Effects of Heat Stress on Expression of Heat Shock Proteins in the Small Intestine of Wenchang Chicks

In this study, immunohistochemistry and real-time fluorescent-based quantitative PCR were used to evaluate the expression of heat shock protein (HSP) 60, HSP70, and HSP90 in the small intestine of Wenchang chicks. Compared with the control group (CK), the positive expression of HSP60 and HSP60 mRNA in the heat stress group (HS) were initially higher and subsequently lower in the duodenum (p<0.01). In the HS jejunum, the levels of HSP60 were higher (p<0.01) and the HSP60 mRNA was lower (p<0.05). Whereas the levels of HSP60 in the HS ileum were higher (p<0.05) and then lower (p<0.01), and the HSP60 mRNA was higher (p<0.01). The levels of HSP70 were higher (p<0.01) and the HSP70 mRNA was lower in the duodenum (p<0.05), while the expression of both HSP70 and HSP70 mRNA was higher in the jejunum (p<0.01) and the ileum (p<0.05) of the HS. In the HS duodenum the levels of HSP90 were lower and then higher (p<0.01), and the HSP90 mRNA was higher (p<0.01). The expression of both HSP90 and HSP90 mRNA was higher in the HS jejunum (p<0.05). The levels of HSP90 were lower while the HSP90 mRNA was higher in the HS ileum (p<0.01). These results indicate that heat stress disturbed the expression of HSP60, HSP70, and HSP90 in the small intestine of chicks.

Effects of Heat Stress on Expression of Heat Shock Proteins in the Small Intestine of Wenchang Chicks

In this study, immunohistochemistry and real-time fluorescent-based quantitative PCR were used to evaluate the expression of heat shock protein (HSP) 60, HSP70, and HSP90 in the small intestine of Wenchang chicks. Compared with the control group (CK), the positive expression of HSP60 and HSP60 mRNA in the heat stress group (HS) were initially higher and subsequently lower in the duodenum (p<0.01). In the HS jejunum, the levels of HSP60 were higher (p<0.01) and the HSP60 mRNA was lower (p<0.05). Whereas the levels of HSP60 in the HS ileum were higher (p<0.05) and then lower (p<0.01), and the HSP60 mRNA was higher (p<0.01). The levels of HSP70 were higher (p<0.01) and the HSP70 mRNA was lower in the duodenum (p<0.05), while the expression of both HSP70 and HSP70 mRNA was higher in the jejunum (p<0.01) and the ileum (p<0.05) of the HS. In the HS duodenum the levels of HSP90 were lower and then higher (p<0.01), and the HSP90 mRNA was higher (p<0.01). The expression of both HSP90 and HSP90 mRNA was higher in the HS jejunum (p<0.05). The levels of HSP90 were lower while the HSP90 mRNA was higher in the HS ileum (p<0.01). These results indicate that heat stress disturbed the expression of HSP60, HSP70, and HSP90 in the small intestine of chicks.(AU)

Expression of PDK1 in malignant pheochromocytoma as a new promising potential therapeutic target.

PURPOSE: Phosphoinositide-dependent kinase 1 (PDK1) is highly expressed in many solid tumors. And several studies have demonstrated that PDK1 has been an emerging and promising target for anti-cancer therapies. However, the role of PDK1 has not been studied so far in malignant pheochromocytoma (PCC). METHODS: In this study, immunohistochemical staining was performed to investigate the protein level of PDK1 in 63 PCC tissue samples, of which 49 were benign and 14 were malignant. In addition, we evaluated the effect of inhibition of PDK1 with siRNA on cell growth, apoptosis and invasive capacity in PC12 cells and identified the underlying mechanisms. RESULTS: We found that PDK1 was overexpressed in malignant PCC tissues, and knockdown of PDK1 with siRNA significantly inhibited cell proliferation, increased apoptosis induction, and attenuated cell migration and invasive capacity in PC12 cells. We also showed that knockdown of PDK1 significantly reduced the phosphorylation of Akt at threonine 308 (p-Akt T308) but did not alter the serine phosphorylation of Akt on the S473 site (p-Akt S473). Furthermore, we found that the p-Akt expression was noticeably decreased after knockdown of PDK1, but the t-Akt expression did not show a significant decrease. CONCLUSION: We have demonstrated for the first time that PDK1 is overexpressed in human malignant PCC and plays an important role in the malignant biological behaviors of PC12 cell. Specifically, we have revealed that knockdown of PDK1 could attenuate activation of the Akt signaling. These data suggest that PDK1 could be a new promising potential therapeutic target in human cancer treatment for malignant PCC.

Clinical significance of serum EGFR gene mutation and serum tumor markers in predicting tyrosine kinase inhibitor efficacy in lung adenocarcinoma.

OBJECTIVE: To study the clinical significance of serum epidermal growth factor receptor (EGFR) gene mutation and serum tumor markers in the prediction of tyrosine kinase inhibitor (TKI) efficacy in patients with lung adenocarcinoma. METHODS: Ninety patients with pathologically diagnosed lung adenocarcinoma were enrolled. Further, 51 out of 90 patients received the EGFR-TKI therapy, oral gefitinib. The correlations among serum EGFR gene mutations in exons 18-21, serum tumor markers such as carcinoembryonic antigen (CEA), carbohydrate antigen 24-2 (CA24-2), carbohydrate antigen 125, carbohydrate antigen 15-3 as well as carbohydrate antigen 19-9 (CA19-9) levels, and EGFR-TKI efficacy were determined. RESULTS: There was a high consistency of EGFR gene mutation rate between serum and tissue samples. The serum EGFR gene mutation rate in female patients or non-smokers was significantly higher than that in male patients or smokers, respectively. Serum CA19-9, CA24-2, and CEA levels were significantly correlated with serum EGFR mutation. After receiving gefitinib, the progression-free survivals (PFSs) of patients with high serum CEA level, high serum CA19-9 level, or serum EGFR gene mutation were significantly higher than those of normal patients, respectively. The PFSs were significantly prolonged in patients with EGFR gene mutation and high serum CEA level or patients with EGFR gene mutation and high serum CA19-9 level compared with those in patients with one abnormal biomarker and normal patients. CONCLUSION: Combined detection of EGFR gene mutations as well as CA19-9 and CEA levels in peripheral blood can predict the efficacy of EGFR-TKI in the treatment of patients with lung adenocarcinoma.

CalliSpheres® drug-eluting beads (DEB) transarterial chemoembolization (TACE) is equally efficient and safe in liver cancer patients with different times of previous conventional TACE treatments: a result from CTILC study.

PURPOSE: To assess the efficacy and safety of drug-eluting beads transarterial chemoembolization (DEB-TACE) in liver cancer patients with different times of previous conventional transarterial chemoembolization (cTACE) treatments. METHODS: 367 liver cancer patients about to receive DEB-TACE treatment were enrolled in this prospective cohort study. All patients were divided into no previous cTACE group (NPC group), 1-2 times previous cTACE group (PC group) and triple or above previous cTACE group (TPC group) according to the times of previous cTACE treatments. RESULTS: There was no difference in complete response (CR) (P = 0.671) and objective response rate (ORR) (P = 0.062) among three groups. Additionally, no difference in overall survival (OS) among groups (P = 0.899) was found. As to liver function, most liver function indexes were deteriorative at 1 week after DEB-TACE operation, but returned to baseline at 1-3 months after DEB-TACE operation in all three groups, while percentage of abnormal total bile acid (TBA) patients was higher in TPC group than NPC and PC groups at 1-3 month post-DEB-TACE (P = 0.018). As for safety profiles, the incidence of pain during DEB-TACE operation was lower in TPC group compared to NPC and PC groups (P = 0.005), while no difference of other adverse events was found during and 1 month post-DEB-TACE treatment among three groups. CONCLUSION: DEB-TACE treatment was equally efficient and tolerated in liver cancer patients with different times of previous cTACE treatments.

Effects of Heat Stress on the Development of GABAergic Neurons in the HPG Axis of Wenchang Chicks

This study conducted an in-depth investigation on the development of GABAergic neurons and their receptors in HPG axis-related target organs of Wenchang chicks under heat stress. One-day-old healthy Wenchang chicks were randomly divided into control (CK) and heat stress (HS) groups. Chicks in the HS group were placed in a 40±0.5°C climatic chamber for HS treatment from 13:00 to 15:00 daily. By immunohistochemistry and Western blotting, GABA and GABAA receptor (GABAAR) expression in the hypothalamus of the HS group was significantly higher (p 0.05), but GABAB receptor (GABABR) expression was significantly lower than that of the CK group (p 0.05). Expression of GABA and its two receptors in the pituitary tissues of the HS group was significantly lower than in the CK group (p 0.05). Expression of GABA and GABABR in ovaries in the HS group was significantly higher, but expression of GABAAR in the testes of the HS group was lower than that of the CK group (p 0.05). In the male chicks, expression of GABA and its two receptors in the hypothalamus, pituitary, and testicular tissues of the HS group was significantly higher than that of the CK group (p 0.05). Western blotting showed that the GABAAR and GABABR expression of the HS group was significantly higher than that of the CK group at 3 and 5 weeks of age. Thus, HS caused GABAergic nervous system disorder in the HPG axis of Wenchang chicks and seriously hindered the normal development of GABAergic neurons in chicks, leading to the disorder of the expression of GABA and its receptors in tissues.

Effects of Heat Stress on the Development of GABAergic Neurons in the HPG Axis of Wenchang Chicks

This study conducted an in-depth investigation on the development of GABAergic neurons and their receptors in HPG axis-related target organs of Wenchang chicks under heat stress. One-day-old healthy Wenchang chicks were randomly divided into control (CK) and heat stress (HS) groups. Chicks in the HS group were placed in a 40±0.5°C climatic chamber for HS treatment from 13:00 to 15:00 daily. By immunohistochemistry and Western blotting, GABA and GABAA receptor (GABAAR) expression in the hypothalamus of the HS group was significantly higher (p 0.05), but GABAB receptor (GABABR) expression was significantly lower than that of the CK group (p 0.05). Expression of GABA and its two receptors in the pituitary tissues of the HS group was significantly lower than in the CK group (p 0.05). Expression of GABA and GABABR in ovaries in the HS group was significantly higher, but expression of GABAAR in the testes of the HS group was lower than that of the CK group (p 0.05). In the male chicks, expression of GABA and its two receptors in the hypothalamus, pituitary, and testicular tissues of the HS group was significantly higher than that of the CK group (p 0.05). Western blotting showed that the GABAAR and GABABR expression of the HS group was significantly higher than that of the CK group at 3 and 5 weeks of age. Thus, HS caused GABAergic nervous system disorder in the HPG axis of Wenchang chicks and seriously hindered the normal development of GABAergic neurons in chicks, leading to the disorder of the expression of GABA and its receptors in tissues.(AU)

Salinomycin enhances doxorubicin sensitivity through reversing the epithelial-mesenchymal transition of cholangiocarcinoma cells by regulating ARK5.

Chemotherapy response rates in patients with cholangiocarcinoma remain low, primarily due to the development of drug resistance. Epithelial-mesenchymal transition (EMT) of cancer cells is widely accepted to be important for metastasis and progression, but it has also been linked to the development of chemoresistance. Salinomycin (an antibiotic) has shown some potential as a chemotherapeutic agent as it selectively kills cancer stem cells, and has been hypothesized to block the EMT process. In this study, we investigated whether salinomycin could reverse the chemoresistance of cholangiocarcinoma cells to the chemotherapy drug doxorubicin. We found that combined salinomycin with doxorubicin treatment resulted in a significant decrease in cell viability compared with doxorubicin or salinomycin treatment alone in two cholangiocarcinoma cell lines (RBE and Huh-28). The dosages of both drugs that were required to produce a cytotoxic effect decreased, indicating that these two drugs have a synergistic effect. In terms of mechanism, salinomycin reversed doxorubicin-induced EMT of cholangiocarcinoma cells, as shown morphologically and through the detection of EMT markers. Moreover, we showed that salinomycin treatment downregulated the AMP-activated protein kinase family member 5 (ARK5) expression, which regulates the EMT process of cholangiocarcinoma. Our results indicated that salinomycin reversed the EMT process in cholangiocarcinoma cells by inhibiting ARK5 expression and enhanced the chemosensitivity of cholangiocarcinoma cells to doxorubicin. Therefore, a combined treatment of salinomycin with doxorubicin could be used to enhance doxorubicin sensitivity in patients with cholangiocarcinoma.

Salinomycin enhances doxorubicin sensitivity through reversing the epithelial-mesenchymal transition of cholangiocarcinoma cells by regulating ARK5

Chemotherapy response rates in patients with cholangiocarcinoma remain low, primarily due to the development of drug resistance. Epithelial-mesenchymal transition (EMT) of cancer cells is widely accepted to be important for metastasis and progression, but it has also been linked to the development of chemoresistance. Salinomycin (an antibiotic) has shown some potential as a chemotherapeutic agent as it selectively kills cancer stem cells, and has been hypothesized to block the EMT process. In this study, we investigated whether salinomycin could reverse the chemoresistance of cholangiocarcinoma cells to the chemotherapy drug doxorubicin. We found that combined salinomycin with doxorubicin treatment resulted in a significant decrease in cell viability compared with doxorubicin or salinomycin treatment alone in two cholangiocarcinoma cell lines (RBE and Huh-28). The dosages of both drugs that were required to produce a cytotoxic effect decreased, indicating that these two drugs have a synergistic effect. In terms of mechanism, salinomycin reversed doxorubicin-induced EMT of cholangiocarcinoma cells, as shown morphologically and through the detection of EMT markers. Moreover, we showed that salinomycin treatment downregulated the AMP-activated protein kinase family member 5 (ARK5) expression, which regulates the EMT process of cholangiocarcinoma. Our results indicated that salinomycin reversed the EMT process in cholangiocarcinoma cells by inhibiting ARK5 expression and enhanced the chemosensitivity of cholangiocarcinoma cells to doxorubicin. Therefore, a combined treatment of salinomycin with doxorubicin could be used to enhance doxorubicin sensitivity in patients with cholangiocarcinoma.

Polymorphic microsatellite loci developed from the Hong Kong oyster (Crassostrea hongkongensis).

Forty polymorphic microsatellite loci were developed from Crassostrea hongkongensis using an enriched partial genomic library with magnetic beads. The polymorphism of these loci was assessed in 30 individuals from a wild population. The allele number of the polymorphic markers ranged from 2 to 13, with an average of 5.8 per locus. The polymorphism information content ranged from 0.032 to 0.891 and 37 loci presented a medium or high level of polymorphism. The observed and expected heterozygosity values ranged from 0.033 to 1.000 and 0.033 to 0.931, respectively. Of the 40 loci, 28 were found to conform to Hardy-Weinberg equilibrium (HWE), whereas the remaining 12 showed a significant departure from HWE. The availability of these markers will aid future genetic studies in C. hongkongensis.

Activation of Src tyrosine kinase in esophageal carcinoma cells in different regulatory environments and corresponding occurrence mechanism.

This study aims at observing the expression of activated Src tyrosine kinase in esophageal squamous cell carcinoma (ESCC), and exploring the relationship of Src tyrosine kinase with the occurrence and progression of ESCC. Immunohistochemistry, immunofluorescence, and immunoblotting are employed to investigate the expression of Src tyrosine kinase in the ESCC tissue. Cellular immunofluorescence is used to measure the expression of activated Src tyrosine kinase in TE1 and TE9 cell lines of human ESCC tissues and EPC1-htert and EPC2-htert cell lines of esophageal epithelial cells. Src tyrosine kinase is overexpressed in ESCC tissue and underexpressed in normal esophageal mucosa. Furthermore, it is overexpressed in the TE1 and TE9 cell lines of human ESCC tissue and underexpressed in the EPC1-htert and EPC2-htert cell lines of esophageal epithelial cells. Src tyrosine kinase shows a higher expression in human ESCC tissue than in normal esophageal mucosa. The difference is statistically significant (P < 0.05). The activation of Src tyrosine kinase plays an important role in the occurrence and development of ESCC.

IFGFA: Identification of featured genes from genomic data using factor analysis.

In this study, a software tool (IFGFA) for identification of featured genes from gene expression data based on latent factor analysis was developed. Despite the availability of computational methods and statistical models appropriate for analyzing special genomic data, IFGFA provides a platform for predicting colon cancer-related genes and can be applied to other cancer types. The computational framework behind IFGFA is based on the well-established Bayesian factor and regression model and prior knowledge about the gene from OMIM. We validated the predicted genes by analyzing somatic mutations in patients. An interface was developed to enable users to run the computational framework efficiently through visual programming. IFGFA is executable in a Windows system and does not require other dependent software packages. This program can be freely downloaded at http://www.fupage.org/downloads/ifgfa.zip.

Protective effect of quercetin on acute lung injury in rats with sepsis and its influence on ICAM-1 and MIP-2 expression.

This study aimed to explore the protective effect of quercetin on acute lung injury (ALI) in rats with sepsis and the related mechanism. Rats were administered different doses of quercetin intraperitoneally, and blood samples and lung tissue were collected at 24 h after treatment. Arterial blood gases, lung water content, protein content, and cell counts in bronchoalveolar lavage fluid (BALF) were measured. Morphological changes in lung tissue pathology were observed under a light microscope. Serum intercellular adhesion molecule (ICAM)-1 and macrophage inflammatory protein 2 (MIP-2) levels were detected and ICAM-1 and MIP-2 mRNA expression in lung tissue was determined. Compared with that in the control model group, arterial blood gases, lung water content, protein content, and cell counts in BALF improved in the high- and low-dose quercetin groups (P < 0.05), with maximal improvement observed for the high-dose quercetin (P < 0.05). Lesions on the lungs improved in the high- and low-dose quercetin groups than those in the control model group, and the high-dose quercetin group showed better improvement than the low-dose group (P < 0.05). Compared with that in the sham-operated group, both serum and lung tissue ICAM-1 and MIP-2 expression increased significantly in the model group (P < 0.05). The quercetin groups presented lower ICAM-1 and MIP-2 expression than the control model group, with the lowest expression observed in the high-dose group (P < 0.05). Quercetin may protect against ALI in rats with sepsis by inhibiting ICAM-1 and MIP-2 expression.

miR-133 inhibits pituitary tumor cell migration and invasion via down-regulating FOXC1 expression.

Many studies have shown that microRNA (miR)-133 functions as a tumor suppressor in a variety of metastatic cancers, including breast cancer, gastric cancer, and liver fibrosis. However, the influence of miR-133 on pituitary tumor malignancy has not yet been reported. The purpose of this study was to explore the role of miR-133 in pituitary tumor cell migration and invasive ability and the molecular mechanisms involved. Our findings suggest that in pituitary adenoma cell lines, through direct targeting and negative control of forkhead box C1 (FOXC1), miR-133 can inhibit pituitary adenoma cell migration and invasion. In addition, epithelial-to-mesenchymal transition can be induced by miR-133. Additionally, a negative correlation was found between FOXC1 and miR-133 expression when comparing their expression levels between cancerous tissue and adjacent normal tissue. This suggests that miR-133 can inhibit cell migration and invasion by directly targeting FOXC1, implying that miR-133 could be a potential therapeutic target for treatment of invasive pituitary adenoma.

Mutations in WT1 in boys with sporadic isolated steroid-resistant nephrotic syndrome.

Mutations in the Wilms' tumor gene, WT1, can lead to syndromic steroid-resistant nephrotic syndrome and isolated steroid-resistant nephrotic syndrome. WT1 mutations have been identified in the majority of children with Denys-Drash or Frasier syndrome. WT1 mutations have not previously been identified in boys with sporadic isolated steroid-resistant nephrotic syndrome, but, recently, four boys with isolated nephrotic syndrome were identified to have WT1 mutations. However, whether boys with sporadic isolated steroid-resistant nephrotic syndrome should be routinely subjected to mutation analysis of WT1 has not been established. We examined 35 boys with sporadic isolated steroid-resistant nephrotic syndrome for mutations in WT1. Mutation analysis of all 10 exons of WT1 was performed by polymerase chain reaction and direct sequencing. Karyotype analysis or Y chromosome identification was performed for all patients. A Y chromosome or a 46, XY karyotype was demonstrated for all 35 patients. No causative WT1 mutation was identified in any of the patients. The WT1 mutation, IVS4+14T>C, which is not predicted to affect splicing, was identified in one patient who achieved complete remission after 8 weeks of oral prednisone treatment, indicating that IVS4+14T>C is not a causative mutation. Five WT1 polymorphisms were also identified in some patients and controls. Our results suggest that mutation analysis of WT1 should not be routinely performed for genetically defined boys with sporadic isolated steroid-resistant nephrotic syndrome.

Characterization of the Microbial Communities in the Ant Lion Euroleon coreanus (Okamoto) (Neuroptera: Myrmeleontidae).

Euroleon coreanus (Okamoto) is widely distributed in China, and the larval stage can be treated as traditional Chinese medicine. However, the host-bacterium relationship remains unexplored, as there is a lack of knowledge on the microbial community of ant lions. Hence, in the current study, we explored the microbial community of the larval ant lion E. coreanus using Illumina MiSeq sequencing. Results indicated that a total of 10 phyla, 126 genera, and 145 species were characterized from the second instars of E. coreanus, and most of the microbes were classified in the phylum Proteobacteria. Cronobacter muytjensii was the most abundant species characterized in the whole body and gut of E. coreanus, and the unclassified species in the genera Brevundimonas and Lactobacillus were relatively more abundant in the head and carcass. In addition, no Wolbachia-like bacteria were detected, whereas bacteria like Francisella tularensis subsp. Holarctica OSU18 and unclassified Rickettsiella were first identified in ant lion E. coreanus.

Cloning and characterization of defense-related genes from Populus szechuanica infected with rust fungus Melampsora larici-populina.

Characterization of defense-related genes is critical for breeding disease-resistant poplar varieties and for better management and control of leaf rust disease. In the present study, full-length cDNAs of five Populus szechuanica defense-related (PsDR) genes, pathogen-related protein 1 (PsPR1), ß-1,3-glucanase (PsGns), thaumatin-like protein 1 (PsTLP1), thaumatin-like protein 2 (PsTLP2), and phenylalanine ammonia-lyase (PsPAL), were cloned from the leaves of P. szechuanica infected with Melampsora larici-populina (MLP). PsPR1 (728 bp), PsGns (1189 bp), PsTLP1 (929 bp), PsTLP2 (885 bp), and PsPAL (2586 bp) were predicted to encode 161, 347, 245, 225, and 711 amino acid residue-containing proteins with isoelectric points of 8.53, 4.96, 4.51, 7.32, and 5.87, respectively. Moreover, the deduced PsDR proteins displayed more than 90% similarity to proteins from other Populus species. In response to the avirulent isolate, Sb052, and the virulent isolate, Th053, of MLP, the expression of PsDR genes was rapidly up-regulated in the leaves of P. szechuanica, peaked at 2 or 7 days post-inoculation (dpi), with levels in the incompatible interaction being higher than those in the compatible interaction. Meanwhile, the expression of PsDR genes (except for PsGns) was also differentially up-regulated at 3, 7, or 18 dpi in the petioles of the infected leaves, leaves next to the inoculated leaves, and in the top buds of the infected plants, respectively, compared to that at 0 dpi. These results suggest that these PsDR genes could play distinctive roles in the defense response of poplar against rust infection.

Analysis of the association between polymorphisms in the vitamin D receptor (VDR) gene and dental caries in a Chinese population.

Environmental influences on the development and progression of dental caries are well known; however, there is little evidence of a genetic component imparting susceptibility to dental caries. The aim of this study was to investigate the relationship between a single nucleotide polymorphism in the vitamin D receptor TaqI locus and dental caries susceptibility in a Chinese population. This case-control study was conducted with a case group (264 patients with dental caries from northwestern China) and a control group (219 individuals without dental caries or systemic disease from the same area). DNA was extracted from the peripheral venous blood of the study participants; the distribution of TaqI locus genotypes and allele frequencies was determined via polymerase chain reaction-restriction fragment length polymorphism. The data obtained were statistically analyzed using the Hardy-Weinberg equilibrium and Chi-square test. The frequency of the Tt genotype in the case group (14.0%) was significantly higher than that in the control group (4.3%), as determined using the genotype TT as the reference. The risk of dental caries was increased 3.8-fold in individuals with the heterozygous Tt genotype compared to that in the individuals with the TT genotype. The proportion of the 't' allele in the case group (7.0%) and the control group (2.1%) was observed to be significantly different [P = 0.0003; OR = 3.592, confidence interval 95% (1.790-7.208)]. Our results therefore suggested that the allele 't' might be a genetic factor determining dental caries susceptibility in individuals from the northwest of China.

B-type natriuretic peptide and cirrhosis progression.

Brain natriuretic peptide (BNP) is used as a marker of cardiac dysfunction to predict heart failure mortality. The significance of the prognostic ability of BNP for liver cirrhosis remains unknown, although the levels of BNP seen in cirrhosis are high. We aimed to determine whether the BNP level is related to the stage of cirrhosis and could serve as a prognostic marker of cirrhosis (predict the 1-year all-cause mortality). We recruited 92 patients at different stages of cirrhosis and 81 controls matched by age and gender for this study. At admission, cardiac physical examination and BNP measurements were performed. Upon discharge, the 89 patients were followed up for 12 months. The median BNP levels of patients with cirrhosis were 167.0 pg/mL, which were significantly higher than those of the control group (167.0 vs 34.8 pg/mL, P = 0.001). Serum BNP levels were positively correlated with the Child score, the grade of esophageal varices, a history of spontaneous bacterial peritonitis, and the presence of ascites and collateral circulation. BNP levels above the median were associated with an increased occurrence of death within 12 months of discharge (log rank P = 0.025), as determined by univariate and multivariate Cox regression analyses. Esophageal varices, large/medium volume ascites, and BNP levels were related to the clinical outcome (P = 0.034, 0.030, and 0.025, respectively). Together, these results suggested that serum BNP levels are significantly correlated with the stage of cirrhosis, suggesting that BNP levels might serve as a significant predictor for 1-year all-cause mortality.

A retrospective analysis of lung metastasis in 64 patients with alveolar soft part sarcoma.

OBJECTIVES: To analyse the lung metastasis and possible factors influencing lung metastasis in alveolar soft part sarcoma (ASPS) patients. METHODS: The medical records of 64 consecutive ASPS patients were reviewed to analyse their treatments, features of lung metastasis, and possible factors influencing lung metastasis. RESULTS: Thirty-six females and 28 males with a median age of 27 years were included. The primary disease sites were the extremities in 51 patients and other locations in 13 patients. The median primary tumour size was 5 cm. Wide local excision of the primary tumour was performed on 56 patients (87.5 %). Thirteen patients (20.3 %) received postoperative adjuvant radiotherapy, and nine patients (14.1 %) underwent adjuvant chemotherapy. Twelve patients (18.8 %) presented with metastatic lung disease. Twenty-nine patients (45.3 %) developed metastatic lung disease during follow-up. Lung metastasis occurred in 64.1 % of the patients. Lung metastasis was detected at a median interval of 20 months after primary ASPS diagnosis. Being male, >20 years of age, having a primary tumour size ≥ 5 cm, and local recurrence were associated with a greater rate of lung metastasis. Median survival after the diagnosis of lung metastasis was 34 months. The 5-year survival rates were 64.1 and 95.2 % for patients with and without lung metastasis (P < 0.001). Thirty-seven patients with metastatic lung disease received anthracycline- and ifosfamide-based chemotherapy. One patient experienced a partial remission. CONCLUSIONS: ASPS patients have a high prevalence of lung metastasis. Sex, age, primary tumour size, and local recurrence are major factors influencing lung metastasis. Chemotherapy is not efficacious in ASPS patients with lung metastasis.