支气管动脉超选择性介入治疗中晚期肺癌

目的 探讨支气管动脉超选择性介入化疗及栓塞治疗肺癌的疗效。方法 58例肺癌病人均行支气管动脉超选择性介入化疗栓塞术，观察治疗前后原发癌灶体积及最大直径与垂直直径的变化，比较肺CT影像学改变；观察栓塞剂用量与癌灶体积之间的关系；观察临床病征、介入并发症等情况，并进行分析。结果 支气管动脉超选择性介入化疗栓塞术治疗肺癌疗效显，术后原发癌灶的体积大多有不同程度缩小，肿瘤最大直径与垂直直径乘积缩小，降低50％以上的占89．66％，栓塞剂用量小，介入并发症出现率低，副反应轻。     

Spontaneous disruption of mycotic aneurysm involving innominate artery

We report a case of ruptured mycotic aneurysm involving innominate artery requiring an urgent surgical treatment. A 62-yr-old woman presented with fever and dyspnea. Previously, she was diagnosed with colon cancer and received right hemicolectomy and one cycle of adjuvant chemotherapy. On echocardiogram, pericardial effusion was noted and emergency pericardiocentesis was performed. CT scan revealed aortic aneurysm involving ascending aorta and innominate artery, and thrombi surrounding those structures. Patch repair of the defect in the ascending aorta and ringed Goretex graft to bypass the innominate and ascending aorta were performed. We believe that this is the first case of ruptured mycotic aneurysm involving innominate artery.     

胃泌素对大鼠胃粘膜环氧合酶及生长因子表达的影响

目的：探讨胃泌素对大鼠胃粘膜环氧合酶（COX）及生长因子表达的影响。方法：雄性SD大鼠皮下注射胃泌素1 μg/kg、10 μg/kg或100 μg/kg，Western blot和免疫组化检查胃粘膜COX-1、COX-2、肝细胞生长因子（HGF）和肝素结合表皮生长因子样生长因子（HB-EGF）表达。评价胃泌素受体拮抗剂YM022对COX-1、COX-2、HGF和HB-EGF表达的影响。结果：胃泌素剂量依赖性地增加大鼠胃粘膜COX-2和HB-EGF表达，而对COX-1和HGF表达无明显影响；YM022阻断胃泌素诱导的COX-2和HB-EGF表达。 结论： 胃泌素调节大鼠胃粘膜COX-2和HB-EGF蛋白表达，提示COX-2和HB-EGF参与与胃泌素相关联的胃粘膜增生和胃癌等的发病过程。     

Distinct roles of pattern recognition receptors CD14 and Toll-like receptor 4 in acute lung injury

Acute lung injury (ALI) induced by lipopolysaccharide (LPS) is a major cause of mortality among humans. ALI is characterized by microvascular protein leakage, neutrophil influx, and expression of proinflammatory mediators, followed by severe lung damage. LPS binding to its receptors is the crucial step in the causation of these multistep events. LPS binding and signaling involves CD14 and Toll-like receptor 4 (TLR4). However, the relative contributions of CD14 and TLR4 in the induction of ALI and their therapeutic potentials are not clear in vivo. Therefore, the aim of the present study was to compare the roles of CD14 and TLR4 in LPS-induced ALI to determine which of these molecules is the more critical target for attenuating ALI in a mouse model. Our results show that CD14 and TLR4 are necessary for low-dose (300-microg/ml) LPS-induced microvascular leakage, NF-kappaB activation, neutrophil influx, cytokine and chemokine (KC, macrophage inflammatory protein 2, tumor necrosis factor alpha, interleukin-6) expression, and subsequent lung damage. On the other hand, when a 10-fold-higher dose of LPS (3 mg/ml) was used, these responses were only partially dependent on CD14 and they were totally dependent on TLR4. The CD14-independent LPS response was dependent on CD11b. A TLR4 blocking antibody abolished microvascular leakage, neutrophil accumulation, cytokine responses, and lung pathology with a low dose of LPS but only attenuated the responses with a high dose of LPS. These data are the first to demonstrate that LPS-induced CD14-dependent and -independent (CD11b-dependent) signaling pathways in the lung are entirely dependent on TLR4 and that blocking TLR4 might be beneficial in lung diseases caused by LPS from gram-negative pathogens.     

Absence of proteinase-activated receptor-1 signaling affords protection from bleomycin-induced lung inflammation and fibrosis

Activation of the coagulation cascade is commonly observed in the lungs of patients with both acute and chronic inflammatory and fibrotic lung disorders, as well as in animal models of these disorders. The aim of this study was to examine the contribution of the major thrombin receptor, proteinase-activated receptor-1 (PAR-1), during the acute inflammatory and chronic fibrotic phases of lung injury induced by intratracheal instillation of bleomycin in mice. Inflammatory cell recruitment and increases in bronchoalveolar lavage fluid (BALF) protein were attenuated by 56 +/- 10% (P < 0.05) and 53 +/- 12% (P < 0.05), respectively, in PAR-1-deficient (PAR-1-/-) mice compared with wild-type (WT) mice. PAR-1-/- mice were also protected from bleomycin-induced pulmonary fibrosis with total lung collagen accumulation reduced by 59 +/- 5% (P < 0.05). The protection afforded by PAR-1 deficiency was accompanied by significant reductions in pulmonary levels of the potent PAR-1-inducible proinflammatory and profibrotic mediators, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor-beta-1 (TGF-beta1), and connective tissue growth factor/fibroblast-inducible secreted protein-12 (CTGF/FISP12). In addition, PAR-1 was highly expressed in inflammatory and fibroproliferative lesions in lung sections obtained from patients with fibrotic lung disease. These data show for the first time that PAR-1 signaling plays a key role in experimentally induced lung injury, and they further identify PAR-1 as one of the critical receptors involved in orchestrating the interplay between coagulation, inflammation, and remodeling in response to tissue injury.     

关于乳腺普通性增生、不典型增生和原位癌相互关系及鉴别诊断的探讨

目的 探讨各种类型乳腺增生症的发病特点、形态学分类、不典型增生与乳腺癌的关系以及不典型增生与乳腺原位癌的鉴别诊断标准。方法 (1)观察本院300例乳腺良性增生性病变的临床发病特点及其病理形态改变。(2)观察86例大切片乳腺癌旁不典型增生病灶与癌灶的关系。结果 乳腺增生症中,纤维腺瘤为主型好发于21～30岁年龄组,而不典型增生病变则多见于40～60岁组。其中囊肿病仅占6．0％,而纤维腺瘤变达25．4％;癌旁组织中不典型增生发生率为65．1％,其中以导管原位癌发生率最高,达74．9％。结论 研究证实了1997年(舟山)“乳腺增生症的组织学分类”(推荐方案)的可行性。乳腺不典型增生与乳腺癌的发生密切相关。乳腺增生症可归纳为普通性增生和不典型增生。不典型增生的特殊增生细胞具有特别的诊断价值。重度不典型增生与原位癌的鉴别诊断有一定困难,但大部分可分。     

川芎嗪对休克血浆所致乳头肌电生理效应的影响

目的探讨川芎嗪（Lig）对休克血浆（SP）所致豚鼠心室乳头肌电生理特性改变的干预作用。方法利用常规玻璃微电极细胞内记录技术，观察SP对豚鼠心室乳头肌动作电位的影响及不同剂量Lig的干预作用。结果（1）用含有SP的灌流液灌流标本时，豚鼠心室乳头肌细胞动作电位的幅值（APA）、超射值（OS）均显著升高（P〈0．05），复极50％、90％时间（APD50、APD90）及动作电位时程（APD）均明显延长（P〈0．05）；（2）Lig可剂量依赖性地降低SP引起的APA、OS升高，延长APD50、APD90及APD，此种干预作用以5．12mmol／L Lig最为明显。结论SP可导致正常豚鼠心室乳头肌电生理特性的改变，而Lig可剂量依赖性地干预此种效应。     

Synthesis and characterization of polyanhydride for local BCNU delivery carriers

p-Carboxyphenoxy propane (CPP) prepolymer consisting of 4 units and sebacic acid (SA) prepolymer consisting of about 10 units were synthesized by reacting CPP and SA in the presence of excess acetic anhydride, respectively. Polyanhydride, poly(CPP-SA) copolymers were copolymerized by a melt polycondensation process with a mixture of CPP and SA prepolymer. Copolymers of average molecular weight up to 110,000 g/mol were achieved. The crystallinity of poly(CPP-SA) copolymers was decreased by the addition of the CPP homopolymer segment to SA homopolymer. Poly(CPP-SA) copolymers gradually degraded for period of 10 days. No large difference of weight loss observed according to molecular weight variation of poly(CPP-SA) copolymers. BCNU release from wafers fabricated by poly(CPP-SA) showed a sustained release pattern with no initial burst and delay of drug release.     

急性冠脉综合症与补体激活

目的： 评价各种类型急性冠脉综合症 (ACS) 病人补体激活的情况和补体激活与心肌损伤的关系。方法： 研究对象分为ACS组110例和正常对照组18人。 ACS组包括ST段抬高型心肌梗死（STEMI）51例，非ST段抬高型心肌梗死（NSTEMI）28例和不稳定性心绞痛（UA）31人。检测病人和正常对照健康人血浆C₃和C₄，CK-MB和肌钙蛋白T (TnT)浓度。结果： STEMI和 NSTEMI病人峰值C₃ 水平［分别为（1 525±302） mg/L和（1 516±289）mg/L］ 和C₄［分别为（423±123） mg/L和（396±68） mg/L］水平高于UA病人和对照组的C₃［分别为（1 275±172） mg/L和（1 072±196） mg/L,P<0.01］ 和C₄［分别为（356±91）mg/L和（182±73） mg/L,P<0.01］。UA病人的 C₃ ［(1 275±172） mg/L］和C₄ ［（356±91） mg/L］均高于对照组（P<0.01）。 ACS病人C₃和C₄水平在住院的前7 d均有明显的变化（P<0.01）。ACS病人峰值C₃和C₄水平与峰值CK-MB（分别为r=0.51和r=0.46，P<0.01）和肌钙蛋白T（分别为r=0.48和r=0.39，P<0.01）呈正相关。结论： ACS病人血浆C₃和C₄均明显升高。C₃和C₄水平与ACS的联系提示补体激活与心肌坏死有关。     

Clonorchis sinensis: molecular cloning and localization of myosin regulatory light chain

One cDNA clone was purified from an adult Clonorchis sinensis cDNA library, and its deduced polypeptide sequence was found to be homologous with myosin regulatory light chain (MRLC) of invertebrates and vertebrates. Two amino-acid residues, Thr and Ser, were conserved at the phosphorylation sites that regulate the function of MRLCs. Recombinant C. sinensis MRLC (rCsMRLC) protein was produced and purified from Escherichia coli, and mouse anti-CsMRLC immune sera recognized a protein of molecular weight 24 kDa from a soluble protein preparation of C. sinensis. The CsMRLC protein was immunohistochemically localized to the muscle fibers of the subtegumental muscle layer and to the muscles of oral and ventral suckers. However, the rCsMRLC protein proved to be less useful antigen for the serodiagnosis of human clonorchiasis.The nucleotide sequence reported herein was submitted to GenBank and assigned accession number AY519356.