The liver is an important organ of the body,with an extraordinary capacity for responding to physical or chemical injuries by regenerating. The mechanisms behind liver regeneration are very complicated as hundreds of substances are involved.However,most of them are not liver-specific,such as HGF,EGF etc. We recently isolated a pure protein with hepatic stimulatory activity from the extract of a weanling calf liver and named its hepatopoietin Cn (HPPCn).This paper,with reference to our own work, mainly reviews the development and bioactivity about hepatic stimulator substance(HSS),augmenter of liver regeneration(ALR),hepassocin(HPS) and HPPCn,which are liver-specific biologically active peptides.

OBJECTIVETo systematically evaluate acupuncture as a treatment for male infertility.

METHODSWe searched Chi na Biology Medical Database (CBM), Wan Fang Medical Information System, China National Knowledge Infrastructure (CNKI), VIP Information Resource System (VIP), and PubMed for published literature on acupuncture as a treatment for male infertility on May 1 2014. Based on the Standards for Reporting Interventions in Clinical Trials of Acupuncture (STRICTA), we evaluated the quality of the reports, conducted meta-analysis on the identified studies via RevMan5.2, and assessed the quality of the evidence in the literature by Grading of Recommendations Assessment, Development, and Evaluation (GRADE).

RESULTSA total of 12 studies involving 2,177 patients were included, the quality of which was evaluated as mediocre. With regard to the cure rate, acupuncture was comparable to traditional Chinese medicine (TCM) (P > 0.05) but better than Western medicine (RR = 4.00, 95% CI 1.63 to 9.82, P < 0.01) while acupuncture + TCM was better than either TCM (RR = 1.77, 95% CI 1.20 to 2.60, P < 0.01) or Western medicine used alone (RR = 2.73, 95% CI 1.51 to 4.93, P < 0.01), and acupuncture + Western medicine was better than Western medicine alone (RR = 1.88, 95% CI 1.17 to 3.02, P = 0.01). The combined use of acupuncture, ear pressure, TCM, and Western medicine showed a higher cure rate than the combination of TCM and Western medicine (RR = 3.45, 95% CI 2.90 to 4.11, P < 0.01). In therapeutic effectiveness, acupuncture was comparable to TCM (P > 0.05) but superior to Western medicine (RR = 1.41, 95% CI 1.12 to 1.71, P < 0.01), acupuncture + TCM was superior to either TCM (RR = 1.14, 95% CI 1.05 to 1.23, P < 0.01) or Western medicine alone (RR = 1.43, 95% CI 1.22 to 1.67, P < 0.01), and acupuncture + Western medicine was superior to Western medicine alone (RR = 1.25, 95% CI 1.05 to 1.49, P = 0.01). In improving sperm concentration, acupuncture was as effective as TCM (P > 0.05) and sham acupuncture (P > 0.05) but outdid Western medicine (RR = 27.00, 95% CI 24.27 to 29.73, P < 0.01) and acupuncture + TCM outdid either TCM (RR = 14.65, 95% CI 7.58 to 21.72, P < 0.01) or Western medicine alone (RR = 1.04, 95% CI--1.43 to 3.51, P > 0.05). In improving grade a sperm, acupuncture exhibited a similar effect to TCM (P > 0.05) and sham acupuncture (P > 0.05), and acupuncture + TCM was more effective than TCM alone (RR = 7.78, 95% CI 3.51 to 12.23, P < 0.01) but equally effective as Western medicine (P > 0.05). In elevating the level of grade a + b sperm, acupuncture + TCM excelled either TCM (RR = 11.00, 95%, CI 3.17 to 18.82, P < 0.01) or Western medicine alone (RR = 12.22, 95% CI 6.87 to 17.57, P < 0. 01), while acupuncture produced a comparable effect with sham acupuncture (P > 0.05). As for the quality of the included studies, only 3 conclusions of the 23 meta-analyses were assessed to be of average quality, while the others of poor or extremely poor quality. Therefore, the recommendation grade of the conclusions was low.

CONCLUSIONFor the treatment of male infertility, acupuncture is reported to be equally effective as TMC and more effective than Western medicine, and its effectiveness is enhanced when applied in combination with either TCM or Western medicine. Acupuncture is distinctively efficacious in improving sperm quality. Nevertheless, the overall quality of the included studies is low.

Objective：This study was designed to establish and optimize the research methods for proteome,and to analyze the proteome components of human lung squamous carcinoma cell line NCI H520. Methods： A series of methods, including immobilized pH gradient two dimensional polyacrylamide gel electrophoresis(2DE), silver staining, PDQuest 2DE analysis software, peptide mass fingerprint based on matrix assisted laser desorption/ionization time of flying mass spectrometry (MALDI TOF MS) and SWISS PROT database searching, were used to separate and indentify the proteome of human lung squarmous carcinoma cell line NCI H520. Results： The good 2DE pattern including resolution and reproducibility was obtained. After silver staining, the 2DE image analysis by PDQuest 2DE software had detected average of 1146± 116 spots, and 851± 95 spots were matched. The average matching rate was 73.3％ . There had a good reproducibility of spot position in 2DE map, with average deviation in IEF direction of 1.52± 0.22 mm， while in SDS PAGE direction it was 1.97± 0.13 mm. Sixty spots were incised from silver staining gel randomly and digested in gel by TPCKtrypsin. Fifty four peptide mass fingerprints (PMF) maps were obtained by MALDI TOF MS. The typic peptide masses were searched in the SWISS PROT database by PeptIdent software. Forty four proteins were preliminarily identified. Some of them were cell cycle related proteins such as Cyclin H, some were signal transduction related proteins such as mitogen activated protein kinase, protein kinase C and receptor protein tyrosine kinase ERBB 2, some were oncogene related proteins such as Ras related protein RAB 36, etc. Conclusions： The main proteome research system including IPG 2DE, image analysis, MALDI TOF MS derived PMFs and database searching has been established. The data of NCI H520 obtained by above methods will be useful for the establishment of human lung squamous cell proteome database.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.

Norepinephrine (NE) modulates synaptic transmission and long-term plasticity through distinct subtype adrenergic receptor (AR)-mediated-intracellular signaling cascades. However, the role of NE modulates glutamatergic long-term potentiation (LTP) in the hypothalamic paraventricular nucleus (PVN) magnocellular neuroendocrine cells (MNCs) is unclear. We here investigate the effect of NE on high frequency stimulation (HFS)-induced glutamatergic LTP in rat hypothalamic PVN MNCs in vitro, by whole-cell patch-clamp recording, biocytin staining and pharmacological methods. Delivery of HFS induced glutamatergic LTP with a decrease in N2/N1 ratio in the PVN MNCs, which was enhanced by application of NE (100 nM).HFS-induced LTP was abolished by the blockade of N-methyl-D-aspartate receptors (NMDAR) with D-APV, but it was rescued by the application of NE. NE failed to rescue HFS-induced LTP of MNCs in the presence of a selective β1-AR antagonist, CGP 20712. However, application of β1-AR agonist, dobutamine HCl rescued HFS-induced LTP of MNCs in the absence of NMDAR activity. In the absence of NMDAR activity, NE failed to rescue HFS-induced MNC LTP when protein kinase A (PKA) was inhibited by extracellular applying KT5720 or intracellular administration of PKI. These results indicate that NE activates β1-AR and triggers HFS to induce a novel glutamatergic LTP of hypothalamic PVN NMCs via the postsynaptic PKA signaling pathway in vitro in rats.