BRAF mutant colorectal cancer cells mediate local immunosuppressive microenvironment through exosomal long noncoding RNAs.

Background: BRAF mutated colorectal cancer (CRC) is prone to peritoneal and distant lymph node metastasis and this correlates with a poor prognosis. The BRAF mutation is closely related to the formation of an immunosuppressive microenvironment. However, the correlation between BRAF mutation and changes in local immune microenvironment of CRC is not clear.

A nomogram model for predicting prognosis of obstructive colorectal cancer.

Background: The prognosis of obstructive colorectal cancer (oCRC) is worse than that of nonobstructive colorectal cancer. However, no previous study has established an individualized prediction model for the prognosis of patients with oCRC. We aimed to screen the factors that affect the prognosis of oCRC and to use these findings to establish a nomogram model that predicts the individual prognosis of patients with oCRC.

Gegen Qinlian decoction enhances immunity and protects intestinal barrier function in colorectal cancer patients gut microbiota.

Background: We previously showed, using the Traditional Chinese Medicine System Pharmacology Database, that Gegen Qinlian decoction (GQD) had a direct antitumor effect, and was combined with programmed cell death protein (PD)-1 inhibitors to treat microsatellite stable (MSS) tumor-bearing mice. However, the effect of GQD on patients with colorectal cancer (CRC) is not clear.

Aim: To determine the therapeutic mechanism of GQD in improving immune function, reducing inflammation and protecting intestinal barrier function.

Effects of PHA-665752 and Cetuximab Combination Treatment on In Vitro and Murine Xenograft Growth of Human Colorectal Cancer Cells with KRAS or BRAF Mutations.

Background: It remains unknown whether blockade of c-Met signaling and epidermal growth factor receptor signaling is effective in suppressing the growth of human colorectal cancer (CRC) cells. In this study, we investigated the effects of the c-Met inhibitor PHA-665752 alone and in combination with cetuximab on the growth of human CRC cells in vitro and in mouse xenografts.

Methods: Human CRC cell lines (Caco2, HCT-116, and HT-29) and mice bearing HCT-116 xenografts were treated with cetuximab in the absence or presence of PHA-665752.

Absence of NF-κB subunit p50 ameliorates cold immobilization stress-induced gastric ulcers.

Stress ulcers are a common complication in critically ill patients, but the underlying mechanism is little known. This study characterized the function of the p50 subunit of NF-κB in an experimental model of cold immobilization stress-induced gastric ulcers. Stress-induced gastric mucosal inflammation and gastric injury were examined in wild-type and NF-κB p50-deficient mice.

[Role of angiotensin II type 1 receptor in activation of nuclear factor-kappaB and activator protein-1 in lung of mice with acute lung injury].

Objective: To explore the role of angiotensin II type 1 (AT1) receptor in activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) in lung of mice with LPS-induced acute lung injury (ALI).

Methods: Eighty-eight BABL/c mice were divided into control group (n = 8), LPS group (n = 40), and LPS + AT1 receptor antagonist ZD7155 group (n = 40) according to the random number table. Puncture of trachea was done in all mice.

Notoginsenoside R1 attenuates renal ischemia-reperfusion injury in rats.

Ischemia-reperfusion (I/R) injury of the kidney is a complex pathophysiological process and a major cause of acute renal failure. It has been shown that I/R injury is related to inflammatory responses and activation of apoptotic pathways. Inhibition of certain elements of inflammatory responses and apoptotic pathway seemed to ameliorate renal I/R injury.

Angiotensin II type-1 receptor antagonist attenuates LPS-induced acute lung injury.

Angiotensin II is able to trigger inflammatory responses through an angiotensin II type 1 (AT1) receptor. The role of AT1 receptor in acute lung injury (ALI) is poorly understood. Mice were randomly divided into three groups (n=40 each groups): NS group; LPS group (2mg/kg LPS intratracheally); and LPS+ZD 7155 group, 10mg/kg ZD 7155 (an AT1 receptor antagonist) intraperitoneally 30 min prior to LPS exposure.

[Endostar reduces the growth and metastasis by inhibiting angiogenesis and lymphangiogenesis in nude mouse models of human cervical cancer].

Objective: To observe the influence of endostar alone or in combination with cisplatin on tumor growth and metastasis, as well as the inhibition of angiogenesis and lymphangiogenesis in nude mouse models of human cervical cancer.

Methods: HeLa cells were inoculated subcutaneously into the hind flank region of female nu/mice to establish xenograft models. The nude mice were randomly divided into 5 groups: (1) sodium chloride (as control); (2) cisplatin alone; (3) endostar alone; (4) cisplatin plus endostar (10 mg/kg); (5) cisplatin plus endostar (20 mg/kg).

Tec kinase mediating IL-8 transcription in monocytes stimulated with LPS.

The purpose of present study was to explore the possibility of Tec kinase as a mediator for IL-8 transcription in monocytes stimulated with LPS. Plasmids of mouse Tec kinase IV or Tec kinase IV with inactivating point mutations generated with QuikChange site-directed mutagenesis were co-transfected with IL-8 promoter driven luciferase construct into RAW264.7 cells, then luciferase activity was measured with a luminometer.

Angiotensin II induces type I collagen gene expression in human dermal fibroblasts through an AP-1/TGF-beta1-dependent pathway.

Angiotensin II is critically involved in skin wound healing, but the underlying mechanism remains unclear. This study investigated the effect of angiotensin II on type I collagen gene activation in human dermal fibroblasts and the possible mechanism involved. Angiotensin II stimulated the mRNA and protein expression of type I collagen and TGF-beta1.

The direct hospitalisation costs of paediatric scalds: 2-year results of a prospective case series.

Objective: To reveal the characteristic and distribution of length of hospital stay (LOS) and direct hospitalisation costs of paediatric scald.

Methods: A prospective case series observation was performed from January 2005 to December 2006 at the Burn Center, Changhai Hospital, Shanghai, China. The information, such as demographics, clinical diagnosis and treatments since admission, of the paediatric scald patients included in the series was recorded.

Epidemiology of pediatric burns requiring hospitalization in China: a literature review of retrospective studies.

Objective: This review was an effort to systematically examine the nationwide data available on pediatric burns requiring hospitalization to reveal burn epidemiology and guide future education and prevention.

Methods: The China Biomedical Disk Database, Chongqing VIP Database, and China Journal Full-Text Database were searched for articles reporting data on children and their burns from January 2000 through December 2005. Studies were included that systematically investigated the epidemiology of pediatric burns requiring hospitalization in China.

Activation of p38 MAPK by reactive oxygen species is essential in a rat model of stress-induced gastric mucosal injury.

Stress ulceration is a common complication in critically ill patients and can result in significant upper gastrointestinal bleeding associated with a high morbidity and mortality. At present, little is known of the molecular mechanisms underlying the incidence of this type of gastric damage. In the present study, we investigated the temporal activation of the redox-sensitive p38 signaling transduction cascade and its roles in a well-defined experimental model of cold immobilization stress-induced gastric ulceration.

Inhibition of p38 mitogen-activated protein kinase attenuates experimental autoimmune hepatitis: involvement of nuclear factor kappa B.

Aim: To investigate the role of p38 mitogen-activated protein kinase (p38MAPK) in murine experimental autoimmune hepatitis (EAH).

Methods: To induce EAH, the syngeneic S-100 antigen emulsified in complete Freud's adjuvant was injected intraperitoneally into adult male C57Bl/6 mice. Liver injury was assessed by serum ALT and liver histology.

Sustained activation of nuclear factor-kappaB by reactive oxygen species is involved in the pathogenesis of stress-induced gastric damage in rats.

Objective: Stress ulceration is a common complication in critically ill patients, but the mechanisms involved are poorly understood. In this study we investigated the temporal activation of the redox-sensitive transcription factor nuclear factor-kappaB and its roles in an experimental model of cold immobilization stress-induced gastric mucosal lesions.

Design: Prospective, controlled, and randomized animal study.

[Activation of nuclear factor-kappaB signaling pathway in rat gastric mucosa during stress ulceration].

Objective: To investigate the time course of nuclear factor-kappaB (NF-kappaB) activation in the process of stress ulcer formation.

Methods: Model of stress ulcer was reproduced by subjecting male Sprague-Dawley rats to water-immersion restraint (WIR) stress. At indicated time after the beginning of WIR stress, animals were sacrificed and cytoplasmic and nuclear protein and total RNA were prepared from gastric corpus mucosal tissues.

Dynamic changes of mitogen-activated protein kinase signal transduction in rats with severe acute pancreatitis.

Objective: To investigate the dynamic changes of mitogen-activated protein kinase (MAPK) signal transduction in rats with severe acute pancreatitis (SAP).

Methods: The SAP model was induced by infusing the bilio-pancreatic duct of 56 Sprague-Dawley rats with 5% sterile sodium taurocholate solution. The rats were randomly divided into seven groups: control group, 0.

Expression of vascular endothelial growth factor-C and the relationship between lymphangiogenesis and lymphatic metastasis in colorectal cancer.

Aim: To investigate the expression of vascular endothelial growth factor-C (VEGF-C) and the relationship between VEGF-C and lymphangiogenesis, lymph node metastasis in colorectal cancer.

Methods: Fifty six cases of colorectal cancer were selected randomly. Expression of VEGF-C was detected by immunohistochemistry, and lymphatic vessels were stained by enzyme histochemical method.