The prognostic values of estimating intraperitoneal pressure in the occurrence of abdominal wall complications in peritoneal dialysis patients.

BACKGROUND: Increased intraperitoneal pressure is associated with abdominal wall complications and technical failure of peritoneal dialysis (PD). Several equations have been developed to estimate intraperitoneal pressure. We aimed to assess the prognostic yield of the intraperitoneal pressure as estimated by current equations on the occurrence of abdominal wall complications in peritoneal dialysis patients. METHODS: This is a retrospective analysis of data from a prospective cohort which recruited 1207 incident PD patients. Estimated intraperitoneal pressure was calculated using four available equations (according to Sigogne, Castellanos, Scanziani and de Jesus Ventura). Abdominal wall complications were recorded during follow-up. Univariate analysis and multivariate analysis with competing risk regression were used to assess the predictive power of the estimates of intraperitoneal pressure in the occurrence of abdominal wall complications. RESULTS: During a median follow-up of 30 months, 66 (5.5%) patients (1.6/100 patient-years) developed abdominal wall complications. The median time to the occurrence of abdominal wall complications was 5.7 months. Only the estimated intraperitoneal pressure by the de Jesus Ventura equation significantly predicted abdominal wall complications by using univariate analyses. Associations between estimated intraperitoneal pressure by the de Jesus Ventura equation and the occurrence of abdominal wall complications disappeared after adjusting for significant clinical factors. CONCLUSIONS: We verified the prognostic value of estimation of intraperitoneal pressure by four available equations in predicting abdominal wall complications in our single-center PD cohort. Due to a low diagnostic yield, a novel equation for estimating the intraperitoneal pressure is urgently needed.

Novel equations for estimating intraperitoneal pressure among peritoneal dialysis patients.

Background: Increased intraperitoneal pressure (IPP) is associated with abdominal wall complications and technical failure in peritoneal dialysis (PD). Since the standard measurement of IPP is limited due to its cumbersome procedures, we aimed to develop and validate equations for estimating IPP. Methods: We performed a cross-sectional study with a total of 200 prevalent PD patients who were divided into development and validation datasets after random sampling matched by body mass index. The IPPs were measured using the Durand method, with whole-body and abdominal anthropometry indices collected. Equations with 2.0-L and 1.5-L fill volumes were generated by stepwise linear regression modelling. The bias, accuracy and precision of the estimated IPP (eIPP) with 2-L and 1.5-L fill volumes were compared with actual IPPs by the Durand method. The eIPP for the 2-L fill volume was also compared with other existing equations. Results: Two new equations incorporating waist circumference and height from the decubitus plane to mid-axillary line were generated. The eIPPs exhibited small biases in relation to the Durand method , with median differences of -0.24 cmH2O and -0.10 cmH2O for 2 L and 1.5 L, respectively. The precisions evaluated by the standard deviation of the absolute value of the differences were 2.59 cmH2O and 2.50 cmH2O, respectively. The accuracies evaluated by the value of the percentage of estimates that differed by >20% for the eIPP were 26% for 2.0 L and 27% for 1.5 L. Better bias, precision and accuracy were observed for the eIPP equation compared with other existing equations for the 2.0-L fill volume. Conclusions: We provided two new equations developed from abdominal anthropometry indices to accurately estimate the IPP in the PD population.

Coagulation Dysfunction in Patients with Liver Cirrhosis and Splenomegaly and Its Countermeasures: A Retrospective Study of 1522 Patients.

Objective: Patients with cirrhosis and splenomegaly often have coagulation dysfunction which affects treatment and prognosis. This study explores the status, grading, and treatment strategies of coagulation dysfunction in patients with liver cirrhosis and splenomegaly. Methods: A retrospective cohort study was conducted on the clinical data on consecutive patients with cirrhosis and splenomegaly treated at Hainan General Hospital, China, from January 2000 to December 2020. Starting research in January 2022. Results: Among 1522 patients included into this study, 297 (19.5%) patients had normal results in all five coagulation tests (prothrombin time, prothrombin activity, activated partial thromboplastin time, thrombin time, and fibrinogen), and 1225 (80.5%) had coagulation dysfunction in at least one of these tests. There were significant differences (P < 0.05) in treatment efficacy on these patients for three of these five coagulation tests, with the exception of prothrombin activity and thrombin time. When coagulation dysfunction was classified into grades I, II, and III based on scores from the three significant coagulation tests, prothrombin time, activated partial thromboplastin time, and fibrinogen, significant differences in surgical outcomes were found among the three grades of coagulation dysfunction and between grades I and III (P < 0.05). The operative mortality rate in patients with grade III in treating liver cancer, portal hypersplenism, and/or splenomegaly was 6.5%. There was no significant difference between patients with grades I and II (P > 0.05). Conclusions: Approximately, 80% of patients with liver cirrhosis and splenomegaly had coagulation dysfunction. Surgery is feasible for grade I and II patients. For grade III patients, nonsurgical treatment should be given first, and surgery should only be considered when the coagulation function returns to normal or near-normal levels after treatment. This trial is registered with MR-46-22-009299.

Establishment and characterization of a multi-drug resistant cell line for canine mammary tumors.

Background and purpose: Canine mammary tumors are the most common tumor disease of female dogs, and adjuvant chemotherapy often results in multi-drug resistance. Currently, the mechanisms underlying the development of tumor multi-drug resistance are unclear. The translation of research applications that can be used to effectively overcome tumor resistance is similarly hampered. Therefore, it is urgent to construct multi-drug resistance models of canine mammary tumors that can be used for research, to explore the mechanisms and means of overcoming resistance. Materials and methods: In this study, the canine triple negative breast cancer cell line CMT-7364 was induced to develop multidrug resistance using doxorubicin by high-dose drug pulse method. The drug resistance and the expression of drug transport pumps of the cells was verified by CCK8 assay, immunoblotting, qPCR and immunofluorescence. Next, we used scratch assay and Transwell invasion assay to compare the migration and invasion abilities of the two cell lines and examined the expression of EMT-related proteins in both using immunoblotting. The differences of transcriptome between parental and drug-resistant cell lines were detected by RNA-seq sequencing. Finally, mouse xenograft models of drug-resistant and parental cell lines were constructed to evaluate the tumorigenic ability. Results: After more than 50 generations of continuous passages stimulated by high-dose drug pulse method, the morphology of drug-resistant cell line CMT-7364/R tended to be mesenchymal-like and heterogeneous under light microscopy compared with the parental cell line CMT-7364/S, and developed resistance to doxorubicin and other commonly used chemotherapeutic drugs. In CMT-7364/R, BCRP was expressed at higher levels at both transcriptional and protein levels, while P-glycoprotein was not significantly different. Secondly, the migration and invasion ability of CMT-7364/R was significantly enhanced, with decreased expression of E-cadherin and increased expression of vimentin and mucin 1-N terminus. Finally, mouse xenograft models were constructed, while there was no significant difference in the volume of masses formed at 21 days. Conclusion: In summary, by using the canine mammary tumor cell line CMT-7364/S as the parental cell line, we successfully constructed a multidrug-resistant CMT-7364/R with high-dose drug pulse methods. Compared to its parental cell line, CMT-7364/R has decreased growth rate, overexpression of BCRP and increased migration and invasion ability due to EMT. The results of this study showed that CMT-7364/R might serve as a model for future studies on tumor drug resistance.

Tetramethylpyrazine-Rhein Derivative inhibits the migration of canine inflammatory mammary carcinoma cells by mitochondrial damage-mediated apoptosis and cadherins downregulation.

BACKGROUND: Canine inflammatory mammary carcinoma (CIMC) has a high incidence of metastasis, high lethality, and poor prognosis, which needs novel adjuvant agents. Tetramethylpyrazine-Rhein Derivative (TRD) has been shown to have antitumor activity, which is a potential research direction for CIMC. PURPOSE: This study evaluated the efficacy of TRD on CIMC in vitro and in vivo, and provided possibilities for the application of active compounds in traditional Chinese medicine. METHODS: In vitro, TRD cytotoxicity was measured with CCK-8. Flow cytometry and transmission electron microscope were used to detect the cell cycle, cell death, and changes in mitochondria. Wound-healing assay, cell invasion assay, and scanning electron microscope were used to evaluate the suppression of cell migration and invasion. Expression changes were detected by RT-qPCR and western blot assay. In vivo, the lung metastasis models were randomly divided into control, low-dose TRD, high-dose TRD, and positive groups. Each group was administered orally once a day for 18 days and took in vivo imaging photos. RESULTS: The IC50 of TRD in CHMp and MDCK were 42.59 and 79.37 µM, respectively. TRD mediated cell apoptosis by mitochondrial damage and caused S and G2/M phase arrest by downregulating cyclin B1. Moreover, TRD reduced filopodia and inhibited cell migration by downregulating cadherins. In CIMC lung metastasis models, TRD could effectively inhibit tumor growth (P < 0.001) in the lungs without significant toxicity. CONCLUSION: TRD showed potential activity to inhibit CIMC lung metastasis with multi-target and low toxicity.

Comparison of tumor-derived total RNA and cell lysate on antitumor immune activity.

Tumor-derived total RNA (TdRNA) and cell lysate (TCL), with almost all the relevant tumor antigens, represent attractive alternative sources of antigens in antitumor immunotherapy. However, the comparison of their capacity to elicit immune responses against breast cancer is still lacking. In this study, the antitumor immune effects of TdRNA and TCL were systematically compared. We isolated TdRNA and TCL from 4T1 mouse breast cancer cells, and found that both sources of antigens could stimulate the maturation of dendritic cells (DCs) at the cellular and in vivo levels, and induce robust cellular immune responses, as evidenced by the increased percentages of both CD4+ and CD8+ T cells in the inguinal lymph nodes and spleen. But TdRNA performed stronger immunoactivities than TCL on the increase of T cell population through DCs activation. Additionally, the synergistic antitumor efficacy of paclitaxel (PTX) with TdRNA and TCL respectively was further evaluated in the murine 4T1 tumor model. Compared with TCL, TdRNA could inhibit tumor growth more effectively with low systemic toxicity when combined with PTX, which was, at least in part, attributable to the improvement of systemic immune function and tumor immune infiltration. Overall, TdRNA outperforms TCL in antitumor immunity, and is expected to be a promising candidate for application as the source of tumor antigens.

Establishment of stable expression of firefly luciferase and EGFP in a canine inflammatory mammary carcinoma cell line and tumor-bearing model in nude mice.

Canine inflammatory mammary carcinoma (CIMC) is a type of canine malignant mammary tumor with a poor prognosis and high mortality. We transduced firefly luciferase and enhanced green fluorescent protein (EGFP) into CHMp, a CIMC cell line, and established CHMp-Luc-EGFP cells. We investigated the characteristics of this cell line in vitro and in vivo. CHMp-Luc-EGFP was passaged continuously 75 times, with stable expression of luciferase and EGFP. Compared with the wild-type, CHMp-Luc-EGFP had similar proliferation, metastasis, histopathology characteristics, and expression of E-cadherin, N-cadherin, and Ki-67. A tumor-bearing model was established by implantation of CHMp-Luc-EGFP cells, and the dynamic changes of tumors were visualized and quantified using the IVIS imaging system. In summary, the cell line we established could reflect the biological characteristics of CHMp cells, visualize the tumor progression in vivo, and provide a powerful tool for the study of CIMC.

Cryotherapy mediates histopathological and microstructural changes during the treatment of skin and subcutaneous tumors in dogs.

The therapeutic effects of cryotherapy on skin and subcutaneous tumors in dogs were retrospectively studied in 20 dogs with 37 tumor lesions, of which 30 were benign and seven were malignant. Our results showed that during follow-up, 94.5% of lesions were completely exfoliated, without relapse or metastasis (mean time = 245.7 days). To investigate the effects of cryotherapy, we compared histopathological observations and microstructural changes in healthy tissues and tumor tissues, before and after cryotherapy. After cryotherapy, both normal skin and tumor tissue exhibited edema and hyperemia, with inflammatory cell infiltration. The cell nuclei exhibited pyknosis, disintegration and necrosis, and tight junctions were decreased in size. Cell morphology was varied, along with fragmented cell nuclear envelopes, crenulated nuclei and indistinct and necrotic intracellular organelles. Vacuoles were apparent in the cytoplasm and intercellular desmosomes were absent. These observations suggested that cryosurgery inhibited skin and subcutaneous tumors via cold-induced injury to cells, and cellular microenvironment changes induced by apoptosis. The results suggested that cryosurgery prevented skin and subcutaneous tumors via cold-induced injury to cells, and cellular microenvironment changes induced by apoptosis. We believe these data will provide general cryotherapy guidance to scientists and veterinary surgeons.

Flavone protects HBE cells from DNA double-strand breaks caused by PM2.5.

Ambient air particulate matter 2.5 (PM2.5) contains many harmful components that can enter the circulatory system and produce reactive oxygen species (ROS) in body. Oxidative stress and DNA damage induced by ROS may affect any cellular macromolecule and lead to DNA double-strand breaks (DSBs). Flavonoids, widely distributed in some herbs and berries, have been proved having anti-oxidative or anti-cancer efficacy. In this study, we investigated whether Flavone, a kind of flavonoids, can protect human bronchial epithelial cells (HBE) from DSBs caused by PM2.5 and how this function is probably implemented. We found that cells exposed to PM2.5 obviously induced viability inhibition, DNA damage and part of apoptosis. However, Flavone treatment prior to PM2.5 apparently improved cell viability, and mitigated the formation of 8-hydroxy-2-deoxyguanosine, the expression of DNA damage-relative protein and cell apoptosis. Our studies demonstrated that PM2.5 induced oxidative DSBs while Flavone ameliorated the DNA damage and increased cell viability probably through influencing DNA repair mechanism of cells.

Peripheral blood cell variations in cirrhotic portal hypertension patients with hypersplenism.

OBJECTIVE: To explore peripheral blood cell variations in hepatic cirrhosis portal hypertension patients with hypersplenism. METHODS: Clinical data of 322 hypersplenism patients with decreased peripheral blood cells, admitted with cirrhotic portal hypertension, was retrospectively studied over the last 17 years. RESULTS: In 64% (206/322) of patients, more than 2 kinds of blood cell were decreased, including 89 cases of pancytopenia (43.2%), 52 cases of WBC + PLT decrease (25.2%), 29 cases of RBC + PLT decrease (14.1%), and 36 cases of WBC + RBC decrease (17.5%); in 36% (116/322) of patients, single type blood cell decrease occurred, including 31 cases of PLT decrease (26.7%), 29 cases of WBC decrease (25%) and 56 cases of RBC decrease (48.3%). Of 227 routine bone marrow examinations, bone marrow hyperplasia was observed in 118 cases (52.0%), the remainder showed no hyperplasia. For the distinct scope and extent of peripheralblood cell decreases, preoperative blood component transfusions were carried out, then treated by surgery, after whole group splenectomy, the peripheral blood cell count was significantly higher (P<0.05). CONCLUSIONS: Of portal hypertensive patients with splenomegaly and hypersplenism, 64% have simultaneous decrease in various blood cells, 36% have decrease in single type blood cells, 52% of patients have bone marrow hyperplasia. A splenectomy can significantly increase the reduction of peripheral blood cells.

Human gastrin-releasing peptide triggers growth of HepG2 cells through blocking endoplasmic reticulum stress-mediated apoptosis.

Gastrin-releasing peptide (GRP) is a kind of neural peptide that plays an important role in the growth of various human cancer cells. However, very little is known about the relationship between GRP and apoptosis in human hepatocellular carcinoma cells. This study investigated the influences of GRP on apoptosis, as well as the mechanism that triggers HepG2 growth. The effects of GRP on cell proliferation were examined by analysis of lactate dehydrogenase. The GRP, caspase 12, and CHOP protein were detected in HepG2 and HL-7702 cells by Western blot, and endoplasmic reticulum (ER) stress-related mRNA transcription was detected by reverse transcription polymerase chain reaction. To explore the specific pathway by which GRP induces the cell growth, we investigated the apoptosis-related pathway. The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription. Three main ER stress-unfolded protein response pathway proteins, including spliced XBP1, cleaved ATF6, IRE1-α, PERK, and eIF2-α, were increased significantly. Furthermore, the cleaved caspase 12 activation was blocked and CHOP expression was inhibited when GRP was expressed either in HepG2 or HL-7702 cells. In conclusion, GRP triggers the growth of HepG2 cells through blocking the ER stress-mediated pathway.

Treatment of malignant melanoma by downregulation of XIAP and overexpression of TRAIL with a conditionally replicating oncolytic adenovirus.

BACKGROUND AND AIM: Currently available systemic therapies for malignant melanoma produce low response rates in patients, and more effective treatment modalities are clearly needed. The tumor necrosis factor (TNF)- related apoptosis-inducing ligand has a significant impact on therapy for patients with X-linked inhibitor of apoptosis protein-downregulation malignant melanoma. The primary objective of this study was to assess its therapeutic potential. MATERIALS AND METHODS: We employed a conditionally replicating oncolytic adenoviral vector, named CRAd5.TRAIL/siXIAP, with the characteristics of over-expression of the therapeutic gene TRAIL and downregulation of XIAP in one vector. B16F10-luc cells were employed to detect anti-tumor activity of CRAd5.TRAIL/siXIAP in vitro and in vivo. RESULTS: CRAd5.TRAIL/siXIAP enhanced caspase-8 activation and caspase-3 maturation in B16F10 cells in vitro. Furthermore, it more effectively infected and killed melanoma cells in vitro and in vivo than other adenoviruses. CONCLUSION: Taken together, the combination of upregulation of TRAIL and downregulation of siXIAP with one oncolytic adenoviral vector holds promise for development of an effective therapy for melanomas and other common cancers.

Gemcitabine resistance induced by interaction between alternatively spliced segment of tenascin-C and annexin A2 in pancreatic cancer cells.

Pancreatic cancer is the fourth leading cause of cancer-related death in the western countries and it is resistant to almost all cytotoxic drugs. In the current study, we explored the gemcitabine resistance induced by the interaction between Annexin A2 (ANXA2) and alternatively spliced segment of tenascin-C (TNfnA-D). In the pancreatic cancer cell culture system in vitro, it was proved that exogenous recombinant TNfnA-D combined with the cell surface ANXA2 specifically and their interaction suppressed gemcitabine-induced cytotoxicity on pancreatic cancer cells in a dose-dependent manner. Meanwhile, the TNfnA-D/ANXA2 interaction increased the phosphorylation of phosphatidylinositol 3-kinase (PI3K), Akt, inhibitory kappaB (IkappaB) kinase alpha/beta (IKKalpha/beta), IkappaBalpha, and p65 nuclear factor-kappaB (NF-kappaB) significantly. Inhibition of Akt and PI3K with their specific inhibitors partially reversed the suppression of gemcitabine-induced cytotoxicity elicited by TNfnA-D/ANXA2 interaction. Activation of p65 NF-kappaB was dependent on the phosphorylation of PI3K/Akt. The phosphorylated IKKalpha/beta induced the phosphorylation and degradation of IkappaBalpha, the sequential phosphorylation, nuclear translocation and activation of p65 NF-kappaB. Pyrrolidine dithiocarbamate (PDTC) effectively blocked the activity of p65 NF-kappaB in response to TNfnA-D. Down-regulation of p65 NF-kappaB with its specific small interfering RNA (siRNA) restored the gemcitabine-induced cytotoxicity suppressed by TNfnA-D/ANXA2 interaction. For the first time, this study show that ANXA2/TNfnA-D interaction induced gemcitabine resistance via the canonical PI3K/Akt/NF-kappaB signaling pathways in pancreatic cancer cells. Therefore, therapy targeting ANXA2/TNfnA-D and/or p65 NF-kappaB may have potential clinical application for patients with pancreatic cancers.

Gastrin-releasing peptide promotes the growth of HepG2 cells via EGFR-independent ERK1/2 activation.

Gastrin-releasing peptide (GRP) plays an important role in regulating tumor growth and migration. However, little is known about its role in human hepatocellular carcinoma (HCC) cells. This study explored the effect of GRP on the growth of HCC HepG2 cells and the underlying mechanisms. Expression of GRP and its cognate receptor (GRPR) were detected by immunocytochemisty, reverse transcription-PCR and Western blotting and compared between two human HCC cell lines (HepG2 and MHCC97H) and a normal hepatic cell line (HL-7702). The effects of GRP on cell proliferation and signaling pathways were examined by Western blotting, MTT assay and flow cytometry. Both GRP and GRPR were overexpressed in HepG2 and MHCC97H cells. GRP activated MAPK/ERK1/2 in HepG2 cells, leading to enhanced proliferation, reduced apoptosis and accelerated cell cycle progression. The effect of GRP on ERK1/2 was effectively attenuated by the GRPR antagonist PD176252 or MEK inhibitor U0126, but not by the TNF-alpha protease inhibitor TAPI-1 or the EGFR tyrosine kinase inhibitor PD153035. The effect of GRP on the growth of HepG2 cells was significantly attenuated by PD176252 or U0126. GRP serves as a mitogen for HepG2 and MHCC97H cells. GRP promotes the growth of HepG2 cells through interaction with GRPR co-expressed in tumor cells, and subsequently activates MAPK/ERK1/2 via EGFR-independent mechanisms.

Gastrin-releasing peptide links stressor to cancer progression.

INTRODUCTION: Gastrin-releasing peptide (GRP) plays an important role in cancer growth and metastasis; however, the mechanisms of how GRP affects cancer progression are not well understood. Recent studies revealed that chronic stress is a major risk factor for cancer progression, and this effect may be mediated by GRP. In this review, we will discuss the mechanisms and implications of GRP linking stressor to cancer progression. MATERIALS AND METHODS: We retrieved the studies of the relationship between GRP, stress and cancers through PubMed using systematic methods to search, select, and evaluate the findings. RESULTS: The results suggested that GRP can mediate the effects of stress on cancers at systemic, tissue and cellular levels: Stress elicits the secretion of GRP in the brain and GRP in turn activates the stress response pathways resulting in an elevation of stress hormones and GRP in the plasma and tissues. GRP in synergy with stress hormones stimulates the growth and invasion of cancer cells by suppressing the anti-tumor immune function and directly activating the pro-proliferative and pro-migratory signaling pathways in cancer cells. CONCLUSION: GRP is a multi-functional peptide, which acts as a stress mediator as well as a growth factor linking stressor to cancer progression. GRP and its high-affinity receptor are useful targets for the diagnosis and treatment of cancers.

The mitogenic effectors of isoproterenol in human hepatocellular carcinoma cells.

Increasing data indicate that stress hormones and their corresponding receptors play an important role in the carcinogenesis and progression of hepatocellular carcinoma (HCC). However, there is presently no study investigating the influence of stress hormones in correlation with beta2-AR on human HCC cells. We examined the expression of alpha1- and beta-ARs in human HCC cell line HepG2 and MHCC97H cells in comparison with that in human normal hepatic cell line HL-7702 cells (L-02), and the influence of isoproterenol (ISO) on the growth of these HCC cells using blocking agents in correlation with beta2-AR and its downstream signaling pathways. We found that alpha1-AR was down-regulated and beta2-AR was up-regulated in HepG2 and MHCC97H cells. ISO dose-dependently promoted the growth of both HepG2 and MHCC97H cells. ISO-induced growth and survival of HCC cells were effectively attenuated by ICI 118551, U0126 and PD153035, but not by H-89 or LY294002. ISO transiently activated MAPK/ERK1/2 in tumor cells which could be blocked either by ICI 118551 or U0126, but not by H-89, LY294002, or PD153035. These findings indicate that ISO mimicking a mitogen promoted the growth of HepG2 and MHCC97H cells via beta2-AR-mediated activation of both MAPK/ERK1/2 dependent and independent signaling pathways, and ISO activated MAPK/ERK1/2 by an EGFR-independent mechanism.

[Historical review of Portal Hypertension].

It has been more than 100 years since the nomenclature Portal Hypertension was put forward, during which the treatment of Portal Hypertension in medical circles experienced a gradual perfection. Reviewing the developmental progress can help to improve the treatment of Portal Hypertension.

Distinct effect of Chrysanthemum indicum Linné extracts on isoproterenol-induced growth of human hepatocellular carcinoma cells.

Chrysanthemum indicum Linné (Asteraceae) is a common Chinese herbal medicine that has been traditionally used for the treatment of inflammation, hypertension and neoplastic diseases in China. However, the mechanism that account for the inhibitory activity of Chrysanthemum indicum Linné against cancer cells is poorly understood. We investigated the effect of Chrysanthemum indicum Linné extracts (CILE) on isoproterenol (ISO) induced growth of human hepatocellar carcinoma (HCC) cells in correlation with the intracellular activity of MAPK/ERK1/2. We found that CILE was effective in attenuating the mitogenic effect of ISO on both HepG2 and MHCC97H cells. The inhibitory effect of CILE was mediated by inhibiting the ISO-induced activation of MAPK/ERK1/2 via beta2-AR in tumor cells. Our findings will be helpful in understanding the anticancer mechanism of CILE.

[Retrospecting the history of intestinal obstructions].

Intestinal obstruction is one of the common and frequently encountered diseases, the treatment of which has a long and tortuous history with a set of valid therapeutic methods accumulated. When a large segment of necrotic intestine, for instance, is to be removed, how do you maintain the patient's nutrition to protect his/her health. The effect of transplant of intestine for a critical intestinal case is even worse than that of the kidney, liver transplants. To solve this problem demands long and indefatigable endeavor. The goal of this article is to review its history, so as to explore the way of thinking and shed some light on its future studies.