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To better understand the behavior of M50NiL steel under carburizing and nitriding duplex treatment, different carburizing temperatures (ranging from 890 to 980 °C) were used for the carburizing pretreatment. The surface microstructures were characterized by X-ray diffraction (XRD), laser scanning confocal microscopy, microhardness testing, scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The results indicate that the proportions of γ′ and large submicron precipitates increase with increasing carburizing temperature, which corresponds to an increase in large primary carbides. The increase in the number/size of large primary carbides promotes the diffusion of nitrogen. The resulting changes in the nanometric precipitates after nitriding lead to different levels of solid solution by nitrogen (reaching a maximum at a 920 °C carburizing pretreatment). The growth mechanism of the submicron precipitates is proposed. The effect of various precipitates and the diffusion behavior of C and solid solution of N on the hardening behavior are discussed.

Nup88 is overexpressed in a number of types of carcinomas and is associated with myometrial invasion, but its exact expression pattern in endometrial cancer and premalignant lesions is unknown.To evaluate the role of Nup88 in endometrial cancers and atypical endometrial hyperplasia and its clinicopathological significance.Nup88 expression was examined by immunohistochemistry in samples from 104 endometrial cancers, 21 atypical endometrial hyperplasia lesions, and 40 normal endometria. All samples were from patients who underwent surgery at the First Hospital of Hebei Medical University (Shijiazhuang, China) between April 2006 and December 2009. Nup88 expression was compared between the groups and associations were assessed between Nup88 and clinicopathological characteristics of the subjects.Nup88 expression in cancer (76% of samples) and atypical hyperplasia (91%) was significantly higher compared to normal endometrium (33%, both P0.001), but there was no significant difference between endometrial cancer and atypical hyperplasia (P=0.237). The expression of Nup88 increased significantly with increasing exposure time to estrogen (P=0.033).Nup88 may be related to the occurrence of endometrial cancers and premalignant lesions. Nup88 might be a useful biomarker for pre-malignant lesions and early-stage endometrial cancer.

This article reports the effect of pre-existing carbides prepared by different heat treatments on the nitriding behaviour during a carburizing and nitriding duplex treatment of an M50NiL steel. The goal was to achieve an improved understanding of the relationship between the pre-existing carbides and nitriding behaviour. The M50NiL steel was carburized at 950 °C, heat treated at different quenching temperatures (ranging from 1000 to 1150 °C) and tempering temperatures (ranging from 500 to 580 °C), and finally nitrided at 500 °C. The surface layers were characterized by means of X-ray diffraction (XRD), laser scanning confocal microscopy (LSCM), scanning electron microscopy (SEM), Vickers microhardness measurement and transmission electron microscopy (TEM). The results show that the formation of intergranular precipitates was greatly related to the presence of pre-existing carbides, which led to a change in the carbon content in the matrix and showed different dissolving capacities. The compound layers consisted of γ′ (Fe4N) and e (Fe2-3N) phases as well as a minor amount of Fe3O4. The pre-existing carbides had no effect on the composition of the compound layer. For the diffusion of nitrogen, a density of pre-existing carbides that was too high or too low was unfavorable, as it greatly decreased the thickness of the nitrided layer. At the quenching temperature of 1100 °C and the tempering temperature of 540 °C, the thickest nitrided layer herein and a good hardness distribution were obtained, which was attributed to the optimum density of pre-existing carbides. This study provides information regarding how to obtain a thick nitrided layer by controlling pre-existing carbides during the duplex treatment of M50NiL steels.

Background: Expression of the meningioma-associated protein (MAC30) was increased in several types of tumors, including esophageal, gastric and colon tumors, compared to normal tissue. MAC30 expression levels gradually increased from normal colorectal mucosa to primary colorectal cancer and colorectal cancer spreading to the lymph nodes. MAC30 expression was related to survival in patients with colorectal cancer. However, there is no study on MAC30 in oral squamous cell carcinoma (OSCC). Methods: Therefore, MAC30 expression in OSCC was investigated and possible associations of MAC30 expression with clinicopathological variables in OSCC have been analyzed. MAC30 expression was immunohistochemically examined in 20 normal oral mucosa and 43 OSCC specimens. Results: Expression levels of MAC30 in the cytoplasm markedly increased from normal oral epithelial cells to primary OSCC. Strong cytoplasmic staining was significantly higher in primary OSCC compared to normal oral mucosa samples (51 vs. 20%, p = 0.019). Furthermore, MAC30 expression levels in primary tumors of patients with lymph node metastasis exceeded levels in those without metastasis (65 vs. 35%, p = 0.048), and MAC30 expression in poorly differentiated tumors was higher than in well-differentiated ones (90 vs. 39%, p = 0.005). Conclusion: Overexpression of MAC30 in the cytoplasm of OSCC may predict nodal metastasis and poor differentiation. Original Publication:BY Yan, DW Wang, ZL Zhu, YH Yang, MW Wang, DS Cui, Hong Zhang and Xiao-Feng Sun, Overexpression of MAC30 in the Cytoplasm of Oral Squamous Cell Carcinoma Predicts Nodal Metastasis and Poor Differentiation, 2010, Chemotherapy, (56), 6, 424-428.http://dx.doi.org/10.1159/000317582Copyright: S. Karger AGhttp://www.karger.com/

FXYD3, interacting with Na+/K+-ATPase, is considered a cell surface regulator modulating the function of ion pumps and ion channels. The FXYD3 gene was originally cloned from murine mammary tumors and then from human breast tumors. However, no study of FXYD3 has been carried out in gliomas; therefore, we examined FXYD3 expression in gliomas and its clinicopathological significance. FXYD3 expression was immunohistochemically examined in 71 primary gliomas, along with 37 matched adjacent normal brain samples and 8 recurred gliomas. The frequency of strong FXYD3 expression was higher in the primary tumors in either unmatched (p = 0.046) or matched cases (p = 0.02), compared to normal brain tissue. FXYD3 expression was significantly more increased in females than males (p = 0.01), and in multiple site gliomas than single sites (p = 0.02). There was no difference of FXYD3 expression regarding age, tumor location, size, histological type, and tumor grade (p > 0.05). The results suggest that FXYD3 expression may be involved in glioma development, especially in multiple gliomas and female patients.

Objectives: Particularly interesting new cysteine-histidine-rich protein (PINCH), as a LIM domain adapter protein, functions in the integrin and growth factor signal transduction pathway, and is upregulated in tumor-associated stroma in several types of cancers. However, no study of PINCH has been carried out in gliomas, therefore we examined PINCH expression in gliomas and its clinicopathological significance. Methods: PINCH expression was immunohistochemically examined in 82 gliomas, along with 26 matched adjacent normal brain samples and 10 recurred gliomas. Results: PINCH was strongly expressed in the primary (35%, p = 0.0001) or recurred tumors (40%, p = 0.004) and weak in normal brain tissue. PINCH expression was significantly increased in high-grade gliomas (55 vs. 24%, high- vs. low-grade gliomas, p = 0.004). There was no association of PINCH expression with gender, age, tumor number, size, histological type and tumor location (p > 0.05). Conclusions: PINCH expression may be involved in glioma development and differentiation.

p33(ING1b), a newly discovered candidate tumor suppressor gene and a nuclear protein, belongs to the inhibitor of growth gene family. Previous studies have shown that p33(ING1b) is involved in the restriction of cell growth and proliferation, apoptosis, tumor anchorage-independent growth, cellular senescence, maintenance of genomic stability and modulation of cell cycle checkpoints. Loss of nuclear p33(ING1b) has been observed in melanoma, seminoma, papillary thyroid carcinoma, oral squamous cell carcinoma, breast ductal cancer and acute lymphoblastic leukemia. Inactivation and/or decreased expression of p33(ING1b) have been reported in various types of cancer, including head and neck squamous cell, breast, lung, stomach, blood and brain malignancies. Since little is known about the clinicopathological significance of p33(ING1b) in esophageal squamous cell carcinoma (ESCC), this study aimed to investigate the association of p33(ING1b) expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in patients with ESCC. p33(ING1b) expression was examined by immunohistochemistry in 20 normal esophageal mucosa and in 64 ESCC specimens. The results revealed that the positive expression of p33(ING1b) protein in normal squamous cells was localized in the nucleus alone and the positive rate was 95%, while in ESCCs, the positive expression was mainly in the cytoplasm, together with nuclear expression, and the positive rate was 36% (P

Objective.To investigate the association of FXYD-3 expression with clinicopathological variables and PINCH in patients with ESCC.Patients and Methods.Expression of FXYD-3 protein was immunohistochemically examined in normal esophageal mucous (n=20) and ESCC (n=64).Results.Expression of FXYD-3 in the cytoplasm markedly increased from normal esophageal epithelial cells to primary ESCC (P=0.001). The expression of FXYD-3 was correlated with TNM stages and depth of tumor invasion. Furthermore, the cases with lymph node metastasis tended to show a higher frequency of positive expression than those without metastasis (P=0.086), and FXYD-3 expression tended to be positively related to the expression of PINCH (P=0.063). Moreover, the cases positive for both proteins had the highest frequency of lymph node metastasis (P=0.001). However, FXYD-3 expression was not correlated with patient’s gender (P=0.847), age (P=0.876), tumor location (P=0.279), size (P=0.7710.771), grade of differentiation (P=0.279), and survival (P=0.113).Conclusion.Overexpression of FXYD-3 in the cytoplasm may play an important role in the tumorigenesis and development in the human ESCC, particularly in combination with PINCH expression.

Objective: Particularly interesting new cysteine-histidine rich protein (PINCH) is an important component of the local adhesion complexes and upregulated in several types of malignancies, and involved in the incidence and development of tumours. PINCH expression is also independently correlated with poorer survival in patients with colorectal cancer. However, there is no study of PINCH in gastric cancer, therefore, the aim of this project was to investigate PINCH expression and its clinicopathological significance in gastric adenocarcinoma.Patients and methods: PINCH expression was immunohistochemically examined in normal gastric mucous (n= 30) and gastric adenocarcinoma (n= 73), from gastric cancer patients.Results: PINCH expression in the associated-stroma of gastric cancers was heterogeneous, and its positive rate (75%) was higher than that of normal gastric mucosa (43%,X2= 9.711,p= 0.002). The stronger staining was observed at the invasive edge of tumour when compared to the inner area of tumour. The rate of positive PINCH (88%) in the cases with lymph node metastasis was higher than that (52%) in the cases without metastasis (X2= 11.151,p= 0.001). PINCH expression was not correlated with patients’ gender, age, tumour size, differentiation and invasion depth (p> 0.05).Comclusion: PINCH protein might play an important role in the tumourigenesis and metastasis of gastric adenocarcinoma.

To study the protective effect of carbon monoxide (CO) inhalation on the serious limb ischemia/reperfusion (I/R) injury, and which effects caused to shock in rats.36 SD rats were randomly divided into I/R, I/R + CO (RC), sham operation (S) groups. I/R injury models were made by the occlusion of the femoral artery for 8 h and the reperfusion for 12 h, 10 d. Before reperfusion of 2 h, RC group started to breathe medical air containing CO (the volume fraction of CO: 0.075%) continuously, until after reperfusion for 4 h, a total of inhalation 6 h. S, I/R groups exposed to air, breathe freely. Caudal artery pressures (CAP), ten days survival rate, serum lactate dehydrogenase (LDH) and creatine kinase (CK) activity, limb wet - to - dry weight ratio (W/D) and the pathologic changes of limb were observed.Once the reperfusion started, the CAP decreased rapidly in I/R group, and the mean reduced to(5.3259 +/- 0.3832) kPa when reperfusion for 8 h. Compared to I/R group, the CAP decreased slower and smaller in RC group, moreover, its mean reduced to (8.3300 +/- 0.4224) kPa when reperfusion for 8 h. The 10 d survival rate in I/R group was that 8 rats died all between reperfusion for 13 - 20 h. Only 1 rat died in RC group and the other 7 rats were still alive when reperfusion for 10 d. Compared to I/R group, the pathological features of the ischemic limb were significant ly improved, and the figures of W/D, serum LDH and CK value were remarkable lower in RC group (P0.05).Inhaling exogenous low-dose CO has a reverse regulation in the blood pressure decline caused by serious limb I/R injury in rats. And at the same time, it can effectively prevent the occurrence of shock, reduce physical damage, significantly increase the survival rate of animals.

To investigate the protective effect of exogenous carbon monoxide (CO) on the liver injury induced by ischemia/reperfusion (I/R) of hind limbs in rats.100 SD rats were divided randomly into sham operated group (S), S+ CO group (SC), I/R group (I/R), I/ R+ CO group (RC). A rat model of ischemia in hind limbs and the reperfusion liver injury was established with the occlusion of the femoral arteries for 4 h and re-opening for 6 - 72 h, 10 d. The rats in SC and RC groups were exposed to air containing CO (the volume traction of CO: 0.05%) for 2 h before and after reperfusion or the corresponding control time point, while the other two groups were exposed to the routine air. The pathologic changes of liver tissue were morphologically observed by HE stain. Serum GPT activity was tested by Automatic Biochemical Analyzer. The percentage of apoptosis, expression levels of bax and bcl-2 protein in liver tissue were detected by Flow Cytometry.There was no difference between S and SC groups. Compared with SC group: (1) Pathological changes in liver tissue were significant in I/R and RC groups. (2) The serum GPT activity of I/R and RC groups was obviously increased. (3) In IR and RC groups, the percentage of apoptosis in liver tissue was all significantly increased. (4) The bax expression level was significantly increased. Compared RC group with I/R group: (1) Pathological change was slight. (2) The serum GPT activity was depressed. (3) The percentage of apoptosis and expression level of bax protein in liver tissue were depressed. (4) The expression level of bcl-2 protein in liver tissue was increased.Exogenous CO could attenuate liver tissue injury induced by limbs I/R in rats.

To study the protective effect of carbon monoxide(CO) inhalation in the limb ischemia/reperfusion (I/R) injury of rats.Forty-four Sprague-Dawley rats were randomly divided into three groups: S, I/R and RC groups. I/R injury model was made by the occlusion of the femoral artery for four hours and the reperfusion for forty-eight hours. RC group was exposed to medical air mixed CO (the volume fraction of CO: 0.05%) during limb reperfusion in rats. The other two groups were exposed to the routine air. Gross morphology of the ischemic limb, wet-to-dry weight ratio (W/D), and skeletal muscle histopathology were observed. The apoptosis index and expression levels of Bax and Bcl-2 in the muscle were assessed with Flow Cytometry. The activities of serum lactate dehydrogenase (LDH) and creatine kinase (CK) were tested by Automatic Biochemical Analyzer.Compared to I/R group, W/D, serum LDH and CK activities, the apoptosis index and Bax expression level in the muscle were all significantly decreased, the Bcl-2 expression level was significantly increased, gross morphology of the ischemic limb and muscle histopathology were obviously improved in RC group.Inhaling exogenous CO can attenuate limb I/R injury.

Background: Particularly interesting new cysteine-histidine rich protein ( PINCH), as an adapter protein of the LIM family for signal transduction in the integrin and growth factor pathway, is upregulated in the stroma of several common types of cancers and involved in promoting tumor progression. In the present study, we examined PINCH expression in normal endometrium, atypical endometrial hyperplasia and endometrioid carcinoma, and further studied the relationships of PINCH expression with clinicopathological variables in cancer patients. Methods: PINCH expression was examined by immunohistochemistry in 23 normal endometrial samples, 18 atypical endometrial hyperplasias and 48 endometrioid endometrial carcinomas. Results: The PINCH expression in the stroma of cancer (71%) was significantly increased compared to either normal endometrium (17%, p andlt; 0.0001) or atypical hyperplasia (39%, p = 0.017), along with 9 cancers that had stronger PINCH expressions at the invasive margin of the cancers compared to the inner cancers. PINCH expression in cancer was higher in the patients with hypertension (p = 0.041) and estrogen exposure time andgt;30 years (p = 0.021). On the other hand, PINCH expression was not related to menopausal status, gravid status, blood sugar/lipid, family background of cancer, histological grade, myometrial invasion, cervical involvement, lymph nodal metastases, growth pattern, estrogen and progestogen receptors (p andgt; 0.05). Conclusion: The results suggest that PINCH seems to play a role, presently unknown, in the tumorigenesis and development of endometrial cancer that merits further study. Original Publication:Hong-Zhen Zhang, Xue-Hui Li, Xia Zhang, Zhi-Yong Zhang, Ya-Li Meng, Shu-Wen Xu, Yan Zheng, Zhen-Long Zhu, Dong-Sheng Cui, Li-Xia Huang, Bao-Yong Yan and Xiao-Feng Sun, PINCH Protein Expression in Normal Endometrium, Atypical Endometrial Hyperplasia and Endometrioid Endometrial Carcinoma, 2010, CHEMOTHERAPY, (56), 4, 291-297.http://dx.doi.org/10.1159/000319953Copyright: S. Karger AGhttp://www.karger.com/

Particularly interesting new cysteine-histidine rich protein (PINCH), as a newly discovered protein of LIM family members, may play a role in signal transduction of integrin and growth factor, and involved in the incidence and development of tumors. PINCH protein is overexpressed in tumor-associated stroma of several types of tumors. However, there is no study of the PINCH in esophageal cancer, therefore we investigated PINCH expression in esophageal squamous cell carcinomas and its clinicopathogical significance in the patients. PINCH expression was immunohistochemically examined in 20 normal esophageal samples and 64 esophageal squamous cell carcinomas. The results showed that PINCH expression in the stroma of cancers was heterogeneous, and its positive rate (56%) was higher than that of normal esophageal mucosa (5%, p0.05). The results suggest that PINCH protein may be a marker of tumor associated-stroma involving tumor development, and predicting the ability of invasion and metastasis of esophageal squamous cell carcinoma. Original publication: Zhenlong Zhu, Yanhong Yang, Yu Zhang, Zhengmin Wang, Dongsheng Cui, Jinting Zhang, Mingwei Wang and Xiao-Feng Sun, PINCH expression and its significance in esophageal squamous cell carcinoma, 2008, Disease Markers, (25), 2, 75-80.http://iospress.metapress.com/content/j38j327k266413x5/. Copyright: IOS Press., http://iospress.metapress.com/

p33(ING1b), as a candidate tumour suppressor gene, has been found to be expressed a proportion of oral squamous cell carcinomas (OSCCs), however, its clinicopathological significance is not studied yet. Our aim was to investigate association of p33(ING1b) expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in OSCCs.p33(ING1b) expression was immunohistochemically examined in 20 normal oral mucosa specimens and 49 OSCCs.Normal squamous cells showed only p33(ING1b )nuclear expression (no cytoplasmic expression), with a rate of 90% positive cases. While 24% of OSCCs appeared cytoplasmic expression (11 of them with weak nuclear staining) and the rest tumours (76%) were negative for p33(ING1b). Furthermore, the cases having lymph node metastasis showed a higher frequency of positive cytoplasmic expression than those without metastasis (P = 0.03). The p33(ING1b) cytoplasmic expression was positively related to PINCH expression (P = 0.04), the cases positive for both proteins had a high rate of the metastasis (P = 0.03).The transfer of p33(ING1b) protein from the nucleus to the cytoplasm may result in loss of normal cellular function of the protein, which might play a role in the tumourigenesis and metastasis of OSCCs.

Particularly interesting new cysteine-histidine rich protein (PINCH), an adapter protein involved in integrin and growth factor signalling, is up-regulated in the stroma of colorectal, breast, prostate, lung and skin cancer. Strong stromal immunostaining for PINCH is an independent prognostic indicator for reduced survival in colorectal cancer, suggesting that PINCH is involved in the signalling that promotes tumour progression. Since no study on PINCH has been carried out in oral squamous cell carcinoma (OSCC), this study aimed to determine PINCH expression in OSCC and its clinicopathological significance. PINCH protein expression was examined by immunohistochemistry in 20 normal oral mucosa and in 57 OSCC specimens. The frequency of strong PINCH immunostaining was higher in tumour-associated stroma of OSCC (37%) as compared to normal oral mucosa (10%) (p=0.02). Strong PINCH stromal immunostaining predicted nodal metastasis: 19/26 (73%) OSCC cases with nodal metastasis had strong PINCH immunostaining compared to 9/31 (29%) cases without nodal metastasis (p=0.02). The PINCH expression in OSCC was more intense in stroma at the invasive edge than in intratumoural stroma. In conclusion, the up-regulation of PINCH protein in stroma may be involved in promoting invasion and metastasis in OSCC.

Aim: To study the expression of cyclooxygenase-2 (COX-2) in human gastric cancer tissues and their paired adjacent mucosa, as well as mucosa from gastric antrum and corpus of the first-degree relatives of the recruited cancer patients. Methods: The expression of COX-2 mRNA in 38 patients with gastric cancer and their 29 first-degree relatives and 18 healthy controls was assessed by the real time RT-PCR. The expression of COX-2 protein was determined by Western blot. Results: A marked increase in COX-2 mRNA expression was found in 20 of 37 (54%) cancerous tissues compared to their respective paired normal mucosa (P, published_or_final_version

To evaluate whether celecoxib, a selective cyclooxygenase 2 (COX-2) inhibitor, could reduce the severity of gastric precancerous lesions following Helicobacter pylori (H pylori) eradication.H pylori-eradicated patients with gastric precancerous lesions randomly received either celecoxib (n = 30) or placebo (n = 30) for up to 3 mo. COX-2 expression and activity was determined by immunostaining and prostaglandin E(2) (PGE(2)) assay, cell proliferation by Ki-67 immunostaining, apoptosis by TUNEL staining and angiogenesis by microvascular density (MVD) assay using CD31 staining.COX-2 protein expression was significantly increased in gastric precancerous lesions (atrophy, intestinal metaplasia and dysplasia, respectively) compared with chronic gastritis, and was concomitant with an increase in cell proliferation and angiogenesis. A significant improvement in precancerous lesions was observed in patients who received celecoxib compared with those who received placebo (P0.001). Of these three changes, 84.6% of sites with dysplasia regressed in patients treated with celecoxib (P = 0.002) compared with 60% in the placebo group, suggesting that celecoxib was effective on the regression of dysplasia. COX-2 protein expression (P0.001) and COX-2 activity (P0.001) in the gastric tissues were consistently lower in celecoxib-treated patients compared with the placebo-treated subjects. Moreover, it was also shown that celecoxib suppressed cell proliferation (P0.01), induced cell apoptosis (P0.01) and inhibited angiogenesis with decreased MVD (P0.001). However, all of these effects were not seen in placebo-treated subjects. Furthermore, COX-2 inhibition resulted in the up-regulation of PPARgamma expression, a protective molecule with anti-neoplastic effects.H pylori eradication therapy followed by celecoxib treatment improves gastric precancerous lesions by inhibiting COX-2 activity, inducing apoptosis, and suppressing cell proliferation and angiogenesis.