Objective To discuss the effect of family nursing intervention on the life quality and pulmary function of patients with chronic obstructive pulmonary disease (COPD). Methods We divided 72 patients with COPD into the test group and the control group with 36 cases in each group.The two groups received routine treatment and nursing but additional family intervention was given to the patients and fam-ily members in the test group.The life quality and pulmonary function after intervention in the two groups were appraised in the two groups. Results The evaluation of life quality and pulmonary function were alleviated after intervention compared with those before intervention (P ＜ 0.05).But the above items in the control group were not significantly improved (P ＞ 0.05). Conclusions Effective family intervention could improve the life quality and pulmonary function of patients with COPD.

Objective To report the experience in diagnosing gastroenteric tuberculosis under en-doscopies, and arose enough attention to avoid missed or mis-diagnosis. Methods Biopsy is taken when lesions, such as gastroenteric mucosal protrusions, nodule, erythema and ulcer are found under endoscopies. Results In 7 cases studied, 2 of them are the gastric tuberculosis (1 ulceration, 1 proliferation) , the rest, colonic tuberculosis (4 proliferation and 1 mixed). Distribution of lesions: gastric antrum 2, each one in terminal ileum, ileocecal valve, terminal ileum plus ileocecum, terminal ileum plus pan colon, and ascending colon. Endoscopic diagnosis: colonic tuberculosis with infiltrative tuberculosis in both lungs 1; colonic malignant tumors 2, mucosal protrusions and ulcerative lesions with undefined nature 4. Caseous necrotic granu-lomas are found in all cases on pathological examination. Conclusion The various appearances of gastroenteral tuberculosis under endoscopies are hard in differentiating from those of colonic carcer, inflammatory bowel diseases ( Crohn' s disease etc. ) , gastric benign or malignant ulceration. The definite diagnosis of gastroenteral tuberculosis is greatly depended on pathological results.

Genome of Arabidopsis has a kind of genes encoding proteins with ARM repeat domains and some of these proteins are known to play important roles in plant development and responses to hormone. An Arabidopsis mutant lfr with a distinct phenotype was got in leaf and flower development. The gene is predicted to encode a protein with ARM repeat domains. In order to study its function and molecular mechanism, recombination expression plasmid pGEX-2TGST∶LFR was constructed and transformed into the host bacteria strain Rosetta. Then IPTG was used to induce the recombinant protein expression in engineering strain. The expression products were detected by 12% SDS-PAGE. The GST∶LFR fusion protein was existed in soluble form with a relative molecular mass 77 ku, which is fit with the molecular mass supposed from gene coding frame. After purification by GST-tag affinity chromatography and electroelution, the fusion protein was used as antigen to prepare polyclonal antiserum in rabbits. After the fifth injection of antigen, the antiserum was obtained and further purified by decreased nonspecific bacteria and GST-tag antibody with method of immuno-precipitation. Western blot analysis showed that the purified antiserum, raised against the recombination LFR protein in rabbits, could react to the recombinant protein expressed in Rosetta specifically. And then the nuclear proteins of Arabidopsis wild type and mutant were extracted and separated by SDS-PAGE. Western blot assays revealed that there was a protein band, with a relative molecular mass 50 ku, indicating that antiserum could react to the native protein expressed in Arabidopsis specifically.

BACKGROUND: Learning and memory disorder exist in diabetic rats,which can be improved by APP 17-mer peptide. However, it is unclear whether learning and memory disorder in diabetes mellitus is caused by influencing neuronal mitochondrial transmembrane potentials and apoptosis in hippocampus or not and what is the related action mechanism of APP17-mer peptide.OBJECTIVE: To observe the effects of APP17-mer peptide on neuronal mitochondrial transmembrane potentials (△ψm) and apoptosis in hippocampal area of diabetic rats.DESIGN: A completely randomized, grouping and controlled trial.SETTING: Beijing Research Laboratory for Brain Aging, Beijing Xuanwu Hospital, Capital University of Medical Sciences; the Department of Endocrine, the First Central Hospital of Baoding.MATERIALS: The data measurement of the experiment was carried out in the Instrument Testing Center, the General Hospital of Chinese PLA between May 2002 and August 2002. The modeling and intervention of the experiment was carried out in the Animal Laboratory of Xuanwu Hospital, Capital University of Medical Sciences. Eighteen male Wistar rats were enrolled and randomized into control group, model group and APP17-mer peptide group with 6 rats in each group.METHODS: ① Diabetic models in the model and APP17-mer peptide groups were established by intraperitoneal injection of 60 mg/kg streptozotocin (pH=4.4) in fasted rats(fasting for 12 hours). Three days later, modeling was successful if blood sugar level in caudal vein was more than 15 mmol/L. Rats in the control group were not subjected to modeling.Then, the rats in the APP17-mer peptide group were subjected to the subcutaneous injection of APP17-mer peptide (3.4 μg for each rat once) three times a week and totally for ten weeks, whereas rats in the other groups were given saline of the same volume. ② After ten weeks, rats were anesthetized and decapitated to take out brain tissues, and then hippocampal tissues were isolated in ice bath for preparation of single cell suspension.JC-1 labeled mitochondrial transmembrane potentials and cell apoptosis in hippocampal area were measured by means of flow cytometry. ③ One-way analysis of variance was adopted in the comparison among groups.RESULTS: Eighteen rats were involved in the results analysis. ①Neuronal mitochondrial transmembrane potential was lower in the model group as compared with the control group [(551.91±53.36) vs (809.88±82.41) △ψm,P＜0.01] while it was higher in the APP17-mer peptide group as compared with the model group [(705.99±89.92) vs (551.91±53.36) △ψm, P ＜ 0.05].There was no difference between the APP17-mer peptide group and control group (P=0.146). ②) Apoptotic percentage of single cell in hippocampus was significantly higher in the model group than in the control and APP17-mer peptide groups [(5.32±1.37)%, (1.03±0.55)%, (2.80±0.92)%, P＜0.01, 0.05].CONCLUSION: Neuronal mitochondrial transmembrane potential and cell apoptosis in hippocampus may be involved in the occurrence and development of diabetes mellitus, and APP17-mer peptide plays an improved role in the process.

AIM To investigate whether pioglitazone can protect cortical neurons from lipopolysaccharides(LPS)-induced neurotoxicity and the mechanisms responsible for this protective effect. METHODS After 7 d cultures，cultured cortical neurons were incubated with LPS 10 mg·L~(-1) for 4-24 h with or without other drugs. In co-incubation experiments, other drugs were added to the neurons 30 min or 1 h prior to incubation with LPS. The cell viability was assessed by MTT assay. The neuronal apoptosis was quantified by scoring the percentage of cells with apoptotic nuclear morphology after Hoechst 33258 staining. The cultured cells were then fixed on the 7th day and immunocytochemically stained with phosphorylated JNK1 antibody. The protein expressions of active caspase 3 and phosphorylated JNK1 were measured by Western blot. Nitric oxide (NO) generation was measured by Griess method. RESULTS The decrease of cell viability and the increase of apoptotic cells in cultured cortical neurons were observed incubated with LPS for 24 h compared with the normal controls. The cell viability of cortical neurons was decreased from (100.0±10.9)% in the normal control group to (72.3±2.1)% in the LPS-treated group and the apoptotic cell percentages were increased from (11.5±4.2)% in the normal control group to (39.5±8.2)% in the LPS group. LPS induced the increases in phospho-JNK1, active caspase 3 expression, and NO generation. Pioglitazone 0.01, 0.1 and 1 μmol·L~(-1), respectively inhibited LPS-induced decrease in cell viability and increase of apoptotic morphology, active caspase 3 expression in cultured neurons. In LPS+pioglitazone 1 μmol·L~(-1) group, cell viability was （97.8±9.7）%, the apoptotic cells percentage was (20.6±5.0)%, NO generation (6.8±1.3)μmol·L~(-1). Furthermore, pioglitazone also inhibited LPS-induced the increase in JNK1 phosphorylation and NO generation. JNK inhibitor SP600125 5 μmol·L~(-1) significantly inhibited LPS-induced neurotoxicity, cell viability was increased from (72.3±2.1)% to (109.8±11.8)%, the apoptotic cells percentage from (39.5±8.2)% decreased to (19.1±4.8)%, NO generation from （21.1±5.0）μmol·L~(-1) decreased to（4.0±1.3）μmol·L~(-1). The PPARγ antagonist GW9662 10 μmol·L~(-1) did not reverse the effects of pioglitazone. In LPS+pioglitazone 1 μmol·L~(-1)+GW9662 10 μmol·L~(-1) group, cell viability was (90.7±6.9)%, the apoptotic cells percentage was (23.4±4.1)%, and NO concentration was (5.8±0.7)μmol·L~(-1). CONCLUSION Pioglitazone protects cortical neurons against LPS insult at least via inhibiting JNK activity and NO generation, but not PPARγ activation.

Objective To establish a transfer model for excess relative risk (ERR) for radiation-related leukemia from Japanese population to Chinese population.Methods Combined ERR of several subtypes of leukemia published in 1994, with the corresponding leukemia baseline incidence rates obtained from Cancer Incidence in Five Continents Vol.Ⅸ (CI5-Ⅸ) for Japanese population and Chinese population, a weighted risk transfer model was employed between an additive model and a multiplicative model, to execute ERR transfer.Results A range of weighing factors was proposed for risk transfer models:weighing factor was 0.4 for male and 0.3 for female, acute lymphoblastic leukemia, acute myeloid leukemia and chronic myeloid leukemia.The uncertainty for ERR transfer was characterized by lognormal distribution.Conclusions Based on the difference of baseline incidence rate for subtypes of leukemia between Japanese population and Chinese population, the transfer model and these weighing factors discussed in the present study could be applicable to transfer ERR for radiation-related leukemia from Japanese population to Chinese population.

Objective To study the relationship of bladder residual urine volume and renal function and urinary tract infection in patients with benign prostatic hyperplasia(BPH). Methods Eighty-one BPH eases from September 2005 to September 2008 were studied retrospectively. All the cases were divided into group A (53 cases, the residual urine volume <60 ml), group B (18 cases, the residual urine volume 60-200 ml),and group C (10 cases, the residual urine volume 200 ml). Blood urea nitrogen(BUN), serum ereatinine (Cr) and urine bacterial culture were observed. Results The BUN and serum Cr in group A, B and C were (5.90 ± 3.01) mmol/L, (90.13 ± 25.08)μmol/L, (7.85±3.53) mmol/L, (128.36 ±30.25) μmol/L and (10.57 ± 4.01)mmol/L, (152.11 ± 36.68) μmol/L, respectively. The BUN and serum Cr in group C were higher than those in group A and B (P < 0.01 or < 0.05). And there was significant difference between group A and group B (P< 0.05). The incidence of urinary tract infection in group A ,B and C was 28.3%(15/53), 44.4%(8/18), 50.0%(5/10), respectively. There was significant difference between group A and group B, C (P < 0.05). But there was no significant difference between group B and group C (P 0.05). Eacherichia was the main bacteria in urinary tract infection. Conclusion The increase of bladder residual urine volume in patients with BPH enhances renal failure and urinary tract infection.

Objective To investigate the changes of autonomic nerve function of coronary heart disease (CHD) patients with panic disorder(PD). Methods All the subjects who met with the diagnostic code of CHD and PD were divided into CHD group(n=40) ,PD group(n=36) ,comorbid CHD and PD group(n=27) ,and 40physical examinee were recruited as normal control group. They had a 24 hours Holter ECG monitoring by time and frequency domain analysis of heart rate variability. ANOVA analysis was utilized to statistic the collected data. Results Compared with normal controls,the patients of others groups had every indexs of HRV were reduced. The indexs of HRV of comorbid CHD and PD were lower than the patients of CHD or PD group. The score of time domain SDNN(70.40 ± 14.74)ms,SDANN(91.72 ± 24.46)ms,PNN50(2.83 ±2.07)%, RMSSD( 15.66 ±7.45)ms,frequency domain LF(647.54 ± 129.24)ms2, HF(596. 16± 127.66) ms2 in comorbid CHD and PD. There were significant differences with others groups(P ＜ 0.05 ). Conclusion The autonomic nervous functional of the patients with CHD and PD were in disorder. The autonomic nervous functional disorder of the patients with comorbid CHD and PD was more severe.

Aim Tostudytheeffectsofferulicacid (FA) on doxorubicin (DOX) induced cellular injury inH9c2ratmyocardialcells.Methods H9c2cells were treated with 1μmol·L-1 DOX treated for 24 h to establish a myocardial injury model. 10, 20, 40μmol ·L-1 FA was added 2 h before DOX treatment. Cell viability was measured by cell counter kit ( CCK-8 ) . Morphological changes were observed by phase contrast microscope. LDH, CK, MDA, SOD levels were detec-ted by biochemical kits. Intracellular level of reactive oxygen species ( ROS) was examined by DCF-DA stai-ning with flow cytometry. Cellular apoptosis was detec-ted by AO-EB staining and DNA agarose gel electro-phoresis. The expression of caspase-3, Bax, Bcl-2 was evaluatedbyWesternblot.Results Exposureof H9c2 cells to DOX led to decrease in cell viability, in-crease in stress and apoptosis. FA pre-treatment im-proved cell viability in a dose-dependent manner, at-tenuated leakage of LDH and CK, and reversed mor-phological changes induced by DOX. FA suppressed DOX-induced oxidative stress as evidenced by reducing ROS and MDA generation and increasing SOD enzyme activity. FA depressed myocardial apoptosis by down-regulating pro-apoptotic protein caspase-3 and Bax, whereas up-regulating apoptosis inhibitory protein Bcl-2.Conclusions FAhasaprotectiveeffectonDOX-induced injury in H9c2 cells. This protection may re-sult from inhibition of myocardial oxidative stress and apoptosis.

Objective To improve the theoretical basis for the typical hemodynamic changes in subclavian steal syndrome (SSS) patients underwent transcranial doppler (TCD) by detailed hemodynamic analysis.Methods Patients with SSS were examined by transcranial doppler and some patients performed tourniquet test.Flow spectrum,flow velocity and pulsatility index (PI) of vertebral artery,basilar artery and middle cerebral artery (MCA) were recorded.Results The flow spectrum of steal side vertebral artery showed that there were 14 cases with systolic notch,18 cases with systolic reverse flow and 3 cases with flow completely reversed.The flow spectrum showed high resistance spectrum in vertebral artery and basilar artery and ipsilateral basilar artery vortex or turbulence in 32 cases.The PI value was higher in contralateral vertebral artery and basilar artery than in anterior circulation (q =9.56,9.98,both P ＜ 0.01),and there was no difference between contralateral vertebral artery and basilar artery (q=0.416,P＞0.05).The tourniquet test were positive in all 22 patients.Conclusions TCD is a convenient,fast,accurate and non-invasive method for hemodynamic examination,which is the first choice for the diagnosis of SSS.