乳母血清泌乳素水平与泌乳量关系的观察

用放射免疫法测定产后40天和60天乳母血清泌乳素基础水平和吸吮后泌乳素最大反应性增值,发现其与乳母泌乳量、婴儿吸吮频率、吸吮时间之间均不存在正相关关系,推测引起泌乳素分泌除吸吮外,还存在其他机理。     

Lobucavir-induced proliferative changes in mice

Nucleoside analogues are used in the treatment of viral infections, including those caused by human immunodeficiency virus, cytomegalovirus, and herpes virus. These drugs are beneficial in the treatment of human disease, but are associated with toxicities that often limit their intended therapeutic use, including anemia, neutropenia, peripheral neuropathy, and myopathy. Some of these compounds have been reported to be carcinogenic in rodents. To investigate the carcinogenic potential of lobucavir, a nucleoside analogue, three groups of 60 male and female mice were orally administered lobucavir at daily doses of 10, 50, and 250 mg/kg (males) or 30, 150, and 750 mg/kg (females) over a period of 104 weeks. Two identical groups of 60 male and female mice each served as controls. The morphology and the incidence of neoplasms is described and compared with the tumor spectrum of other nucleoside analogues. Light microscopically, lobucavir-induced neoplastic lesions consisted of upper digestive tract squamous cell neoplasia in males and females; cervical, vaginal, and cutaneous squamous cell neoplasia in females; and Hardarian gland adenomas and adenocarcinomas in male mice. These results suggest that long-term administration of lobucavir causes neoplasia in mice, the spectrum of which resembles that observed after long-term administration of zidovudine or ganciclovir.     

Horner syndrome

Horner syndrome is an uncommon but important clinical entity, representing interruption of the sympathetic pathway to the eye and face. Horner syndrome is almost always diagnosed clinically, though pharmacological testing can be used to confirm the diagnosis. Imaging modalities such as PET, CT and MRI are important components of work‐up for patients presenting with acquired Horner syndrome. Our patient’s presentation with Horner syndrome unmasked the causative superior sulcus squamous cell carcinoma and a coincidental lower lobe adenocarcinoma. Successful radical treatment of these cancers resulted in complete resolution of the syndrome and disease‐free survival at 18 months. We review the anatomy and pathophysiology underlying this and other causes of Horner syndrome.     

668颗后牙镍铬合金PFM边缘适合性的临床观察

目的：观察采用2种边缘形式的后牙烤瓷熔附金属全冠边缘适合性和对牙龈健康的影响.方法：对668颗后牙,分别采用2种边缘形式的后牙烤瓷熔附金属全冠（单冠或桥的基牙）在修复2年后进行复查,检测其边缘适合性及牙龈指数（GI）和牙周探诊深度（PD）,用统计学方法分析修复体边缘形式与牙龈病变间的关系.结果：采用羽状边缘360°金属脚边的PFM边缘适合性明显优于凹面肩台型边缘PFM,凹面肩台型边缘的PFM的牙龈病变发生率,明显高于羽状边缘360°金属脚边的PFM,而边缘适合性差者较适合性好者牙龈病变发生率显著增高.结论：后牙PFM的边缘采用羽状边缘360°金属脚边是一种好的选择.     

Syringomyelia with Arnold Chiari I malformation: a report of four cases

4 cases of syringomyelia with type I Arnold Chiari malformation was seen presenting mainly with dissociated sensory loss, weakness of hands and upper motor neurone signs in the lower limbs. The first patient improved with posterior fossa decompression. The second and fourth patient appeared not to have improved after surgery, and the third case refused operation. One patient showed cord atrophy on myelogram presumably due to a collapse of the syrinx. One of the patients was unusual in that the syrinx extended down to segment T11. Magnetic resonance imaging of the posterior fossa and the cervical cord, to date, is the most useful procedure for diagnosis.     

辛伐他汀对早期糖尿病大鼠视网膜白细胞黏附的影响

目的 观察辛伐他汀（Sim）对白细胞在早期糖尿病大鼠视网膜毛细血管中黏附、堆积的影响,探索他汀类药物可能的非调脂性治疗作用.方法 Wistar大鼠40只,随机分为正常对照组、糖尿病组（DM）、糖尿病Sim组（DMsim）和糖尿病生理盐水组（DM saline）.腹腔注射链脲佐菌素（STZ）建立糖尿病模型,成模后Sim组予以Sim15 mg/（kg·d）;DMsim组等量灌胃,2周后处死动物,取右眼制备视网膜石蜡切片,行形态学观察及CD45-MAb免疫组织化学研究.结果 CD45在正常大鼠视网膜血管内皮细胞胞膜中有表达,DM组CD45的表达明显增加,与正常对照组、DMsim组比较差异有统计学意义（P＜O.05）.结论 早期糖尿病大鼠视网膜白细胞黏附性增加,Sim可显著地抑制白细胞在视网膜中的黏附和堆积,改善糖尿病大鼠视网膜微循环.     

3,4-Dichlorobenzyloxyacetic acid is extensively metabolized to a taurine conjugate in rats

The metabolism of the antisickling agent 3,4-dichlorobenzyloxyacetic acid (3,4-DCBAA) was examined after ip administration to rats. Within 5 days after administration of radiolabeled 3,4-DCBAA, 77.4 +/- 4.6% of the dose was recovered in the urine and only 3.2 +/- 0.5% was recovered in the feces. Metabolites in the urine were isolated and characterized by HPLC, electron impact MS, and LC/MS, and their identities were confirmed by comparing their spectra with those of synthetic standards. Quantitation of these urinary metabolites revealed that the majority of the radioactive dose was excreted as a taurine conjugate (60.1 +/- 4.4%), while lesser amounts were excreted as 3,4-dichlorohippurate, unchanged 3,4-DCBAA, the glycine conjugate of 3,4-DCBAA, and a polar unknown which is believed to be glycolic acid. A pathway involving an initial O-dealkylation at the benzyl carbon of 3,4-DCBAA and proceeding through the glycine conjugation of 3,4-dichlorobenzoic acid has been proposed to explain the formation of 3,4-dichlorohippurate and the polar unknown. The extensive conjugation of 3,4-DCBAA with taurine is an unprecedented observation in rats, which usually utilize glycine for amino acid conjugation reactions. Further studies with 3,4-DCBAA may provide insight into the enzymatic mechanisms of taurine conjugation, which are not well defined at this time.     

Steady-state fluctuation and variability of betaxolol and atenolol plasma levels

Twenty-four nonsmoking male volunteers took 50 mg atenolol or 10 mg betaxolol orally once a day for 9 days in a two-period, four-sequence, randomized, crossover study. Plasma concentrations reached steady state after day 5. Percent fluctuation in plasma concentration defined as (Cmax-Cmin)/Cavg (% fluctuation 1) was 97% on day 9 for betaxolol and 343% for atenolol; thus atenolol fluctuation was more than threefold that of betaxolol. A 10-fold difference in plasma level fluctuation was observed when fluctuation was defined as (Cmax-Cmin)/Cmin (% fluctuation 2). The intersubject variances for % fluctuation 1 and % fluctuation 2 were 4.1 and 85.5 times greater for atenolol than for betaxolol; these differences were marginally statistically significant for % fluctuation 1 and significant for % fluctuation 2. The intrasubject variabilities for area under the curve and plasma level fluctuations were statistically greater for atenolol than for betaxolol. Atenolol intrasubject variances were 25 and 271 times greater than for betaxolol for % fluctuation 1 and % fluctuation 2, respectively. Thus, betaxolol exhibited less fluctuation in plasma levels with substantially less intersubject and intrasubject variability. These factors would be expected to provide a more consistent therapeutic response and more dependable dosage adjustment.