蛋黄磷脂中磷脂酰乙醇胺的薄层扫描测定

将超临界ＣＯ２萃取法得到的蛋黄粉中的磷脂经薄层色谱分离，采用双波长薄层扫描仪对其磷脂酰乙醇胺进行测定。平均回收率为９７．６７％，ＲＳＤ为２．３１％。     

格林—巴利综合症血清唾液酸、磷脂、胆固醇的测定及其临床意义

本文应用硫代巴比妥酸(TBA)法对34例格林—巴利综合征(GBS)患者51次血清唾液酸(SA)测定。结果显示:患者血清SA含量显著高于50例对照组,血清SA阳性率亦显著高于对照组;GBS患者四肢肌力与血清SA呈负相关;以重型GBS血清SA含量显著高于轻型,病程初期高于患病后期;血清磷脂含量GBS明显高于对照组,而血清胆固醇两组变化无显著性意义。本文提示GBS血清SA含量变化能够反映周围神经损伤的程度。     

Renewal of the membrane complex of Schistosoma mansoni is closely associated with lipid metabolism

Metabolic pathways leading to lipid biosynthesis in four different developmental stages of Schistosoma mansoni were explored and quantified by incubation in the presence of labeled precursors in a chemically defined medium. At the schistosomulum stage and in male, female, or paired worms, glycerol and oleate incorporation into neutral lipids, mainly in the form of triacylglycerols, was greater than into phospholipids, whereas in 11-and 15-day-old worms, synthesis mainly led to phospholipids. Incorporation into phospholipids was recovered largely in phosphatidylcholine, and distribution into other phospholipids depended on the developmental stage. Incorporation of choline and ethanolamine into their respective phospholipids represented up to 15% of the parasitic phospholipid content. The formation of phosphatidylcholine by phosphatidylethanolamine methylation occurred mainly in the immature parasitic stages. Inositol incorporation was also measurable, whereas [14C]serine incorporation was low or undetectable. Addition of 1-palmitoyl-2-[14C]oleyl phosphatidylcholine revealed a very high uptake of this phospholipid by the immature stages but further metabolism was not detectable. In contrast, adult S. mansoni were completely unable to take up or absorb this exogenous phospholipid. The most striking aspect of this study was the relatively high metabolic activity in 11-day-old worms and the lower but sustained activity on day 15 and at the schistosomulum stage. By comparison, biosynthetic activity in adult S. mansoni, on which research studies have been focused until now, was very low. We also discuss the participation of lipid metabolism in the constant renewal of the membrane complex which is essential to parasitism by S. mansoni.     

Phosphatidylglycerolphosphate synthase encoded by the PEL1/PGS1 gene in Saccharomyces cerevisiae is localized in mitochondria and its expression is regulated by phospholipid precursors

The PEL1/PGS1 gene of the yeast Saccharomyces cerevisiae is essential for the viability of rho ^–/rho° mutants and the normal cardiolipin content of cells. The PEL1-GFP fusion gene has been found to complement the pel1/pgs1 mutation and its fluorescent protein was localized to mitochondria similarly to the β-galactosidase activity of a protein encoded by the PEL1-lacZ fusion gene. The expression of the PEL1-lacZ reporter gene was repressed in cells grown in the presence of inositol and choline, reduced in the ino2 and ino4 strains, but constitutive in the opi1 null-mutant strain. The results demonstrate that Pel1p, playing a vital role in cells impaired in the mitochondrial DNA, is localized in the mitochondria and expressed in response to inositol and choline. Received: 15 June / 15 July 1998     

Major phospholipids and phosphatidylcholine synthesis in adult Schistosoma mansoni

The major phospholipids present in the phospholipid extract of Schistosoma mansoni were phosphatidylcholine (28%), phosphatidylethanolamine (25%), phosphatidylserine (15%) and phosphatidylglycerol (8%). The synthesis of phosphatidylcholine in S. mansoni adults occurred by the choline to phosphatidylcholine or Kennedy pathway. Incorporation of CDPcholine and choline into the phosphatidylcholine of worm slices appeared linear over time with no demonstrable sex differences in choline incorporation. A slight difference in the incorporation of CDPcholine by separate sexes was evident. Methylation of phosphatidylethanolamine to phosphatidylcholine could not be demonstrated.     

PLPP2: Potential therapeutic target of breast cancer in PLPP family

PLPPs (Phospholipid phosphatases) are widely expressed in different human tissues, regulate cell signal transduction, and are overexpressed in cancers such as gliomas, pancreatic adenocarcinoma, lung adenocarcinoma, and so on. As a member of the PLPP family, PLPP2 (phospholipid phosphatase 2) plays a vital role in the occurrence and development of breast cancer, but its mechanism is still unclear. Our research found that PLPP2 was overexpressed in breast cancer, and the higher expression level of PLPP2 showed a worse prognosis for breast cancer patients. Further analysis showed that overexpression of PLPP2 affected the expression of CDC34 (cell-division cycle 34), LSM7 (Like-Smith 7), and SGTA (small glutamine-rich tetratricopeptide repeat-containing protein alpha) through EMT (epigenetic-mesenchymal transition) related pathways to promote the occurrence and development of breast cancer. In vitro, silencing PLPP2 significantly reduced the proliferation, invasion, and migration abilities of human breast cancer cells MDA-MB-231. ER+ is a common subtype of breast cancer. Furthermore, we found that the overexpression of PLPP2 was significantly related to the poor prognosis of ER+ breast cancer. These results indicate that PLPP2 has value as a potential therapeutic target for breast cancer, especially for ER+ breast cancer.     

低分子肝素经大鼠胃肠道吸收的研究

目的考察低分子肝素(LMWH)溶液及乳剂在麻醉大鼠胃肠道的吸收情况以及磷脂对LMWH的促吸收作用.方法在体大鼠胃中给药、小肠及小肠各肠段循环液给药,一定时间后测定血液凝固时间的变化及循环液中药量的变化,以反映药物的吸收情况.结果LMWH在体小肠和十二指肠循环溶液及乳剂循环一定时间后,药量显著减少,血液凝固时间明显延长.结论LMWH在胃中无明显吸收,部分被破坏;在小肠中吸收,十二指肠吸收最好.磷脂乳剂对LMWH有一定的保护和促吸收作用.     

失火烟雾吸入与肺损伤

目的　观察失火烟雾吸入引起肺损伤的表现。方法　对 117例失火烟雾吸入者的临床表现进行分析 ,并进行了相应的大鼠染毒实验。结果　临床上主要表现为上呼吸道和肺部的刺激和炎症反应 ,动脉血氧分压降低。染毒大鼠支气管肺泡灌洗液中细胞总数及中性白细胞数增高 ,磷脂组分改变。病理形态学可见炎症浸润、间质水种及肺水肿。结论　失火烟雾吸入可致急性呼吸道损伤 ,表现为刺激性气道炎、肺泡炎及肺水肿。     

Inhibition of fibroblast cell adhesion on substrate by coating with 2-methacryloyloxyethyl phosphorylcholine polymers

Fibroblast adhesion and growth behavior were examined on various polymers coated on a poly(ethylene telephthalate) (PET) substrate. The polymers are poly[2-methacryloyloxyethyl phosphorylcholine (MPC)-co-n-butyl methacrylate copolymer (PMB)s with different MPC unit compositions, and poly(2-hydroxyethyl methacrylate). Surface analysis by dynamic contact angle measurement revealed that the mobility of the polymer chain on the PET substrate depended on the MPC unit composition, but there was no significant difference between the PMBs with 3-10 mol% MPC units and poly(HEMA). Fibronectin adsorption on the polymer surface from a cell culture medium was determined by immunoassay. The adsorbed fibronection was evenly distrubuted in every polymer, however, the amount was reduced with an increase in the MPC unit composition in the PMB. This result suggested that the MPC unit could weaken the interaction between the polymer surface and proteins. When fibroblast L-929 cells, were cultured on the polymers, the cells adhered and the number of cells increased on not only the hydrophobic poly(BMA) but also on the hydrophilic poly(HEMA). However, the number of cells that adhered on the PMB surface decreased with an increase in the MPC unit composition. This was a result of the fibronectin adsorption behavior. Thus, it could be concluded that since the PMB could suppress cell adhesion proteins e.g. fibronectin, the PMB showed excellent cell adhesive resistance properties.     

Adsorption of Surfactant to Bronchial Epithelium: Possible Role of Receptor ‘Unmasking’ in Asthma

Background.?In a recent study in animals it has been shown how surface-active phospholipid (SAPL) in the form of a commercially available micronized (5 µmφ) dry powder (ALEC^T/Pumactant^T) was able to reduce afferent neural feedback to the brainstem in response to a methacholine challenge by the same order of magnitude as drugs commonly prescribed for asthma. The underlying theory assumed that adsorption of SAPL to bronchial epithelium masked irritant receptors eliciting the bronchoconstrictor reflex, thus providing a barrier to noxious stimuli entering the lungs. Objective.?To test the underlying assumption that SAPL was actually adsorbed (i.e., bound to bronchial epithelium), especially the major and most surface-active component of lung surfactant, namely dipalmitoyl phosphatidylcholine (DPPC). A secondary objective was to investigate any role of phosphatidylglycerol (PG) in promoting the adsorption of DPPC. Methods.?Radiolabeled DPPC dispersed ultrasonically in saline was used to incubate excised sections of porcine bronchial epithelium. The adsorbed DPPC was then quantified by rigorously rinsing the tissue of adhering fluid and then digesting it for β-scintillation counting. Each test (n = 8 runs) was repeated for ratios of DPPC:PG of 9:1, 7:3 (as per ALEC^T/Pumactant^T) and 1:1 for both dipalmitoyl PG (DPPG) and EggPG (as incorporated in ALEC^T/Pumactant^T). Results.?Despite rigorous rinsing postincubation, bronchial epithelium was found to adsorb DPPC at a level roughly equivalent to one close-packed monolayer; whereas both DPPG and EggPG promoted the adsorption of DPPC in a dose-dependent manner, reaching an approximate threefold increase for 7:3 DPPC:PG. Conclusion.?DPPC adsorbs to bronchial epithelium in amounts necessary for the masking of receptors, and this adsorption (probably chemisorption) is quite strongly promoted by PG either in its indigenous state (DPPG) or in the form (EggPG) used in ALEC^T to suppress the sensitivity of bronchial irritant receptors in our previous study and in clinical trials just completed.