古文唐“瘦”宋“肥”论——以朱东润《中国历代文学作品选》与姚鼐《古文辞类纂》为考察对象

通过对朱东润主编《中国历代文学作品选》与姚鼐《古文辞类纂》中所选的唐宋古文进行随机抽样做定量分析,我们发现:宋代古文在句子长度上比唐代古文多约1个字,每百字所使用的语气虚词比唐代古文多1.17个字;在篇幅上,宋代赠序比唐代多约20个字,墓志则比唐代多300字以上。这一定量分析的结果证实了古文确实是唐"瘦"宋"肥"。在此基础上,我们从三个方面分析了唐、宋古文风格上的差异,并对明代散文艺术形式上的演变及其复杂生态进行了一定程度的解释。

Leptin: a multifunctional hormone

Leptin is the protein product encoded by the obese (ob)gene. It is a circulating hormone produced primarily by the adipose tissue. ob/ob mice with mutations of the gene encoding leptin become morbidly obese, infertile, hyperphagic, hypothermic,and diabetic. Since the cloning of leptin in 1994, our knowledge in body weight regulation and the role played by leptin has increased substantially. We now know that leptin signals through its receptor, OB-R, which is a member of the cytokine receptor superfamily. Leptin serves as an adiposity signal to inform the brain the adipose tissue mass in a negative feedback loop regulating food intake and energy expenditure. Leptin also plays important roles in angiogenesis, immune function, fertility and bone formation. Humans with mutations in the gene encoding leptin are also morbidly obese and respond to leptin treatment,demonstrating that enhancing or inhibiting leptin’s activities in vivo may have potential therapeutic benefits.

Effects of acute or prolonged exposure to leptin on hepatic glucose oxidation

Objective To observe the short-term and long-term effects of leptin on hepatic glucose oxidation and glucokinase gene expression. Methods Rat hepatic cell line BRL was incubated with leptin of different doses (range from 10?ng/ml-200?ng/ml) for 1?h or 24?h. Glucose oxidation was determined by liquid scintillation counting. Glucokinase gene expression (corrected by β-actin) was determined by reverse transcription semi-quantitative polymerase chain reaction. Results Treatment with leptin 10?ng/ml for 1?h had no significant effects on glucose oxidation in hepatic cells. However, at the doses ranging from 50?ng/ml to 200?ng/ml, leptin significantly inhibited glucose oxidation. These effects disappeared when the hepatic cells were exposed to leptin for 24?h. Glucokinase mRNA expression was reduced significantly after both 1?h and 24?h exposure to leptin (100?ng/ml) as compared to that of the control group. Conclusion A low dose of leptin has no significant effect on glucose oxidation in hepatic cells. A relatively high dose of leptin has an acute inhibitory effect on the glucose oxidation in hepatic cells. This effect may likely involve the inhibition of glucokinase gene expression. The inhibitory effect on glucose oxidation is transient and disappears with prolonged exposure time.

Fatness and thinness of uniform Cantor sets for doubling measures

Let E = E({nk},{ck}) be a fat uniform Cantor set. We prove that E is a minimally fat set for doubling measures if and only if (nkck)p = ∞ for all p < 1 and that E is a fairly fat set for doubling measures if and only if there are constants 0 < p < q < 1 such that (nkck)q < ∞ and (nkck)p = ∞. The classes of minimally thin uniform Cantor sets and of fairly thin uniform Cantor sets are also characterized.

Influence of catgut implantation at acupoints on leptin and insulin resistance in simple obesity rats

OBJECTIVES:To investigate the influence of catgut implantation at acupoints on leptin resistance(LR) and insulin resistance(IR) in the simple obesity rat.METHODS:Rats were made obese with high-fat diets,after which surgical catgut was implanted at Zusanli(ST 36) and Neiting(ST 44) acupoints once a week for 4 weeks(implantation group).Rats from the implantation group were compared with normal rats and unoperated obese rats(control group).Gene expression of the leptin receptor(OB-R) was evaluated using RT-PCR and northern blot.Serum and hypothalamus leptin and insulin(INS) levels were determined by radioimmunoassay.Body weight,Lee's index,body fat,serum and hypothalamus leptin and INS levels,and hypothalamic OB-R gene expression were determined before and after treatment.RESULTS:Body weights,Lee's index,body fat,and serum leptin and INS levels were significantly higher in obese than in normal rats.Hypothalamic leptin and INS levels and OB-R gene expression were significantly lower in obese rats.Catgut implantation at acupoint promoted weight loss and decreased serum leptin and INS levels.Hypothalamic leptin and INS levels and OB-R gene expression increased significantly.CONCLUSIONS:Catgut implantation at acupoint adjusts central and peripheral leptin and promotes hypothalamic OB-R gene expression.This may be an important method for regulation of LR,IR and abnormal endocrinology and metabolism.

A high-fat diet increases body fat mass and up-regulates expression of genes related to adipogenesis and inflammation in a genetically lean pig

Because of their physiological similarity to humans, pigs provide an excellent model for the study of obesity. This study evaluated diet-induced adiposity in genetically lean pigs and found that body weight and energy intake did not differ between controls and pigs fed the high-fat （HF） diet for three months. However, fat mass percentage, adi- pocyte size, concentrations of total cholesterol （TC）, triglyceride （TG）, high-density lipoprotein cholesterol （HDL-C） and low-density lipoprotein cholesterol （LDL-C）, insulin, and leptin in plasma were significantly higher in HF pigs than in controls. The HF diet increased the expression in backfat tissue of genes responsible for cholesterol synthesis such as Insig-1 and Insig-2. Lipid metabolism-related genes including sterol regulatory element binding protein lc （SREBP-lc）, fatty acid synthase 1 （FASN1）, diacylglycerol O-acyltransferase 2 （DGAT2）, and fatty acid binding protein 4 （FABP4） were significantly up-regulated in backfat tissue, while the expression of proliferator-activated receptor-α（PPAR-α） and carnitine palmitoyl transferase 2 （CPT2）, both involved in fatty acid oxidation, was reduced. In liver tissue, HF feeding significantly elevated the expression of SREBP-lc, FASN1, DGAT2, and hepatocyte nuclear factor-4α （HNF-4α） mRNAs. Microarray analysis further showed that the HF diet had a significant effect on the expression of 576 genes. Among these, 108 genes were related to 21 pathways, with 20 genes involved in adiposity deposition and 26 related to immune response. Our results suggest that an HF diet can induce genetically lean pigs into obesity with body fat mass expansion and adipose-related inflammation.