Evaluation of silicone elastomer catheters for long-term intravenous chemotherapy

We evaluated the efficacy and the complications of 65 silicone elastomer catheters inserted percutaneously for long-term venous access for administration of chemotherapy, antibiotics, and blood products in patients with metastatic cancer. Treatments were administered either in the hospital or in the outpatient clinic, using a portable infusion pump. The median indwelling time of catheters was 238 days (range, two to 521). The projected duration of catheter function, when the electively removed catheters were censured, was 310 days. Twenty-three catheters were removed because of malfunction, while the remaining either were discontinued electively (20) or were functioning at the conclusion of the study (22). The problems necessitating removal of 23 catheters were inadvertent dislodgement from loose sutures (eight), mechanical damage to the catheters (four), sepsis (four), phlebitis (four), intraluminal blockage with a clot (two), and cellulitis (one). We conclude that silicone elastomer catheters are safe and reliable for extended venous access for cancer chemotherapy. They are easy to insert and remove and can be replaced with a guide wire without requiring surgical intervention.     

Interfacial properties of polymethyl alpha-cyanoacrylate and polybutyl alpha-cyanoacrylate.

Several physical properties of two polyalkyl alpha-cyanoacrylates relevant to their use in pharmaceutical dosage forms have been investigated. Formation of polymer films at several oil-water interfaces reveals films of diverse morphology. The retardation of solute transfer across an oil-water interface caused by the presence of polymer films formed in situ from the monomers has revealed that the methyl derivative forms the more effective barrier to the test solute, gentian violet. The emulsion-stabilizing properties of the methyl polymer have been studied, and the film-forming properties of the monomers spread from benzene onto water surfaces have been examined using a surface balance.     

Study of the effects of progesterone therapy on the stilboestrol-induced sensitivity of isolated uteri of hypophysectomized rats

1. In intact rats progesterone (50 mg/kg) antagonized the effect of stilboestrol (100 μg/kg) on the vaginal smears and the uterine sensitivity. The uterine sensitivity to acetylcholine, oxytocin and 5-hydroxytryptamine was decreased by 6·8, 64 and 14·8 times, respectively, as compared with uteri removed after stilboestrol injections.

2. Progesterone therapy in hypophysectomized rats also antagonized the effect of stilboestrol on the vaginal mucosa and on the uterine sensitivity to drugs. The sensitivity to acetylcholine, oxytocin and 5-hydroxytryptamine was decreased by 6·2, 50 and 14·5 times, respectively. Similar results were obtained on uteri removed from sham-hypophysectomized rats.

3. On the basis of these results it is suggested that the hypophysis does not play any part in the desensitization of the myometrium to the oxytocic drugs and in the changes found in the vaginal mucosa after progesterone therapy.

     

Comparison of the effectiveness of two liquid-based Papanicolaou systems in the handling of adverse limiting factors, such as excessive blood

BACKGROUND: Excessive blood may compromise gynecologic Papanicolaou (Pap) smears. Liquid-based cytologic techniques have been developed in part to address this problem. In the current study, conditions of excessive blood were simulated to compare the ability of two liquid-based systems, ThinPrep and SurePath, to satisfactorily process specimens in the presence of this potentially limiting factor. METHODS: Equal volumes of washed epithelial cells derived from pooled residues of liquid Pap vials were added to a series of ThinPrep and SurePath vials. Increasing volumes of freshly drawn, packed erythrocytes were added to the vials in progressive amounts from 50 microL or 100 microL up to 3000 microL. The vials were processed on their respective instruments according to U.S. Food and Drug Administration-approved procedures for a total of six test runs. The cellularity of the slides was measured by averaging epithelial cell counts in a total of five 40x fields. RESULTS: SurePath preparations were uncompromised by blood until aliquots from 1000 microL to 3000 microL were reached. The ThinPrep system invariably was overwhelmed by the first 50-microL or 100-microL aliquot of blood, with epithelial cell counts dropping immediately to near zero. CONCLUSIONS: The cell enrichment process of the SurePath system capably handled significantly greater amounts of potentially obscuring blood than the membrane filtration method of the ThinPrep system, which was compromised by as little as 相似文献   

Diagnosis of human rotavirus in stool specimens: comparison of different methods

A total of 345 stool specimens of hospitalized children below 5 years of age with acute gastroenteritis were tested for the presence of rotavirus by Polyacrylamide gel electrophoresis (PAGE), a monoclonal antibody based enzyme immunoassay (EIA) and a latex agglutination test (LAT). Detection rate for PAGE and EIA were 24.9% (345/86) and 20.9% (345/70) respectively. Using PAGE as the standard, the sensitivity and specificity of EIA were 75.6% and 98.1% respectively. The sensitivity of LAT was 70.9% with 100% specificity (LAT was done in only PAGE positive specimens). LAT appeared as the simplest and economic for both bed side and field use.     

Lactosylceramide recruits PKCalpha/epsilon and phospholipase A2 to stimulate PECAM-1 expression in human monocytes and adhesion to endothelial cells

Despite the importance of platelet/endothelial cell adhesion molecule-1 (PECAM-1, CD31) in the adhesion and diapedesis of monocytes/lymphocytes, little is known about the mechanisms by which it is regulated. We explored the role of a glycosphingolipid, lactosylceramide (LacCer), in modulating PECAM-1 expression and cell adhesion in human monocytes. We observed that LacCer specifically exerted a time-dependent increase in PECAM-1 expression in U-937 cells. Maximal increase in PECAM-1 protein occurred after incubation with LacCer for 60 min. LacCer activated PKCalpha and -epsilon by translocating them from cytosol to membrane. This was accompanied by the activation of phospholipase A(2) (PLA(2)) and the increase of cell adhesion, which were abrogated by chelerythrine chloride, 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl)-maleimide and 12-(2-cyanoethyl)-6,7,12,13-tetrahydro-13-methyl-5-oxo-5H-indolo(2,3-a)pyrrolo(3,4-c)-carbazole (GO 6976) (PKC inhibitors). Similarly, bromoenol lactone (a Ca(2+)-independent PLA(2) inhibitor) and methyl arachidonyl fluorophosphonate (an inhibitor of cytosolic PLA(2) and Ca(2+)-independent PLA(2)) inhibited LacCer-induced PLA(2) activity. Bromophenacyl bromide (a PLA(2) inhibitor) abrogated LacCer-induced PECAM-1 expression, and this was bypassed by arachidonic acid. Furthermore, the arachidonate-induced up-regulation of PECAM-1 was abrogated by indomethacin [a cyclooxygenase (COX)-1 and -2 inhibitor] or N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (a COX-2 inhibitor) but not nordihydroguaiaretic acid (a lipoxygenase inhibitor). In sum, PKCalpha/epsilon are the primary targets for the activation of LacCer. Downstream activation of intracellular Ca(2+)-independent PLA(2) and/or cytosolic PLA(2) results in the production of arachidonic acid, which in turn serves as a precursor for prostaglandins that subsequently stimulate PECAM-1 expression and cell adhesion. These findings may be relevant in explaining the role of LacCer in the regulation of PECAM-1 and related pathophysiology.