Pluronic modified polyamidoamine (PAMAM) conjugate (PF127-PAMAM) was prepared and the inhibiting effect of MDR against MCF-7/ADR was investigated with doxorubicin (DOX) as model drug. 1H NMR and FTIR spectra showed that the conjugate was synthesized successfully. Element analysis accurately measured that 27.63% amino of per PAMAM was modified by pluronic (PAMAM : PF127, 1 : 35.37 mole ratio). PF127-PAMAM showed an increased size and a reduced zeta potential compared to PAMAM. PF127-PAMAM had lower hemolytic toxicity and cytotoxicity due to the reduced zeta potential and the protection of PF127. Each PF127-PAMAM molecular could load 19.58 DOX molecules, and the complex exhibited sustained and pH-sensitive release behavior. PF127-PAMAM/DOX exhibited weaker cytotoxicity than free DOX in MCF-7 cells; while the complex showed much stronger reverse effect of drug resistance in MCF-7/ADR cells, and resistance reversion index (RRI) was as high as 33.15.

Objective To explore the effects of cisplatin on the proliferation and autophagy of endometrial carcinoma Ishikawa cells.Methods Ishikawa cell proliferation was detected by MTS assay after the cells were treated with CDDP.To assess the level of autophagy,transmission electron microscope and Western blot were used to detect LC3 and Beclin1 expression;fluorescence microscopy was used to observe the fluorescence aggregation of green fluorescent protein and microtubule associated protein 1 light chain 3 fusionprotein (GFP-LC3).Results Cisplatin of 10 g/mL inhibited the proliferation of Ishikawa cells,with an increase of time and concentration,the inhibition of cell proliferation was significantly elevated (P ＜ 0.01).Transmission electron microscopy showed that under a condition of cisplatin on Ishikawa endometrial cancer cell,autophagy occurred.With an increase of concentration and dosage,Western blot showed that autophagy related protein LC3 expression was up-regulated,but becline-1 had no obvious change.LC3 expression level was higher in 12h-treatment with 20 μg/mL cisplatin group than in the control group,and was higher in 24h-treatment group than in 12h-treatment group.Conclusions Cisplatin inhibits proliferation of Ishikawa cells and induces autophagy of the cells in a time-and dose-dependent manner.Autophagy related MAP-LC3 is involved in the molecular mechanisms of autophagy induced by cisplatin in endometrial carciHom.

Objective To investigate the effects of Dermatophagoides pteronyssinus ( Der p) on the expression of TLR4 and IL-4 in P815 mast cells and to further analyze the immunoregulatory effects of 1,25-(OH)2D3 on Der p treated P815 mast cells.Methods Different concentrations of Der p and 1,25-( OH) 2 D3 were used alone or in combination to stimulate P815 mast cells.The supernatants of the stimulated cell culture were analyzed by enzyme-linked immunosorbent assay ( ELISA) for the detection of IL-4.The stimulated cells were collected and analyzed by real-time PCR and Western blot assays for the detection of TLR4atmRNAandproteinlevels,respectively.Results (1)TLR4expressionwasdetectedinP815 cells.The expression of TLR4 was enhanced in P815 cells treated with various concentrations of Der p.A significant dose-dependent up-regulation of TLR4 was observed in P815 cells after incubation with Der p for 36 h.(2) Der p promoted the release of IL-4 in P815 cells (P<0.05).(3) No significant differences with the expression of TLR4 and IL-4 were observed among 1,25(OH)2D3 treatment groups as compared with the control group (P>0.05).(4) 10-8 mol/L of 1,25(OH)2D3 promoted the Der p-induced expression of TLR4 in P815 cells (P<0.01).However, 1,25(OH)2D3 inhibited the release of IL-4 in a dose-dependent manner(P<0.05orP<0.01).Conclusion (1)Derpcouldpromotetheinflammationandallergicreac-tion through up-regulating TLR4 and IL-4 in mast cells.(2) The possible mechanism for the inhibitory of 1, 25(OH)2D3 on Der p-induced immune responses was due to the suppression of Th2-type immune responses through inhibiting the synthesis and secretion of IL-4 in mast cells.

Background and purpose:Tumor budding is a poor prognostic factor in colorectal cancer. In this study, we studied the tumor budding by counting the actual number in 10 high power fields and evaluated itsclinical application in predicting lymph node metastasis of T1 colorectal cancer.Methods:Tissue specimens from 307 patients with histologically conifrmed T1 colorectal cancer were enrolled. The clinicopathological characteristics including tumor budding were evaluated for their predictive value in lymph node metastasis. A formula was created to calculate the risk score for prediction of lymph node metastasis which was validated by 14 new cases.Results:In the multivariate analysis, it showed that tumor grade, lymphovascular invasion and the number of tumor budding were signiifcantly associated with lymph node metastasis. The probability of lymph node metastasis was calculated using the following equations:Z=1.571×(lymphovascular state: invasion, 1; no invasion, 0)+2.661×(tumor grade: high grade, 1; low grade, 0)+0.024×(budding counts)-3.885; Probability=1/1+e-Z. The high scores were correlated with the lymph node metastasis in the validations.Conclusion:We can accurately assess the risk of lymph node metastasis by counting the number of tumor budding in 10 high power fields. Therefore tumor budding could potentially assist treatment decision making in T1 colorectal cancer patients with high-risk lymph node metastasis.

Objective:To investigate the effects of compound insulation measure in operation room on hypothermia of cesarean section of very low birth weight infant (VLBWI).Methods:A total of 96 VLBWI, who were born with cesarean section in the People`s Hospital of Guangxi Zhuang Autonomous Region from January 2018 to October 2020 and admitted to the neonatal intensive care unit were enrolled in the present study. They were assigned to observation group and control group according to the enrolled time, each group was 48 cases. The control group received routine protocol, the observation group implemented the compound insulation measures. The body temperature, heart rate, blood oxygen saturation (SpO 2), end tidal carbon dioxide partial pressure (P ETCO 2) were measured at birth, 10 min after birth and before entering the transfer incubator. The incidence of hypothermia, hypoglycemia and hypoxemia in premature infants were compared between the two groups. Results:At 10 min after birth and before entering the transfer incubator, the body temperature, SpO 2, P ETCO 2 were (36.58 ± 0.49) ℃, 0.95 ± 0.02, (37.17 ± 3.15) mmHg (1 mmHg =0.133 kPa) and (36.50 ± 0.55) ℃, 0.94 ± 0.02, (38.08 ± 3.85) mmHg in the observation group, which were significantly higher than those in the control group (36.27 ± 0.57) ℃, 0.93 ± 0.02, (35.85 ± 3.14) mmHg and (35.75 ± 0.48) ℃, 0.93 ± 0.01, (36.63 ± 3.17) mmHg, the differences were statistically significant ( t values were 2.03-7.13, all P<0.05). Before entering the transfer incubator, the heart rate was (140.25 ± 8.67) times/min in the observation group, which was significantly lower than that in the control group (145.89 ± 9.23) times/min, the difference was statistically significant ( t value was 3.09, P<0.05). The incidence of hypothermia, hypoglycemia and hypoxemia were 16.7%(8/48), 8.3%(4/48) and 12.5%(6/48) in the observation group, which were significantly lower than those in the control group 37.5%(18/48), 22.9%(11/48) and 29.2%(14/48), the differences were statistically significant ( χ2=5.28, 3.87, 4.04, all P<0.05). Conclusions:Evidence-based operation room compound insulation measure can effectively maintain the constant body temperature in VLBWI, reduce the incidence of hypothermia, hypoglycemia and hypoxemia.

Herpes simplex virus (HSV), including HSV-1 and HSV-2, is an important pathogen that can cause many diseases. Usually these diseases are recurrent and incurable. After lytic infection on the surface of peripheral mucosa, HSV can enter sensory neurons and establish latent infection during which viral replication ceases. Moreover, latent virus can re-enter the replication cycle by reactivation and return to peripheral tissues to start recurrent infection. This ability to escape host immune surveillance during latent infection and to spread during reactivation is a viral survival strategy and the fundamental reason why no drug can completely eradicate the virus at present. Although there are many studies on latency and reactivation of HSV, and much progress has been made, many specific mechanisms of the process remain obscure or even controversial due to the complexity of this process and the limitations of research models. This paper reviews the major results of research on HSV latency and reactivation, and discusses future research directions in this field.
Herpes Simplex ; virology ; Herpesvirus 1, Human ; physiology ; Humans ; Virus Activation ; physiology ; Virus Latency ; physiology ; Virus Replication