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Accumulating evidence suggested that the irreversible tyrosine kinase inhibitors (TKIs) have potential to override the acquired resistance to target-based therapies. Herein, we reported IC-4 as a novel irreversible TKI for epidermal growth factor receptor (EGFR). IC-4 potentially suppressed proliferation, induced apoptosis and a G2/M cell cycle arrest in breast cancer cells, correlating with inhibition of EGF-induced EGFR activation, but independent of DNA damage. In addition, IC-4 exhibited anti-angiogenetic activities both in vitro and in vivo. It suppressed cell viability and proliferation induced by various growth factors in human umbilical vein endothelial cells (HUVECs). IC-4 also inhibited HUVECs migration and tube formation. In transgenic zebrafish embryo model, IC-4 was shown to suppress formation of intersegmental vessel and development of subintestinal vessels. Taken together, these results demonstrated that IC-4 is a new irreversible EGFR-TKI, exhibiting potent anti-breast cancer and anti-angiogenetic effects.

Triterpenoids isolated from Ganoderma lucidum are a class of naturally occurring compounds and structurally highly oxidized lanostanes. Accumulated data show that triterpenoids exhibit a broad spectrum of anti-cancer properties, including anti-proliferative, anti-metastatic and anti-angiogenic activities. A systematic summary and knowledge of future prospects are necessary to facilitate further studies on this species.This review aims to summarize and analyze the current knowledge on the anti-cancer properties and mechanisms of G. lucidum triterpenoids (GLTs) and discuss the future prospects of the application of GLTs in cancer treatment.Extensive research over the last 10 years has provided evidence of the anti-cancer activities of GLTs in different stages of carcinogenesis. These activities include cell cycle arrest, induction of apoptosis and autophagy, and suppression of metastasis and angiogenesis. However, the exact molecular mechanisms involved in these processes remain unclear. Androgen receptor, nuclear factor-kappa B, activator protein-1, p53 and 14-3-3 are reportedly involved in the anti-cancer properties of GLTs. Animal models further shed light on the development of GLTs as anti-cancer agents. However, more research and clinical trials are necessary to exploit these compounds.

Solasodine, a steroidal alkaloid isolated from solanaceous species, exhibits anticancer activities on several cell lines. This study aimed to explore the antitumor potential of solasodine on ovarian cancer cells. The MTT assay, lactate dehydrogenase release assay, Hoechst 33342 staining, 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine staining assay, and Annexin V/PI assay were conducted to investigate the antiproliferation and apoptosis-inducing effects of solasodine. Monodansylcadaverine staining was performed to label the acidic puncta on ovarian cancer HEY cells. A wound healing assay and Transwell assay were carried out to determine whether solasodine elicits an antimetastatic effect on HEY cells. A gelatin zymography assay was applied to detect the enzymatic activities of matrix metalloproteinases. Western blot was employed to examine relevant protein expression. Results revealed that solasodine inhibited cell viabilities in a time- and dose-dependent manner, triggered apoptotic body formation, reduced cell mitochondrial membrane potential, and interfered with autolysosome degradation in ovarian cancer cells. Solasodine also suppressed the migration and invasion of HEY cells by downregulating matrix metalloproteinase expression and activities. This study could be used as a basis for further studies on the molecular mechanisms of the antiproliferation, apoptosis-inducing, autophagy-modifying, and antimetastatic activities of solasodine.

Ganoderma lucidum (Fr.) Karst is a traditional Chinese herb that has been widely used for centuries to treat various diseases including cancer. Herein, an ethanol-soluble and acidic component (ESAC), which mainly contains triterpenes, was prepared from G. lucidum and its anti-tumor effects in vitro were tested on human breast cancer cells. Our results showed that ESAC reduced the cell viability of MCF-7 and MDA-MB-231 cells in a concentration-dependent manner with IC50 of about 100 μg/mL and 60 μg/mL, respectively. DNA damage was detected by Comet assay and the increased expression of γ-H2AX after ESAC treatment was determined in MCF-7 cells. Moreover, ESAC effectively mediated G1 cell cycle arrest in both concentration- and time-dependent manners and induced apoptosis as determined by Hoechst staining, DNA fragment assay and Western blot analysis in MCF-7 cells. In conclusion, ESAC exerts anti-proliferation effects by inducing DNA damage, G1 cell cycle arrest and apoptosis in human breast cancer cells.

Background Platycodin D (PD), a triterpenoid saponin isolated from the Chinese medicinal herb Platycodonis radix, possesses anti-cancer effects in several cancer cell lines. The aim of this study was to evaluate its anti- cancer activities in hepatocellular carcinoma cells. Materials and methods MTT and colony formation assays were performed to evaluate cell proliferation, along with flow cytometry and Western blotting for apoptosis. Cell adhesion was tested by observing cellular morphology under a microscope, while the transwell assay was employed to investigate the cell migration and invasion. Results PD concentration-dependently inhibited cell proliferation in both HepG2 and Hep3B cells, and significantly suppressed colony formation and induced apoptosis in HepG2 cells. The protein levels of cleaved poly ADP-ribose polymerase (PARP) and Bax were up-regulated while that of survivin was down-regulated after treatment with PD. Moreover, PD not only obviously suppressed the adhesion of HepG2 cells to Matrigel, but also remarkably depressed their migration and invasion induced by 12-O-tetradecanoylphorbol 13-acetate (TPA). Conclusions PD presents anti-cancer potential in hepatocellular carcinoma cells via inducing apoptosis, and inhibiting cell adhesion, migration and invasion, indicating promising features as a lead compound for anti-cancer agent development.

In this study we aimed to assess the feasibility and safety of fast-track surgery (FTS) combined with laparoscopy for treating patients with rectal cancer and compare the results with those of the conventional perioperative intervention group.A total of 120 patients with rectal cancer were prospectively randomly assigned to the FTS combined with laparoscopy group and the conventional perioperative intervention plus laparoscopy group from November 2011 to November 2012. All patients received radical anterior resection with total mesorectal excision. Their baseline characteristics and the perioperative outcomes were recorded for analyses.Compared with the conventional perioperative intervention group, the fast-track protocol combined with laparoscopy could shorten the time to the first flatus (53.44 ± 23.64 h vs 67.85 ± 20.12 h, P = 0.001) and first defecation (65.23 ± 22.24 h vs 86.98 ± 24.85 h, P = 0.000) after operation, accelerate the decrease of white blood cell count (P 0.05), inhibit body temperature augmentation (P 0.05) and reduce postoperative complication rate (16.9% vs 3.5%, P = 0.030). In addition, the length of postoperative stay was also shortened (5.05 ± 1.38 days vs 6.98 ± 2.26 days, P = 0.000). The medical cost of hospitalization was also reduced in the FTS group.FTS in combination with laparoscopy may accelerate the clinical recovery of patients with rectal cancer after surgery.

To evaluate the effect of health education on prevention from schistosome infection in engineering construction workers in Poyang Lake area.The workers for constructing "De Chang" highway in Poyang Lake area were divided randomly into an experiment group and a control group, "health education + protective skill training" was carried out in the experiment group, whereas, no intervention was implemented in the control group.In the experiment group, the awareness rates of schistosomiasis control knowledge were 7.96% and 96.39% before and after the intervention, respectively; the rates of contacting infested water were 100% and 1.77% pre- and post-intervention, respectively; the work protective rates increased from zero before the intervention to 100% after the intervention; there was no person infected with schistosome after the intervention. However, in the control group, all the indexes above-mentioned had no significant changes.The intervention model "health education + protective skill training", can effectively prevent from schistosome infection in engineering construction workers in Poyang Lake area.

Furanodiene (FUR) is a natural terpenoid isolated from Rhizoma Curcumae, a well-known Chinese medicinal herb that presents anti-proliferative activities in several cancer cell lines. Herein, we systematically investigated the effects of FUR on the significant processes of tumor progression with the relatively low concentrations in 95-D lung cancer cells. FUR concentration-dependently inhibited cell proliferation and blocked the cell cycle progressions in G1 phase by down-regulating the protein levels of cyclin D1 and CDK6, and up-regulating those of p21 and p27 in 95-D cells. FUR also affected the signaling molecules that regulate apoptosis in 95-D cells revealed by the down-regulation of the protein levels of full PARP, pro-caspase-7, survivin, and Bcl-2, and the up-regulation of cleaved PARP. Further studies showed that FUR enhanced the expression of light chain 3-II (LC3-II) in the protein level, indicating that autophagy is involved in this process. Besides, the adhesion ability of 95-D cells to matrigel and fibronectin was slightly inhibited after FUR treatment for 1 h in our experimental condition. FUR also slightly suppressed cell migration and invasion in 95-D cells according to the data from wound healing and Transwell assays, respectively. Taken together, FUR activated the signal molecules regulating G1 cell cycle arrest, apoptosis and autophagy, while slightly affecting the key steps of cell metastasis in 95-D lung cancer cells in the relatively low concentrations.

Celastrol is one of the principal active ingredients of Tripterygium wilfordii Hook.f., a toxic Chinese medical herb traditionally prescribed for controlling pain and inhibiting inflammation in various chronic inflammatory diseases, including rheumatoid arthritis (RA). Resistance to apoptosis of fibroblast-like synoviocytes is considered a major characteristic of RA. In this study, we test celastrol's cytotoxic effect and potential mechanisms in human rheumatoid synovial fibroblasts (RA-FLS). In the cytotoxic assay, we found that celastrol dose-dependently decreased RA-FLS viability and increased LDH release. The apoptotic nuclear morphology was observed after celastrol treatment as determined by DAPI fluorescence staining. Flow cytometry analysis with PI and Annexin V revealed that celastrol induced RA-FLS cell cycle arrest in the G2/M phase and apoptosis. Furthermore, celastrol dramatically increased expression of Bax/Bcl-2, proteolytic cleavage of Caspase-3, -9, PARP, and decreased expression of FasR. In addition, celastrol treatment resulted in DNA damage. Collectively, we concluded that celastrol inhibits RA-FLS proliferation by inducing DNA damage, cell cycle arrest, and apoptosis in vitro, which might provide data for its application in RA treatment.

Oridonin, a natural tetracycline diterpenoid isolated from Chinese herb Rabdosia rubescens, has been reported to be a potent cytotoxic agent against a wide variety of tumors. However, its effect on highly metastatic breast cancer cells has not been addressed. In this study, we investigated the effects of oridonin on growth, migration and invasion of highly-metastatic human breast cancer cells. Our results showed that oridonin induced potent growth inhibition on human breast cancer cells MCF-7 and MDA-MB-231 in a time- and dose-dependent manner. According to the flow cytometric analysis, oridonin suppressed MCF-7 cell growth by cell cycle arrest at the G2/M phase and caused accumulation of MDA-MB-231 cells in the Sub-G1 phase. The induced apoptotic effect of oridonin was further confirmed by a morphologic characteristics assay and TUNEL assay. Oridonin triggered the reduction of Bcl-2/Bax ratio, caspase-8, NF-κB (p65), IKKα, IKKβ, phospho-mTOR, and increased expression level of cleaved PARP, Fas and PPARγ in a time-dependent manner. Immunofluorescent analysis showed that γH2AX-containing nuclear foci were significant in oridonin-treated MDA-MB-231 cells. Meanwhile, oridonin significantly suppressed MDA-MB-231 cell migration and invasion, decreased MMP-2/MMP-9 activation and inhibited the expression of Integrin β1 and FAK. In conclusion, oridonin inhibited the growth and induced apoptosis in breast cancer cells, which might be related to DNA damage and activation of intrinsic or extrinsic apoptotic pathways. Moreover, oridonin also inhibited tumor invasion and metastasis in vitro possibly via decreasing the expression of MMPs and regulating the Integrin β1/FAK pathway in MDA-MB-231 cells.

To investigate the effect of hepatocyte growth factor (HGF) and transforming growth factor-β(1) (TGFβ(1)) on the expression of α-smooth muscle actin (α-SMA) and collagen I in human atrial fibroblast in vitro, and to explore the possible molecular mechanism of atrial fibrosis in patients with atrial fibrillation (AF).Human atrial fibroblast, isolated from aseptic right atrial appendage tissues of 10 sinus rhythm (SR) and 10 chronic atrial fibrillation (CAF) patients, were cultured with HGF and TGFβ(1). mRNA expressions of collagen I and α-SMA were detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), the protein expression of α-SMA was determined by immunofluorescence and Western blot.(1) Compared with SR group, left atrium was significantly dilated in CAF group (t = 2.692, P0.05), the mRNA expression of collagen I and α-SMA of atrial fibroblasts were significantly upregulated (all P0.01), mRNA expression of collagen I was positively correlated with left atrial dimension (LAD) (r = 0.836, P = 0.014), AF duration (r = 0.739, P = 0.045) and α-SMA mRNA level (r = 0.886, P = 0.012). (2) Compared with SR group, the expression of α-SMA protein in CAF atrial fibroblasts were significantly increased (P0.01). (3) TGFβ(1) further stimulated while HGF significantly attenuated the expression of collagen I and α-SMA in CAF atrial fibroblasts (all P0.01).Increasing expression of collagen I and α-SMA in human atrial fibroblasts might promote atria remodeling leading to the development and sustaining of AF. HGF is involved in the negative regulation on the expression of α-SMA and collagen I.

Cell adhesion, migration and invasion are critical steps for carcinogenesis and cancer metastasis. Ganoderma lucidum, also called Lingzhi in China, is a traditional Chinese medicine, which exhibits anti-proliferation, anti-inflammation and anti-metastasis properties. Herein, GAEE, G. lucidum extract mainly contains ganoderiol A (GA), dihydrogenated GA and GA isomer, was shown to inhibit the abilities of adhesion and migration, while have a slight influence on that of invasion in highly metastatic breast cancer MDA-MB-231 cells at non-toxic doses. Further investigation revealed that GAEE decreased the active forms of focal adhesion kinase (FAK) and disrupted the interaction between FAK and SRC, which lead to deactivating of paxillin. Moreover, GAEE treatment downregulated the expressions of RhoA, Rac1, and Cdc42, and decreased the interaction between neural Wiskott-Aldrich Syndrome protein (N-WASP) and Cdc42, which impair cell migration and actin assembly. To our knowledge, this is the first report to show that G.lucidum triterpenoids could suppress cell migration and adhesion through FAK-SRC-paxillin signaling pathway. Our study also suggests that GAEE may be a potential agent for treatment of breast cancer.

The E2F1 transcription factor is a well known regulator of cell proliferation and apoptosis, but its role in response to DNA damage is less clear. 8-Chloro-adenosine (8-Cl-Ado), a nucleoside analog, can inhibit proliferation in a variety of human tumor cells. However, it is still elusive how the agent acts on tumors. Here we show that A549 and H1299 cells formed DNA double-strand breaks after 8-Cl-Ado exposure, accompanied by E2F1 upregulation at protein level. Overexpressed wild-type (E2F1-wt) colocalized with double-strand break marker γ-H2AX and promoted G2/M arrest in 8-Cl-Ado-exposed A549 and H1299, while expressed S31A mutant of E2F1 (E2F1-mu) significantly reduced ability to accumulate at sites of DNA damage and G2/M arrest, suggesting that E2F1 is required for activating G2/M checkpoint pathway upon DNA damage. Transfection of either E2F1-wt or E2F1-mu plasmid promoted apoptosis in 8-Cl-Ado-exposed cells, indicating that 8-Cl-Ado may induce apoptosis in E2F1-dependent and E2F1-independent ways. These findings demonstrate that E2F1 plays a crucial role in 8-Cl-Ado-induced G2/M arrest but is dispensable for 8-Cl-Ado-induced apoptosis. These data also suggest that the mechanism of 8-Cl-Ado action is complicated.

Background Dihydroartemisinin (DHA) exhibits potent anti-malarial and anti-cancer activities. This study aimed to investigate the anti-proliferative effects of a combination of DHA and doxorubicin (DOX) on human breast cancer cells. Methods MTT assay and the combination index (CI) were used to show the anti-proliferative effects and calculate the synergism potential, respectively. Flow cytometry assay was used to detect apoptosis and the intracellular accumulation of DOX. JC-1 staining was used to determine the mitochondrial membrane potential. Western blot analysis was used to detect the protein expression of some apoptosis-related molecules. Results Asynergistic anti-proliferative effect was found, and the enhanced anti-cancer activity was observed to be accompanied by the prompt onset of apoptosis in MCF-7 cells. The combinative treatment remarkably decreased the mitochondrial membrane potential and activated caspase cascades more than the mono-treatment. Pretreatment with DHAalso did not influence the accumulation of DOX in MCF-7 cells. Conclusion This study presented a new opportunity to enhance the effectiveness of future treatment regimens of breast cancer using DOX.

Ganoderic acid DM (GADM) is a triterpenoid isolated from Ganoderma lucidum, a well-known edible medicinal mushroom. In the present study, we found that GADM effectively inhibited cell proliferation and colony formation in MCF-7 human breast cancer cells, which was much stronger than that of MDA-MB-231 breast cancer cells. GADM both concentration- and time-dependently mediated G1 cell cycle arrest and significantly decreased the protein level of CDK2, CDK6, cycle D1, p-Rb and c-Myc in MCF-7 cells. Moreover, GADM obviously induced DNA fragmentation and cleavage of PARP which are the characteristics of apoptosis and decreased the mitochondrial membrane potential in MCF-7 cells. Besides, we also showed that GADM elicited DNA damage as measured by comet assay which is a sensitive method for DNA damage detection. γ-H2AX, a marker of DNA damage, was also slightly up-regulated after treated with GADM for 6h, suggesting that the G1 cell cycle arrest and apoptosis induced by GADM may be partially resulted from GADM-induced DNA damage. These results have advanced our current understandings of the anti-cancer mechanisms of GADM.

This study explored the anatomic relationship of the popliteus complex (PC) and collected anatomic data of PC in a Chinese population. The anatomic study was performed using 81 formalin-fixed knees. The femoral attachment of the popliteus tendon could be classified into three types with respect to femoral attachment of the lateral collateral ligament. The popliteofibular ligament presented as ligament (87.7%) or fascia (12.3%), originating from the musculotendinous junction of the popliteus muscle or just proximal to it. Given the great variability of the posterolateral structures, reconstructive surgeons should design a method based on individual anatomic features, rather than a fixed reconstructive surgery.

To explore the anatomic features of the fabella and its relationship with the common peroneal nerve and the fabellofibular ligament, so as to provide anatomical evidence for clinical diagnosis and treatment of fabella diseases in a Chinese population. Sixty-one formalin-fixed knee specimens were obtained for anatomic dissection. Structural features of the fabella were investigated by radiological and histological tests. There were 53 cases (86.89%) with fabellae in the lateral head of the gastrocnemius muscle, including 34 bony ones (55.74%), whereas only 6 cases had fabellae in the medial head (9.84%). The fabellae were accompanied by common peroneal nerves on their surfaces in 11 cases (20.8%), and the presence of the fabella was not generally predictive of a fabellofibular ligament. As much as 57.9% of the cartilage fabellae were not visualized on radiograph. The structure of the ossified fabella is similar to a typical long bone. Fabellae were mainly present in the lateral head of the gastrocnemius muscle in a large proportion of the Chinese population. More than half of the cartilage fabellae were not visualized on radiograph. Its clinical significance could not be ignored by physicians and anatomists.

In order to determine the curative effect of small dose heparin for treatment of chronic idiopathic thrombocytopenic purpura (CITP), a total of 12 CITP patients, who were failed with prednisone and immunosuppressants over 6 months, had been treated with subcutaneous injection of small dose heparin. The curative effects were seen in 8 patients and there were no exacerbation of hemorrhage during the therapy. The results showed that it is effective and safe to use this treatment for CITP.

Cucurbitacins are a class of triterpenoids widely distributed in plant kingdom with potent anti-cancer activities both in vitro and in vivo by inducing cycle arrest, autophagy, and apoptosis. Cucurbitacin B (Cuc B), could induce S or G2/M cell cycle arrest in cancer cells while the detailed mechanisms remain to be clear. This study was designed to precisely dissect the signaling pathway(s) responsible for Cuc B induced cell cycle arrest in human lung adenocarcinoma epithelial A549 cells. We demonstrated that low concentrations of Cuc B dramatically induced G2/M phase arrest in A549 cells. Cuc B treatment caused DNA double-strand breaks (DSBs) without affecting the signal transducer and activator of transcription 3 (STAT3), the potential molecular target for Cuc B. Cuc B triggers ATM-activated Chk1-Cdc25C-Cdk1, which could be reversed by both ATM siRNA and Chk1 siRNA. Cuc B also triggers ATM-activated p53-14-3-3-σ pathways, which could be reversed by ATM siRNA. Cuc B treatment also led to increased intracellular reactive oxygen species (ROS) formation, which was inhibited by N-acetyl-l-cysteine (NAC) pretreatment. Furthermore, NAC pretreatment inhibited Cuc B induced DNA damage and G2/M phase arrest. Taken together, these results suggested that Cuc B induces DNA damage in A549 cells mediated by increasing intracellular ROS formation, which lead to G2/M cell phase arrest through ATM-activated Chk1-Cdc25C-Cdk1 and p53-14-3-3-σ parallel branches. These observations provide novel mechanisms and potential targets for better understanding of the anti-cancer mechanisms of cucurbitacins.

To investigate the role of interleukin (IL)-17 in small bowel allograft rejection.We detected the expression of helper T cell 17 (Th17) cells in biopsy specimens from 3 cases of living small bowel transplantation in our department through immunofluorescence stain. We then established a rat heterotopic small bowel transplantation model. The rats were sacrificed on the 1(st), 2(nd), 3(rd), 5(th), and 7(th) d after small bowel transplantation. The degrees of transplantation rejection in rat intestine graft were examined through hematoxylin eosin (HE) stain, and the expression of Th17 cells in rat intestine graft were detected through immunofluorescence stain. In addition, the recipient rats undergoing intestinal transplantation were administrated with mouse-anti-rat IL-17 monoclonal antibody (mAb), and the survival of rats was analyzed. The recipient rats which received mouse-anti-rat IL-17 mAb treatment were sacrificed on the 1(st), 2(nd), 3(rd), 5(th), and 7(th) d after small bowel transplantation. The degrees of transplantation rejection and the expression of Th17 cells in rat intestine graft were detected through HE and immunofluorescence stain. The expression of IL-17, IL-1β, tumor necroses factor receptor-α (TNF-α), IL-6, and IL-8 in the intestine graft or serum were also detected.The expressions of Th17 cells ran parallel with the degree of acute rejection in human intestine grafts. The intestine graft rejection of rats was aggravated with prolonged duration after intestinal transplantation, and the expressions of Th17 cells were also correlated with the degree of acute rejection in rat intestine grafts. Administration of mouse-anti-rat IL-17 mAb prolonged the survival of rats after small bowel transplantation (P0.001). Furthermore, we found that the administration of mouse-anti-rat IL-17 mAb significantly decreased the intensity of CD4+IL-17+ Th17 cells in intestine grafts on the 2(nd), 3(rd), 5(th), and the 7(th) d (97.22 ± 4.05 vs 12.45 ± 2.02 on the 7(th) d, P0.0001), and suppressed the severity of acute rejection. The expression of IL-17 in the intestine graft declined after mouse-anti-rat IL-17 mAb administration on the 2(nd), 3(rd), 5(th), and the 7(th) d (0.88 ± 0.03 vs 0.35 ± 0.02 on the 7(th) d, P0.0001). We also detected the IL-17 serum level and found that the IL-17 level reduced from the 1(st) d to the 7(th) d (6.52 ± 0.18 ng/mL vs 2.04 ± 0.15 ng/mL on the 7(th) d, P0.0001). No significant difference in the level of IL-17 mRNA in the intestine graft was identified between the two groups. The levels of IL-1β, TNF-α, IL-6, and IL-8 mRNA in the intestine graft after the administration of mouse-anti-rat IL-17 mAb were also tested. We found that on the 3(rd), 5(th), and 7(th) d after intestinal transplantation, administration of mouse-anti-rat IL-17 mAb significantly inhibited the levels of IL-1β (12.11 ± 1.16 vs 1.27 ± 0.15 on the 7(th) d, P0.001), TNF-α (27.37 ± 2.60 vs 1.06 ± 0.26 on the 7(th) d, P0.001), IL-6 (21.43 ± 1.79 vs 1.90 ± 0.32 on the 7(th) d, P0.001), and IL-8 (20.44 ± 1.44 vs 1.34 ± 0.20 on the 7(th) d, P0.001) mRNA in the intestine graft.IL-17 may act as a promising and potent target for inhibiting acute rejection after small bowel transplantation.

AIM: To assess the impact of fast-track surgery (FTS) on hospital stay, cost of hospitalization and complications after radical total gastrectomy. METHODS: A randomized, controlled clinical trial was conducted from November 2011 to August 2012 in the Department of Digestive Surgery, Xijing Hospital of Digestive Diseases, the Fourth Military Medical University. A total of 122 gastric cancer patients who met the selection criteria were randomized into FTS and conventional care groups on the first day of hospitalization. All patients received elective standard D2 total gastrectomy. Clinical outcomes, including duration of flatus and defecation, white blood cell count, postoperative pain, duration of postoperative stay, cost of hospitalization and complications were recorded and evaluated. Two specially trained doctors who were blinded to the treatment were in charge of evaluating postoperative outcomes, discharge and follow-up. RESULTS: A total of 119 patients finished the study, including 60 patients in the conventional care group and 59 patients in the FTS group. Two patients were excluded from the FTS group due to withdrawal of consent. One patient was excluded from the conventional care group because of a non-resectable tumor. Compared with the conventional group, FTS shortened the duration of flatus (79.03 ± 20.26 h vs 60.97 ± 24.40 h, P = 0.000) and duration of defecation (93.03 ± 27.95 h vs 68.00 ± 25.42 h, P = 0.000), accelerated the decrease in white blood cell count [P < 0.05 on postoperative day (POD) 3 and 4], alleviated pain in patients after surgery (P < 0.05 on POD 1, 2 and 3), reduced complications (P < 0.05), shortened the duration of postoperative stay (7.10 ± 2.13 d vs 5.68 ± 1.22 d, P = 0.000), reduced the cost of hospitalization (43783.25 ± 8102.36 RMB vs 39597.62 ± 7529.98 RMB, P = 0.005), and promoted recovery of patients. CONCLUSION: FTS could be safely applied in radical total gastrectomy to accelerate clinical recovery of gastric cancer patients.

AIM: To report the comprehensive diagnosis and treatment of acute rejection in the first case of living-related small bowel transplantation with a long-term survival in China. METHODS: A 18-year-old boy with short gut syndrome underwent living-related small bowel transplantation, with the graft taken from his father (44-year old). A segment of 150-cm distal small bowel was resected from the donor. The ileo-colic artery and vein from the donor were anastomosed to the infrarenal aorta and vena cava of the recipient respectively. The intestinal continuity was restored with an end-to-end anastomosis between the recipient jejunum and donor ileum, and the distal end was fistulized. FK506, MMF and prednisone were initially used for post-transplant immunosuppression. Endoscopic observation and mucosal biopsies of the graft were carried out through the terminal ileum enterostomy; serum was collected to detect the levels of IL-2R, IL-4, IL-6 and IL-8. The change of the graft secretion and absorption was observed. RESULTS: Acute rejection was diagnosed promptly and cured. The patient was in good health, 5 years after living-related small bowel transplantation. CONCLUSION: The correct diagnosis and treatment of acute rejection are the key to the long-term survival after living-related small bowel transplantation.