[New records of distribution of medical plants in Anhui province].

During the fourth national survey of Chinese material medica resources inventory, 9 species of medical plants in Huangshan area of Anhui Province were newly recorded, including Microlepia calvescens, Dryopteris hangchowensis, Fatoua pilosa, Girardinia chingiana, Lecanthus peduncularis, Galium kamtschaticum, Carpesium minus,Cirsium racemiforme, Globba racemosa, which belong to seven families and nine genera. Among these, 3 genera (Girardinia, Lecanthus, Globba) are new geographical distribution in Anhui Province. All of voucher specimens are preserved in ACM. These discoveries enrich the content of flora in Anhui and provide fundamental materials for studying the plants of Anhui.

[Development of rapid setting-drying device for herbarium specimens and its application in survey of Chinese materia medica resources in Anhui].

Herbarium specimens are the basis for the plant classification and indispensable media in teaching, scientific research and resources investigation. They have also played an important role in identifying and producing traditional Chinese medicine. High-quality herbarium specimens shall meet high requirements for integrity, smoothness, color and fabricating efficiency. Therefore, we designed a rapid setting and drying device for herbarium specimens, which could make the herbarium specimens smooth, colorful and not easy to mildew. In this paper, we pointed out the deficiency of traditional methods in making herbarium specimens, and introduced the structure and working principle of the device. Besides, we also discussed the effect of the device in setting and drying herbarium specimens and its application in the fourth national survey of the Chinese material medica resources (CMMR) in Anhui province. As a result, the device provides new ideas for producing herbarium specimens, with a reasonable design, good uniformity, high efficiency, safety and portability, and so is worthy of promotion and application in the national survey of CMMR.

[Historical evolution and development countermeasures of uncommon-territorial herbs].

As an important part of Chinese medicinal materials, uncommon-territorial herbs are also the most complex parts in the herbal medicine markets. Through years of investigation on the key markets of Chinese herbal medicine, the meaning of uncommon-territorial herbs, their historical evolution, origin and characteristics were clarified in this paper, and some countermeasures were put forward for its development.

Infection rate of Eperythrozoon spp. in Chinese population: a systematic review and meta-analysis since the first Chinese case reported in 1991.

BACKGROUND: Eperythrozoonosis is an important animal health problem worldwide, it not only has a major impact on the economic viability, but also makes a significant impact on public health issues. The present systemic review intends to collate all relevant published data to assess the burden of Eperythrozoon infection in Chinese population and discuss the implications of these findings for public health policy. METHODS: A meta-analysis was conducted to review the published studies that reported Eperythrozoon spp. in Chinese population. Inclusion criteria comprised of the use of microscopic venous blood smear examination for Eperythrozoon detection and a detailed description of sampling techniques. RESULTS: Twenty-four cross-sectional studies with 52,433 participants and 14,951 positive cases, within the range of China mainland, were included in the present analysis. The infection rate of Eperythrozoon varied from 0 to 97.29% with geographical and seasonal variations, people with mild infection intensity contributed the major part (68.93%). The infection rates were highest in the children and adolescents group, significantly increased risk of Eperythrozoon infection was found among herdsmen. CONCLUSIONS: The current study raises awareness about the human eperythrozoonosis in China, which is a newly emerging zoonosis. The majority of Eperythrozoon infection intensity was asymptomatic mild infection. The infection rate of Eperythrozoon in Chinese population varied by geographical region, season, age and occupation. These factors need to be considered when conducting health education campaigns and comparing the surveillance results from different studies.

Nitric oxide regulates pulmonary vascular smooth muscle cell expression of the inducible cAMP early repressor gene.

Nitric oxide (NO) regulates vascular smooth muscle cell (VSMC) structure and function, in part by activating soluble guanylate cyclase (sGC) to synthesize cGMP. The objective of this study was to further characterize the signaling mechanisms by which NO regulates VSMC gene expression using transcription profiling. DNA microarrays were hybridized with RNA extracted from rat pulmonary artery smooth muscle cells (RPaSMC) exposed to the NO donor compound, S-nitroso-glutathione (GSNO). Many of the genes, whose expression was induced by GSNO, contain a cAMP-response element (CRE), of which one encoded the inducible cAMP early repressor (ICER). sGC and cAMP-dependent protein kinase, but not cGMP-dependent protein kinase, were required for NO-mediated phosphorylation of CRE-binding protein (CREB) and induction of ICER gene expression. Expression of a dominant-negative CREB in RPaSMC prevented the NO-mediated induction of CRE-dependent gene transcription and ICER gene expression. Pre-treatment of RPaSMC with the intracellular calcium (Ca(2+)) chelator, BAPTA-AM, blocked the induction of ICER gene expression by GSNO. The store-operated Ca(2+) channel inhibitors, 2-ABP, and SKF-96365, reduced the GSNO-mediated increase in ICER mRNA levels, while 2-ABP did not inhibit GSNO-induced CREB phosphorylation. Our results suggest that induction of ICER gene expression by NO requires both CREB phosphorylation and Ca(2+) signaling. Transcription profiling of RPaSMC exposed to GSNO revealed important roles for sGC, PKA, CREB, and Ca(2+) in the regulation of gene expression by NO. The induction of ICER in GSNO-treated RPaSMC highlights a novel cross-talk mechanism between cGMP and cAMP signaling pathways.

The Effect of Phase Separation on the Mechanical Behavior of the Co-Cr-Cu-Fe-Ni High-Entropy Alloy.

Phase separation phenomena in high-entropy alloys (HEAs) have attracted much attention since their discovery, but little attention has been given to the dynamics of the deformation mechanism of this kind of HEA during uniaxial tension, which limits their widespread and practical utility. In this work, molecular dynamics simulation was used to study the effect of phase separation on the mechanical properties of an HEA under uniaxial tensile loading. Moreover, the associated deformation behavior of the Co-Cr-Cu-Fe-Ni HEA was investigated at the nanoscale. Models with Cu-rich grain boundaries or grains were constructed. The results showed that Cu-rich grain boundaries or grains lowered the strength of the Co-Cr-Cu-Fe-Ni HEA, and Cu-rich grain boundaries significantly reduced ductility. This change of mechanical properties was closely associated with a deformation behavior. Furthermore, the deformation behavior was affected by the critical resolved shear stress of Cu-rich and Cu-depleted regions and the uneven stress distribution caused by phase separation. In addition, dislocation slipping and grain boundary sliding were the main mechanisms of plastic deformation in the Co-Cr-Cu-Fe-Ni HEA.

Nitric oxide-dependent suppression of thioredoxin-interacting protein expression enhances thioredoxin activity.

OBJECTIVE: Cellular redox balance is regulated by enzymatic and nonenzymatic systems and freely diffusible nitric oxide (NO) promotes antioxidative mechanisms. We show the NO-dependent transcriptional regulation of the antioxidative thioredoxin system. METHODS AND RESULTS: Incubation of rat pulmonary artery smooth muscle cells (RPaSMC) with the NO donor compound S-nitroso-glutathione (GSNO, 100 micromol/L) suppressed thioredoxin-interacting protein (Txnip), an inhibitor of thioredoxin function, by 71+/-18% and enhanced thioredoxin reductase 2.7+/-0.2 fold (n=6; both P<0.001 versus control). GSNO increased thioredoxin activity (1.9+/-0.5-fold after 4 hours; P<0.05 versus control). Promoter deletion analysis revealed that NO suppression of Txnip transcription is mediated by cis-regulatory elements between -1777 and -1127 bp upstream of the start codon. Hyperglycemia induced Txnip promoter activity (3.9+/-0.2-fold; P<0.001) and abolished NO effects (-37.4+/-1.0% at 5.6 mmol/L glucose versus 12.4+/-2.1% at 22.4 mmol/L glucose; P<0.05). Immunoprecipitation experiments demonstrated that GSNO stimulation and mutation of thioredoxin at Cys69, a site of nitrosylation, had no effect on the Txnip/thioredoxin interaction. CONCLUSIONS: NO can regulate cellular redox state by changing expression of Txnip and thioredoxin reductase. This represents a novel antioxidative mechanism of NO independent of posttranslational protein S-nitrosylation of thioredoxin.

[Relationship between Tpeak-Tend interval and coronary artery stenosis and effects of percutaneous transluminal coronary angioplasty on Tpeak-Tend].

OBJECTIVE: To explore the relationship between Tpeak-Tend interval (Tpe) and the extent and severity of coronary artery stenosis, and evaluate the effect of percutaneous transluminal coronary angioplasty and stent implantation (PCI) on Tpe in the patients with coronary heart disease (CHD). METHODS: The ECG data were collected from 187 CHD patients undergoing coronary angiography and PCI to evaluate the extend and severity of coronary artery stenosis before and after the interventions. RESULTS: The Tpe of patients with severe stenosis increased significantly as compared with that in patients with moderate stenosis (138.9-/+16.2 ms vs 116.5-/+13.7 ms, P<0.05), and a significant difference was also noted between the moderate stenosis and mild stenosis (86.4-/+12.9 ms) groups (P<0.05). The Tpe decreased significantly in the patients in the order of multi-vessel involvement (140.7-/+17.8 ms), double vessel involvement (118.6-/+14.9 ms), singly vessel involvement (100.5-/+13.2 ms), and stenosis-free (84.3-/+12.4 ms) groups (P<0.05). Tpe was correlated to the extent and severity of coronary artery stenosis (r>0.4). In patients with severe stenosis, the Tpe was significantly reduced at 1 h, 24 h, and 1 week after PCI (115.8-/+14.5, 92.7-/+12.9, and 88.2-/+11.3 ms, respectively, P<0.05). CONCLUSION: The Tpe can reflect the severity and range of coronary artery stenosis, which can be reduced by PCI. Tpe can be a new index for evaluating myocardial ischemia in CHD patients.

[Clinical assessment of Tpeak-end interval for prediction of myocardial infarction].

OBJECTIVE: To assess the value of Tpeak-end interval (Tpe) in predicting myocardial infarction (MI). METHODS: Tpe and Tpeak-end internal after correcting the heart rate (TpeRR) were measured and analyzed in 234 MI patients, who were followed-up for an average of 32 ± 10 months. RESULTS: Clinical events occurred in 45 (19.2%) patients at the end TpeRR of the follow-up. Tpe and of the patients with clinical events were significantly higher than those in patients without the clinical events (P < 0.001). The incidence of clinical events in patients with Tpe > 140 ms were significantly higher than that in patients with Tpe ≤ 140 ms by Kaplan-Meier analysis (P < 0.001). With clinical event as the end point, the proportional hazards rate was 2.48 in univariate COX analysis (P < 0.01). After controlling for risk factors, the hazards rate was 2.66 by multvariate COX regression (P < 0.01). CONCLUSION: Tpe is positively correlated to the prognosis of MI and serves as an new index for predicting the clinical events in MI patients.

Nitric oxide induces phosphodiesterase 4B expression in rat pulmonary artery smooth muscle cells.

Phosphodiesterases (PDE) metabolize cyclic nucleotides limiting the effects of vasodilators such as prostacyclin and nitric oxide (NO). In this study, DNA microarray techniques were used to assess the impact of NO on expression of PDE genes in rat pulmonary arterial smooth muscle cells (rPASMC). Incubation of rPASMC with S-nitroso-l-glutathione (GSNO) increased expression of a PDE isoform that specifically metabolizes cAMP (PDE4B) in a dose- and time-dependent manner. GSNO increased PDE4B protein levels, and rolipram-inhibitable PDE activity was 2.3 +/- 1.0-fold greater in GSNO-treated rPASMC than in untreated cells. The soluble guanylate cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one, and the cAMP-dependent protein kinase inhibitor, H89, prevented induction of PDE4B gene expression by GSNO, but the protein kinase G (PKG) inhibitors, Rp-8-pCPT-cGMPs and KT-5823, did not. Incubation of rPASMC with IL-1beta and tumor necrosis factor-alpha induced PDE4B gene expression, an effect that was inhibited by l-N(6)-(1-iminoethyl)lysine, an antagonist of NO synthase 2 (NOS2). The GSNO-induced increase in PDE4B mRNA levels was blocked by actinomycin D but augmented by cycloheximide. Infection of rPASMC with an adenovirus specifying a dominant negative cAMP response element binding protein (CREB) mutant inhibited the GSNO-induced increase of PDE4B gene expression. These results suggest that exposure of rPASMC to NO induces expression of PDE4B via a mechanism that requires cGMP synthesis by sGC but not PKG. The GSNO-induced increase of PDE4B gene expression is CREB dependent. These findings demonstrate that NO increases expression of a cAMP-specific PDE and provide evidence for a novel "cross talk" mechanism between cGMP and cAMP signaling pathways.

Nerve growth factor induces anti-apoptotic heme oxygenase-1 in rat pheochromocytoma PC12 cells.

Nerve growth factor (NGF) and heme oxygenases (HOs) both exert neuroprotective effects. To characterize the role of HOs in the prevention of apoptosis by NGF, we investigated the effect of NGF on the expression of HOs in serum-deprived PC12 cells. Serum deprivation (SD) led to a rapid decrease in HO-1 gene expression followed by induction of apoptosis. Incubation of serum-deprived PC12 cells with NGF prevented apoptosis and increased HO-1 mRNA and protein levels, as well as HO enzyme activity. HO-2 gene expression was unaffected by SD or NGF. Incubation of cells with mitogen-activated protein kinase kinase (MEK) inhibitors (PD98059 or U0126) attenuated the ability of NGF to increase HO-1 expression and to protect PC12 cells against SD-induced apoptosis. NGF augmented HO-1 gene transcription but did not alter HO-1 mRNA stability. HO inhibitors or antisense HO-1 RNA decreased the ability of NGF to prevent cell apoptosis. Inhibition of HO activity enhanced intracellular reactive oxygen species (ROS) production and attenuated NGF-induced reduction of ROS in serum-deprived PC12 cells. These results demonstrate that NGF enhances HO-1 gene transcription via MEK activation and that the induction of HO-1 plays an important role in the antioxidative and antiapoptotic effects of NGF in serum-deprived PC12 cells.

Strategic advantages of insulin-like growth factor-I expression for cardioprotection.

BACKGROUND: Insulin-like growth factor-I (IGF-I) peptide has beneficial effects on cardiomyocyte function and survival, many of which are mediated through the serine-threonine kinase, Akt. However, concerns about systemic effects of IGF-I peptide limit its clinical application. The present study tested whether local IGF-I expression could mediate cardioprotection without elevating serum [IGF-I]. METHODS: The ability of a recombinant adenovirus encoding IGF-IB (Ad.IGF-I) to activate Akt and protect cardiomyocytes from hypoxia-induced apoptosis in vitro was compared with the effects of IGF-I peptide or expression of constitutively active Akt (myr-Akt). In vivo, cardiac IGF-I gene transfer was performed prior to ischemia-reperfusion injury (IRI). Effects on the ischemic and infarcted areas were assessed while serum [IGF-I] was measured by radioimmunoassay. RESULTS: Compared with IGF-I peptide, Ad.IGF-I achieved more sustained activation of Akt and reduced hypoxia-induced apoptosis at lower media IGF-I concentrations. In a co-culture system, Ad.IGF-I protected both infected and uninfected cells from hypoxic injury, while myr-Akt protected only infected cells. In vivo cardiac injection of Ad.IGF-I mediated significant local IGF-I expression, without affecting serum [IGF-I] levels. After IRI, Ad.IGF-I did not affect the ischemic area but reduced infarct size approximately 50% (32 +/- 13 vs. 64 +/- 14% AAR in Ad.GFP rats, p < 0.003), although the transgene was expressed in only approximately 15% of the ischemic region, consistent with possible paracrine benefit. CONCLUSIONS: Somatic gene transfer of IGF-I may offer strategic advantages over both systemic delivery of IGF-I peptide and expression of cell autonomous cardioprotective transgenes such as Akt by mediating autocrine and paracrine cardiomyocyte protection without elevating serum [IGF-I] levels.