Volume 86  ·   Issue 38  ·  2006

Helicobacter pylori (Hp) was studied as early as 100 years ago, but it was not until 1982 that Australian scholars Warren and Marshall successfully isolated "unidentified Campylobacter" from human stomach. It was renamed several times, and it was officially named Hp in 1989. In recognition of their outstanding achievements in the discovery of Hp, the Nobel Prize in Physiology and Medicine was awarded to these two scientists in 2005. The discovery of Hp is a major event in the history of medicine. The Nobel Prize won by Warren and Marshall is a glory and a milestone in the research of gastroenterology.

In the early 1990s, it was reported that the incidence of reflux esophagitis increased after the eradication of Hp. Subsequently, the clinical research on the relationship between gastroesophageal reflux disease (GERD) and Hp attracted widespread attention.

Objective to explore the value of a new surgical method: fistula-jejunostomy in the treatment of external pancreatic fistula.Methods From May 2002 to March 2005, a total of 8 patients with external pancreatic fistula were treated with fistula-jejunostomy in which the fistula was separated 2cm into the abdominal cavity and a silicone tube was implanted in the fistula. The distal end of the jejunum was dissected, and the distal end of the jejunum was valged 3 cm. The mucosa of the jejunum was destroyed with carbonic acid, and the fistula was sutured with the end of the mucosa. The jejunum was turned up to cover the fistula, and tied around the jejunum with thick silk thread for one week. The silicone tube was led out of the body through the abdominal wall through the jejunostomy. Results 8 patients recovered smoothly after operation without complications such as pancreatic fistula.

Objective to investigate the effects of SrhCD40L-mediated CD40 ligandation on the biological behavior of human Burkitt lymphoma CA46 cells and its possible molecular mechanism.Methods The effects of SrhCD40L-mediated CD40 ligandation on the proliferation, cell cycle and apoptosis of human Burkitt lymphoma CA46 cells were detected by tetramethylazole salt colorimetry, cell cycle analysis, Annexin-V apoptosis detection and terminal deoxynucleotide mediated nick end labeling (TUNEL). Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and immunoblotting were used to detect the effects of SrhCD40L-mediated CD40 ligandation on the expression of survivin gene and protein in human Burkitt lymphoma CA46 cells. Results CD40 was highly expressed in human Burkitt lymphoma CA46 cells; SrhCD40L-mediated CD40 ligandation induces homotypic aggregation, inhibits cell proliferation and induces apoptosis in CA46 cells.The effect on cell cycle is that S phase is blocked from entering G2/M phase.SrhCD40L-mediated CD40 ligandation can cause down-regulation of survivin gene and protein expression in CA46 cells.Conclusion SrhCD40L-mediated CD40 ligandation can inhibit the proliferation and induce apoptosis of Burkitt lymphoma CA46 cells; Survivin gene and protein may be one of the molecular mechanisms involved in SrhCD40L-mediated CD40 ligandation inhibiting proliferation and inducing apoptosis of CA46 cells.

Objective to study prospectively the efficacy of cyclosporine A (CsA) in the treatment of myelodysplastic syndrome (MDS). Methods 33 cases of MDS were treated with CsA, including 24 cases of refractory anemia (RA), 2 cases of refractory anemia with circular sideroblastosis (RAS), and 7 cases of refractory anemia with blastosis (RAEB). Methods of administration: 3~5 mg · kg-1 · d-1, divided into two doses. During the course of treatment, the dose was adjusted according to the blood concentration of CsA and the curative effect, and the course of treatment was more than 3 months. Results At 3 months of treatment, according to the evaluation criteria of MDS International Working Group, the total hematological improvement rate of 32 patients was 18/32 (56.3%). At the end of follow-up, the median follow-up period was 14 months, and the natural course of disease changed in 4 cases (4/32): 1 case was in complete remission, 3 cases were in partial remission, and 16 cases were in hematological improvement, with the total effective rate of 20/32 (62.5%). Conclusion This paper confirms that CsA is effective in the treatment of patients with RA and RAEB type, and it is effective for both hypoplastic and active hyperplastic myelodysplastic syndrome.

Objective to investigate the diagnostic value of neurological symptom/neurological deficit score (NSS/NDS), Michigan neuropathy screening method (MNSI), vibration sensory threshold examination (VPT) and 10 g nylon wire examination in diabetic peripheral neuropathy (DPN). Methods Nerve conduction velocity (NCV) examination, NSS/NDS score, MNSI score, VPT examination and 10 g nylon wire examination were performed in 240 patients with type 2 diabetes mellitus who met the criteria. The sensitivity, specificity, positive predictive value, negative predictive value, accuracy and Kappa value (κ value) of the four simple methods were calculated using NCV as the "gold standard". Results The sensitivity, specificity and accuracy of MNSI>2 were 78.15%, 88.43% and 83.33%, respectively, which were highly consistent with NCV examination (κ value was 0.67). The sensitivity and accuracy of NSS/NDS score and VPT examination were lower than those of MNSI screening method, but better than those of NCV examination (κ value was 0.52 and 0.60, respectively), but lower than those of MNSI screening method.10 It can be used for outpatient and inpatient DPN initial screening and epidemiological investigation.

Objective to investigate the effects of chronic hepatitis B virus (HBV) infection on human liver cytochrome enzyme 3A4 (CYP3A4), and to provide guidance for safe medication in patients with chronic HBV infection. Methods Liver tissue samples from patients with chronic HBV infection and normal subjects were collected, homogenized and prepared into microsomes by differential centrifugation. Using testosterone as probe substrate, a technical platform for the detection of CYP3A4 enzyme metabolism in vitro was established by high performance liquid chromatography (HPLC), and the enzyme activity of CYP3A4 in liver tissue samples of the two groups was detected. The difference of expression of CYP3A4 protein in liver tissue samples of the two groups was determined by Western blot method. Results HPLC detection showed that the index Vmax reflecting enzyme activity was (493±297) pmol·min-1·mg-1 in chronic HBV infection group and (741±189) pmol·min-1·mg-1 in normal control group. The difference between the two groups was statistically significant (P =0.03), while the characteristic constant Km value of enzyme system was (0.142±0.057) μ The expression of CYP3A4 protein in the chronic HBV infection group was 3.0±1.6, which was lower than that in the normal group (5.7±1.5). The correlation coefficient between enzyme activity and protein expression in each sample was 0.7683 (P<0.01), indicating that there was a good correlation between enzyme activity and protein expression. Conclusion Chronic HBV infection can reduce the expression of CYP3A4 enzyme protein in the liver, resulting in a decrease in enzyme activity, but no effect on the structure of enzyme.

Objective to observe the effect of fusion gene of human vascular endothelial growth factor 165 (hVEGF165) and chimeric hirudin (FH) on restenosis after carotid artery injury in rabbits, and to provide a new idea for gene therapy of restenosis. Methods The fusion gene of hVEGF165 and FH (hVEGF165-FH) was constructed by gene recombination. The model of restenosis after common carotid artery angioplasty in rabbits was prepared. The fusion gene was transfected locally from the injury as the treatment group, and pcDNA3.0 empty plasmid was transfected locally as the control group. The results showed that the degree of vascular stenosis in the treatment group was significantly reduced compared with the control group by angiography and pathological analysis. Pathological analysis showed that the degree of luminal stenosis in the treatment group was significantly reduced compared with the control group (1 week: 11.50% vs 33.25%; 3 weeks: 19.75% vs 52.25%, P<0.05); The degree of intimal hyperplasia (intima/media, I/M) was significantly reduced in the treatment group compared with the control group (1 week: 0.12 vs 0.50; 3 weeks: 0.35 vs 1.07, P<0.05). At the same time, the fusion gene had an inhibitory effect on thrombosis at the site of vascular injury, but had no effect on systemic coagulation index, and there was no systemic hemorrhage complication.Conclusion the fusion gene hVEGF165-FH can effectively prevent restenosis after carotid angioplasty in rabbits.Based on endothelial repair, the construction of dual-target or even multi-target fusion gene may be an effective strategy for the prevention and treatment of restenosis in the future.

Helicobacter pylori (Hp) is a major pathogenic bacterium that causes chronic gastritis, peptic ulcer, gastric cancer and mucosa-associated lymphoid tissue (MALT) lymphoma [1]. The cag pathogenic island (PAI) of Hp [2] and IgG antibody produced by one of the immune antigens, CagA, have been proved to be related to gastric mucosal atrophy and gastric cancer caused by Hp infection [3]. There are also a certain number of Hp infected people in Schistosoma japonicum infected populations in China, and it is still unclear whether these co-infected populations have special clinical consequences. This study examined whether Schistosoma japonicum infection regulates the humoral immune response against Hp and delays the occurrence of atrophic gastritis through the existing serological data.

Objective to determine the differential proteins of Helicobacter pylori (Hp) in gastric cancer, peptic ulcer and gastritis. Methods Hp was isolated and cultured from gastric mucosal tissues biopsied by gastroscopy, the bacterial proteins of Hp were extracted by lysates and ultrasonic disruption method, and then the bacterial proteins were quantified by Bradford method. The bacterial proteins of Hp were obtained by bidimensional electrophoresis. The differential proteins of Hp in gastric cancer, peptic ulcer and gastritis were found by Imagemaster 5.0 image analysis software. The differential proteins were identified by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF) and quadrupole time-of-flight electrospray tandem mass spectrometry (Q-TOF). Results Three cases of Hp in gastric cancer, peptic ulcer and gastritis were selected for two-dimensional electrophoresis. Compared with gastric ulcer and gastritis, four protein spots in Hp of gastric cancer were highly expressed. The results of mass spectrometry were thioredoxin, adenylate kinase, single-stranded DNA binding protein and ribosomal protein, 50 S, L7/L12, with Mowse scores of 94, 286, 139 and 132, respectively, and the sequence coverage rate was 77%, 33%, 33% and 28%, respectively. Conclusion Thioredoxin has the functions of antioxidant and inhibiting apoptosis, which may be related to the carcinogenic effect of Hp. Proteomics research has a wide application prospect in the research field of the relationship between Hp and gastric cancer.

Objective to study the expression of peroxisome proliferation factor-activated receptor γ (PPAR-γ) and cyclooxygenase 2 (COX-2) in Helicobacter pylori (Hp) infection and its related diseases and their relationship to explore the pathogenesis of Hp. Methods Two-step immunohistochemical method was used to detect the expression of COX-2 and PPAR-γ in gastric mucosa of 209 patients with endoscopic biopsy. 209 cases included 75 cases of superficial gastritis (CSG) (including 50 cases of Hp positive and 25 cases of Hp negative), 24 cases of atrophic gastritis (CAG) (including 13 cases of Hp positive and 11 cases of Hp negative), 90 cases of intestinal metaplasia and dysplasia (IM + DYS) (including 45 cases of Hp positive and 45 cases of Hp negative) and 20 cases of Hp negative gastric mucosa with roughly normal histology. Meanwhile, the expression of COX-2 and PPAR-γ in gastric mucosa of 36 patients with CSG who had been infected with Hp for more than 10 years before and after 10 years was also detected. Results (1) From control group → CSG → CAG → IM + DYS, the expression of COX-2 in glandular cells was gradually stronger, The positive rates of COX-2 in inflammatory cells were 0, 32%, 29.2% and 36.7%, respectively, and were higher in all disease groups than in the control group (all P<0.05). (2) The expression of COX-2 in glandular cells and inflammatory cells of Hp-positive patients in CSG group and IM + DYS group were significantly higher than those of Hp-negative patients (P<0.01 or P<0.05). (3) The positive rates of PPAR-γ in glandular cells were 0, 18.7%, 29.2% and 45.6% from control group → CSG → CAG → IM + DYS, respectively (P<0.01 or P<0.05); The positive rates of PPAR-γ in inflammatory cells were 0, 22.5%, 20.8% and 22.2%, respectively (P>0.05). (4) The expression of PPAR-γ in inflammatory cells in CSG group and IM + DYS group was significantly higher than that in Hp negative group (P<0.01); The expression of PPAR-γ in glandular cells was significantly higher in Hp positive patients in CSG group and IM + DYS group than in Hp negative patients (P<0.05). (5) The expression of COX-2 in inflammatory cells of CSG patients with persistent Hp infection was significantly lower after 10 years than that of 10 years ago (P<0.05), but there was no significant difference in the expression of PPAR-γ in inflammatory cells before and after 10 years (P>0.05). (6) The expression of COX-2 and PPAR-γ in glandular cells of CSG patients with persistent Hp infection after 10 years was significantly higher than that of 10 years ago (P<0.01). (7) There was no correlation between the expression of COX-2 and PPAR-γ in inflammatory cells of Hp negative disease groups (r =0.006 and 0.149, both P>0.05); The expression of COX-2 and PPAR-γ in glandular cells showed a significant positive correlation in IM + DYS group (r =0.336, P<0.05), but there was no correlation between the expression of COX-2 and PPAR-γ in other disease groups (r =0.035 and 0.126, both P>0.05). (8) The expression of COX-2 and PPAR-γ in inflammatory cells and glandular cells in Hp-positive disease groups showed a significant positive correlation with each other (r =0.348 and 0.645, P<0.05 or P<0.01). Conclusion (1) Hp infection can induce the over-expression of COX-2 and PPAR-γ in gastric mucosal inflammatory cells and glandular cells, and Hp may be involved in the early progression of gastric cancer by up-regulating the expression of COX-2 and PPAR-γ. (2) The expression of COX-2 induced by Hp infection is related to acute inflammation caused by Hp infection; With the prolongation of infection time, the expression changes of COX-2 and PPAR-γ may reflect the pathological process of CSG → CAG → IM → DYS → gastric cancer caused by Hp infection earlier than pathological examination.

Objective to investigate the effects of resistant strains of Helicobacter pylori (Hp), gender, age and different clinical diseases on Hp eradication therapy, and to clarify the main reasons for the failure of Hp eradication therapy. Methods The minimum inhibitory concentration (MIC) of Hp strains against metronidazole and clarithromycin was determined by E-test in patients with positive Hp culture who came to the gastroscopy room of Peking University First Hospital for upper gastrointestinal symptoms. All the enrolled patients were treated with lansoprazole, metronidazole and clarithromycin for 7 days. Results A total of 157 patients entered the study and completed the treatment. The resistance rates of Hp to metronidazole and clarithromycin were 45.9% (72/157) and 18.5% (29/157), respectively. The eradication rate of Hp in 157 patients was 61.8% (97/157), and the difference of Hp eradication rate among patients with different genders, ages and different clinical diseases was not statistically significant (all P>0.05); The eradication rates of metronidazole-sensitive strains and drug-resistant strains were 89.4% (76/85) and 29.2% (21/72) (P<0.01), respectively. The eradication rates of clarithromycin-sensitive strains and drug-resistant strains were 72.7% (93/128) and 16.0% (4/29) (P<0.01), respectively.

Objective to study the effects of Helicobacter pylori (Hp) infection on the type of gastritis and esophageal acid exposure, especially the relationship between colonization density of Hp and reflux esophagitis (RE), and further explore the role of Hp in the pathogenesis of reflux esophagitis (RE). Methods 223 patients with gastroesophageal reflux disease with typical symptoms such as acid reflux and heartburn were examined by gastroscopy and gastric mucosal biopsy for pathological examination, and gastroesophageal pH monitoring for 24 hours. RE or non-erosive reflux disease (NERD) were diagnosed according to the presence or absence of erosion of esophageal mucosa under gastroscopy. Combined with gastroscopy and pathology, gastritis was divided into 4 groups: chronic non-atrophic antrum gastritis group (CNAA group, chronic non-atrophic inflammation of gastric antrum was mainly, and gastric mucosa was basically normal); Chronic non-atrophic gastritis group (CNAG group, there were obvious chronic non-atrophic inflammation in gastric antrum and body); Chronic atrophic antral gastritis group (CAA group, chronic atrophic inflammation of gastric antrum); In the chronic atrophic gastritis group (CAG group, chronic multifocal atrophic inflammation of gastric antrum and body), Hp infection was diagnosed by WS staining, and it was divided into mild, moderate and severe infection according to the colonization density of Hp. DeMeester score ≥15 was used as the positive diagnostic criterion in 24 h pH monitoring. Results Among 223 patients with GERD, 62 (27.8%) were confirmed as RE by gastroscopy, and the remaining 161 (72.2%) were NER.67 (30.0%) were Hp positive, and there was no statistically significant difference in age, gender, incidence of RE, positive rate of pH monitoring and DeMeester score between Hp positive and Hp negative patients. Among the 223 patients, 45 (20.2%) had CNAA, 88 (39.5%) had CNAG, 65 (29.2%) had CAA, and 25 (11.2%) had CAG. The Hp-positive patients showed obvious non-atrophic chronic inflammation of gastric antrum and gastric body (56.7%), which was significantly different from the Hp-negative patients (P<0.05). The proportion of CAG in RE group was lower than that in NERD group (6.5% vs 13%); Among 67 patients with Hp-positive GERD, the positive rate of 24-h pH monitoring and the mean pH value of stomach in the moderate to severe gastric infection group were significantly different from those in the mild infection group (46.4% vs 73.5% and 2.3±0.8 vs 2.0±1.1, P<0.05). Conclusion Hp infection has obvious influence on the type and location of gastritis; The site and degree of Hp infection also significantly affected the acidity of stomach and the exposure of esophageal acid; Diffuse atrophic gastritis may have a certain protective effect on the occurrence of RE.

Objective to study the effects of Helicobacter pylori (Hp) and its related cytokines on the apoptosis of gastric epithelial cells in order to explore the pathogenic mechanism of Hp. Methods Human gastric immortalized epithelial cell line (GES-1) and human gastric cancer cell line (AGS) were used as the research objects. The effects of Hp virulent strain (NCTC 11637) alone and in combination with Hp related cytokines [interleukin (IL) -1 β, IL-8 and IL-10] on the apoptosis of the two cell lines were detected by flow cytometry; The effects of IL-1 β, IL-8 and IL-10 on the apoptosis induced by exogenous Fas ligand (FasL) in two cell lines were detected by reverse transcription-polymerase chain reaction. The effects of Hp and its related cytokines (IL-1 β, IL-8 and IL-10) on the basal expression of Fas mRNA in two cell lines were detected by reverse transcription-polymerase chain reaction. Results (1) The apoptosis induced by Hp in GES-1 and AGS cells increased by 113.0% and 47.0% (both P<0.05); IL-1 β and IL-10 could inhibit Hp-induced apoptosis of GES-1 (29.6%, 25.8%) and AGS (19.7%, 21.1%) cells (all P<0.05); IL-8 could enhance Hp-induced apoptosis in GES-1 cells (19.9%, P<0.05). (2) Hp could up-regulate the basal expression of Fas mRNA in GES-1 and AGS cells (89.0% and 36.0%, P<0.05); IL-1 β and IL-10 had no significant effect on the basal expression of Fas mRNA in the two cells (P>0.05); IL-8 can up-regulate the basal expression of Fas mRNA in GES-1 cells (33.0%) (P<0.05). (3) IL-1 β and IL-10 can inhibit the apoptosis of GES-1 cells (30.3%, 32.5%) and AGS cells (44.2%, 51.5%) induced by FasL (P<0.05); IL-8 can enhance FasL-induced apoptosis of GES-1 cells (100%, P<0.05). Conclusion Hp can directly mediate gastric epithelial cell apoptosis by upregulating Fas receptor expression. HP-related cytokine IL-8 may enhance HP-induced gastric epithelial cell apoptosis by upregulating Fas receptor expression. IL-1 β and IL-10 may inhibit Hp-induced gastric epithelial cell apoptosis through other mechanisms.

The patient was a 29-year-old married female who was admitted to the Department of Endocrinology of Peking Union Medical College Hospital on June 2, 2002 due to episodic dizziness and fatigue in the morning for 5 years and aggravated for 1 year. The patient had occasional dizziness and fatigue in the morning with palpitations since 1997, which was relieved after eating. After that, the symptoms gradually aggravated and the attacks became more and more frequent, every 5 to 6 days. The symptoms were comatose in the morning, sweating profusely, weakness and fatigue after waking up, and obvious hunger. The symptoms improved after eating or taking sugar, and the body weight increased by 7.5 kg every year from 55kg in 1997 and 12.5 kg in 2001. In early 2002, he went to a local hospital. The blood glucose was between 1.87 and 5.25 mmol/L in glucose tolerance test, the synchronous insulin level was between 15.4 and 123 mIU/L, and the C-peptide was between 3.0 and 15.1 mg/L. The B-ultrasound of liver, gallbladder, pancreas, spleen, kidney and adrenal gland showed no abnormalities. The uterus size was normal, the bilateral ovaries were enlarged, and follicle-like structures of different sizes were visible. Pituitary CT showed pituitary tumor, which was for further diagnosis

The 3rd National Conference on Organ Transplantation, sponsored by the Organ Transplantation Group of the Surgery Branch of the Chinese Medical Association, and hosted by the Second Affiliated Hospital of Kunming Medical College and the First People's Hospital of Kunming, was held at the Expo Garden Hotel in Kunming from May 27 to 29, 2006. 370 delegates from all over the country attended the conference, and 181 papers were received.

In 1970, Swan and Ganz first applied Pulmonary-Artery Catheter (PAC) to clinical practice. Since then, Pulmonary-Artery Catheter is often called Swan-Ganz Catheter or floating Catheter, and it has been rapidly popularized in clinical practice.

With the publication of the results of several large clinical studies of anastrozole, letrozole and exemestane in the field of adjuvant therapy, it has been more and more used in adjuvant endocrine therapy for postmenopausal breast cancer patients [1]. Its long-term application improves the disease-free survival of patients, but there is also the risk of bone loss and osteoporosis. One case of this adverse reaction observed by us and its management are reported as follows.

Na-K-2Cl cotransporter-1 (NKCC1) is a kind of membrane transporter widely distributed in animal cells. Its function is to transport Na +, K + and Cl-in an electrically neutral transmembrane ratio of 1:1:2.

The enhanced spiral CT scanning method does not need to make hypothesis on ventricular cardiac function, and has high accuracy and good repeatability in evaluating left ventricular cardiac function. However, spiral CT under 16 slices is difficult to evaluate cardiac function because of the few rows of detectors, slow scanning speed, low temporal resolution and Z-axis spatial resolution. 64 slice spiral CT can be used for evaluating cardiac function because of its large coverage range, fast scanning speed and high temporal resolution.