Objective To investigate the method and effect of free autogenous palmaris longus tendon transplantation in the treatment of moderate and severe cicatricial ectropion.Methods The autogenous palmaris longus tendon was obtained through a small lateral proximal wrist band incision (lengths from 4 cm to 6 cm).The graft was properly sutured to the exposed tarsus and the attachments of inner and outer canthus.Local skin flap was rotated to cover the tendon and to repair the wound.Results Six man (8 eyes) with moderate and severe cicatricial ectropion were treated in our department,all case of ectropion were rectified after operation.The eyeballs were well contacted with lower eyelid and no recurrence of eetropion,epiphora and corneal exposure during 6 to 18 months' follow-up.The tension of the lower eyelid was abiding with satisfied effects.Conclusions The palmaris longus tendon is easy to obtain and there is no harm to the donor site.The cicatricial ectropion could be repaired with self-palmaris longus tendon transplantation with lasting effect and the recurrence rate is lower,which is well worthy popularizing.

This study was aimed to establish an effective method for the simultaneous content determination of strychnine and brucine in rat plasma.The Wistar rat plasma samples were processed by liquid-liquid extraction and separated on a UPLC BEH C18 column.The mobile phase was acetonitrile - acid water (17?83).The acid water was 0.02 mol·L-1.The potassium dihydrogen phosphate and 0.014 8 mol·L-1 sodium heptane sulfonate was mixed with equal amount.The 10% phosphonic acid was used to adjust the system to the pH of 2.8.The detection wavelength was set at 260 nm.The results showed that foreign materials in the Wistar rat plasma did not interfere with the content determination of samples.The calibration curve of strychnine was in good linearity within the range of 0.067 84-3.392 00μg·mL-1.The calibration curve of brucine was in good linearity with the range of 0.052 48-2.624 00μg·mL-1.The intra-and inter-day precisions were less than 10%.The mean extraction recoveries were more than 85%.The stability results met the requirements for biopharmaceutical analysis.It was concluded that the UPLC detection method was sensitive and precise,which can be used in the pharmacokinetics study of strychnine and brucine in Tong-Mai(TM) pill.

BACKGROUND:Interleukin-1 receptor-associated kinase 4 activity-induced inflammations and infection have been extensively accepted. However, there was no report concerning its effects on flap ischemia-reperfusion injury. OBJECTIVE:To explore the significance of interleukin-1 receptor-associated kinase 4 activity in flap ischemia-reperfusion injury. METHODS:A total of 36 adult male Sprague-Dawley rats were randomized into sham-operated group (n=12), ischemia-reperfusion group (n=12) and interleukin-1 receptor-associated kinase 4 group (n=12). The models of right lower abdominal island flap ischemia-reperfusion injury were set up. Interleukin-1 receptor-associated kinase 4 group was intraperitoneal y injected with 1 mL of interleukin-1 receptor-associated kinase 4 (100μmol/L) before reperfusion. The flaps were col ected at 1, 2, 4, and 6 hours after ischemia-reperfusion injury for histopathhological observation. At 1 hour after ischemia-reperfusion, protein expression of interleukin-1 receptor-associated kinase 4 was detected in flaps. The proportion of flap survival was calculated at 7 days after surgery.RESULTS AND CONCLUSION:Histopathological observation demonstrated that compared with the ischemia-reperfusion injury group, neutrophil infiltration and edema was evidently improved, and the protein expression of interleukin-1 receptor-associated kinase 4 was gradual y reduced in the interleukin-1 receptor-associated kinase 4 group. Flap survival proportions were respectively (51.70 ±7.62)%and (86.56±12.23)%in the ischemia-reperfusion injury group and interleukin-1 receptor-associated kinase 4 group at 7 days after surgery. There were significant differences in the flap survival proportion between the two groups (P<0.01). These results showed that after flap ischemia-reperfusion injury, the inhibition of interleukin-1 receptor-associated kinase 4 activities could elevate the survival rate of transplanted flap.

ObjectiveTo study the mechanism of myocardial dielectric property changes in radio frequency during hypothermic preservation and explore myocardial viability evaluative method. Methods Hybrid young pigs (20-30 kg) were used in the experiment. Heart arrest was induced with GIK solution. According to preservative temperature, the animals were divided into three groups: group A (4 ℃),group B (15 ℃) and group C (25 C). The heart was preserved in saline for 12,6 and 4 h respectively. Myocardial dielectric properties and ATP content were tested every 5 and 30 min during hypothermic preservation respectively. The relationship between tanoδm and ATP content was analyzed. ResultsTanδm of three groups was decreased significantly at the beginning, most slightly in group A and most obviously in group C. There was no significant difference in Tanδm between group B and group C with group A at 1 h,but there was obvious difference at 2,3 and 4 h (P＜0. 05,P＜0. 05,P＜0. 01 ). There was correlation between tanδm and ATP in the three groups. ConclusionTanδm in three groups is dropped with preservation time and temperature, and tanδm had a correlation with ATP content. Detection of myocardial dielectric property in radio frequency is a kind of quick, accurate and noninvasive method.

Objective:To investigate the factors associated with delay in anticoagulant therapy in patients with cerebral venous sinus thrombosis (CVST) and its effect on outcome.Methods:Patients with CVST admitted to Changhai Hospital, Naval Medical University from January 2010 to August 2021 were retrospectively enrolled. Patients were divided into early anticoagulation group and late anticoagulation group by the median time interval from first symptom to initiation of anticoagulation. The modified Rankin Scale was used for outcome assessment at 90 d after onset. 0-2 scores were defined as good outcome and 3-6 were defined as poor outcome. Demographic and clinical data were compared for the early versus late anticoagulation group and for the good versus poor outcome groups. Multivariable logistic regression was used to identify independent influencing factors of delay in anticoagulation and the correlation of delay in anticoagulation with poor outcome. Results:A total of 131 patients were included, their age was 40.07±15.11 years old, and 68 (51.91%) were male. Of these, 65 patients (49.62%) were in the early anticoagulation group and 14 (10.69%) were in the poor outcome group. Compared with the late anticoagulation group, the early anticoagulation group had a significantly higher proportion of patients with seizures and brain parenchymal damage as well as higher D-dimer levels on admission, while the proportion of patients with visual impairment/papilloedema was significantly lower (all P<0.05). Compared with the good outcome group, the poor outcome group had significantly higher proportions of patients with seizures, dyskinesia, impaired consciousness, low Glasgow Coma Scale score, and brain parenchymal damage as well as higher D-dimer, total cholesterol and low density lipoprotein cholesterol levels, sites of thrombus involvement were more common in the superior sagittal and straight sinuses, and significantly lower proportions of patients with headache and lower albumin levels on admission (all P<0.05). Multivariate logistic regression analysis showed that visual impairment/papilloedema (odds ratio [ OR] 0.119, 95% confidence interval [ CI] 0.030-0.473; P=0.002) and brain parenchymal damage ( OR 1.341, 95% CI 1.042-1.727; P=0.023) were independently associated with a delay in anticoagulation treatment, and a delay in anticoagulation treatment ( OR 6.102, 95% CI 1.185-30.504; P=0.030) and D-dimer level on admission ( OR 1.299, 95% CI 1.141-1.480; P<0.001) were the independent predictors of poor outcome in patients with CVST. Conclusions:Visual impairment/papilloedema and absence of brain parenchymal damage on cranial imaging are the independent risk factors for delay in anticoagulation in patients with CVST. The delay in anticoagulation is strongly associated with the poor outcome in patients with CVST.

Objective To study the immunomodulatory effect of polysaccharides (CRPS25-Ⅱ) derived from Chroogomphus rutilus on mouse mononuclear macrophages, RAW264.7 cells. Methods RAW264.7 cells were resuspended and cultured, cell suspension was prepared. The blank control group and CRPS25-Ⅱ groups with different mass concentrations (1, 20, 40, 80 and 160 μg/ml) were set up. MTT assay was used to determine the cytotoxicity of CRPS25-Ⅱ on RAW264.7 cells. RT-PCR was used to detect the effects of CRPS25-Ⅱ on the secretion of immune regulatory factors IL-6 and TNF-α from RAW264.7 cells. Western blot was used to detect the effects of CRPS25-Ⅱ on the expression of p-P65 protein in NF-κB pathway of RAW264.7 cells. Results The results showed that CRPS25-Ⅱ (1−160 μg/ml) had no obvious cytotoxicity. CRPS25-Ⅱ (1−160 μg/ml) increased the secretion of cytokines, and thus promoted the mRNA expression of IL-6 and TNF-α. CRPS25-Ⅱ increased the phosphorylation of p-P65 protein and activated the NF-κB signaling pathway, and thus promoted the immune regulation of cells. CRPS25-Ⅱ (1−160 μg/ml) could increase the p-P65 protein, and the promoting effects of CRPS25-Ⅱshowed an upward trend in the concentration range of 1−40 μg/ml and gradually weakened in the concentration range of 40−160 μg/ml. Conclusion Polysaccharides derived from chroogomphus rutilus had no cytotoxicity to mouse macrophages, and could promote the secretion of inflammatory factors IL-6 and TNF-α and activate the NF-κB signaling pathway, thus playing an immunomodulatory role.

Aberrant activation of oncogenic signaling pathways in tumors can promote resistance to the antitumor immune response. However, single blockade of these pathways is usually ineffective because of the complex crosstalk and feedback among oncogenic signaling pathways. The enhanced toxicity of free small molecule inhibitor combinations is considered an insurmountable barrier to their clinical applications. To circumvent this issue, we rationally designed an effective tumor microenvironment-activatable prodrug nanomicelle (PNM) for cancer therapy. PNM was engineered by integrating the PI3K/mTOR inhibitor PF-04691502 (PF) and the broad spectrum CDK inhibitor flavopiridol (Flav) into a single nanoplatform, which showed tumor-specific accumulation, activation and deep penetration in response to the high glutathione (GSH) tumoral microenvironment. The codelivery of PF and Flav could trigger gasdermin E (GSDME)-based immunogenic pyroptosis of tumor cells to elicit a robust antitumor immune response. Furthermore, the combination of PNM-induced immunogenic pyroptosis with anti-programmed cell death-1 (αPD-1) immunotherapy further boosted the antitumor effect and prolonged the survival time of mice. Collectively, these results indicated that the pyroptosis-induced nanoplatform codelivery of PI3K/mTOR and CDK inhibitors can reprogram the immunosuppressive tumor microenvironment and efficiently improve checkpoint blockade cancer immunotherapy.