结构功能:黑社会犯罪与我国刑法配置分析

黑社会犯罪是一种以追求非法经济利益为动因的特殊集团犯罪,它以犯罪动因为核心,构筑了犯罪动因、犯罪行为、犯罪安全保护三层级的犯罪结构模式。因此,要控制这种危害性极大的社会犯罪,就必须构筑起以抑制犯罪动因为核心的刑法结构功能体系。我国刑事立法已按照社会控制与犯罪对应的要求,建构了自己的结构体系而与黑社会犯罪形成了刺激与反应的互动关系,但这个结构体系尚存在着不完善之处,因此有必要对这个结构体系进行整合。

Expressions of MMP-2,-9,TIMP-1,-2,-3 mRNA in Rat Uterus during Estrous Cycle

Zymography and in situ hybridization were used to investigate matrixmetalloproteinase -2, -9 (MMP -2, MMP-9) activities and expressions of MMP -2, -9 and TIMP1, -2, -3 (tissue inhibitors of matrix metallo-proteinases) mRNA in the rat uterus during estrouscycle. The relative activity was semiquanted by using densitometric analysis. The MMP-2(67 kDa) activity in every stage during estrpus cycle was detected by zymography. MMP-2activity was highest at proestrus; higher at estrus and metaestrus; lowest at diestrus. Throughin situ hybridization, MMP -2, -9, TIMP -1~ -3 mRNA mainly in hasal stroma cells of uterineendometrium were detected. The positive signals of MMP -2 and -9 mRNAs in hasal stromacells were shown stronger at proestrus, estrus and metaestrus while they showed the weakest atdiestrus. The expression of MMP -2 mRNA coincided with MMP -2 activity change. MMP-2and -9 mRNAs were also highly expressed in uterine circular muscle at estrus. Weak signals ofMMP -9 mRNA were detected in uterine luminal and glandular epithelial cells at estrus.TIMP -1 mRNA in hasal stroma cells was shown as the strongest expression at estrus andmetaestrus; stronger at proestrus and the weakest at diestrus. TIMP-2 mRNA in basal stromacells was stronger at estrus and diestrus; weaker at proestrus and metaestrus. TIMP -1 and -2mRNAs were also highly expressed in uterine luminal and glandular epithelial cells at estrus.TIMP -3 mRNA in hasal stroma cells revealed the strongest expression at estrus; stronger atdiestrus and metaestrus and showed the weakest at proestrus. The mRNA was also highlyexpressed in uterine circular muscle at estrus. In short, our present results provide evidencethat MMP -2, -9 and TIMP -1~ -3 were involved in rat uterine endometrium reconstructionduring estrous cycle.

Effects of Periodical Salinity Fluctuation on the Growth, Molting, Energy Homeostasis and Molting-Related Gene Expression of Litopenaeus vannamei

To determine the response of Litopenaeus vannamei to periodical salinity fluctuation, a 30-day experiment was conducted in laboratory. In this experiment, two salinity fluctuation amplitudes of 4(group S4) and 10(group S10) were designed. The constant salinity of 30(group S0) was used as the control. Levels of shrimp growth, molting frequency(MF), cellular energy status(ATP, ADP and AMP), as well as the expression of genes encoding molt-inhibiting hormone(MIH), crustacean hyperglycemic hormone(CHH), ecdysteroid-regulated protein(ERP), and energy-related AMP-activated protein kinase(AMPK) were determined. The results showed that periodical salinity fluctuation significantly influenced all indicators except MF which ranged from 13.3% in group S10 to15.4% in group S4. In comparison with shrimps cultured at the constant salinity of 30, those in group S4 showed a significant elevation in growth rate, food conversion efficiency, cellular energy status, ERP and MIH gene transcript abundance, and a significant reduction in CHH and AMPK transcript abundance(P < 0.05). However, salinity fluctuation of 10 only resulted in a significant variation in MIH and CHH gene expression when compared to the control(P < 0.05). According to our findings, L. vannamei may be highly capable of tolerating salinity fluctuation. When ambient salinity fluctuated at approx. 4, the increased MF and energy stores in organisms may aid to promoting shrimp growth.

Pharmarcogenetic Mechanism of ACE liD Polymorphism Adversely Responding to ACE Inhibitors in Regulating the ACE Promoter Activity in Neurons

The ACE （angiotensin converting enzyme） inhibitors are not only drugs widely prescribed drugs in cardiovascular diseases, but also potentially therapeutic agents in dementia. Based on the findings that the ACE inhibitors could activate the c-Jun N-terminal kinase signal to increase the ACE gene expression and that the Alu element of the human ACE gene involved in regulating ACE promoter activity, we aimed to investigate whether there are different pharmacogenetic responses of ACE I/D polymorphism to the ACE inhibitors in neurons. The three reporter vectors, pACEpro（0-SEAP, p-I-ACEpro-SEAP, and p-D-ACEpro-SEAP were used to examine the transcriptional activity of the vectors responding to the lisinopril treatment using a transient-transfection method in SH-SY5Y cells. Our results showed that lisinopril increased the promoter activity of an ACE gene by 16.7%. Additionally, we found the lisinopril enhanced the ACE promoter activity of the I-form vector by 17.2%, but adversely reduced that of the D-form vector by 16.8%, as compared with the respective control without the lisinopril treatment. Firstly, our findings had proved that the UD polymorphism of ACE gene contrarily responds to the ACE inhibitors in regulating the ACE expression in neurons, which provide a novel insight suggesting genetic testing to tailor the treatment regimens in AD （Alzheimer＇s disease） patients.

Reactive protein, plasminogen activator inhibitor type-1 （PAI-1） levels, PAI-1 promoter 4G/5G polymorphism and acute myocardial infarction

Objective To investigate the relationship between CRP, plasminogen activator inhibitor type 1 （PAI-1） levels, PAI-1 gene promoter 4G/5G polymorphism and the type of acute myocardial infarction （ST elevation myocardial infarction, STEMI vs the non-ST elevation Myocardial infarction, NSTEMI）. Methods One hundred seventy-six consecutive patients with AMI were included for the study, of whom 60 had STEMI and 56 had NSTEMI, and 60 adults without cardiovascular and cerebrovascular disease were selected as controls. Blood samples were obtained from patients within 6 h of AMI and the plasma PAI-1, CRP, and the gene polymorphism were measured. Results Plasma levels of PAI- 1 and CRP were higher in AMI groups, compared those in the control group, and plasma levels of PAI-1 were significantly higher in patients with STEMI compared to those with NSTEMI （80.12ng/ml VS.73.01ng/ml, P 〈0.01）, while CRP levels were not significantly different between patient with STEMI and NSTEMI （3.87 ± 0.79 mg/ml VS.4.01 ±0.69mg/ml, P〉0.05）. PAI-1 levels presented a significant correlation with CRP levels in the NSTEMI subjects. However, PAI-1 and CRP levels could explain the lack of a significant relationship between them in control and STEMI subjects.The frequencies of 4G/4G genotype in the AMI group were higher than those in the control group and higher in patient with STEMI than in patient with NSTEMI. Plasma levels of PAI-1 in subjects with 4G/4G genotype were significantly increased as compared to those in subjects with 4G/5G and 5G/5G genotype. Conclusions Plasma PAI-1 levels were associated with different myocardial infarction type, and PAI-1 promoter 4G/5G polymorphisms and CRP may be related to plasma PAI-1 levels

Inhibition Mechanism of Hydroxyproline-like Small Inhibitors to Disorder HIF-VHL Interaction by Molecular Dynamic Simulations and Binding Free Energy Calculations

Protein-protein interactions are vital for a wide range of biological processes.The interactions between the hypoxia-inducible factor and von Hippel Lindau(VHL)are attractive drug targets for ischemic heart disease.In order to disrupt this interaction,the strategy to target VHL binding site using a hydroxyproline-like(pro-like)small molecule has been reported.In this study,we focused on the inhibition mechanism between the pro-like inhibitors and the VHL protein,which were investigated via molecular dynamics simulations and binding free energy calculations.It was found that pro-like inhibitors showed a strong binding affinity toward VHL.Binding free energy calculations and free energy decompositions suggested that the modification of various regions of pro-like inhibitors may provide useful information for future drug design.