Objective To compare the effect of different gastrointestinal motility drugs on capsule endoscopy. Methods Seventy-one patients with suspected small bowel disease were randomly divided into metoclopramide group (24 patients), mosapride group(25 patients) and control group (22 group). The patients in metoclopramide group swallowed capsule endoscopy immediately after intramuscularly injecting 10 mg metoclopramide, the patients in mosapride group swallowed capsule endoscopy 15 min after taking 5 mg mosapride, and the patients in control group did not take any of the gastrointestinal motility drugs. Three groups had the same bowel preparation before checking. The finishing rate of small bowel examinations, stomach and small intestinal transit time, intestinal cleanliness and the detection rates of lesions in three groups were compared. Results The total small bowel examination finishing rate was 94.4%(67/71). The small bowel examination finishing rate in metoclopramide group, mosapride group, and control group was 95.8%(23/24), 96.0%(24/25), and 90.9% (20/22), and there was no significant difference(P>0.05). The stomach transit time in metoclopramide group, mosapride group and control group was(27.5 ± 20.7), (28.1 ± 20.9) and (52.3 ± 33.5) min. The stomach transit time in metoclopramide group and mosapride group had no significant difference (P>0.05), but it was significantly lower than that in control group (P<0.05). The small intestinal transit time in three groups had no significant difference (P>0.05). The image class scores in metoclopramide group, mosapride group and control group was (2.5 ± 0.4), (2.7 ± 0.4) and (1.7 ± 0.3) scores.The scores in metoclopramide group and mosapride group had no significant difference (P>0.05), but they were significantly higher than that in control group (P<0.05). The detection rate of lesions in metoclopramide group, mosapride group and control group was 45.8%(11/24), 56.0%(14/25) and 18.2%(4/22). The detection rate of lesions in metoclopramide group and mosapride group had no significant difference (P>0.05), but it was significantly higher than that in control group (P<0.05). Conclusions The use of gastrointestinal motility drugs before capsule endoscopy can improve the quality of inspection, and metoclopramide and mosapride shows no significant difference.

BACKGROUNDBisphosphonates have been used to treat many bone diseases in clinic. Bisphosphonates have also been proven useful in the management of bone metastasis in patients with breast and prostate carcinoma as demonstrated in a number of trials in vitro and in vivo, but, it is little known that the effect of bisphosphonates on lung cancer, one of the most common bone metastatic malignant tumors. This study is to investigate the effect of several bisphosphonates on inhibiting proliferation of different lung cancer cell lines in vitro, and to validate whether this inhibitive effect is comprehensive or selective.

METHODSThe cytotoxic effect of bisphosphonates on lung cancer cells and human normal liver cells was determined by sulforhodamine B (SRB) assay.

RESULTSAfter incubation of lung cancer cells with bisphosphonates for 72h, the proliferation was inhibited in different degrees. The inhibiting activity of medronate (MDP) was the lowest, while the activity of ibandronate and incadronate (YM175) was between MDP and alendronate. The effects of bisphosphonates on human normal liver cells were different. The toxicity of MDP, ibandronate and YM175 was low, while alendronate had high toxicity. The sensitivity of lung cancer cells to bisphosphonates was also different. The sensitivity of H446 and SPC-A1 was comparatively lower, while H460 and A549 were more sensitive.

CONCLUSIONSBisphosphonates can inhibit the proliferation of lung cancer cells and human normal liver cells in different degrees. The inhibiting effect is associated with the kind and concentration of bisphosphonates, and also the kind of lung cancer cells.

Objective:To investigate the predictive value of albumin/fibrinogen ratio (AFR) for 28-d mortality in patients with sepsis.Methods:A total of 186 patients with sepsis admitted to the Intensive Care Unit of the First Affiliated Hospital of Xinjiang Medical University from January 2019 to December 2021 were studied retrospectively. They were divided into the survival group ( n=124) and death group ( n=62) according to the 28-d survival conditions. Clinical data of each group within 24 h after admission were recorded, including age, sex, underlying diseases, white blood cell count, albumin, fibrinogen (FIB), PCT, CRP and other laboratory examination indexes. APACHEⅡ scores and SOFA scores were recorded at the time of admission. Cox regression was used to analyze the influence of each index on the prognosis of patients. Receiver operating characteristic (ROC) curve was used to analyze the predictive value of AFR for 28-d mortality in patients with sepsis. Kaplan-Meier method was used to draw survival curves under different AFR levels for survival analysis. Pearson correlation was used to analyze the relationship between AFR and APACHEⅡ score. Rseults:Age, number of patients with septic shock, mechanical ventilation, APACHEⅡ score, SOFA score, blood lactic acid and fibrinogen increased significantly in the death group ( P<0.05), while albumin and AFR were significantly decreased ( P<0.001). ROC curve analysis showed that the area under the curve of AFR in predicting 28-d mortality risk of patients with sepsis was 0.900. When the cut-off value of AFR was 7.64, the sensitivity was 80.0% and the specificity was 85.5%. Kaplan-Meier survival analysis showed that patients with AFR >7.64 had better prognosis. Cox regression analysis showed that AFR, APACHEⅡ score and the presence of septic shock were independent risk factors affecting the prognosis of patients with sepsis. AFR was strongly correlated with APACHEⅡ score ( r=-0.462, P<0.001). Conclusions:As a simple, effective and safe biomarker, AFR has a certain predictive value for 28-d mortality risk in patients with sepsis.

Objective:Establishment of a new model of human primary colon cancer transplantation tumor in normal immune mice and to provide a reliable experimental animal model for studying the pathogenesis of colon cancer under normal immunity.Methods:Human colon cancer cells come from colon cancer patients who underwent surgery in the Affiliated Hospital of Jining Medical College in 2017. The mice in the cell control group were inoculated with phosphate buffered solution (PBS) containing colon cancer cells, the microcarrier control group was inoculated with PBS containing microcarrier 6, and the cell-microcarrier complex group was inoculated with the PBS containing colon cancer cell-microcarrier complex. The cells of each group were inoculated under the skin of the right axilla of mice by subcutaneous injection, and the time, size, tumor formation rate and pathological changes under microscope were recorded. The transplanted tumor tissue was immunohistochemically stained with the EnVisiion two-step method, and the tumor formation rate of the transplanted tumor was judged according to the proportion of positive cells in the visual field. The polymerase chain reaction (PCR) method was used to detect the expression of human-specific Alu sequence in mice tumor tissue.Results:After inoculation with tumor cells, the mice in the cell control group and the microcarrier control group did not die and did not form tumors; the mice in the cell-microcarrier complex group had palpable subcutaneous tumors in the right axillary subcutaneously on the 5th to 7th days after inoculation, and tumor formation rate is 67% (10/15), and the tumor volume can reach about 500 mm 3 2 to 3 weeks after vaccination. The immunohistochemistry results showed that CK20, CDX-2 and carcinoembryonic antigen were all positively expressed. The PCR results showed that the expression of human-specific Alu sequence can be detected in the transplanted tumor tissue of tumor-bearing mice. Conclusion:Human primary colon cancer cells used microcarrier 6 as a carrier to form tumors in normal immunized mice, and successfully established a new model of human colon cancer transplantation tumor in normal immune mice.

Objective:Establishment of a new model of human primary colon cancer transplantation tumor in normal immune mice and to provide a reliable experimental animal model for studying the pathogenesis of colon cancer under normal immunity.Methods:Human colon cancer cells come from colon cancer patients who underwent surgery in the Affiliated Hospital of Jining Medical College in 2017. The mice in the cell control group were inoculated with phosphate buffered solution (PBS) containing colon cancer cells, the microcarrier control group was inoculated with PBS containing microcarrier 6, and the cell-microcarrier complex group was inoculated with the PBS containing colon cancer cell-microcarrier complex. The cells of each group were inoculated under the skin of the right axilla of mice by subcutaneous injection, and the time, size, tumor formation rate and pathological changes under microscope were recorded. The transplanted tumor tissue was immunohistochemically stained with the EnVisiion two-step method, and the tumor formation rate of the transplanted tumor was judged according to the proportion of positive cells in the visual field. The polymerase chain reaction (PCR) method was used to detect the expression of human-specific Alu sequence in mice tumor tissue.Results:After inoculation with tumor cells, the mice in the cell control group and the microcarrier control group did not die and did not form tumors; the mice in the cell-microcarrier complex group had palpable subcutaneous tumors in the right axillary subcutaneously on the 5th to 7th days after inoculation, and tumor formation rate is 67% (10/15), and the tumor volume can reach about 500 mm 3 2 to 3 weeks after vaccination. The immunohistochemistry results showed that CK20, CDX-2 and carcinoembryonic antigen were all positively expressed. The PCR results showed that the expression of human-specific Alu sequence can be detected in the transplanted tumor tissue of tumor-bearing mice. Conclusion:Human primary colon cancer cells used microcarrier 6 as a carrier to form tumors in normal immunized mice, and successfully established a new model of human colon cancer transplantation tumor in normal immune mice.

Objective: This study aimed to explore the role of SGK-1 in the occurrence of temporomandibular joint(TMJ) osteoarthritis(TMJ-OA). Methods: Sixteen rats were randomly divided into Control group(Control group) and TMJ-OA group(TMJ-OA group), and TMJ-OA group was injected with sodium iodoacetate(MIA) intra articular cavity while Control group was injected with 0.9% sodium chloride solution. Pain behavior was assessed by measuring the head withdrawal threshold(HWT) with a von-Frey apparatus. Hematoxylin-eosin(HE) and Safranin O-fast green stains were used to observe the histological structure changes of the condyle of TMJ-OA rats. Real-time PCR was performed to exam the expression levels of mRNA of SGK-1, MMP-13, IL-1β, COX-2 in mandibular condylar cartilage(MCC). HE stain was used to observe the histological structure changes of the trigeminal ganglion(TG) of TMJ-OA rats. Real-time PCR was performed to exam the expression levels of mRNA of SGK-1, COX-2 in TG. Results: MIA injection induced typical OA-like lesions in the TMJ within 28 days. Administration of MIA led to the significant decrease in HWT, disordered of the condyle cartilage and subchondral bone structure, demyelination aggravated of nerve fibers in TMJ rats. Compared with rats in Control groups, the expression levels of SGK-1 in MCC and TG of rats in TMJ-OA group were upregulated. Conclusion In the pathological process of TMJ-OA, SGK-1 may plays an important role not only in cartilage structural damage but also in pain transmission.

Objective To establish a new patient-derived xenograft (PDX) model of human liver cancer by inoculating the complex of human primary liver cancer cells and a novel microcarrier (microcarrier 6) into mice with normal immune function. Methods Primary liver cancer cells were isolated and extracted from the fresh human liver cancer tissue of five patients and were then co-cultured with microcarrier 6 to construct a three-dimensional tumor cell culture model in vitro . According to the type of graft, 75 male C57BL/6 mice were divided into cell control group, microcarrier control group, and experimental group (each sample corresponded to three groups, with 15 groups in total and 5 mice in each group). The liver cancer cell-microcarrier complex was implanted into the mice by subcutaneous inoculation, and tumor formation time, tumor formation rate, and histopathological manifestations were observed. The Fisher's exact test was used for comparison of categorical data between two groups. Results As for the liver cancer cells from the five patients, tumor formation was observed in the mice corresponding to three patients. In these three experiments, tumor formation was not observed in the control groups and was only observed in the experimental groups, and 12 of the 15 mice in the experimental groups had successful tumor formation, with a tumor formation rate as high as 80%, which was significantly different from that in the cell control groups and the microcarrier control groups (all P < 0.05). The tumor formation time was 5-7 days; the xenograft tumor grew rapidly, and HE staining showed nested or flaky cells with obvious heteromorphism, with the presence of pathological mitosis; immunohistochemical staining showed positive CK8/18, Hep, and Gpc-3, which was in accordance with the characteristics of human liver cancer cells. Conclusion This experiment successfully establishes a new PDX model of human liver cancer based on the complex of microcarrier 6 and human primary liver cancer cells in mice with normal immunity. This model can be used to better elucidate the mechanism of the development and progression of liver cancer in the body with normal immunity, and besides, it also provides a new animal model with higher value for the precise treatment of liver cancer.