A matched case-control study in Taiwan to evaluate potential risk factors for prostate cancer.

The rising incidence rate of prostate cancer (PCa) worldwide has become a public health concern. PCa has a multifactorial etiology, and the link between human papillomavirus (HPV) and PCa has been widely investigated by numerous case-control studies. This age-matched, case-control study included 143 PCa patients and 135 benign prostatic hyperplasia (BPH) patients, with prostatic specimens testing negative for malignancy, as control. Study participants were recruited from four major hospitals in Taoyuan City, Taiwan, period 2018-2020, looking into HPV infection and other PCa risk factors, including dietary habits, family history, personal lifestyle, and sexual behavior. Multiple logistic regression analysis and forward stepwise selection analysis were conducted to identify potential risk factors for PCa. HPV DNA was found in 10 of the 143 PCa cases (7%) and 2 of the 135 BPH controls (1.5%) (OR = 6.02, 95% CI = 1.03-30.3, p = 0.046). This association was slightly significant, and furthermore, high risk HPV was not found to be associated with PCa. Higher body mass index (BMI) (OR = 1.15, 95% CI = 1.05-1.27, p = 0.003), more total meat consumption (OR = 2.74, 95% CI = 1.26-5.94, p = 0.011), exhibited association to PCa. However, PCa family history only presented a statistically significant difference by forward stepwise analysis (OR = 3.91, 95% CI = 1.17-13.12, p = 0.027). While much focus has been on the association between HPV and PCa, the results of this study indicate that more efforts should be directed towards investigating dietary habits, personal lifestyle and family history as factors for PCa. These results could serve as a basis for designing PCa prevention strategies.

Diel Fluctuation Superimposed on Steady High pCO2 Generates the Most Serious Cadmium Toxicity to Marine Copepods.

Coastal systems experience diel fluctuation of pCO2 and cadmium (Cd) pollution; nevertheless, the effect of fluctuating pCO2 on Cd biotoxicity is poorly known. In this study, we initially performed the isotopically enriched organism bioassay to label Tigriopus japonicus with 113Cd (5 µg/L) to determine the Cd accumulation rate constant (kaccu) under ambient (400 µatm) and steadily (1000 µatm) and fluctuatingly elevated (1000 ± 600 µatm) pCO2 conditions for 48 h. Next, T. japonicus was interactively subjected to the above pCO2 exposures at Cd (control, 5, and 500 µg/L) treatments for 7 d. Biochemical and physiological responses for copepods were analyzed. The results showed that steadily increased pCO2 facilitated Cd bioaccumulation compared to ambient pCO2, and it was more under fluctuating acidification conditions. Despite compensatory reactions (e.g., increased energy production), Cd ultimately induced oxidative damage and apoptosis. Meanwhile, combined treatment exhibited higher toxicity (e.g., increased apoptosis) relative to Cd exposure, and even more if fluctuating acidification was considered. Intriguingly, fluctuating acidification inhibited Cd exclusion in Cd-treated copepods compared to steady acidification, linking to higher Cd kaccu and bioaccumulation. Collectively, CO2-driven acidification could aggravate Cd toxicity, providing a mechanistic understanding of the interaction between seawater acidification and Cd pollution in marine copepods.

Calreticulin Regulates ß1-Integrin mRNA Stability in PC-3 Prostate Cancer Cells.

Prostate cancer (PCa) is the major cause of cancer-related death among aging men worldwide. Recent studies have suggested that calreticulin (CRT), a multifunctional chaperon protein, may play an important role in the regulation of PCa tumorigenesis and progression. However, the underlying mechanisms are still unclear. Integrin is an important regulator of cancer metastasis. Our previous study demonstrated that in J82 bladder cancer cells, CRT affects integrin activity through FUBP-1-FUT-1-dependent fucosylation, rather than directly affecting the expression of ß1-integrin itself. However, whether this regulatory mechanism is conserved among different cell types remains to be determined. Herein, we attempted to determine the effects of CRT on ß1-integrin in human prostate cancer PC-3 cells. CRT expression was suppressed in PC-3 cells through siRNA treatment, and then the expression levels of FUT-1 and ß1-integrin were monitored through RT-PCR. We found that knockdown of CRT expression in PC-3 cells significantly affected the expression of ß1-integrin itself. In addition, the lower expression level of ß1-integrin was due to affecting the mRNA stability. In contrast, FUT-1 expression level was not affected by knockdown of CRT. These results strongly suggested that CRT regulates cellular behavior differently in different cell types. We further confirmed that CRT directly binds to the 3'UTR of ß1-integrin mRNA by EMSA and therefore affects its stability. The suppression of CRT expression also affects PC-3 cell adhesion to type I collagen substrate. In addition, the levels of total and activated ß1-integrin expressed on cell surface were both significantly suppressed by CRT knockdown. Furthermore, the intracellular distribution of ß1-integrin was also affected by lowering the expression of CRT. This change in distribution is not lysosomal nor proteosomal pathway-dependent. The treatment of fucosydase significantly affected the activation of surface ß1-integrin, which is conserved among different cell types. These results suggested that CRT affects the expression of ß1-integrin through distinct regulatory mechanisms.

Dosimetric comparison of helical tomotherapy, volumetric-modulated arc therapy, intensity-modulated radiotherapy, and field-in-field technique for synchronous bilateral breast cancer.

PURPOSE: To compare the dosimetric characteristics of helical tomotherapy (HT), volumetric-modulated arc therapy (VMAT), intensity-modulated radiotherapy (IMRT), and tangential field-in-field technique (FIF) for the treatment of synchronous bilateral breast cancer (SBBC). METHODS AND MATERIALS: Ten patients with early-stage unilateral breast cancer were selected for simulating the patients with SBBC in this retrospective analysis. Treatment plans with HT, VMAT, IMRT, and FIF were generated for each patient with a total dose of 50.4 Gy in 28 fractions to the target. Plan quality, namely conformity index (CI), homogeneity index (HI), dose-volume statistics of organs at risk (OARs), and beam-on time (BOT), were evaluated. RESULTS: HT plans showed a lower mean heart dose (3.53 ± 0.31Gy) compared with the other plans (VMAT = 5.6 ± 1.36 Gy, IMRT = 3.80 ± 0.76 Gy, and FIF = 4.84 ± 2.13 Gy). Moreover, HT plans showed a significantly lower mean lung dose (p < 0.01) compared with the other plans: mean right lung doses were 6.81 ± 0.67, 10.32 ± 1.04, 9.07 ± 1.21, and 10.03 ± 1.22 Gy and mean left lung doses were 6.33 ± 0.87, 8.82 ± 0.91, 7.84 ± 1.07, and 8.64 ± 0.99 Gy for HT, VMAT, IMRT, and FIF plans, respectively. The mean dose to the left anterior descending artery was significantly lower in HT plans (p < 0.01) than in the other plans: HT = 19.41 ± 0.51 Gy, VMAT = 25.77 ± 7.23 Gy, IMRT = 27.87 ± 6.48 Gy, and FIF = 30.95 ± 10.17 Gy. FIF plans showed a worse CI and HI compared with the other plans. VMAT plans showed shorter BOT (average, 3.9 ± 0.2 minutes) than did HT (average, 11.0 ± 3.0 minutes), IMRT (average, 6.1 ± 0.5 minutes), and FIF (average, 4.6 ± 0.7 minutes) plans. CONCLUSIONS: In a dosimetric comparison for SBBC, HT provided the most favorable dose sparing of OARs. However, HT with longer BOT may increase patient discomfort and treatment uncertainty. VMAT enabled shorter BOT with acceptable doses to OARs and had a better CI than did FIF and IMRT.

Dihydropyrazothiazole derivatives as potential MMP-2/MMP-8 inhibitors for cancer therapy.

MMP-2/MMP-8 is established as one of the most important metalloenzymes for targeting cancer. A series of dihydropyrazothiazole derivatives (E1-E18) bearing a salicylaldehyde group linked to Pyrazole ring were designed, synthesized, and evaluated for their pharmacological activity as MMP-2/MMP-8 inhibitors. Among them, compound E17 exhibited most potent inhibitory activity (IC50 = 2.80 µM for MMP-2 and IC50 = 5.6 µM for MMP-8), compared to the positive drug CMT-1 (IC50 = 1.29 µM). Compounds (E1-E18) were scrutinized by CoMFA and CoMSIA techniques of Three-dimensional quant. structure-activity relationship (3D-QSAR), as well as a docking simulation. Moreover, treatment with compound E4 could induce MCF-7 cell apoptosis. Overall, the biological profile of E1-E18 may provide a research basis for the development of new agents against cancer.

Expression of soluble vascular endothelial growth factor receptor-1 and placental growth factor in fetal growth restriction cases and intervention effect of tetramethylpyrazine.

OBJECTIVE: To investigate the expression of soluble vascular endothelial growth factor receptor-1 (sFlt-1) and placental growth factor (PLGF) in the fetal growth restriction (FGR) cases and the intervention mechanism of tetramethylpyrazine. METHODS: A total of 60 fetal growth restriction cases that admitted to our hospital were randomly divided into ligustrazine intervention group (group A) and nutritional support group (group B). A total of 50 healthy pregnant women were also enrolled as control group (group C). Expression level of maternal serum sFlt1, PLGF and fetal growth parameters including HC, AC, FL, BPD, EFW as well as placenta PLGF, sFlt-1 mRNA expression were recorded and compared among the three groups. A total of 15 SD rats were selected and were divided into three groups, TMP group, alcohol and tobacco group and blank control group. Three groups of rats were dissected on the twentieth day of gestation. RESULTS: Expression level of sFlt-1 and PLGF in group A was not significantly different from that of group C (P>0.05); but significant difference in SFlt1 and PLGF expression level was observed between group C and group B (P<0.05). Before treatment, HC, AC, FL, BPD and EFW of group A and group B were significant lower than those of group C, but after treatment, those parameters in group A were significantly improved (P<0.05). In the animal experiment there was no significant difference in sFlt-1 between treatment group and FGR group without treatment or control group (P>0.05). There was significant difference in PLGF between FGR group with treatment and FGR group without treatment or control group (P<0.01). CONCLUSIONS: PLGF level is decreased and sFlt-1 increased in patients suffered from fetal growth restriction, and FGR rats show increased sFlt-1 and decreased PLGF, thus they can be indicator of the fetal growth restriction. Ligustrazine can effectively improve sFlt-1, PLGF expression level in fetal growth restriction cases, which can be used as treatment for FGR.

RTN4 3'-UTR insertion/deletion polymorphism and susceptibility to non-small cell lung cancer in Chinese Han population.

Nogo protein, encoded by gene reticulon-4 (RTN4), includes three major isoforms by different splicing, named Nogo-A Nogo-B and Nogo-C. Nogo proteins play an important role in the apoptosis of cells, especially in tumor cells. RTN4 single nucleotide polymorphisms (SNPs) can influence the efficiency of transcription and translation thus being related with an individual's predisposition to cancer. The CAA insertion/deletion polymorphism (rs34917480) within RTN4 3'-UTR has been reported to be associated with many cancer types. In order to investigate the relationship between this polymorphism and susceptibility to non-small cell lung cancer (NSCLC) in the Chinese population, we conducted the present case-control study including 411 NSCLC patients and 471 unrelated healthy controls. The genotype distributions were significantly different between cases and controls (p=0.014). We found that the del allele could significantly increase NSCLC risk (ins/ins vs ins/del: p=0.007, OR 1.46, 95%CI=1.11-1.93; dominant model: p=0.004, OR 1.47, 95%CI=1.13-1.92 and allele model: p=0.008, OR 1.35, 95%CI=1.08-1.67). This association was stronger in participants over 60 years old, males and smokers. We therefore conclude that the CAA insertion/deletion polymorphism (rs34917480) contributes to non-small cell lung cancer risk in Chinese population. Age, sex and environmental exposure are also related to carcinogenic effects of rs34917480.

Indole-3-acetic acid reverses the harpin-induced hypersensitive response and alters the expression of hypersensitive-response-related genes in tobacco.

Harpin proteins stimulate hypersensitive response (HR) in plants. However, the mechanism by which HR is regulated is not clear. The role of the auxin, indole-3-acetic acid (IAA), in the control of harpin-stimulated HR was investigated. IAA was used to inhibit HR that was stimulated by purified fusion harpin(Xoo) protein in tobacco. Semi-quantitative PCR and qRT-PCR were employed to detect the expression of HR related genes. IAA at 100 µM reversed harpin-induced HR which was inhibited by 500 µM 2,3,5-triiodobenzoic acid (TIBA). Semi-quantitative PCR and qRT-PCR showed the combined application of 100 µM IAA and harpin protein from Xanthomonas oryzae enhanced the expression of HR marker gene, hsr203J, but weakened the expression of the disease-defense gene, chia5. TIBA also decreased the expression of hsr203J but increased the expression of chia5. Thus, the auxin can reverse harpin(Xoo)-induced HR.

Role of PTEN in cholera toxin-induced SWO­38 glioma cell differentiation.

Malignant gliomas persist as a major disease responsible for high morbidity and mortality rates in adults. Differentiation therapy has emerged as a promising treatment modality. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene function is commonly lost in primary gliomas, particularly in glioblastomas, and this is associated with tumor differentiation. PTEN gene deletion is one of the main molecular events in gliomas. In this study, we aimed to explore the effect and mechanisms of PTEN on cholera toxin (CT)­induced SWO-38 glioma cell differentiation. It has been shown that transfection of the exogenous PTEN gene induces glioma cell differentiation; however, the underlying mechanism remains to be elucidated. Results of the present study showed that CT-induced SWO-38 glioma cell differentiation was characterized by morphological changes, the increased expression of glial fibrillary acidic protein (GFAP), an accumulation of cells in the G0/G1 phase of the cell cycle, the decreased expression of cyclin D1 and a decreased invasion and migration capacity. Silencing of the PTEN protein using RNA interference resulted in suppressed cell differentiation. Furthermore, inhibition of the PI3K/AKT pathway by the inhibitor LY294002 led to attenuated differentiation, while differentiation remained stable with the inhibition of the MAPK/ERK pathway by PD0325901. Thus, PTEN may be important in glioma cell differentiation.

High expression of KIF26B in breast cancer associates with poor prognosis.

To date, a great number of studies have demonstrated that altered expression of kinesins is associated with development and progression of various human cancers. Kinesin family member 26B (KIF26B), a member of the kinesin superfamily proteins (KIFs), is essential for kidney development. However, the role of KIF26B during tumorigenesis and progression is limited. Here, we demonstrate that both KIF26B mRNA and protein are overexpression in breast cancer tissues by RT-qPCR and western blot. Immunohistochemistry revealed that KIF26B expression significantly correlated with clinicopathological factors, including tumor size (P = 0.011), grade (P = 0.017), lymph node status (P = 0.009) and ER status (P = 0.012). Moreover, the Kaplan-Meier analysis indicated that breast cancer patients with high KIF26B expression had a shorter survival than those with low KIF26B expression. In addition, multivariate analysis indicated that KIF26B is an independent prognostic for outcome in breast cancer (HR, 2.356; 95%CI, 1.268-4.378; P = 0.007). Collectively, our study demonstrated that KIF26B was overexpression in breast cancer and could be served as a potential prognostic marker.

Effect of sex on biomechanical properties of the proper hepatic artery in pigs and humans for liver xenotransplant.

OBJECTIVES: This study investigated the relation between biomechanical properties of the proper hepatic artery and sex in pigs and humans to provide the theoretical basis for selecting suitable donor in pig-to-human liver xenotransplant. MATERIALS AND METHODS: The proper hepatic arteries of 32 Chinese Hubei white pigs (8 males, 8 females, 8 castrated males, and 8 ovariectomized females) and 10 deceased donors (5 human men, 5 human women) were obtained. The pressure-diameter relations of the proper hepatic arteries were measured on biomechanical test equipment to calculate the incremental elastic modulus (Einc), pressure-strain elastic modulus (Ep), volume elastic modulus (Ev), and compliance. Each sample was sliced into 5-µm frozen sections and stained with hematoxylin-eosin. RESULTS: There were significant differences in Einc (F=10.24; P = .001), Ep (F=3.75; P = .001), and Ev (F=3.41; P = .002) of the proper hepatic arteries of female, male, and gonadectomized pigs; females had the lowest elastic modulus and the gonadectomized group had the highest (P < .01). There was a significant difference in compliance of the porcine proper hepatic arteries between the sexes, highest in the female group and lowest in the gonadectomized group (P < .01). No difference in the elastic modulus and compliance of the proper hepatic artery between the male pig and the human man. There was no difference between the female pig and the human woman. CONCLUSIONS: There were differences in the biomechanical properties of the proper hepatic arteries of the female, male, and gonadectomized pigs. The biomechanical properties of the human men/women proper hepatic artery match those of the porcine male/female hepatic artery. The correlation between sex and biomechanical properties of the proper hepatic artery in pigs could imply that a pig of the same sex should be chosen for pig-to-human liver xenotransplant.

Effects of sargentgloryvine stem extracts on HepG-2 cells in vitro and in vivo.

AIM: To observe the effects of sargentgloryvine stem extracts (SSE) on the hepatoma cell line HepG-2 in vitro and in vivo and determine its mechanisms of action. METHODS: Cultured HepG-2 cells treated with SSE were analysed by 3-(4,5-Dimethyl-thiazol-2-yl)-2,5-Diphenyltetrazolium bromide and clone formation assay. The cell cycle and apoptosis analysis were conducted by flow cytometric, TdT-Mediated dUTP Nick End Labeling and acridine orange/ethidium bromide staining methods, and protein expression was examined by both reverse transcriptase-polymerase chain reaction and Western blotting. The pathological changes of the tumor cells were observed by haematoxylin and eosin staining. Tumor growth inhibition and side effects were determined in a xenograft mouse model. RESULTS: SSE treatment could not only inhibit HepG-2 cell proliferation in a dose- and time-dependent manner but also induce apoptosis and cell cycle arrest at the S phase. The number of colonies formed by SSE-treated tumor cells was fewer than that of the controls (P < 0.05). SSE induced caspase-dependent apoptosis accompanied by a significant decrease in Bcl-xl and Mcl-1 and elevation of Bak expression (P < 0.05). Tumor necrosis factor α in the xenograft tumor tissue and the liver functions of SSE-treated mice showed no significant changes at week 8 compared with the control group (P > 0.05). Systemic administration of SSE could inhibit the HepG-2 xenograft tumor growth with no obvious toxic side effects on normal tissues. CONCLUSION: SSE can induce apoptosis of HepG-2 cells in vitro and in vivo through decreasing expression of Bcl-xl and Mcl-1 and increasing expression of Bax.

Differentiation of SWO-38 glioma cells induced by CDA-2 is mediated by peroxisome proliferator-activated receptor gamma.

Glioma remains one of the most lethal human tumors in spite of the progress in radiotherapy, chemotherapy, and surgical techniques. Cell differentiation agent-2 (CDA-2) is an extraction from healthy human urine consisting of primary organic acids and peptides, and it has been demonstrated to inhibit growth and induce differentiation in glioma and other cell lines. However, the mechanism remains unclear. Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptors (NHRs) which are involved in cellular differentiation and proliferation. In this study, we investigated if CDA-2 induced differentiation of SWO-38 glioma cells is mediated by PPARgamma. CDA-2 induced differentiation of SWO-38 cells was characterized by typical morphological changes, increased expression of GFAP, inhibition of proliferation and G(0)/G(1) cell cycle arrest. CDA-2 also triggered up-regulation of PPARgamma, GFAP and PTEN protein and a reduction of COX-2 protein. However, the effects of CDA-2 on SWO-38 cells could be partly reversed by GW9662, an irreversible PPARgamma antagonist. Our investigation demonstrated that CDA-2 could be a potential drug for tumor differentiation therapy, and activation of the PPARgamma pathway might be a crucial factor in glioma differentiation induced by CDA-2.

Biochemical response of the copepod Tigriopus japonicus Mori experimentally exposed to cadmium.

The response of the copepod (Tigriopus japonicus Mori) to cadmium (Cd) additions was investigated under laboratory-controlled conditions in a 12-day exposure. Superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), acetylcholinesterase (AchE), reduced glutathione (GSH), the ratio of reduced to oxidized glutathione (GSH/GSSG), and metallothionein (MT) were analyzed for Cd treatments (0, 10, 20, 40, and 100 microg/L) after exposure for 1, 4, 7, and 12 days. Additionally, thiobarbituric reactive species assay was used to evaluate lipid peroxidation (LPO) of the copepod after the 12-day exposure. The results indicated that Cd treatments significantly influenced the biochemical indexes (SOD, GPx, GST, AchE, GSH, and GSH/GSSG) after certain exposure times. Exposure to Cd induced LPO in the treated copepods, hinting that the copepods had suffered from oxidative damage. During exposure, the Cd initiated an induced MT synthesis in the copepods by day 7, which peaked at day 12 and which was probably responsible for Cd detoxification. Thus, Cd exposure significantly affected the detoxification process and antioxidant system of this copepod, and T. japonicus could be used as a suitable bioindicator of exposure to Cd using SOD, GPx, GST, LPO, and GSH/GSSG as biomarkers.

Effects of macronutrient additions on nickel uptake and distribution in the dinoflagellate Prorocentrum donghaiense Lu.

The influences of macronutrient additions on nickel (Ni) uptake and distribution in the subcellular structures and macromolecular components of the dinoflagellate Prorocentrum donghaiense Lu were examined using a radioisotope tracer method. The results showed that nitrate addition enhanced the uptake of Ni by P. donghaiense, whereas phosphate addition inhibited Ni uptake at high-Ni concentration. Nitrate or phosphate addition significantly affected Ni distribution in the subcellular structures and components. The majority of Ni was found in the soluble substances (>70%) and in the proteins (55.0-79.6%) of the algal cells. Urea reduced the Ni content in the amino acid-carbohydrate but elevated its content in proteins, and shown significantly correlated with the protein content of the algal cells. Thus, nutrient enrichment could influence both metal uptake and its distribution in the subcellular structures and components of the phytoplankton, as well as its subsequent transfer in marine food chains.

[Artesunate suppresses human endometrial carcinoma RL95-2 cell proliferation by inducing cell apoptosis].

OBJECTIVE: To investigate the inhibitory effect of artesunate on human endometrial carcinoma RL95-2 cell line proliferation in vitro and the possible mechanisms. METHODS: The inhibitory effect of artesunate on the cell proliferation was assessed with MTT assay. Transmission electron miscrosopy was used to observe the morphological change of the cells after the treatment. Flow cytometry was performed to examine the changes in the cell cycle, reactive oxygen species (ROS) levels (with DCFH-DA labeling) and mitochondrial membrane potential (rhodamine123 staining), and caspase-3 activity was detected by immunohistochemistry. RESULTS: Artesunate inhibited the proliferation of RL95-2 cells with an IC(50) of 26.29 microg/ml. Transmission electron microscopy revealed early apoptotic changes of the cells with obvious chromatin fragmentation. The cell cycle arrest at G(0)/G(1) phase was observed by flow cytometry, and immunohistochemistry demonstrated caspase-3 positivity in cytoplasm. ROS generation in the cells increased obviously after treatment with artesunate for 72 h, which also resulted in lowered mitochondrial membrane potential. CONCLUSION: Artesunate suppressed the proliferation of RL95-2 cells in vitro possibly by inducing cell apoptosis.

[Expression of peroxisome proliferator-activated receptor gamma in glioma].

OBJECTIVE: To investigate the expression and significance of peroxisome proliferators-activated receptor gamma (PPAR gamma) in human glioma. METHODS: Immunohistochemical staining for PPAR gamma was performed using biopsy specimens of human glioma of various histological types. Expression of PPAR gamma and GFAP in glioma cell lines SWO-38, U251 and SHG-44 were analyzed using Western blotting and reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Immunohistochemical study showed that PPAR gamma was expressed in glioma tissues with positive rate of 37.5%. Western blotting and RT-PCR showed that PPAR gamma was expressed in both glioma cell lines SWO-38 and U251, but not in SHG-44 cells. However, high expression of GFAP was detected in SHG-44 cells. CONCLUSION: PPAR gamma is associated with carcinogens of glioma. Actived PPAR gamma by agonist may be a novel approach to the treatment of glioma.

[Effects of exogenous human chorionic gonadotropin on nude mice bearing endometrial carcinoma].

OBJECTIVE: To observe the effects of exogenous human chorionic gonadotropin (hCG) on nude mice bearing transplanted endometrial carcinoma. METHODS: Human endometrial carcinoma xenograft was transplanted in nude mice, and the effects of hCG injection on the tumor growth was evaluated according to tumorigenesis and xenograft weights. The expression of Ki-67 in the tumor was determined by immunohistochemistry, and HE staining was performed for morphological observation and measurement of the necrosis area in the tumor. The effect of hCG on fibrosis in the tumor was evaluated with Masson staining. RESULTS: Compared to normal saline-treated tumor-bearing mice, the mice with hCG treatment showed increased tumor weight. HE staining for tumors in HCG-treatment group visualized tumor cell arrangement in glandular structure with smaller necrosis area, and Masson staining identified thick and compact collagen fibers as compared with the thin and loosely arranged fibers in saline-treated group. No significant difference was found in the Ki-67 expression in the tumors between the two groups. CONCLUSION: Exogenous hCG can promote the differentiation of the endometrial carcinoma cells in vivo.

Influence of N, P additions on the transfer of nickel from phytoplankton to copepods.

We examined the influence of macronutrient (nitrate and phosphate) additions on Ni uptake by phytoplankton (Prorocentrum donghaiense and Skeletonema costatum) and its subsequent transfer to marine copepods (Calanus sinicus and Labidocera euchaeta). Ni uptake by phytoplankton after 24h of exposure was markedly dependent on nutrient conditions, with a higher nutrient quota facilitating Ni accumulation in the algae. Trophic transfer was quantified by measurements of the Ni assimilation efficiency in C. sinicus and L. euchaeta, feeding on the algae under different nutrient treatments. Ni assimilation efficiency generally increased with an increase of nutrient concentration in the algae. A significant positive-correlation was found between the Ni assimilation efficiencies of the copepods and the %intracellular Ni in the algal cells. However, ambient nutritional conditions had little effect on the physiological turnover rate constant of Ni by copepods. Thus, nutrient enrichment may lead to an increase in Ni uptake and transfer in marine plankton.