Volume 90  ·   Issue 30  ·  2010

The emergence of coronary drug-eluting stents (DES) has made a milestone progress in percutaneous coronary intervention (PCI). Compared with bare metal stents (BMS), DES has shown obvious advantages in different types of coronary artery lesions [1], and greatly reduced the target lesion reconstruction rate (TLR). However, when DES began to be widely used in clinic, the problem of late thrombosis in DES stents has emerged [2].

Vascular disease is a systemic disease involving important organs in the whole body. It is associated with many risk factors of metabolic abnormalities such as hypertension, hyperlipidemia, diabetes, hyperuric acid and homocysteine elevation, and leads to progressive vascular injury and eventually vascular events, including acute myocardial infarction, stroke, advanced renal disease, peripheral vascular disease, etc., with high mortality and disability rate [1-2]. However, the above diseases are not caused by diseases of organs such as heart or brain, but diffuse sclerosis, atherosclerosis and local obstruction of blood vessels supplying the above organs.

Objective To evaluate the long-term efficacy and safety of DES in the setting of primary PCI in our single center. Methods From September 2004 to November 2008, 464 patients undergoing primary PCI for STKMI were included at the 28th Division in Beijing Anzhen Hospital. The adverse events were compared among different types of DES. Results The major adverse cardiac events[ MACE, including sudden cardiac death, stent thrombosis, target lesion revascularization ( TLR ) , target vessel revascularization (TVR), reinfarction and coronary artery bypass graft], all-cause death, major bleeding, anti-platelet therapy and secondary prevention of coronary heart disease of different types of DES were no significant differences. The cumulative incidence of MACE and stent thrombosis were 9.3% and 1.1% respectively, different types of DES were 9. 4% , 5. 1% , 5. 9% , 6. 6% ( P = 0. 483 ) and 3. 1% , 0. 0% , 0. 0% , 0. 0% ( P = 0. 092) respectively. The patients in the DES group had longer duration of dual antiplatelet therapy(average 16. 2 ±6. 7 months). No major bleeding occurred in all patients with the longterm and low-dose aspirin ( 100 mg). Conclusions Different types of DES have the same results in the setting of primary PCI, and were long-term safe and effective with a reasonable strategy for anti-platelet therapy and secondary prevention.

Objective To assess the therapeutic effect and safety of drug eluting stent for the patients with anterior wall myocardial infarction by left anterior descending artery occluded abruptly. Methods From January 2004 to December 2008, 302 patients with anterior wall myocardial infarction in 12 hours from chest pain to treatment were treated. But only 189 patients were recruited and randomly divided into drug eluting stent group (n=95) and bare metal stent group (n =94). The occurrence of cardiac death, stent thrombosis, reinfarction, target vessel revascularization and re-hospitalization because of heart function failure was compared. Results There was no difference in cardiac death [3 /95 (3% ) vs 7 /94 (7% ) , P = 0. 206 ] , reinfarction [1/95 ( 1 % ) vs 5 /94 ( 5 % ) , P = 0. 112 ] and re-hospitalization because of heart function failure[8( 8% ) vs 5 (5% ), P = 0. 434]. Compared with those in bare metal stent group, the patients in drug eluting stent group has a lower rate of target vessel revascularization [2(2% ) vs 13 (14% ) , P = 0. 009 ] and composite therapeutic effect endpoints [12(13%) vs 25 ( 27% ) , P = 0. 011 ]. There was no difference in safety endpoint or stent thrombosis [1(1%) vs 4 (4% ), P = 0. 204 ]. Conclusion In patients with anterior wall myocardial infarction by left anterior descending artery occluded abruptly, drug eluting stent decreases the rate of target vessel revascularization. But it has no increased stent thrombosis.

Objective To investigate the impact of gender on outcomes in patients with non-ST segment elevation acute coronary syndrome undergoing intervention treatment. Methods In a multi-center randomized trial, the patients diagnosed as non-ST segment elevation acute coronary syndrome were randomly assigned to undergo early intervention ( coronary angiography ≤ 24 h after randomization) or delayed intervention ( coronary angiography ≥ 36 h after randomization) . The primary outcome was a composite of death, myocardial infarction or stroke at 180 days. The secondary outcomes were death, myocardial infarction, refractory ischemia, stroke or revascularization at 180 days. Results Among 815 patients (545 males, 270 females) , the incidences of primary and secondary outcome were equivalent for both genders ( P > 0. 05). Males of the early intervention group had a greater incidence of the primary outcome (7. 1 % vs 14. 8% , P=0. 00). The secondary outcome was a composite of death, myocardial infarction or refractory ischemia occurring in 12. 5% of males in early intervention group and 21. 2% in delayed intervention group. Significant difference existed ( P = 0. 00 ). The incidence of another secondary outcome as a composite of death, myocardial infarction, refractory ischemia, stroke or revascularization was equivalent for males in early intervention group and delayed intervention group (26.8% vs 32.4% , P>0. 05). The incidences of primary outcome ( 12. 6% vs 14. 3% , P > 0. 05 ) and secondary outcome ( 18. 5% vs 23. 5% P > 0. 05 ; 28. 5% vs 27. 7% P > 0. 05 ) were equivalent for females in early intervention group and delayedintervention group (P > 0.05). Conclusion Patients with non-ST segment elevation acute coronary syndrome undergoing intervention demonstrate no significant gender differences in efficacy and safety. Early intervention reduces the rate of myocardial infarction for males, but it is not superior to delayed intervention for females.

Objective To analyze the clinical efficacy of combined therapy in the treatment of advanced adrenal cortical adenocarcinoma. Methods The clinical data of 12 cases with advanced adrenal cortical adenocarcinoma at our hospital from 1986-2006 were analyzed. And the relevant literatures were reviewed. Results Eleven patients underwent operation to remove primary lesions. Only 1 case received a biopsy. All cases were treated with chemotherapy or chemotherapy pulse post-operative radiotherapy. Pathological diagnosis was all of adrenal cortical adenocarcinoma. According to the staging criteria of Jacques and Brennan, all 12 cases were of Ⅳ stage. The follow-up duration was 6-40 months. According to evaluation criterion of chemotherapeutic effect by WHO in 1987, the results were; CR (complete remission) (n=0), PR (partial remission) (n=7), SD (stable disease) (n=3) and PD (progressive disease) (n=2). The effective rate was 58.3% (7/12). The median survival time was 14 months and median progression-free survival time 9 months. Conclusion Combined therapy of adrenal cortical adenocarcinoma is effective to prolong the patient lifespan. Radiotherapy offers partial symptomatic relief for those with osseous metastasis. Making an early diagnosis and offering a novel therapy yield a better outcome.

Objective To study the clinical features of 9 patients with X-linked adrenal hypoplasia congenita (AHC) by gene sequencing so as to provide diagnostic rationales. Methods The patients were 9 cases of X-linked AHC treated at our hospital from July 2007 to June 2009. The clinical manifestations were analyzed. The blood biochemistry tests and the hormone examinations including luteinizing hormone-releasing hormone ( LHRH) stimulation tests and human chorionic gonadotropin ( HCG) stimulation tests were conducted to evaluate the functions of gonads. And CT scans of adrenal glands and gene tests of DAX1/ NR0B1 were performed. Results Nine AHC patients from 8 families were studied. All patients had DAX1/ NR0B1 gene mutations. The main clinical features were; (1) some patients (3 families) had a family history of X-linked recessive inheritance; (2) the ages of onset were all below 10 years old (from 2 month after birth to 9 years old) and ages of being treated at our hospital were from 15 to 34 years old; (3) all patients had adrenocortical hypofunctions, but clinical situations were different, most of them had pigmentation (n = 9) , nausea and vomiting (n = 8) , hypotension (n = 6) , Addisonian crisis (n =4). Others were debility, hypoglycemia and cold susceptibility. laboratory tests indicated that all patients had hyponatremia at the onset and higher blood adrenocorticotropic hormone level, lower blood 17hydroxyprogesterone level compared to normal controls; (4) none of the patients had puberty and there was no responses to LHRH stimulation tests, 3 of them had normal responses to HCG stimulation tests; (5) small bilateral adrenal glands were displayed on CT scans. Conclusions The main clinical features of Xlinked AHC are adrenocortical hypofunetion and hypogonadotropic hypogonadism. But the phenotypes vary greatly in different patients. So male children with adrenal cortical hypofunetion should be suspected of Xlinked AHC and DAX1/NR0B1 gene tests should be performed. The sexual development of the patients also should be followed up.

Objective To investigate the correlation between excision repair cross-complementing 1 ( ERCC1) expression and cisplatin sensitivity in non-small cell lung cancer ( NSCLC). Methods A total of 168 NSCLC patients were selected from our hospital from January 2005 to December 2007. The expression of ERCC1 protein was analyzed by immuohistochemistry and ERCC1 mRNA tested by RT-PCR. Analyses were performed to determine the correlation between expression of ERCC1 and chemotherapeutic sensitivity in NSCLC. Results A positive expression of F.RCC1 protein was found in 99 ( 58. 93% ) patients. The expression of ERCC1 had no correlation with gender, age, stage and pathological types ( P >0. 05). Among all patients, 133 were followed up for about 3-5 years and 91 cases belonged to the responding group. Three cases with stage I a-I b underwent only operation without chemotherapy. And 76 (58. 46% ) patients were positive for ERCC1 expression in 130 cases. In the responding group, 38 (43. 18% ) cases had a positive expression of ERCC1 and 50 (56. 82% ) cases a negative expression of ERCC1. In the non-responding group, 37 (88. 10%) cases had a positive expression of ERCC1 and 5 ( 11.90%) cases a negative expression of ERCC1. The expression of ERCC1 decreased in the responding group versus the nonresponding group (x2 =23. 50, P <0. 01). The expressions of ERCC1 mRNA were (0. 624±0.275)and (2.758±0.771) in the responding and non-responding groups respectively (t = 11.54, P =0.013).Conclusion An elevated expression of ERCC1 is an important factor for cisplatin insensitivity in NSCLC. Itmay provide an useful reference for designing individualized chemotherapeutic regimens for NSCLC patients.repair cross-complementing 1; Cisplatin

Objective To explore the clinical experiences of combined palliative procedures for cyanotic congenital heart defects with intractable hypoplasia of pulmonary arteries. Methods From August 2001 to September 2009, 31 patients with cyanotic congenital heart defects and intractable hypoplasia of pulmonary arteries underwent surgical procedures. Among them, 26 patients were pulmonary atresia with ventricular septal defect and the other 5 cases complicated congenital heart defects with pulmonary stenosis. Different kinds of palliative procedures were performed according to the morphology of right and left pulmonary arteries in every patient. If the pulmonary artery was well developed, Glenn procedure was performed. Modified Blalock-Taussig or Waterston shunt was performed if pulmonary arteries had hypoplasia. If the pulmonary arteries were of severe hypoplasia, Melbourne shunt was performed. Systemic-pulmonary artery shunts were performed bilaterally in 23 cases. Systemic-pulmonary shunt was performed in one side and Glenn procedure contralaterally in 8 cases. Results There was one early death because of cardiac arrest. The number of patients suffered from low cardiac output syndrome, perfusion lung and pulmonary infection postoperatively was 5, 3 and 2, respectively. Systemic-pulmonary shunts were reperformed after theoriginal operation in 3 cases because of occlusion of conduits. The mean follow-up time was 25 ± 16 months (6-72 months). I>eft pulmonary index(8. 1 ±3.7 vs 14. 9 ±6. 2), right pulmonary index (12. 7 ±8. 1 vs 17.7 ±7. 8)and pulmonary index(20. 9 ±9.4 vs 32. 6 ± 11. 7) increased significantly (all P<0. 001). The pulmonary diameter increased significantly after modified Blalock-Taussig shunt (5. 5 ± 1. 0 vs 7. 0 ±2. 0) , modified Waterston shunt (5. 7 ± 4. 0 vs 9. 2 ± 3. 6) and melbourne shunt (2. 2 ± 0. 4 vs 7.4 ± 2. 5) (all P < 0.05) . Bilateral pulmonary arteries developed well compared with that of preoperative condition. Hemoglobin decreased from (194±27) g/L to (174±24) g/L (P<0.05) and peripheral oxygen saturation increased from (65 ±11)% to (84 ±6)% ( P < 0. 001 ) . During the follow-up ultimate complete repair were performed in 3 cases and one patients underwent Glenn procedure. Conclusions The procedures should be considered for hypoplasia of pulmonary arteries in cyanotic congenital heart defects. Combined palliative operation is an adequate therapy.

Objective To explore the clinical feasibility and features of adopting a low-collar arcshaped incision for minimally invasive near total thyroidectomy. Methods From April 1998 to March 2007, the procedure was accepted by 53 patients with thyroidal nodules, including nodular goiter (n=34 ) , thyroid adenoma ( n = 12 ) and thyroid carcinoma ( n=7). Near total thyroidectomy was performed through a 2-4 cm low-collar horizontal skin incision by conventional instrumentation. Results The incision yielded excellent cosmetic results because the small and lower incisions were completely hidden by clothing collar. The recurrent laryngeal nerve and parathyroid glands were easily identified and preserved. The mean operation time was 62. 2 minutes (range: 58-112). No complication occurred. The mean bleeding amount was 25 ml ( min: 10, max:100). The drainage was extracted at Day 2 or 3 postoperatively. The mean postoperative stay was 7.6 days (range: 7-12) while the post-operative follow-up 2 months to 9 years. Conclusion Such technique is feasible, safe, minimally invasive, less time-consuming and cosmetically ideal. It is suitable for young and middle-aged women.

Objective To study the effect of hypoxia on the proliferation of human bone marrow mesenchymal stem cells (hBMSCs). Methods The method of density gradient centrifugation was employed to isolate and culture hBMSCs. And flow cytometry ( FCM) was employed to detect the cell surface marker. After establishing the experimental model of CoCl2-chemical hypoxia, MTT method and flow cytometry were applied to evaluate the proliferation and the proliferation index of hBMSCs at different time points with various CoCl2 concentrations. Results The proliferations of hBMSCs was inhibited within the first 12 hours under chemical hypoxia condition. Compared with the normal group, the hBMSCs of each CoCl2 group were remarkably proliferated 1 ,2,4 days after chemical hypoxia with CoCl2,but 300 u,mol/L CoCl2 group showed no significant difference (P >0.05). 100 μmol/L CoCl2 group (0. 139 ±0. 003, 0. 178 ±0. 005, 0. 224 ±0. 005) and 150 μmol/L CoCl2 group (0. 202 ± 0.020, 0. 224 + 0.019, 0. 263 ± 0. 004) proliferation was significantly higher than that of the control group (0. 134 ± 0. 005, 0. 167 ± 0. 004, 0. 206 ± 0. 005 ) . Compared with the normal group, the hBMSCs were remarkably proliferated 24 hours after chemical hypoxia with CoCl2 concentration of 150 )μmol/L (all P < 0.05). At Day 6 , the 100,150 u.mol/1. CoCl2 group (0. 258 ±0. 020, 0. 264 ±0.008) cells was still higher than that of normal group (0. 248 ±0. 004), but the advantage gradually diminished ( P < 0.05 ) .At Day 7 , the proliferative effects of hypoxia disappeared. Conclusion CoCl2 -induced chemical hypoxia may promote the proliferation of hBMSCs.

Objective To elucidate the molecular mechanism of norcantharidin ( NCTD) in inducing apoptosis of liver cancer cells so as to provide basic rationales for its application in liver cancer treatment Methods Liver cancer cell lines of SMMC-7721 and BEL-7402 were treated with NCTD. The cell growth inhibition was measured by MTT [ 3-( 4, 5-dimethylthiazol-2-yl )-2, 5-diphenyltetrazolium bromide] assay, cell death detected by trypan blue exclusion assay and apoptosis examined by Annexin V/PI staining and flow cytometry. The cleavage of caspase-9, -3 and PARP, and the expression of the antiapoptotic Bcl-2 proteins were analyzed by Western blot. Results The MTT results showed that, after a treatment with NCTD for 24, 48 and 72 h, the 1C50 of NCTD in SMMC-7721 cell line was 12, 6 and 1. 6μg/ml respectively; in BEL-7402, the IC50 10, 4 and 2μg/ml respectively. Trypan blue exclusion assay showed that NCTD mediated substantial cell death in two cancer cell lines. Apoptosis assay showed that, after a 12 h treatment with 10 μg/ml NCTD, 27% of SMMC-7721 cells were induced to undergo apoptosis, an increment of 20% over the untreated control cells (7% ) ; 30% of BEL-7402 cells became apoptotic, an increment of 22% over the untreated control cells (8% ). Western blot analysis showed that NCTD treatment potently induced the activation of caspase-9, -3 and the cleavage of PARP, and markedly down-regulated the expression of Bcl-2, Bcl-XL and Mcl-1. Conclusion NCTD strongly inhibits liver cancer cell growth and potently induces apoptotic cell death in two liver cancer cell lines. The strong anticancer activity of NCTD may be induced through targeting multiple Bcl-2 anti-apoptotic family members.

Objective To construct a eukaryotic expression vector of stathmin gene and investigate its effect on esophageal squamous cell carcinoma ( ESCC) EC9706 cell line. Methods Stathmin cDNA coding sequence was amplified by RT-PCR and cloned into a eukaryotic expression vector pcDNA3. 1( + ). EC9706 cells were transfected with this recombinant plasmid pcDNA3. 1-stathmin by lipofectamine. And the stable transfectants were selected with G418 medium. Stathmin protein expression was detected with Western blot in transfected EC9706 cell lines. Morphologic change of stable transfectants was observed under microscope. The proliferation of transfected cells was measured by cell counting, MTT and in vitro formation assay of flat Flow cytometry was used to detect the cell cycle. Nude mice were adopted to investigate the in vivo tumorigenic characteristics of the transfected cells. Results A 450 bp coding sequence of stathmin cDNA was amplified by RT-PCR and then cloned into pcDNA3. 1 ( + ) plasmid to harvest the recombinant plasmid pcDNA3. 1-stathmin. The recombinant plasmid pcDNA3. 1-stathmin and blank vector were transfected respectively into EC9706 cells. The up-regulated expression of stathmin protein was validated by Western blot ( P < 0. 01 ) . Compared with control, EC9706 cells transfected with pcDNA3. 1-stathmin appeared swollen and multi-nuclear with a cell mitotic arrest; doubling generation time of pcDNA3. 1stathmin transfectants was prolonged(25 -28 h); The in vitro cell proliferation ability and clone formation rate (34.5% +-6.9%) decreased, cell cleavage was blocked at G2/M phase (21. 7% +- 3. 4% ) and the oncogenicity of inoculated cells in nude mice decreased ( all P < 0. 01). Conclusions The up-regulated expression of stathmin protein triggered by the recombinant plasmid pcDNA3. 1-stathmin can inhibit the proliferation and oncogenicity of ESCC EC9706 cells. TTiis molecule may be a promising therapeutic target in ESCC patients.

Objective To establish the murine xenograft model of human prostate cancer by grafting tumor tissues beneath the renal capsule of intact male athymic mouse. Methods Fifteen SCID mice were randomly divided into 3 groups ( n = 5 each ). Tissue recombinants were prepared in vitro with newborn BALB/c murine seminal vesicle mesenchyme (SVM) and surgical isolated human prostate cancer tissues by using recombination technique and then grafted beneath the renal capsule of intact male athymic mouse. At Week 4 after initial implantation, grafts were harvested and tumor sizes calculated. The expressions of human specific markers CK8/18 and vimentin were evaluated by immunohistochemistry to identify the human prostatic origin in grafts. P63 protein, a basal cell marker, was detected in prostate basal membrane to identify whether it was benign or malignant tissue. And the study control was prepared by implanting prostate cancer tissues alone under the renal capsule in SCID mouse. Results Of all 78 implantation cases in 15 mice, the tumor-forming rates were 100% (39/39)and 94. 1% (37/39)respectively in the recombination and prostate cancer alone grafting groups. The recombination group was shown to be more efficient in terms of tumor size and weight in comparison with the prostate cancer alone group [ ( 9. 7 +- 3. 1 ) vs ( 6. 8 +- 2. 0) mm3, (12. 1 +-3. 6) vs (8. 2 +-2. 2) (u,)g, P <0. 01 ]. There was no difference in serum PSA level between two groups. Grafts were confirmed as human prostate cancer tissues with the expressions of CK8/18 and vimentin. No expression of P63 was detected. Conclusion The xenograft murine model of human prostate cancer is successfully established. It contains stroma components and is particularly suitable for studying the interaction of stroma and epithelia in the in vivo progression of prostate cancer.

Objective To construct the human cytochrome P-450 CYP2E1 (CYP2E1) recombinant adenovirus vector and detect its anti-tumor effects in combination with chemotherapeutic drugs so as to provide rationales for gene directed enzyme prodrug therapy ( GDEPT) . Methods CYP2E1 cDNA was cloned from human liver and a recombinant adenovirus vector constructed at a titer of 1 x 1012 pfμ/ml. Human bone marrow-derived mesenchymal stem cells ( BMSCs) were separated, cultured, purified and detected. The tropism of BMSCs for cancer cells was detected by Transwell technique. These recombinant vectors were transferred into BMSCs and A375 cells and the expressions of EGFP and CYP2E1 detected by fluorescence microscope, RT-PCR and Western blot respectively. Inverted microscope, MTT and Annexin V-FTTC/PI were employed to detect the anti-tumor effect of CYP2E1 recombinant adenovirus vectors in combination with chemotherapeutic prodrug dacarbazine ( DTIC) . Results The recombinant adenovirus vectors pAd5CMV-NpA-CYP2El and pAd5CMV-NpA-EGFP were constructed successfully. BMSCs were successfully separated and they could migrate in vitro through a polycarbonate filter toward K562 and A375 cells in the lower chamber. Fluorescence microscope was used to detect the expression of EGFP while both RT-PCR and Western blot revealed a high expression of CYP2E1 in gene-transfected group cells. The dead cell counts of co-culture group of gene-transfected BMSCs and wild type A375 cells were significantly higher than those of the control under inverted microscope. The results of MTT showed that the growth inhibition of gene-transfected group cells was increased with DTIC concentration in a concentration dependent manner. IC50 of group BMSCs-CYP2El + A375 was (0. 17 ±0. 13) mmol/L, and that of the control group was ( 0. 65 ± 0. 20) mmol/L ( P < 0. 01). The DTIC concentration at which BMSCs were relatively safe might be selected at 0.05 mmol/L. Annexin V-FITC/PI confirmed that the apoptosis rate of BMSCs-CYP2E1 + A375 group was significantly higher than that of the control group after a 48-hour treatment of 0. 05 mmol/L DTIC (26. 8 ±2. 0 vs 8. 7 ± 1. 3, P < 0. 01). Conclusion With an in vitro tropism for cancer cells, BMSCs transferred with CYP2E1 recombinant adenovirus vectors have anti-tumor effects probably synergistically with chemotherapeutic drugs.

Objective To investigate the anti-tumor effect of interventional chemotherapy with liposome doxorubicin for hepatic metastasis of pancreatic tumor in nude mice. Methods After the establishment of hepatic metastatic model of pancreatic tumor, the nude mice received various formulations via a spleen injection to imitate the interventional chemotherapy. In each of two following experiments, 42 nude mice were randomly divided into 6 groups. They received liposomal doxorubicin ( including high, intermittent and low-dose), free doxorubicin, gemcitabine plus cisplatin and control respectively. In the first experiment, the doses were 6,3,1.5,3,3 mg/kg and 100 μl 10% glucose for each group respectively. And in the second experiment, 9, 6, 3, 6, 6 mg/kg, and 100 μl 10% glucose respectively. The efficacies of interventional injection of liposomal doxorubicin with different doses were examined in terms of tumor growth retardation for the hepatic metastatic foci of pancreatic tumor. Results In the first experiment, the difference of median hepatic tumor volume was significant among the three groups of mice receiving liposomal doxorubicin with incremental doses in a dose-dependent manner [ high dose: ( 3 ± 1 ) mm3, middle dose: (55 ± 18) mm3, low dose: (90 ± 23) mm3, P < 0.05 ]. The liposomal doxorubicin led to a substantial delay of tumor growth as compared to the free drug or gemcitabine plus cisplatin at the same dose ( both P <0.05). In addition, all animals were well-tolerated with no obvious acute toxiciry. In the second experiment, significant difference was obtained for the mice injected with different doses of liposomal doxorubicin [ (11 ±4)mm3, (13±4)mm3, (50 ± 18)mm3 ,P<0.05]. It was correlated with tumor growth delay. The mice administered with either 9 mg/kg or 6 mg/kg were more efficacious to retard tumor growth than those given 3 mg/kg ( P < 0. 05 ) . Despite its enhanced effectiveness as compared to mice in gemcitabine plus cisplatin group (P < 0. 05 ) , the liposomal doxorubicin at a dose of 6 mg/kg resulted in a marginally delayed tumor growth compared to those of free doxorubicin at the same dose ( P > 0. 05 ). No evident acute toxic response was observed for each group of mice receiving liposomal doxorubicin. In contrast, approximately half of the animals receiving either free doxorubicin or gemcitabine plus cisplatin died of toxic responses. Conclusion Liposomal doxorubicin may be a potential interventional chemotherapeutic agent for hepatic metastasis of pancreatic tumor because of improved anti-tumor efficacy and reduced toxicity in comparison to free doxorubicin and gemcitabine plus cisplatin.

Case Abstract A 42-year-old male was admitted to the hospital on December 23, 2009 due to "abdominal pain with melena for 1 d". The patient developed abdominal pain without obvious inducement 1 d ago, with persistent distension and pain around the umbilicus and left upper abdomen, accompanied by melena for 4 times, dark red rotten stool at first, and then black soft stool, with a total of about 500 g. The abdominal pain after defecation could be slightly relieved, but he still felt abdominal distension, and vomited three times at the same time, non-jetting, the vomit was stomach content, no hematemesis, accompanied by syncope once, which relieved spontaneously after about a few seconds, without disturbance of consciousness. He had no fear of cold and fever, no chest tightness and shortness of breath, no expectoration and hemoptysis. He came to the emergency department of our hospital and was admitted to the hospital with "abdominal pain and melena to be examined" after receiving symptomatic and supportive treatment such as hemostasis and fluid rehydration.

primary aldosteronism (PA) is a common clinical disease, and it is more common in urology, cardiovascular department and endocrinology department.The incidence of PA is 0.5% ~2% in general population and 5% ~12% in hypertensive patients.It is one of the common causes of refractory hypertension [1]. Besides, aldosterone itself can also cause cardiac and cerebral lesions,vascular inflammation,target organ damage, etc. [2-4]. Human adrenocortical cancer cell H295R cell has the characteristics of stable secretion of aldosterone and other steroid hormones, and is one of the few adrenocortical cell lines. Because H295R cell is closest to primary cultured human adrenocortical cells in hormone secretion and cell characteristics, H295R cell has become the main cell or even the only cell in human adrenocortical research at present [5].

There are only more than 100 cases of congenital X-linked adrenal hypoplasia congenita (AHC) with hypogonadotrophic hypogonadism (HH) caused by DAX1 gene mutation reported worldwide. Our hospital first diagnosed two domestic cousins with this disease in 2007 [1], and then diagnosed three patients. Because of the difficulty in diagnosing this disease and the lack of corresponding diagnosis and treatment routine, the diagnosis and treatment experience of these three patients is reported as follows.