Objective:To explore the effective drug and the best way of administration of the drug in the relief of moderate or severe cancer pain,so as to attain the best effect.Methods:30 patients with moderate or later period cancer orally take 30 mg Morphine tablet every 12 hours. The initial dose was 60 mg,and then it was adjusted according to the effect till the most appropriate dose was reached.Results:After taking Morphine tablet,the rate of complete relief and moderate relief of moderate or severe cancer pain were 70%(21/30),26.7%(8/30),respectively. The total effective rate was 96.7%.Conclusion:Effect of Morphine tablet for cancer pain treatment was sure and reliable,the administration of 30 mg Morphine tablet every 12 hours was safe and effective.

Objective To study the effects of platelet activation on the metastasis and prognoies of lung cancer. Methods Radio-immunity and ELISA were employed to detect the TXB_2,DH-TXB_2,TSP, β-TG, GMP-140,CGMP and FN of 168 cases of lung cancer patients (lung cancer group) and 80 cases of healthy persons control group. The lung cancer group included two subgroups: earlier and metaphase group (n=51) and advanced group (n=17), 39 cases in the former group underwent operation (after operation group). Results (1)Compared with control group, the levels of DH-TXB2,TSP,β-TG,GMP-140,CGMP in group of earlier and metaphase lung cancer increased and FN decreased. TXB2,DH-TXB2,TSP,β-TG,GMP-140,CGMP in advanced group increased and FN decreased;DH-TXB2 and GMP-140 increased in group of after operation. (2)Compared with group of earlier and metaphase lung cancer,the levels of DH-TXB2,TSP,β-TG,GMP-140,CGMP in group of after operation increased and FN decreased; In advanced group, levels of TXB2, DH-TXB2,TSP,β-TG,GMP-140,CGMP increased and FN decreased. (3)In the lung cancer group, CGMP was positively correlated with DH-TXB2,TSP,β-TG and GMP-140. (4)Compared with control group,TXB2, DH-TXB2, TSP,β-TG,GMP-140 and CGMP in group glandular cancer and small cell carcinoma cases increased,FN decreased;In squamous cancer, the levels of TXB2, DH-TXB2,GMP-140 and CGMP increased and FN decreased. (5)Compared with small cell carcinoma cases, DH-TXB2 decreased in cases of glandular cancer; GMP-140 decreased in squamous cancer. Conclusions Activations of platelet generally emerged with lung cancer patients, platelet activation was severe in advanced cancer patients. Activations of platelet, after operation, is obviously eased. The level of platelet activation marker is possibly related with histological classification of lung cancer.

Objective To investigate the adhesion molecule expression and functional status of platelets in lung cancer patients, and their relations with disease progression. Methods Using flow cytometry to measure the expression of surface antigens and functional status of platelets in 60 healthy control group, and 164 lung caneer patients. Results Comparing with control group, the expression in early group and mid term group(A group) of CD31, CD36, CD62, CD63 increased, and there is no significant meaning in the differences of surgery group (B group) of CD31, TSP, CD36, CD62, CD63. The expression in advanced group (C group) of CD31, TSP, CD36, CD62, CD63 increased. Comparing with A Group, the expression in B Group of CD36, CD62, CD63 decreased. The expression in C group of CD31, TSP, CD36, CD62, CD63 increased. Comparing with the small cell lung cancer, the expression of adenocareinorna of TSP, CD36,, CD62, CD63, squamous cell carcinoma of CD31, CD62, CD63, and alveolus cancer of CD31, TSP, CD63, all decreased. Conclusion The high level expression of platelet activation exists in patients with lung cancer of different stage, and decreased after operation. Platelet activation expressed significantly in the advanced stage of small cell lung cancer.

Objective To investigate the effects of morroniside on fibrinogen (Fib), prothrombin time (PT), activated partial thromboplastin time (APTT) and thrombin time (TT) in focal cerebral ischemia/reperfusion in rats. Methods The animal model was induced with occlusion of middle cerebral artery (MCAO) with suture embolus, and morroniside was then administered intragastrically at the dose of 30, 90 and 270 mg/kg for 7 d. Acetyl salicylic acid was taken as positive control drug. The content of Fib, and PT, APTT and TT were measured withrelated kits. Results Compared with the sham-operated group, the concentration of Fib significantly increased (P<0.001) and PT, APTT and TT significantly shortened in the model group (P<0.001); however, compared with the model group, morroniside significantly decreased Fib content (P<0.01) and prolonged PT, APTT and TT (P<0.05). Conclusion Morroniside can antagonize the coagulation function in focal cerebral ischemia/reperfusion in rats.

Parkinson's disease is a common progressive neurodegenerative disorder among old people, characterized by progressive loss of dopamine-producing neurons in the substantia nigra pars compacta and accordingly low level of dopamine in the nigrostriatal pathway.Neuroinflammation and even systemic inflammation have been suggested to be involved in the demise of dopaminergic neurons. Anti-inflammatory treatment could protect brain from inflammatory injury and prevent the progressive course of Parkinson's disease, which suggests a potential new strategy for Parkinson's disease treatment.

Objective:To investigate HER2 mRNA expression in breast cancer with HER2 immunohistochemistry (IHC) 0 and to analyze the feasibility of distinguishing between the tumor with HER2 μltra-low expression and the one without expression of HER2 (no staining by IHC) by HER2 mRNA level preliminarily.Methods:HER2 mRNA was analyzed by reverse transcription digital PCR in 41 cases of formalin-fixed paraffin-embedded surgical tissue samples of invasive breast cancer obtained between January 2020 and March 2023 at Peking Union Medical College Hospital. The cohort included 21 HER2 IHC 1+ and 20 IHC 0 (12 ultra-low and 8 non-expression of HER2). HER2 mRNA expression level was quantitatively evaluated by the FAM (HER2)/VIC (reference gene) ratio.Results:The expression of HER2 mRNA for the cases with 1+, ultra-low, and non-expression of HER2 by IHC was 0.30 to 1.78 (average 0.90, median 0.82), 0.55 to 1.51 (average 0.93, median 0.90) and 0.22 to 0.78 (average 0.41, median 0.36), respectively. For the mean and median HER2 mRNA levels, there was no significant difference between HER2 IHC 1+ and HER2 ultra-low expression diseases ( P=0.757). A remarkable difference in HER2 gene expression was found between the tumors with 1+ and non-expression of HER2 by IHC ( P=0.002). And, HER2 ultra-low cases contained statistically higher levels of HER2 mRNA compared with non-expression of HER2 subgroup by IHC ( P=0.001). Conclusions:Based on HER2 mRNA, HER2 non-expression and HER2 weak expression (including HER2 IHC 1+ and ultra-low) belong to two different types of the tumor and the disease with HER2 IHC 1+ and HER2 ultra-low expression may be the same. It is necessary to further test the performance of HER2 mRNA detection for stratifying the HER2 weak expression subgroup and to determine the threshold.

AIM:To investigate the role of phosphoenolpyruvate carboxykinase 1(PCK1)in the proliferation and migration of mouse vascular smooth muscle cells(VSMCs)and the underlying mechanism.METHODS:The prolif-eration and migration of mouse VSMCs were induced by platelet-derived growth factor(PDGF)-BB.The cells were divided into a vehicle group and a PDGF-BB group.The expression of PCK1 was detected by Western blot and immunofluores-cence staining.The mouse Pck1 siRNA(si Pck1)were transfected into mouse VSMCs to silence PCK1.The cells were di-vided into the vehicle,si Pck1+vehicle,PDGF-BB and si Pck1+PDGF-BB groups.The protein level of PCK1 was detected by Western blot.The proliferation was explored by Ki-67 immunofluorescence staining and the viability was detected by CCK-8 assay.The migration was determined by a scratch test.Mitochondrial dynamics were observed via transmission electron microscopy.A lentivirus carrying dynamin-related protein 1(Drp1)gene(lenti-Drp1)was transfected into VSMCs to induce them to overexpress DRP1.The cells were divided into the PDGF-BB,si Pck1+PDGF-BB,lenti-Drp1+PDGF-BB and lenti-Drp1+si Pck1+PDGF-BB groups.Proliferation,migration and mitochondrial dynamics were measured as described above.RESULTS:PDGF-BB increased the protein expression of PCK1 and DRP1,cell viability,the per-centage of Ki-67-positive cells,the wound healing rate and mitochondrial division in VSMCs.These effects were sup-pressed when PCK1 protein expression was silenced.After DRP1 was overexpressed,the inhibitory effects of PCK1 silenc-ing on cell viability,the percentage of Ki-67-positive cells,the wound healing rate and mitochondrial division were signifi-cantly reversed.CONCLUSION:PCK1 promotes the mitochondrial division,proliferation and migration of VSMCs in mice by upregulating the expression of DRP1.