Volume 85  ·   Issue 23  ·  2005

The first difficulty in the treatment of severe burn patients is shock, because a large amount of plasma components are extravasated within 48 hours after burn, and blood cells are destroyed, which is very easy to produce hypovolemic shock.

Objective to investigate the multidrug resistance reversal effect of schisandrin B (SchB) on human breast cancer cells MCF-7 transfected with multidrug resistance 1 gene (MDR1) and its related mechanism.Methods Human MDR1 gene was introduced into MCF-7 cells to form drug-resistant cell line MCF-7/MDR1. This cell line was used as a model to evaluate the multidrug resistance reversal effect of SchB in vitro. The IC50 of chemotherapy drugs alone or in combination with SchB was compared by MTT assay, and the reversal factor was calculated. Results The transfected cells showed high expression of P glycoprotein and increased resistance to doxorubicin, vincristine, paclitaxel and homoharringtonide; SchB (25 μ mol/L) significantly reduced the IC50 of doxorubicin, vincristine, paclitaxel and homoharringtonide on MCF-7/MDR cells, and the reversal fold was 6.03-23.94 times; SchB (25 μ mol/L) increased the intracellular accumulation of rhodamine 123 in MCF-7/MDR cells by about 5 times, and the effect was comparable to that of verapamil at 10 μ mol/L; However, SchB (25 μ mol/L) did not affect the expression of P-glycoprotein in MCF-7/MDR cells. Conclusion SchB can effectively reverse the multidrug resistance of MCF-7 cells transfected with MDR1, and the mechanism may be that it inhibits the efflux activity of P-glycoprotein.

Objective to establish a method for the detection of platelet derived microparticles (PMPs) by cytometric bead array (CBA) and evaluate its methodology.Methods the detection microspheres coated with monoclonal antibody against platelet membrane glycoprotein Ⅲa (CD61) were used to capture PMPs, and the captured PMPs were combined with CD41 PE, and the microsphere-PMPs-CD41 PE complex was detected by flow cytometry.The detection conditions were optimized by experiment; The repeatability and detection linearity of the method were evaluated.The levels of PMPs in 45 healthy subjects were detected.The results showed that the detection microspheres could be kept stably at 4℃ for more than 90 days with a variation coefficient of 0.65%, which basically met the requirements of clinical detection.The samples collected by CTAD anticoagulant tube could effectively inhibit the release of PMPs in vitro; The maximum binding of PMPs can be achieved by reaction at room temperature for 4h; The non-specific adsorption of PMPs by the detection microspheres can be removed by washing with PBS. The coefficient of variation within the batch of the method is 6.8%; The coefficient of variation between batches was 10.4%, which showed good repeatability; The PMPs in the activated platelet supernatant were detected by this method, and the linearity was good between 0 and 200 μ L (r =0.9962). The reference range of PMPs in 45 healthy adults was 1.031~1.766 (relative fluorescence intensity). Conclusion Flow microsphere technique can detect PMPs simply, quickly and accurately, which is of great significance for the diagnosis and treatment of clinical hemorrhage and thrombotic diseases.

Objective to establish an adrenal implant-containing kidney transplantation model and to explore the protective effect of adrenal implant on kidney transplantation. Methods on the basis of successfully preparing adrenal implant-containing kidney donor, allogeneic kidney transplantation was performed. The experimental animals were divided into group Ⅰ (adrenal implant-containing kidney transplantation group) and group Ⅱ (simple kidney transplantation group), all of which were not treated with any immunosuppressant, and the recipient's right kidney (left side was transplanted kidney) was removed 7 days after operation; The survival time of recipients after right nephrectomy was observed, and the morphological changes of adrenal implants and kidney transplantation, serum corticosterone, creatinine and urea nitrogen concentrations were measured at different time points before and after adrenal implantation and right nephrectomy. Results 7 weeks after adrenal implantation, adrenal implants survived well and recovered endocrine function; 7 days after right nephrectomy, the adrenal implants gradually showed atrophy, degeneration and punctate necrosis, but the survival time of 10.2 days ± 2.2 days in group Ⅰ was significantly longer than that of 7.3 days ± 1.2 days in group Ⅱ, and the morphological observation and functional status of the former were significantly better than that of the latter.Conclusion Adrenal implants have protective effects on kidney transplantation in the early stage after transplantation.

Objective to investigate the protective effect of rosiglitazone on renal interstitial fibrosis and its mechanism.Methods Using unilateral ureteral obstruction (UUO) in rats as a model, the contents of renal interstitial matrix on the obstructed side were observed at different time points (3d, 7d, 14d); Macrophage infiltration of renal cortex in each group; Expression of Fibrogenic Transforming Growth Factor-β 1 (TGF-β 1); The mRNA expression of connective tissue growth factor (CTGF), bone morphogenetic protein 7 (BMP-7), Smad6 signal protein and the protein expression of BMP-7 and PAI-1 in renal cortex related to renal fibrosis. Results Rosiglitazone could improve the degree of renal interstitial fibrosis induced by UUO (P<0.05); Significantly reduced the number of interstitial macrophage infiltration; The expression of TGF-β 1 in renal tissue was down-regulated (P<0.05); Decrease the expression of fibrogenic factors CTGF and PAI-1 downstream of TGF-β 1; Conclusion Rosiglitazone can protect against renal interstitial inflammation and fibrosis induced by UUO, and its possible mechanisms include inhibiting the infiltration of renal interstitial inflammatory cells; Reduce the expression of TGF-β 1, prevent TGF-β signal transduction, inhibit the expression of TGF-β 1 downstream effector factors CTGF and PAI-1, and increase the expression of BMP-7 protein with anti-fibrotic and anti-inflammatory effects, so as to block the fibrogenic effect of TGF-β 1 from multiple layers.

Objective to investigate the mutation frequency and characteristics of rhodopsin gene (RHO) and retinitis pigmentosa 1 (RP1) gene in Hong Kong Han nationality patients with retinitis pigmentosa (RP), and to further explore their potential interaction in the pathogenesis of RP. Methods 151 Han nationality RP probands and 150 controls in Hong Kong were detected by high-throughput conformation sensitive gel electrophoresis and direct sequencing. The mutation of RHO and RP1 gene in the whole coding region and adjacent split region was detected. 46 relatives of 12 RP probands were further separated and analyzed. The effects of RHO and RP1 gene on RP were studied by univariate analysis, multivariate analysis and genotype family imbalance analysis. Results the mutation detection rates of RHO gene and RP1 gene were 1.3% each. R872H in RP1 gene could reduce the risk of RP. Multivariate Logistic regression analysis revealed that there was an interaction between IVS4-23G>A of RHO gene and N985Y and C2033Y of RP1 genes, respectively. Conclusion The mutation rate of RHO and RP1 gene in Han RP patients in Hong Kong is lower than that of other RP patients. Besides pathogenic gene mutation, the sequence change of non-coding region can also change the susceptibility of RP.

Objective to evaluate the feasibility, safety and efficacy of radiofrequency ablation (RFA) in the treatment of hepatic cavernous hemangioma (HCH), and to explore the best way of radiofrequency therapy. Methods From March 2001 to June 2004, a total of 104 HCH lesions in 68 patients were treated with RFA. Among them, 19 cases were treated with percutaneous RFA, 29 cases were treated with laparoscopic RFA, and 20 cases were treated with open RFA. During laparoscopic and open RFA therapy, 7 cases of lesions with a diameter greater than 7 cm were treated with Pringle method to block intrahepatic blood flow. Postoperative ultrasonography and spiral CT scan were used to evaluate the efficacy of RFA. Results Two new lesions were found in laparoscopic RFA and 4 new lesions were found in open RFA. All cases completed RFA successfully. After blocking intrahepatic blood flow with Pringle method, the mean intraoperative blood loss was significantly reduced (P<0.01), the average radiofrequency treatment time of single lesion was significantly shortened (P<In laparoscopic RFA, 15 cases underwent simultaneous cholecystectomy due to chronic calculous cholecystitis, 2 cases underwent cholecystectomy due to the involvement of the gallbladder bed, 3 cases underwent fenestration and drainage of hepatic cyst. In open RFA, 5 cases underwent simultaneous cholecystectomy due to gallbladder lesions, 1 case underwent partial resection of hepatic cyst, and 3 cases underwent common bile duct exploration due to common bile duct stones. 29 cases showed postoperative fever and serum transaminase increases, and 1 case developed transient hematuria. No serious complications related to RFA treatment were found. After 6-36 months follow-up, the complete necrosis rate of lesions was 99% (103/104). 1 case found marginal residual lesions 6 months after percutaneous RFA treatment, and percutaneous RFA treatment was performed again. Conclusion RFA is safe and feasible in the treatment of HCH, and the efficacy is affirmative. According to the size, number, location and clinical status of patients, percutaneous, laparoscopic or open RFA treatment can be selected. Laparoscopic or open RFA treatment after blocking intrahepatic blood flow can reduce the bleeding volume and improve the curative effect.

Objective to investigate the changes of hospitalization composition ratio and mortality of patients with pulmonary thromboembolism (PTE), and to provide reference for the prevention and treatment of PTE. Methods The data of 442 inpatients with PTE admitted to Fuwai Cardiovascular Hospital from 1974 to 2002 were retrospectively analyzed. Results The annual number of inpatients with PTE and the inpatient composition ratio increased gradually from less than 5 cases per year and 0.1152% per year in early 1970s to 48~79 cases per year and 0.5866% per year in early 21st century. The peak incidence of PTE was in winter, and the incidence was significantly higher than other seasons (P<The mortality rate of patients with PTE decreased significantly from 20% in the 1970s to 5.8% in the beginning of the 21st century. The mortality rate of patients with PTE was 12.5% before 1990 and 4.5% after 1990, the difference was statistically significant (P =0.005). The mortality rate of patients with PTE was 4.6% in male and 8.6% in female, the difference was not statistically significant (P =0.09). The mortality rate of patients with PTE was 5.5% in PTE less than 70 years old and 19.0% in patients ≥70 years old, the difference was statistically significant (P<Conclusion PTE is an important common disease and should be paid more attention to.

Objective to investigate the relationship between the expression of CT120A and the growth of lung cancer cells. Methods the RNA interfering plasmid small hairpin RNA (shRNA) -H was constructed and transfected into lung adenocarcinoma cell line SPC-A-1. The expression of CT120A was determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Cell proliferation in vitro was analyzed by BrdU-TdR incorporation assay and soft agar clone formation assay; The tumorigenic ability of SPC-A-1 cells in vivo was determined after the down-regulation of CT120A gene expression in nude mice. RNA interfering expression plasmid shRNA-H could effectively inhibit the expression of CT120A gene, reducing the expression of CT120A mRNA by 50% ~70% and protein by 80%. The down-regulation of CT120A gene inhibited the proliferation of SPC-A-1 cells in vitro, reduced the ability of SPC-A-1 cells to form clones in soft agar and tumor in nude mice, and increased the sensitivity of SPC-A-1 cells to UV-induced apoptosis. Conclusion CT120A gene has a close relationship with the growth of lung cancer cells, and CT120A gene may be used as a new target for drug treatment of lung cancer.

Objective to investigate the relationship between adenovirus vector (Ad) -mediated anti-tumor immunity induced by xenogeneic melanoma-associated antigen tyrosinase-associated protein 2 (TRP2) and autoimmune damage.Methods C57BL/6 mice were intradermally immunized with AD-encoded human or mouse TRP2 (Ad hTRP2 or Ad mTRP2), and the mice were divided into normal control group (d170-3), Ad hTRP2 and Ad mTRP2 immunization groups.CTL killing activity and IFN-γ production were analyzed by in vivo cytotoxic T lymphocyte (CTL) killing assay and intracellular interferon γ (IFN-γ) staining (ICS) (3 mice per group); B16.F10 melanoma cells (10 mice in each group) were inoculated subcutaneously to observe the survival of tumor-bearing mice. Results the CTL killing activity of mice induced by Ad hTRP2 was correlated with the immunization time, the activity reached the maximum 1 week after immunization, and then gradually decreased; The killing activity of CTL induced by Ad hTRP2 was dose-responsive. The killing rate of CTL in mice immunized with Ad hTRP2 was 94% ± 5% at 6 hours after 1 week, and the CD8+ T cells producing IFN-γ in spleen accounted for 0.87% ± 0.12% of the total CD8+ T cells, while Ad mTRP2 was 22% ± 8% and 0.15% ± 0.05% respectively. The mice immunized with Ad hTRP2 inoculated with 1×106 B16.F10 cells showed 100% tumor-free growth after 3 months, but vitiligo formed at the virus injection site; However, the survival rate of mice immunized with Ad mTRP2 inoculated with 1×105 B16.F10 cells at 3 months was only 20%, and there was no local vitiligo formation. Conclusion AD-mediated xenogeneic TRP2 can effectively break the immune tolerance to self-TRP2, induce strong antigen-specific cellular immune response, and at the same time, it is accompanied by autoimmune damage.

Objective to investigate the role of serum and glucocorticoid-induced protein kinase-1 (SGK1) in the production of fibronectin (FN) in human glomerular mesangial cells (HMC) induced by high glucose, and to explore the mechanism of SGK1 in glomerular sclerosis in diabetic nephropathy (DN). Methods Plasmid with SGK1 dominant activated mutant (pIRES2-EGFP-S422D SGK1 mutant, SD) was transiently transfected into HMC; At the same time, the mRNA and protein expression of SGK1 and FN were observed by RT-PCR and Western blot. Results the expression of SGK1 mRNA in HMC transfected with SD was significantly higher than that in HMC transfected with FP and NT (0.704 vs 0.497, 0.491, P<0.01), SGK1 protein overactivation (1 178 497 vs 193 875, 195 597, P<0.01), the expression of FN mRNA and protein increased significantly (0.749 vs 0.463, 0.475, P<0.01; 659 550 vs 342 354, 340 428, P<Conclusion In diabetic nephropathy, high glucose can induce FN synthesis in human mesangial cells through SGK1-mediated signaling pathway. This newly discovered signaling pathway indicates that SGK1 may be involved in the occurrence of glomerular fibrosis in diabetic nephropathy.

Recently, during the mid-term inspection or final review of some major clinical research projects, the national scientific research management department found that although the quality of research design scheme of the evaluation projects has improved obviously, there are still many problems in project implementation, which are highlighted by the poor compliance of researchers, that is, the researchers can't strictly follow the design scheme, which leads to the decline of data quality.

"Subglottic" refers to the upper airway space between the lower edge of the vocal cords and the lower edge of the cricoid cartilage. Benign subglottic stenosis can occur after trauma, and it is more common in iatrogenic (mainly after endotracheal intubation) [1], followed by inflammation, inhalation burn and idiopathic lesions of unknown nature, and a few are congenital [2]. The pathological manifestations are fibrocicatricial changes, and some can involve the glottis upward, upper glottis, and upper trachea downward (i.e. combined lesions), and the lumen is often obstructed by more than 70%. Patients with obvious dyspnea usually need to stay in the tracheotomy catheter for a long time. X-ray film of the neck, CT scan and magnetic resonance all show images of total circumferential stenosis. Endoscopic stenosis can be seen below the vocal cords and cannot be extended. Because of the traditional view that transverse subglottic airway at the level of cricoid cartilage will lead to bilateral recurrent laryngeal nerve paralysis [3], endoscopic dilatation, laser vaporization, tracheotomy and laryngoplasty with internal support are mostly used in treatment [4-6].

Prostate cancer, especially well differentiated adenocarcinoma, is difficult to distinguish from prostatic hyperplasia or adenopathy in histology. We observed the expression of p504s-p63 mixed antibody in prostate cancer and benign hyperplasia tissues by immunohistochemistry, and explored the specific marker of prostate cancer and the differential diagnosis method of prostate cancer.

Meningeal metastasis of solid tumors is rare in clinic, but it has increased by about 4% ~15% in recent 20 years [1, 2]. However, meningeal metastasis of breast cancer has shown a downward trend, which is probably related to the increasing neoadjuvant chemotherapy [2]. Meningeal metastasis caused by solid tumors is more common in breast cancer about 12% ~34%,lung cancer 17% ~25%,melanoma 17% ~25%,and malignant tumors of digestive system 4% ~14% [3]. Between 1995 and 1999, we treated 80 cases of leatheroid gastric cancer in Gustave Roussy Cancer Treatment Center in France. Among them, 4 cases were complicated with meningeal metastasis, all of which were between 48 and 58 years old, including 3 males and 1 female. No abnormalities were found in preoperative examination, and 3 patients underwent surgical treatment, and 1 patient was found to have peritoneal metastasis at the time of diagnosis. The clinical diagnosis and treatment process is reported as follows.

The patient, a 26-year-old woman, felt pain in her right middle abdomen at night two days ago, showing persistent colic, aggravated during activity, without nausea, vomiting and diarrhea. Physical examination showed clear consciousness, poor spirit, painful appearance, no yellowing stain of skin and sclera, flat and soft abdomen, tense right abdominal muscle, and a mass of 15 cm ×10 cm in the right middle and upper abdomen, soft texture, clear border, obvious tenderness, no rebound pain, not subcostal of liver and spleen. Body temperature: 38 ℃. Blood routine: white blood cells 11.4×109/L, red blood cells 3.61×1012/L, neutral 0.81, lymph 0.10. Liver and kidney function were normal. Clinical diagnosis: inflammatory mass in the right abdominal cavity.

A 14-year-old female was seen in Fuzhou General Hospital of Nanjing Military Region in early November 2002 for "repeated fever, cough, expectoration and chest pain for 3 months". During physical examination, a protuberant mass of about 2.5 cm ×2.0 cm was found on the right chest wall, with obvious inflammatory exudation around it, desquamation and a little secretion on the surface, and soft texture. Other superficial lymph nodes and liver and spleen were not enlarged. CT showed: right middle and lower chest wall soft tissue and pleural cavity lesions, right rib bone destruction and right pleural effusion. Intraoperative frozen section pathology showed lymphoma. Considering the wide cumulative range, the possibility of radical resection of chest wall lesions was small, and thoracic reconstruction was difficult, so right chest wall incision and closed drainage was given. Postoperative pathology showed: anaplastic large cell lymphoma; Immunohistochemistry: CD20 (-), CD3 (-), CD15 (-), CD30 (+ +), ALK (+), EMA (+ +), vimentin (+).

A 28-year-old male was admitted to the hospital mainly because of "repeated bone pain for 4 years". In 2000, the patient developed dull pain in right hip joint without obvious trigger, and the symptoms gradually aggravated and claudication appeared. In the local hospital, the blood calcium and phosphorus were "low", and pelvic X-ray showed "bilateral old fracture of femoral neck", and was diagnosed as "hypophosphatemia and anti-vitamin D rickets". After treatment with calcitriol, calcium carbonate and neutral phosphorus solution, the symptoms gradually alleviated. In early 2002, the right mandible was found to have a bone bulge of about 2.0 cm ×1.0 cm. In April 2002, the patient developed weakness of both lower limbs. X-ray in the local hospital showed "bilateral femoral head necrosis, embedded femoral neck fracture, and multiple double concave deformations of vertebral body".

The basic and clinical research of atrial fibrillation (AF), completed by Professor Huang Congxin of Wuhan University People's Hospital, Professor Ma Changsheng of Beijing Anzhen Hospital affiliated to Capital Medical University, Professor Yang Yanzong of the First Affiliated Hospital of Dalian Medical University and Professor Zhang Shu of Fuwai Cardiovascular Hospital of Chinese Academy of Medical Sciences, won the second prize of National Science and Technology Progress Award not long ago.

primary biliary cirrhosis (PBC) and autoimmune hepatitis (AIH) are two common autoimmune liver diseases with their own unique clinical manifestations. However, in recent years, it has been found that some patients have the characteristics of these two diseases simultaneously, which are called "overlapping syndrome". The clinical, biochemical and therapeutic responses of 11 patients with PBC/AIH overlapping syndrome were analyzed in this paper.

Thromboembolism, especially stroke, is the main cause of disability and death in atrial fibrillation, but the mechanism of thrombosis has not been completely elucidated. Nitric oxide has powerful antithrombotic and anti-arteriosclerotic effects, and it is closely related to many cardiovascular diseases [1], but its role in atrial fibrillation is still unclear. In this study, we will use competitive PCR to quantitatively determine the expression of plasminogen activator inhibitor-1 (PAI-1) mRNA in atrial intima of atrial fibrillation dogs, and use nitric oxide sensitive electrode to directly determine the content of nitric oxide in endocardium.

Hereditary antithrombin (AT) deficiency is caused by AT gene mutation, which can be divided into two types: Type I is mainly manifested by the synchronous reduction of AT antigen (AT:Ag) and activity (AT:A) levels, and Type II is caused by AT structure abnormality [1]. More than 300 cases have been reported abroad, with more than 130 types of gene mutation; However, we have only reported one case in China [2]. In this paper, another family of AT deficiency was studied, and it was found that this family was hereditary AT deficiency type I, caused by the heterozygous mutation of AT gene C2757T.

The RHD and RHCE genes located on human chromosome 1 (1p34-36) encode RHD and RHCE, the core proteins of Rh blood group system, respectively [1]. Among them, D antigen has important clinical significance because of its strong immunogenicity. At present, most of the studies on the molecular mechanism and frequency distribution of weak D phenotype are concentrated in European population, while there are few studies on this aspect in Chinese population [2-7]. We studied a case of D mutant and found a new RHD allele, which is reported as follows.