Search

•A signature consisting of 5 genes (CLIC5, ENTPD8, PACSIN3, HGD, and GNG7) was selected to construct a prognostic model in TCGA rectal cancer cohort and validated in the GSE133057 cohort.•It showed that overall survival is significantly low in the high-risk group (P = 0.0044, log-rank = 6.328).•It was differentially involved in the immune-related analyses between the high- and low-risk groups in rectal cancer, which correlated with immune inhibitors.•It showed significant correlations between the high- and low-risk groups with differentiation, apoptosis, and quiescence at the single-cell level in rectal cancer.

To explore the relationship between Insulin-like growth factor (IGF)-I, −II and lung development in neonatal rats. 80 timed pregnant Sprague-Dawley (SD) rats were randomly divided into 4 groups (n=20): group A (Control group), group B (Dexamethasone (DEX) 1 group), group C (DEX 2 group), group D (retinoic acid (RA) group). 20 pregnant rats in group A, B and D were injected subcutaneously or intraperitoneally with vehicle (NS), DEX, or RA respectively during gestational day 16 to 18. All newborn rats in group C were subcutaneously injected with DEX at day 1 to 3 after birth. The lung tissue was obtained at the following times: fetuses at gestational ages of 18, 20 and 21 days, and 1, 3, 5, 7, 10, 14 and 21 days after birth. Lung tissues were used for histopathological study, the polypeptides analysis of IGF-I, −II (immunohistochemistry and Western blot) and mRNA analysis (RT-PCR). The results showed that the strongest expression of IGF-I in group A and D occurred at ages of 5–7 days (alveolar stage). The stronger their expressions, the better the alveolar develop. The peak stage of expression in group B occurred earlier, on the day 3 after birth. Compared with group A, the expression of IGF-I during gestation age of 18 days to age of 3 days in group B were significantly higher (P<0.01), but significantly lower at other time points (P<0.01). The expression of IGF-I was lower in group C all the time and always higher in group D than those in group A (P<0.01). The peak expression of IGF-II took place at the gestation age of 18 days, then gradually dropped to trace. During 18 days of gestation to age of 3 days, the expression IGF-II in group B was significantly higher than that in group A (P<0.01). No difference was found among all other groups. The change in the expression of IGF-I, −II mRNA in all 4 groups was similar to that of their polypeptides. The results suggested that there is a close linking between IGF-I, −II and lung development in newborns. The IGF-II works at early stage and the that of IGF-I works at the stage of new septa formation and alveoli maturation. The stronger their expressions, the more mature the lung development.

Eleven hundred patients who underwent laparoscopic primary hernioplasty from 2002 to 2007 at our hernia center are included in our prospective study. A modified transabdominal preperitoneal (TAPP) prosthetic technique was applied in 1100 cases of hernioplastic operations. The modified technique consisted of using the needle with thread and needle-hook to close the hernia ring and partial preperitoneal dissecting to place the mesh. A self-made mesh is used. The lift-insert technique is applied to fix the mesh. There were 882 indirect and 218 direct hernias. Mean operative time is 20 minutes for 1-sided hernia and 35 minutes for two-sided hernia. A total of 1002 (95) patients were discharged within 48 hours. No mesh infection or migration has been reported. No postoperative adhesive ileus has been reported. Ten patients have been treated with analgesic medication. There are 9 recurrences (0.9) reported with a 98 follow-up over 1–6 years. We find that the modified laparoscopic transabdominal preperitoneal hernioplasty is a safe and efficacious treatment option for primary inguinal hernia.

To explore the mechanism of Notch in hyperoxia-induced preterm rat lung injury, 2-days-old preterm SD rats were randomized into control and hyperoxia group (FiO2≥0.85). On day 1, 7, 14 and 21, 8 rat pups of each time point were used to assess histopathological changes of lung with HE staining and to evaluate the expression of Notch1 and Notch3 with immunohistochemistry. Notch1, Notch3, Aquaprin5 (AQP5) and surfactant protein C (SP-C) mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). The results showed that the lung injury in the hyperoxia group was characterized by retarded lung alveolization and differentiation of alveolar epithelial type II cells (AEC II). Positive staining of Notch1 in hyperoxia group was weaker than controls at every time point (except for day 7), while positive staining of Notch3 was much stronger (P,0.05,P<0.01). Notch1, Notch3 mRNA level showed similar change as protein level. AQP5, SP-C mRNA decreased significantly as compared with that of the controls (P<0.01). We are led to conclude that hyperoxia results in abnormal expression of Notch, which is likely to contribute to the pathogenesis of lung injury through regulating proliferation and transdifferentiation of alveolar epithelial cells.

The influence of platelet-derived growth factor (PDGF) on lung development in newborn rats and the effect of retinoic acid (RA) on PDGF in lung development were investigated. Newborn Sprague-Dawley (SD) rats were randomly assigned to two groups: control group and RA group. The rats in RA group was intraperitoneally injected with all trans-retinoic acid (500 μg/kg every day) for consecutive 3 days after birth, while those in the control group were not subjected to intervention. Immunohistochemical assay was performed to locate the expression of PDGF. mRNA levels of PDGF were measured by reverse transcription polymerase chain reaction (RT-PCR) at age of 1, 3, 5, 7, 10, 14, 21 days. The method of radial alveolar counts (RAC) was used to measure the amount of the alveoli of the lungs. It was found that with increasing days, levels of PDGF-A and PDGF-B changed to verying degrees. RA could elevate significantly the expression levels of PDGF-A mRNA and protein (P<0.01), but not affect the expression levels of PDGF-B mRNA and protein markedly (P>0.05). It is suggested that PDGF might play an important role in lung development. RA can stimulate lung development through increasing the expression levels of PDGF-A mRNA and protein.

The pathogenesis of hyperoxia lung injury and the mechanism of amygdalin on type 2 alveolar epithelial cells (AEC2) isolated from premature rat lungsin vitrowere investigated. AEC2 were obtained by primary culture from 20-days fetal rat lung and hyperoxia-exposed cell model was established. Cell proliferating viability was examined by MTT assay after treatment of amygdalin at various concentrations. DNA content and the proliferating cell nuclear antigen (PCNA) protein expression of AEC2 were measured by using flow cytometry and immunocytochemistry respectively after 24h of hyperoxia exposure or amygdalin treatment. The results showed that hyperoxia inhibited the proliferation and decreased PCNA protein expression in AEC2 of premature ratin vitro. Amygdalin at the concentration range of 50–200 μmol/L stimulated the proliferation of AEC2 in a dose-dependent manner, however, 400 μmol/L amygdalin inhibited the proliferation of AEC2. Amygdalin at the concentration of 200 μmol/L played its best role in facilitating proliferation of AEC2sin vitroand could partially ameliorated the changes of proliferation in hyperoxia exposed AEC2 of premature rat. It has been suggested that hyperoxia inhibited the proliferation of AEC2s of premature rat, which may contribute to hyperoxia lung injury. Amygdalin may play partial protective role in hyperoxia-induced lung injury.