAIRM1 down-expression promoted HEPG2 cell growth and metastasis, which was further strengthened following the co-transfection of miR-125b. Furthermore, overexpressed HOTAIRM1 inhibited HCC-LM3 cell growth and metastasis and a complete reversal of the results seen when transfected with miR-125b. CONCLUSIONS: For the first time, we found that RIZ1 was upregulated in liver cancer cells and RIZ1-mediated H3K9me1 enrichment on the HOTAIRM1 promoter regulated the growth and metastasis of liver cancer cells by targeting miR-125b, which could further accelerate tumor proliferation, migration and invasion. It may serve as a therapeutic marker for liver cancer treatment.

MicroRNA-378 inhibits the development of smoking-induced COPD by targeting TNF-α.

OBJECTIVE: To explore the mechanism microRNA-378 in smoking-induced airway inflammation and mucus hypersecretion. MATERIALS AND METHODS: Human bronchial epithelial (HBE) cells were treated with cigarette smoke extract (CSE) to construct the in vitro COPD model. Expression levels of microRNA-378, inflammatory factors and MUC5AC in CSE-treated HBE cells were determined by quantitative real-time polymerase chain reaction (qRT-PCR), Western blot and enzyme-linked immunosorbent assay (ELISA). The regulatory effects of microRNA-378 on expressions of inflammatory factors and mucin 5AC (MUC5AC) were observed in CSE-treated HBE cells overexpressing microRNA-378. We verified whether tumor necrosis factor-α (TNF-α) was the target gene of microRNA-378 through dual-luciferase reporter gene assay. Expression levels of TNF-α and p-p65 in CSE-treated HBE cells were examined. Finally, CSE-treated HBE cells were co-overexpressed with microRNA-378 and TNF-α to elucidate whether microRNA-378 exerted its function in regulating the development of COPD through targeting TNF-α. RESULTS: CSE treatment downregulated microRNA-378 expression, but upregulated expressions of inflammatory factors and MUC5AC in HBE cells. MicroRNA-378 overexpression markedly inhibited the elevated levels of inflammatory factors and MUC5AC in CSE-treated HBE cells. Dual-luciferase reporter gene assay verified that TNF-α was the target gene of microRNA-378. Moreover, TNF-α expression in CSE-treated HBE cells was time-dependently elevated. TNF-α overexpression partially reversed the decreased levels of inflammatory factors and MUC5AC in HBE cells overexpressing microRNA-378. CONCLUSIONS: MicroRNA-378 inhibits the inflammatory response by targeting TNF-α, which may be a potential therapeutic target for COPD.

MicroRNA-486-5p inhibits ovarian granulosa cell proliferation and participates in the development of PCOS via targeting MST4.

OBJECTIVE: To explore whether microRNA-486-5p affected the proliferation of ovarian granulosa cells by targeting MST4 (silk/threonine protein kinase 4), thereby promoting the development of polycystic ovary syndrome (PCOS). MATERIALS AND METHODS: The level of microRNA-486-5p in PCOS tissues and adjacent normal tissues was detected by quantitative real-time polymerase chain reaction (qRT-PCR). After microRNA-486-5p up-regulation in KNG cells, the mRNA and protein level of related genes was examined using qRT-PCR and western blot assay, respectively. Meanwhile, cell proliferation and cell cycle were analyzed by cell counting kit-8 (CCK-8) assay and flow cytometry. After insulin treatment of KNG cells, expressions of microRNA-486-5p and MST4, cell proliferation as well as cell cycle, were detected by qRT-PCR, CCK-8 and flow cytometry, respectively. Furthermore, cell proliferation and cycle situation were examined after simultaneous up-regulation of MST4 and microRNA-486-5p in vitro. RESULTS: MicroRNA-486-5p expression in PCOS tissues was significantly lower than that of normal tissues. In KNG cells, up-regulation of microRNA-486-5p significantly inhibited cell proliferation and cell cycle. The levels of cycle-associated proteins including CDK2 and CCNB1 decreased significantly. The results of dual-luciferase reporter gene assay showed that microRNA-486-5p could bind to MST4. After up-regulating microRNA-486-5p, both the mRNA and protein levels of MST4 decreased remarkably. MST4 expression was found significantly elevated in PCOS tissues as well. After overexpression of MST4, cell proliferation was enhanced, cell cycle was promoted, and expressions of cycle-related proteins increased. After treatment with different concentrations of insulin in KNG cells, the expression level of microRNA-486-5p decreased in a concentration-dependent manner. However, opposite results were observed in MST4 level. Meanwhile, the proliferation ability and cell cycle of insulin-treated cells were significantly enhanced. In addition, the inhibitory effect of microRNA-486-5p on cell proliferation and cell cycle could be partially reversed by simultaneous up-regulation of MST4 and microRNA-486-5p. CONCLUSIONS: MicroRNA-486-5p can bind to MST4 in a targeted manner and inhibit the proliferation of ovarian granulosa cells, thereby inhibiting the development of PCOS.

Long non-coding RNA ANRIL down-regulates microRNA-7 to protect human trabecular meshwork cells in an experimental model for glaucoma.

OBJECTIVE: Although the potential involvements of INK4 locus reported in glaucoma, the effects of long non-coding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) on trabecular meshwork (TM) cells remain unclear. In this study, we aimed to explore the effects of lncRNA ANRIL on the oxidative injury of human TM cells as well as the underlying mechanisms. MATERIALS AND METHODS: Oxidative injury of human TM cells was induced by H2O2 stimulation. Cell viability, apoptotic cells, expression of proteins related to apoptosis, and reactive oxygen species (ROS) level were testified by CCK-8 assay, flow cytometry assay, Western blot analysis, and DCFH-DA staining, respectively. LncRNA ANRIL was overexpressed, and its effects on H2O2-injured TM cells were analyzed. Afterward, miR-7 expression in lncRNA ANRIL overexpressing-cells was determined by RT-qPCR. Moreover, it was verified whether lncRNA ANRIL affected H2O2-treated TM cells via miR-7, followed by the measurements of the involved signaling pathways. RESULTS: H2O2-induced decrease of cell viability and the increases in apoptosis and ROS generation were significantly attenuated by lncRNA ANRIL overexpression. miR-7 expression was down-regulated by lncRNA ANRIL, and miR-7 overexpression abrogated the effects of lncRNA ANRIL on H2O2-treated TM cells. Phosphorylation levels of the key kinases in the mTOR and MEK/ERK pathways were enhanced by lncRNA ANRIL via down-regulating miR-7 in H2O2-treated TM cells. CONCLUSIONS: LncRNA ANRIL attenuated oxidative injury of human TM cells and activated the mTOR and MEK/ERK pathways, possibly through down-regulating miR-7.

The JAK2/STAT3 signaling pathway is required for inflammation and cell death induced by cerulein in AR42J cells.

OBJECTIVE: The study was designed to investigate the JAK2/STAT3 signaling pathway in pancreatitis and its association with inflammation and cell death to provide a potential treatment method for pancreatitis. MATERIALS AND METHODS: The rat pancreatic acinar AR42J cells were used for the study, and they were transfected with JAK2 and STAT3 siRNAs to mimic knockdown condition. Cerulein was used to treat AR42J cells. Western blot and ELISA were employed to detect the expression of related proteins. Flow cytometry was done to analysis the necrosis of AR42J cells. RESULTS: In this study, we found that cell death and the secretion of IL-6 and TGF-ß1 were significantly increased, and the JAK2/STAT3 signaling pathway was activated in cerulein-induced AP. To determine the role of JAK2 and STAT3, JAK2 siRNA and STAT3 siRNA were used to block JAK2 and STAT3, respectively. The levels of IL-6 and TGF-ß1 levels in the medium were lower in JAK2 siRNA and STAT3 siRNA-treated cells compared with controls. Flow cytometry analysis showed that the level of cell death, expression of cleaved caspase-3, and the release of LDH were decreased following JAK2 siRNA and STAT3 siRNA treatment. CONCLUSIONS: These findings point to a novel role for the JAK2/STAT3 signaling pathway in the progression of cerulein-induced AP.

Down-regulation of LncRNA NR027113 inhibits cell proliferation and metastasis via PTEN/PI3K/AKT signaling pathway in hepatocellular carcinoma.

OBJECTIVE: Hepatocellular Carcinoma (HCC) is a worldwide common and malignant tumor. It is discovered in recent years that long non-coding RNAs (lncRNAs) participate in many biological processes of HCC. However, their specific role in HCC has not been entirely clarified yet. In this research, we aimed to explore biological functions, clinical significance and the underlying molecular mechanisms of lncRNA NR027113 in HCC. PATIENTS AND METHODS: qRT-PCR was performed to test the expression of NR027113 in HCC tissue samples and HCC cell lines. The association of NR027113 expression with overall survival, disease-free survival and clinicopathological factors was analyzed. MTT assays, Colony formation assay, flow cytometry and transwell invasion assays were performed to determine the effect of NR027113 in the regulation of biological behaviors of HCC cells. Western blot was performed to determine the activation of the PTEN/PI3K/AKT signaling pathway. RESULTS: In the present study, we proved that is significantly up-regulated in HCC tissues and cell lines. HCC patients with higher NR027113 expression were associated with significantly shorter overall survival and disease-free survival. NR027113 knockdown inhibited the proliferation and metastasis of HCC cells in vitro. In addition, NR027113 knock-down was found to inhibit the activity of the PI3K/Akt signaling pathway and restrain the EMT process. Furthermore, we found that PTEN silencing could reverse the inhibitory effect of NR027113 knockdown on Akt phosphorylation and HCC cells function. CONCLUSIONS: A brand new lncRNA NR027113 was found, which can promote the proliferation, invasion and metastasis of HCC via the PTEN/PI3K/AKT signaling pathway, and may be a potential therapeutic target in the future treatment of HCC.

Adiponectin partially rescues high glucose/high fat-induced impairment of mitochondrial biogenesis and function in a PGC-1α dependent manner.

OBJECTIVE: Plasma adiponectin (APN) levels are decreased in diabetic patients. Dysfunctional mitochondrial biogenesis is involved in type 2 diabetes (T2DM) pathogenesis, by unclear mechanisms. The present study determined (1) whether myocardial mitochondrial biogenesis was impaired in cardiomyocytes exposed to a high glucose/high fat (HGHF) medium (a T2DM in vitro model), (2) the effects of APN administration upon mitochondrial biogenesis in cardiomyocytes affected by HGHF incubation, and 3) the involved underlying mechanisms. MATERIALS AND METHODS: Neonatal rat ventricular myocytes (NRVMs) were isolated and incubated in HGHF medium. Mitochondrial function was assessed by ATP content, and fluorescent microscopic analysis of myocardial apoptosis was determined by TUNEL staining and caspase-3 activity. RESULTS: HGHF treatment reduced mitochondrial biogenesis, altered mitochondrial structure, and induced mitochondrial dysfunction in NRVMs. Administration of APN partially rescued these effects. However, siRNA-mediated knockdown of peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1α) significantly blocked the beneficial effects of APN in mitochondria and cardiomyocytes subjected to hypoxia/reoxygenation injury. CONCLUSIONS: In the current study, we have provided the direct in vitro evidence that APN partially rescues HGHF-induced impairment of mitochondrial biogenesis and function via PGC-1α-mediated signaling.

Effects of donor cells' sex on nuclear transfer efficiency and telomere lengths of cloned goats.

The aim of this study was to investigate the effects of donor cells' sex on nuclear transfer efficiency and telomere length of cloned goats from adult skin fibroblast cells. The telomere length of somatic cell cloned goats and their offspring was determined by measuring their mean terminal restriction fragment (TRF) length. The result showed that (i) reconstructed embryos with fibroblast cells from males Boer goats obtained significantly higher kids rate and rate of live kids than those of female embryos and (ii) the telomere lengths of four female cloned goats were shorter compared to their donor cells, but five male cloned goats had the same telomere length with their donor cells, mainly due to great variation existed among them. The offspring from female cloned goats had the same telomere length with their age-matched counterparts. In conclusion, the donor cells' sex had significant effects on nuclear transfer efficiency and telomere lengths of cloned goats.

Serum angiopoietin-like 4 is over-expressed in COPD patients: association with pulmonary function and inflammation.

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is both a pulmonary and systematic disease, which will cause abnormal expression of some circulating factors. Angiopoietin-like protein 4 (ANGPTL4) has been reported to play important role in inflammatory responses and several diseases. However, whether it contributes to COPD is an open question. The aim of this study is to explore the potential relationship between ANGPTL4 and COPD. PATIENTS AND METHODS: In this study, circulating levels of ANGPTL4, C-reactive protein (CRP), adiponectin, tumor necrosis factor (TNF)-α, matrix metalloproteinase (MMP)-9 and monocyte chemotactic protein (MCP)-1 in 73 COPD patients and 40 healthy volunteers were investigated using multiplex enzyme-linked immunosorbent assay Kits. Then, we analyzed the correlations between ANGPTL4 with other inflammatory mediators and pulmonary function. RESULTS: Serum ANGPTL4 levels were significantly elevated in COPD patients compared with healthy controls (122.86 ± 38.59 ng/mL versus 99.03 ± 31.84 ng/mL, p = 0.001). Besides, serum ANGTPL4 levels were much higher in ever-smokers with COPD than in never-smokers with COPD (131.71 ± 32.92 ng/mL versus 113.25 ± 42.34 ng/mL, p = 0.03). More importantly, the concentrations of circulating ANGPLT4 correlated inversely with forced expiratory volume in 1 second (FEV1) % predicted, an index of lung function in COPD (r = -0.450, p < 0.001) and in all participants (r = -0.369, p < 0.001), while correlated positively with CRP (r = 0.312, p = 0.007 for COPD; r = 0.404, p < 0.001 for total subjects), adiponectin (r = 0.266, p = 0.004 for total subjects), and MMP-9 (r = 0.254, p = 0.03 for COPD). CONCLUSIONS: Our results suggest that circulating ANGPTL4 levels are up-regulated in COPD patients, and have correlations with pulmonary function and systematic inflammation in COPD, which provides a novel idea to further dig the pathogenic mechanisms of COPD, and justifies more studies to determine how ANGPTL4 contributes to COPD.

Effects of Herceptin on circulating tumor cells in HER2 positive early breast cancer.

The objective of this study was to determine the changes in peripheral blood circulating tumor cells in HER2-positive early breast cancer before and after Herceptin therapy, and to explore the effects of the HER2 gene and Herceptin on circulating tumor cells. CK19 mRNA expression in peripheral blood was evaluated by qRT-PCR as an index of circulating tumor cells in 15 cases of HER-2-positive breast cancer and 18 cases of HER2-negative breast cancer before, and after chemotherapy as well. Ten cases of HER2-positive breast cancer continued on Herceptin therapy for 3 months after chemotherapy, and their peripheral blood was again drawn and assayed for CK-19 mRNA expression. Preoperatively, all cases of HER2-positive cancer were positive for CK19 mRNA in peripheral blood, but 6 cases of HER2-negative breast cancer were positive (33.3%), where there was a substantial difference between the two groups. After 6 cycles of adjuvant chemotherapy, CK19 positive rates in cases of HER2-positive and -negative breast cancer reduced by 93.3 and 11.1%, respectively, with a significant difference still existing. After 3 months of Herceptin therapy, expression of CK19 mRNA declined considerably in 10 cases of HER2 positive breast cancer (113.66 ± 88.65 vs 63.35 ± 49.27, P = 0.025). HER-2 gene expression closely correlated with circulating tumor cells in peripheral blood of early breast cancer patients. Moreover, Herceptin, a monoclonal antibody for HER2, can reduce the number of circulating tumor cells, which can be an early predictive factor for Herceptin therapy effectiveness against breast cancer.

The effects of germacrone on lipopolysaccharide-induced acute lung injury in neonatal rats.

Germacrone is one of the main bioactive components in the traditional Chinese medicine Rhizoma curcuma and has been shown to possess an anti-inflammatory activity. Our present study aimed to investigate the protective effects of germacrone on lipopolysaccharide (LPS)-induced acute lung injury in neonatal rats. Results showed that germacrone treatment significantly decreased the expression of pro-inflammatory cytokines IL-6 and TNF-α. Meanwhile, the expression of anti-inflammatory mediators TGF-ß1 and IL-10 was obviously increased following germacrone administration. The LPS-induced pathological changes in neonatal rats were also attenuated by germacrone treatment. In vitro, MTT and EdU incorporation assay indicated that germacrone administration significantly increased the A549 cell viabilities in a dose-dependent manner. Besides, flow cytometry and TUNEL analysis showed that the cell apoptosis rate was significantly reduced in a concentration-dependent manner after germacrone injection. At the molecular level, we found that germacrone treatment promoted the expression of claudin-4 both in vivo and in vitro as shown by real time PCR and western blot. Collectively, our study demonstrated that germacrone protected neonatal rats against LPS-induced ALI partially by modulation of claudin-4.