Objective To explore the diagnosis and treatment of clinical possible organizing pneumonia.Methods The medical records of 31 patients with clinical probable organizing pneumonia were retrospectively analyzed.The clinical presentation,radiographic results and treatment were collected and analyzed.Results Thirty-one patients with non-response to antibiotics were preliminary diagnosed as organizing pneumonia.By percutaneous lung biopsy or transbronchial lung biopsy the tuberculosis,fungi,suppurative inflammation,lung cancer and other diseases were ruled out in 24 patients,and 7 patients were diagnosed by perfect effect of corticosteroids treatment.Twenty-one patients had typical CT findings.All the patients responded rapidly and completely to the administration of corticosteroids.Six patients relapsed after the reduction or stop of corticosteroid in a follow-up time of 6-25 months.Conclusions Non-response to antibiotics,the typical imaging findings and lung biopsy ruling out other diseases are important for diagnosing organizing pneumonia.Rapid response to administration of corticosteroids may be helpful to the diagnosis.Decreasing the dose of corticosteroid too early may cause recurrence of organizing pneumonia.

Objective:To investigate the effect of DNA vaccine expressed Helicobacter pylori(Hp) oipA on protecting against Hp infection.Methods:The ORFs of Hp oipA had been inserted into the eukaryotic expressing vector pVAX1 and SGC-7901 cells had been transfected with recombinant plasmid pVAX1-oipA. The expression of oipA had been detected by RT-PCR and ELISA. After extracted and purified, pVAX1-oipA had been injected into BALB/c mice through muscles of right leg one time each week for three weeks(100 ?g each mouse). pVAX1 blank and normal saline had been used as the control groups. Titer of antibodies had been detected by ELISA two months after the last immunization. Based on the confirmation of immunological response in the pVAX1 groups, mice had been given orogastric challenged with live Hp Sydney strain three times(0.5?108/0.5 ml each mouse). Four weeks after challenge, mice had been sacrificed. Histological change and the colonization of Hp in the gastric mucosa had been detected by urease test, the culture of Hp, and electronic microscopy.Results:SGC-7901 cells transfected with pVAX1-oipA had expressed corresponding production at the level of transcription and translation. Immunized mice had been induced anti-oipA antibodies. After challenged with bacterium, as contrast to immunized mice groups injected with pVAX1-oipA, pVAX1 blank, normal saline, the positive rate of urease test of gastric mucosa was 0(0/10), 90%(9/10), 100%(5/5)respectively,the positive rate of cultures of Hp was 20%(2/10), 90%(9/10), 100%(5/5)respectively. Histological findings: the different degree of erosion had been observed in control group, but 80%(8/10)of gastric mucosa were normal in immunized mice.Conclusion:oipA DNA could induce effective immune response in protection against Hp infection.

This article was aimed to study the therapeutic effects and anti-inflammatory effects of Chinese and west-ern medicine ointment on fungal infection animals. Guinea pig models which were infected with Trichophyton rubrum or Microsporum lanosum were applied to observe the effects of antifungal infections on She-Zhi Qin-Xian (SZQX) ointment by transdermal administration. The ointment is the combination of miconazole nitrate, snake oil and Sophora flavescens which is traditional Chinese medicine (TCM). Simultaneously, the models of croton oil-induced mouse ear swelling and carrageenan-induced rat paw swelling were established to observe the curative effect of SZQX ointment. The results showed that the SZQX ointment had a protective role on both guinea pig models. The microscopic scale of localized lesions in infected guinea pigs was significantly decreased (P< 0.01). The effect of SZQX ointment was better than the single using of Chinese or western medicine. The SZQX ointment was also able to significantly reduce the croton oil-induced mouse ear swelling and carrageenan-induced rat paw swelling (P< 0.05, or P< 0.01) with distinct anti-inflammatory effect. And the effect of SZQX ointment was superior to the single using of either Chinese or western medicine. It was concluded that the SZQX ointment had significant antifungal infection and anti-inflam-matory effect.

This study was aimed to establish an HPLC method for the content determination ofepimedin A, epimedinB,epimedinC,epimedium glycoside,baohuosideI in epimedium flavonoids capsule. The elusion was performed on an Eclipse Plus C18column (250 mm× 4.6 mm, 5μm). The mobile phase was composed of acetonitrile and water with a gradient elution. The flow rate was set at 1 mL·min-1. The detection wave length was set at 270 nm. The column temperature was 25℃. The results showed that the linear ranges of epimedin A,epimedinB,epimedinC,epimedium glycoside,baohuosideI were 3.10-62.00μg·mL-1, 5.70-114.00μg·mL-1, 9.14-182.80μg·mL-1, 15.20-304.00μg·mL-1, and 1.56-31.20μg·mL-1, respectively. The correlation coefficientr was more than 0.999 3. The average recoveries were 101.06% (RSD = 1.05%,n = 6), 100.78% (RSD = 1.08%,n = 6), 99.17% (RSD = 1.14%,n = 6), 100.23% (RSD = 0.68%,n = 6), and 99.09% (RSD = 1.30%,n = 6), respectively. This experiment was precise, reproducible and stable. It was concluded that the method was simple and accurate, which provided a certain reference value for the multi-component assaying of epimedium flavonoids capsule.

Objective To investigate the effect and underlying mechanism of radioactive 125I seed implantation on the angiogenesis of transplanted human lung adenocarcinoma in nude mice.Methods An animal model of transplantd human lung adenocarcinoma was established by subcutaneous implanting A549 cells into nude mice.Twenty four tumor-bearing nude mice were randomly divided into 4 groups with different irradiation doses of blank control (without any treatment) and 0 MBq,22.2 MBq,29.6 MBq and by embedding radioactive 125I seeds with an 18 G implant needle.Tumor volumes were measured every 4 days until all mice were terminated 30 d later and the tumor growth curve was drawn.The microvessel density (MVD) in the tumor tissue was detected by immunohistochemistry S-P assay.The mRNA and protein levels of VEGF and HIF-1α of each group were detected by RT-PCR and Western blot,respectively.Results After embedding of 125I seeds,the tumor volumes of 22.2 MBq group (886 ± 97) and 29.6 MBq group (590 ± 107) were significantly smaller than those of control group (2 297 ± 149) at 54 d after administration (q =14.117,17.075,P ＜ 0.05),but there were no significant differences among 0 MBq group and control group,22.2 MBq and 29.6 MBq groups (P ＞ 0.05).The immunohistochemical CD34-positive staining demonstrated that MVD in 22.2 MBq group (522 ± 119) and 29.6 MBq group (491 ± 121) were decreased significantly compared with control group (922 ± 260) (q =4.826,5.197,P ＜0.05),but there were no significant differences among 0 MBq and control groups,22.2 MBq and 29.6 MBq groups(P ＞0.05).The mRNA expressions of VEGF and HIF-1α in 22.2 MBq group (0.279±0.0659,0.370 ±0.0857) and 29.6 MBq group (0.215 ±0.0620,0.278 ±0.0651) were significantly lower than those in the control group (q VEGFmRNA =18.881,17.211,q HIF-1αmRNA =15.376,14.733,P ＜0.05),but there were no significant differences among 0 MBq and control groups,22.2 MBq and 29.6 MBq groups(P ＞0.05).At the same time,the expression levels of VEGF and HIF-1α protein after 125I seed implantation were also obviously decreased in 22.2 MBq and 29.6 MBq groups (qvEGr =5.848,6.263,q HIF-1α =6.560,7.576,P ＜ 0.05),and no significant difference between 0 MBq and control groups(P ＞ 0.05) and between 22.2 MBq and 29.6 MBq groups (P ＞ 0.05).Conclusions Interstitial implantation with 125I seeds may potently inhibit angiogenesis in human lung adenocarcinoma xenografts of nude mice.

To explore the correlation between the C807T polymorphism of platelet membrane gly- coprotein Ⅰa (GPⅠa) gene and aspirin resistance in Chinese people, 200 patients with high-risk of atherosclerosis took aspirin (100 mg/d) for 7 days. Platelet aggregation function was detected using adenosine diphosphate (ADP) and arachidonic acid (AA) before and after the administration of aspi- fin. Then the subjects were divided into three groups according to the results of platelet aggregation function: an aspirin resistant (AR) group, an aspirin semi-responder (ASR) group and an aspi- fin-sensitive (AS) group. Platelet GPⅠa gene 807CT polymorphism was examined by means of po- lymerase chain reaction-sequence specific primers (PCR-SSP). The results showed that T allelic fre- quency in AR group and ASR group were higher that of AS group (P<0.005), and the prevalence of genotypes (TT+TC) of these two groups was significantly higher than that in AS group (P<0.05). Platelet GPⅠa T allele was significantly associated with aspirin resistance as revealed by multiple logistic regression (OR=3.76, 95% CI: 2.87-9.58). The results suggest that inherited platelet GPⅠa variations may have an important impact on aspirin resistance and the presence of GPⅠa T allele may be a marker of genetic susceptibility to aspirin resistance.

OBJECTIVETo summarize the experience of minimally invasive treatment in 520 patients with intracranial aneurysms on a retrospective study.

METHODSThe measures used in the treatment of 520 patients were reviewed in terms of timing of surgery, induced-hypotensive anesthesia, brain protection combined with temporal occlusion of the feeding artery, external drainage of CSF, dynamic monitoring of intracranial pressure, blood flow velocity, serum osmolality and CT scanning, anti-vasospasm therapy as well as selected interventional endovascular embolization of aneurysms.

RESULTSOf the 520 patients, 485 were treated with either direct clipping or endovascular embolization and 35 patients were treated non-surgically. In 449 patients undergoing direct clipping and 36 undergoing endovascular embolization, intraoperative rupture of aneurysm occurred in 27 (6.0%) and 0%, respectively. Death occurred in 13 (2.6%), hemiplegia in 8 (1.6%), and vegetative state in 2 (0.4%). The operative mortality of direct clipping was 3.8% in 210 patients before 1990 and 1.8% in 275 patients after 1990 (36 patients undergoing endovascular embolization, the operative mortality was 0%).

CONCLUSIONThe outcome of patients with intacranial aneurysms can be markedly improved and the operative mortality can be lowered by minimally invasive treatment.

Adult ; Aneurysm, Ruptured ; mortality ; therapy ; Embolization, Therapeutic ; Female ; Follow-Up Studies ; Humans ; Intracranial Aneurysm ; mortality ; surgery ; Intraoperative Complications ; mortality ; Male ; Microsurgery ; Middle Aged ; Minimally Invasive Surgical Procedures ; Retrospective Studies ; Survival Rate ; Treatment Outcome

Background: s/Aims: Transmembrane 6 superfamily member 2 (TM6SF2) E167K variant is closely associated with the occurrence and development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the role and mechanism of TM6SF2 E167K variant during MASLD progression are not yet fully understood. Methods: The Tm6sf2167K knock-in (KI) mice were subjected to high-fat diet (HFD). Hepatic lipid levels of Tm6sf2167K KI mice were detected by lipidomics analysis. Thin-layer chromatography (TLC) was used to measure the newly synthesized triglyceride (TG) and phosphatidylcholine (PC). Results: The TM6SF2 E167K variant significantly aggravated hepatic steatosis and injury in HFD-induced mice. Decreased polyunsaturated PC level and increased polyunsaturated TG level were found in liver tissue of HFDinduced Tm6sf2167K KI mice. Mechanistic studies demonstrated that the TM6SF2 E167K variant increased the interaction between TM6SF2 and PNPLA3, and impaired PNPLA3-mediated transfer of polyunsaturated fatty acids (PUFAs) from TG to PC. The TM6SF2 E167K variant increased the level of fatty acid-induced malondialdehyde and reactive oxygen species, and decreased fatty acid-downregulated cell membrane fluidity. Additionally, the TM6SF2 E167K variant decreased the level of hepatic PC containing C18:3, and dietary supplementation of PC containing C18:3 significantly attenuated the TM6SF2 E167K-induced hepatic steatosis and injury in HFD-fed mice. Conclusions The TM6SF2 E167K variant could promote its interaction with PNPLA3 and inhibit PNPLA3-mediated transfer of PUFAs from TG to PC, resulting in the hepatic steatosis and injury during MASLD progression. PC containing C18:3 could act as a potential therapeutic supplement for MASLD patients carrying the TM6SF2 E167K variant.

Background: s/Aims: Transmembrane 6 superfamily member 2 (TM6SF2) E167K variant is closely associated with the occurrence and development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the role and mechanism of TM6SF2 E167K variant during MASLD progression are not yet fully understood. Methods: The Tm6sf2167K knock-in (KI) mice were subjected to high-fat diet (HFD). Hepatic lipid levels of Tm6sf2167K KI mice were detected by lipidomics analysis. Thin-layer chromatography (TLC) was used to measure the newly synthesized triglyceride (TG) and phosphatidylcholine (PC). Results: The TM6SF2 E167K variant significantly aggravated hepatic steatosis and injury in HFD-induced mice. Decreased polyunsaturated PC level and increased polyunsaturated TG level were found in liver tissue of HFDinduced Tm6sf2167K KI mice. Mechanistic studies demonstrated that the TM6SF2 E167K variant increased the interaction between TM6SF2 and PNPLA3, and impaired PNPLA3-mediated transfer of polyunsaturated fatty acids (PUFAs) from TG to PC. The TM6SF2 E167K variant increased the level of fatty acid-induced malondialdehyde and reactive oxygen species, and decreased fatty acid-downregulated cell membrane fluidity. Additionally, the TM6SF2 E167K variant decreased the level of hepatic PC containing C18:3, and dietary supplementation of PC containing C18:3 significantly attenuated the TM6SF2 E167K-induced hepatic steatosis and injury in HFD-fed mice. Conclusions The TM6SF2 E167K variant could promote its interaction with PNPLA3 and inhibit PNPLA3-mediated transfer of PUFAs from TG to PC, resulting in the hepatic steatosis and injury during MASLD progression. PC containing C18:3 could act as a potential therapeutic supplement for MASLD patients carrying the TM6SF2 E167K variant.