One-Pot Synthesis of Benzoazole-Substituted Thioenamines via a Cross Dehydrogenation Coupling (CDC) Reaction.

An iodine-catalyzed synthesis of benzoazole-substituted thioenamines in a one-pot manner was reported. Using 2-aminothiophenols (or 2-aminophenols or 1,2-phenylenediamines), tetramethylthiuram disulfide (TMTD), and enamines (mainly indoles) as starting materials, the target C(sp2)-S formation products (benzoazole-substituted thioenamines) could be furnished smoothly in good yields. The reaction might proceed through an electrophilic substitution pathway in a cross dehydrogenation coupling (CDC) manner. The protocol is metal-free and features easy performance, a one-pot manner, a good functional group tolerance, and good yields.

General Layer-by-Layer Assembly of Multilayered Photoanodes: Triggering Tandem Charge Transport toward Photoelectrochemical Water Oxidation.

Modulation of photoinduced charge separation/migration and construction of controllable charge transfer pathway over photoelectrodes have been attracting enduring interest in semiconductor-based photoelectrochemical (PEC) cells but suffer from sluggish charge transport kinetics. Here, we report a general approach to fabricate NP-TNTAs/(TMCs QDs/PSS)n (X = Te, Se, S) photoanodes via a facile and green electrostatic layer-by-layer (LbL) self-assembly strategy, for which transition-metal chalcogenides quantum dots (TMCs QDs) [CdX (X = Se, Te, S)] and poly(sodium 4-styrenesulfonate) (PSS) were periodically deposited on the nanoporous TiO2 nanotube arrays (NP-TNTAs) via substantial electrostatic force, resulting in the continuous charge transfer pathway. NP-TNTAs/(TMCs QDs/PSS)n photoanodes demonstrate significantly enhanced solar-driven photoelectrochemical (PEC) water oxidation activities, relative to NP-TNTAs and TMCs QDs under visible and simulated sunlight irradiation, predominantly because of the suitable energy level configuration between NP-TNTAs and TMCs QDs, unique integration mode, and high-speed interfacial charge separation rate endowed by LbL assembly. The ultrathin PSS intermediate layer functions as "molecule glue" for pinpoint and uniform self-assembly of TMCs QDs on the framework of NP-TNTAs and photosensitization effect of TMCs QDs triggers the unidirectional charge transfer cascade, synergistically boosting the charge separation/transfer efficiency. Our work offers an efficacious approach to craft multilayered photoelectrodes and spur further interest in finely tuning the spatial charge flow in PEC cell for solar-to-hydrogen conversion.

Charge Transport Surmounting Hierarchical Ligand Confinement toward Multifarious Photoredox Catalysis.

Metal nanoparticles (NPs) have been deemed an imperative sector of nanomaterial for triggering the Schottky-junction-driven electron flow in photoredox catalysis, but they suffer from sluggish charge-transfer kinetics, rendering efficient charge flow difficult. Here, we report the construction of unidirectional charge-transfer channel in a metal/semiconductor heterostructure via a ligand-triggered self-assembly method, by which hierarchically branched ligands (DMAP)-capped Pd NPs were controllably attached on the WO3 nanorods (NRs) scaffold, resulting in the well-defined Pd@DMAP/WO3 NRs heterostructures. The pinpointed deposition of Pd@DMAP on the WO3 NRs endows the Pd@DMAP/WO3 NRs heterostructure with conspicuously improved photoactivities for organic pollutant mineralization, as well as the capacities for photocatalytic selective oxidation of aromatic alcohols to aldehydes and photoreduction of chromium ions under the irradiation of simulated sunlight and visible light, far surpassing the applicability of blank WO3 NRs. This is due to the imperative contribution of Pd@DMAP as efficient electron reservoir in accelerating the unidirectional flow of electrons from Pd@DMAP to WO3 NRs, overcoming the confinement of spatially hierarchically branched ligand and interface configuration. Moreover, interfacial charge transport efficiency is finely tuned by the interface configuration engineering. The active species in the multifarious photoreactions were unveiled, and a linker-triggered photoredox catalysis mechanism was put forward. It is hoped that our current work would afford new strategies for strategically constructing metal/semiconductor heterostructures for versatile photocatalytic applications.

Confinement of Quantum Dots in between Monolayered Graphene Nanosheets for Arousing Boosted Multifarious Photoredox Selective Organic Transformation.

Transition metal chalcogenide quantum dots (TMC QDs) represent promising light-harvesting antennas because of their fascinating physicochemical properties including quantum confinement effect and suitable energy band structures. However, TMC QDs generally suffer from poor photoactivities and photostability due to deficiency of active sites and ultrafast recombination rate of photoinduced charge carriers. Here, we demonstrate how to rationally arouse the charge transfer kinetic of TMC QDs by close monolayered graphene (GR) encapsulation via a ligand-dominated layer-by-layer (LbL) assembly utilizing oppositely charged TMC QDs and GR nanosheets as the building blocks. The assembly units were spontaneously and intimately integrated in an alternate integration mode, thereby resulting in the multilayered three-dimensional (3D) TMC QDs/GR ensembles. It was unveiled that multifarious photoactivities of TMC QDs/GR nanocomposites toward versatile photoredox organic catalysis including photocatalytic aromatic alcohols oxidation to aldehydes and nitroaromatics reduction to amino derivatives under visible light irradiation are conspicuously boosted because of spatially multilayered monolayered GR encapsulation which are superior to those of TMC QDs counterparts. The substantially enhanced photoactivities of TMC QDs/GR nanocomposites arise from reasons including improved light absorption and enhanced charge separation efficacy because of GR encapsulation together with unique stacking mode between TMC QDs and GR endowed by LbL assembly. Our work would provide a promising and efficacious route to smartly accelerate the charge transfer kinetic of TMC QDs for solar energy conversion.

Layer-by-Layer Self-Assembly of Metal/Metal Oxide Superstructures: Self-Etching Enables Boosted Photoredox Catalysis.

The capability of noble metal nanoparticles (NPs) as efficient charge transfer mediators to stimulate Schottky-junction-triggered charge flow in multifarious photocatalysis has garnered enormous attention in the past decade. Nevertheless, fine-tuning and controllable fabrication of a directional charge transport channel in metal/semiconductor heterostructures via suitable interface engineering is poorly investigated. Here, we report the progressive fabrication of a tailor-made directional charge transfer channel in Pt nanoparticles (NPs)-inlaid WO3 (Pt-WO3) nanocomposites via an efficient electrostatic layer-by-layer (LbL) self-assembly integrated with a thermal reduction treatment, by which oppositely charged metal precursor ions and polyelectrolyte building blocks were intimately and alternately assembled on the WO3 nanorods (NRs) by substantial electrostatic interaction. LbL self-assembly buildup and in situ self-etching-induced structural variation of WO3 NRs to a microsized superstructure occur simultaneously. We found that such exquisitely crafted Pt-WO3 nanocomposites exhibit conspicuously enhanced and versatile photoactivities for nonselective mineralizing of organic dye pollution and reduction of heavy metal ions at ambient conditions under both visible and simulated sunlight irradiation, demonstrating a synergistic effect. This is attributed to the imperative contribution of Pt NPs as electron traps to accelerate the directional high-efficiency electron transport from WO3 to Pt NPs, surpassing the confinement of electron transfer kinetics of WO3 owing to low conduction level. More intriguingly, photoredox catalysis can also be triggered simultaneously in the same reaction system. The primary in situ produced active species in the photocatalytic reactions were specifically analyzed, and underlying photocatalytic mechanisms were determined. Our work would provide a universal synthesis strategy for constructing various metal-decorated semiconductor nanocomposites for widespread photocatalytic utilizations.

Partially Self-Transformed Transition-Metal Chalcogenide Interim Layer: Motivating Charge Transport Cascade for Solar Hydrogen Evolution.

Directional and high-efficiency charge transport to the target active sites of photocatalyst is central to boost the solar energy conversion but is retarded by the sluggish charge transfer kinetics and deficiency of active sites. Here, we report the elaborate design of cascade unidirectional charge transfer channel over spatially multilayered CdS@CdTe@MoS2 dual core-shell ternary heterostructures by partial transformation of CdS to CdTe interim layer followed by seamless encapsulation with an ultrathin MoS2 layer. The suitable energy-level alignment and unique coaxial multilayered assembly mode among the building blocks accelerate the interfacial charge separation and transport, endowing the CdS@CdTe@MoS2 heterostructures with conspicuously enhanced visible-light-driven photocatalytic hydrogen generation performances along with good photostability. The integrated roles of ultrathin CdTe intermediate layer in passivating the defect sites of CdS NWs framework, mediating the unidirectional charge transfer cascade and prolonging the charge lifetime, were ascertained. Besides, the crucial role of the outermost MoS2 layer as the metal-free cocatalyst in enriching the surface active sites for hydrogen evolution was also determined. Our work would provide new alternatives for finely tuning the charge flow toward promising solar-to-hydrogen conversion efficiency.

Precise Tuning of Coordination Positions for Transition-Metal Ions via Layer-by-Layer Assembly To Enhance Solar Hydrogen Production.

Finely tuning the charge transfer constitutes a central challenge in photocatalysis, yet exquisite control of the directional charge transfer to the target reactive sites is hindered by the rapid charge recombination. Herein, dual separated charge transport channels were fabricated in a one-dimensional transition-metal chalcogenide (TMC)-based system via an elaborate layer-by-layer (LbL) self-assembly approach, for which oppositely charged metal-ion-coordinated branched polyethylenimine (BPEI) and MoS2 quantum dots (QDs) were alternately integrated to fabricate the multilayered TMC@(BPEI/MoS2 QDs)n heterostructures with controllable interfaces. Photocatalytic hydrogen generation performances of such ternary heterostructures under visible light irradiation were evaluated, which unravels that the BPEI layer not only behaves as "molecule glue" to enable the electrostatic LbL assembly with MoS2 QDs in an alternate stacking fashion on the TMC frameworks but also acts as a unidirectional hole-transfer channel. More significantly, transition-metal ions (Fe2+, Co2+, Ni2+, Cu2+, and Zn2+) coordinated on the outmost BPEI layer are able to function as interfacial electron transfer mediators for accelerating the interfacial cascade electron transport efficiency. These simultaneously constructed dual high-speed electron and hole-transfer channels are beneficial for boosting the charge separation and enhancing the photocatalytic hydrogen evolution performances.

Evidence for conformational movement and radical mechanism in the reaction of 4-thia-L-lysine with lysine 5,6-aminomutase.

We demonstrate that the steady state reaction of lysine 5,6-aminomutase with substrate analogue 4-thia-l-lysine generates a radical intermediate, which accumulates in the enzyme to an electron paramagnetic resonance (EPR) detectable level. EPR line width narrowing of approximately 1 mT due to [4'-(2)H] labeling of the pyridoxal-5'-phosphate (PLP), an isotropic hyperfine coupling of 40 MHz for the proton at C4' of PLP derived from (2)H electron nuclear double resonance (ENDOR) measurement, and spin density delocalization onto the (31)P of PLP realized from observations of the (31)P ENDOR signal provide unequivocal identification of the radical as a substrate-PLP-based species. X- and Q-band EPR spectra fittings demonstrate that this radical is spin coupled with the low spin Co(2+) in cob (II) alamin and the distance between the two species is about 10 A. These results provide direct evidence for the active site motion upon substrate binding, bringing the adenosylcobalamin to the proximity of substrate-PLP for subsequent H-atom abstraction and for the notion that lysine 5,6-aminomutase functions by a radical mechanism. Observation of (2)H-ENDOR signal also provides a reliable hyperfine coupling constant for future comparison with quantum-mechanical-based calculations to gain further insight into the molecular structure of this steady state radical intermediate.

[Clinical implication of blood somatostatin determination in critically ill patients].

OBJECTIVE: To investigate the relationship between contents of blood somatostatin (SST) and inflammatory reaction or severity of illness in critically ill patients, and its value in the evaluation of prognosis. METHODS: Sixty critically ill patients were divided into three groups according to the acute physiology and chronic health evaluation II (APACHE II) score as mild (<16, 23 cases), mediate (16 - 20, 20 cases) and severe (>20, 17 cases) group; and also divided as dead (D, 13 cases) or survival group (S, 47 cases) according to the final outcome; 20 healthy volunteers served as control. The blood SST concentration was detected by radioimmunoassay, while the levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured by enzyme linked immunosorbent assay (ELISA). RESULTS: The SST concentration in critically ill patients was significantly lower than normal control [(18.2+/-17.6) ng/L vs. (224.8+/-130.2) ng/L, P<0.05], while the levels of TNF-alpha and IL-6 were significantly higher [TNF-alpha: (32.4+/-14.2) ng/L vs. (14.2+/-5.7) ng/L, IL-6: (131.6+/- 42.7) ng/L vs. (65.8+/-24.3) ng/L, both P<0.05]. The SST concentration in severe group was significantly lower than that of mild and mediate group [(8.1+/-7.2) ng/L vs. (24.7+/-15.9) ng/L and (19.2+/-22.1) ng/L, both P<0.05], while the levels of TNF-alpha and IL-6 were significantly higher than mild group [TNF-alpha: (39.0+/-16.4) ng/L vs. (28.9+/-10.9) ng/L, IL-6: (156.0+/-49.6) ng/L vs. (111.5+/-32.6) ng/L, both P<0.05]. A negative correlation was found between SST and TNF-alpha, IL-6, also between SST and APACHE II score (r(1)=-0.682, r(2)=-0.894, r(3)=-0.327, P<0.05 or P<0.01). The SST concentration in D group was significantly lower than S group [(6.4+/-5.5) ng/L vs. (21.5+/-18.4) ng/L, P<0.05]. CONCLUSION: The SST level in blood can reflect the severity of illness in critically ill patients and shows clinical value in evaluation of prognosis.

Self-transformation of ultra-small gold nanoclusters to gold nanocrystals toward boosted photoreduction catalysis.

Glutathione-protected Aux nanoclusters uniformly and intimately embedded at the interface of CdSe QDs and graphene were in situ self-transformed to Au nanocrystals (NCs) via a facile thermal reduction strategy. The inlaid Au NPs substantially accelerate the interfacial directional charge transfer toward multifarious photoreduction catalysis under visible light irradiation.

Differential expression of genes associated with cell proliferation and apoptosis induced by okadaic acid during the transformation process of BALB/c 3T3 cells.

Okadaic acid (OA) is a tumor promoter in two-stage carcinogenesis experiments. Nevertheless, the effects of OA on cell transformation, cell proliferation and apoptosis vary widely, and the molecular events underlying these effects of OA are not well understood. In the present study, we examined the promoting activity and the associated effects on cell growth and apoptosis mediated by OA in BALB/c 3T3 cells, and evaluated alterations of gene transcriptional expression by microarray analysis. The promoting activity of OA was estimated by a two-stage transformation assay, in which cells were treated first with a low dose of the initiator N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and then with OA for 14 days. It showed that OA, at concentrations of 7.8-31.3 ng/ml, enhanced the transformation of MNNG-treated cells. In the promotion phase, cells exposed to OA (7.8 ng/ml) grew slowly for the first 2 days and subsequently died. As determined by Hoechst 33342 fluorescent dye and Annexin-V/PI dual-colored flow cytometry, OA induced morphologically apoptotic cells and increased the percentage of early apoptotic cells. The gene expression profile induced by OA at five time points in the promotion phase was determined by use of a specific mouse toxicological microarray containing 1796 clones, and a total of 177 differentially expressed genes were identified. By gene ontology analysis, 31 of these were determined to be functionally involved with cell growth and/or maintenance. In this group, numerous genes associated with the cell proliferation and cell cycle progression were down-regulated at early and/or middle time points. Among these was a subset of genes associated with apoptosis, in which Bnip3, Cycs, Casp3 and Bag1 genes are involved in the mitochondrial pathway of apoptosis. Ier3, Mdm2 and Bnip3 genes may be p53 targets. Furthermore, real-time PCR confirmed the expression changes of five genes selected at random from the differentially expressed genes. We conclude that OA induces cell growth inhibition and apoptosis in the two-stage, MNNG-initiated transformation of BALB/c 3T3 cells. The results of gene expression profile analysis imply that multiple molecular pathways are involved in OA-induced proliferation inhibition and apoptosis. Mitochondrial and p53-associated apoptotic pathways also may contribute to OA-induced apoptosis.

[Changes of vasoactive intestinal polypeptide and vasoactive intestinal polypeptide receptor 1 in small intestine and liver during macaque development].

The present study was aimed to investigate the changes of vasoactive intestinal polypeptide (VIP) and VIP receptor 1 (VIPR1) in small intestinal and hepatic tissues during macaque development. The tissue samples of small intestine, liver and blood samples from peripheral and portal vein of 4 macaques of 6-month fetus, 2-day neonate, 45-day neonate and adult were obtained after anesthetization. The concentration of VIP in blood or tissues of macaques was measured by radioimmunoassay. The distribution of VIP in small intestinal or hepatic tissues was visualized by immunohistochemical staining. The expression of VIPR1 was detected by in situ hybridization. The results showed that: (1) VIP concentration in intestinal tissue of 6-month fetus was (20.7+/-14.3) ng/mg protein, and a few VIP-positive nerve fibers first appeared in intestinal villus root and submucosal layer but not in muscle layer. The intestinal concentration of VIP increased gradually with macaque development and reached (514.8+/- 49.2) ng/mg protein in adult, significantly higher than that in 6-month fetus (P<0.01). (2) In adult animal, VIP-positive nerve fibers became thicker and gradually extended into the mucosal crypt, submucosal layer nerve, myenteric nerve plexus of annular muscle and indulge muscle, and annular muscle. Correspondingly, the expression of VIPR1 in intestine was up-regulated during development. (3) On the contrary, the levels of VIP and VIPR1 in liver were gradually decreased during development. (4) VIP concentration in small intestinal tissue was higher than that in hepatic tissue during development. The VIP level in portal vein was also significantly higher than that in peripheral blood during development. In conclusion, the levels of VIP and VIPR1 in mucosal crypt, submucosal layer nerve, myenteric nerve plexus of annular muscle and indulge muscle increase rapidly after birth. Most of VIP from intestinal tract is degraded in portal vein before entering liver, suggesting that VIP does not metabolize and decompose in liver, and that VIPR1 is only present in embryo hepatic blood vessels.

[The inhibitive effects of celecoxib combined with octreotide on the metastasis of human gastric cancer in vivo].

OBJECTIVE: To investigated if cyclooxygenase-2 (COX-2) inhibitor celecoxib in combination with somatostatin (SST) analog octreotide is able to inhibit the metastasis of human gastric cancer (GC) in vivo. METHODS: Seventy five patients with GC were randomly divided into 3 equal groups: control group, taking no anti-tumor medicine before GC resection; celecoxib group, receiving celecoxib orally 200 mg/d for 7 days before surgery; and combination group, receiving celecoxib orally 200 mg/d and octreotide 100 microg injected subcutaneously for 7 days before operation. The resected specimens were studied for the expression of epithelial cadherin (E-Cad) and matrix metalloproteinase (MMP) by using immunohistochemical staining. MMP-2 and MMP-9 were also quantified with Western blotting. The GC cells from the resected gastric cancer specimens were isolated by immunomagnetic separation. Modified Boyden chamber membrane invasion culture system coated with Matrigel was used to observe the migration and invasion of the GC cells. RESULTS: The abnormal staining rates of E-Cad of GC tissue in the combination group and the celecoxib group were 28.0% and 44.0%, significantly lower than that in the control group (56.0%, both P < 0.05). The grey level of MMP-2 and MMP-9 in the combination and celecoxib groups were (99 +/- 20, 89 +/- 13) and (260 +/- 15, 180 +/- 13) respectively, both significantly lower than that of the control group [(314 +/- 11, 241 +/- 12), P < 0.05]. The number of GC cells that penetrated the membrane was (2.75 +/- 0.58)/10(3) cells in the combination group, (2.29 +/- 0.58)/10(3) cells, the migration rate of the combination group was lower by 38% compared with that of the control group (F = 6.44, P < 0.05). CONCLUSION: The metastasis of human gastric carcinoma cells may be inhibited by the combinative treatment of celecoxib and octreotide.

[Effects of selective and non-selective cyclooxygenase-2 inhibitor on the growth of colon cancer cells].

OBJECTIVE: To evaluate the effects of selective and non-selective cyclooxygenase-2 on the growth and apoptosis of colon cancer cell lines in vitro. METHODS: The proliferation of colon cancer cells was determined by MTT assay, and the cell cycle progression was analyzed by flow cytometric assay. Annexin V/PI staining in combination with flow cytometric assay was used to detect apoptosis induced by NSAIDs. RESULTS: It was found that celecoxib, meloxicam and aspirin could inhibit the growth of HT-29 or SW480 cell and showed a concentration dependent pattern. COX-2 protein was expressed in HT-29 and LS174-T, but not in SW480 cells. In addition, PCNA levels in both HT-29 cell and SW480 cells were reduced by aspirin and celecoxib. Both aspirin (10 mmol/ L) and celecoxib (50 micromol/L) induced apoptosis of HT-29 and SW480 colon cancer cells, the apoptosis rates were 4.8%, 17.7% and 5.1%, 20.4% respectively. CONCLUSION: Both COX-2 selective and non-selective inhibitors can potentially inhibit the growth of colon cell lines and such inhibitory effect on COX-2 negative colon cancer cells is also evident.

[Initial research for effects of vasoactive intestinal polypeptide (VIP) on differentiation of human umbilical cord blood derived CD34+ cells into hepatic related cells].

OBJECTIVE: To investigate the effect of vasoactive intestinal polypeptide (VIP) on differentiation of hematopoietic stem cells (HSC) into hepatic related cells and probe into the possibility that VIP affects HSC transdifferentiation. METHODS: Mini MACS assay was used to purify human CD34+ cells from mononuclear cell (MNC), the purity of the CD34+ cells was evaluated by flow cytometry. Alpha fetal proteins(AFP) in cultured CD34+ cells and their supernatant were measured with ELISA assay. Liver tissue markers on CD34+ cells, AFP, albumin (ALB) and CK-19, were measured by immunohistochemistry. Western blot assay was used to detect the expression of ALB on CD34+ cells. Nest RT-PCR was used to measure the expression of AFP mRNA and ALB mRNA on CD34+ cells, the product of ALB was chosen to measure the sequence. RESULTS: Immunohistochemistry showed that human CD34+ cell contained AFP and albumin but no CK-19 protein. When human CD34+ cells were cultured with VIP for 14 days, the concentration of AFP within CD34+ cells was decreased from (270.00 +/- 11.37) pg/mL to (165.00 +/- 8.51) pg/mL (P < 0.05). Western blot revealed that albumin in CD34+ cells treated with VIP faded, compared to that of control. Both human cord blood MNC and CD34+ cells expressed AFP mRNA and albumin mRNA; the sequence of the product of nest RT-PCR for albumin matched completely with the sequence of albumin in GenBank. CONCLUSION: Human cord blood CD34+ cells have been note to express hepatocyte related markers such as AFP and albumin, although there is no evidence of CK-19 expression. These findings suggests the possibility that human HSC could be transdifferentiated into hepatocyte. The expressions of AFP and albumin on human CD34+ cells depressed by VIP indicate that VIP might inhibit the transdifferentiation of HSC.

[Therapeutic effect of somatostatin on acute respiratory distress syndrome in experimental rats].

OBJECTIVE: This study was aimed to assess the effects of somatostatin (SST) and its analog Octreotide on the treatment of acute respiratory distress syndrome (ARDS) in rat model. METHODS: ARDS rat model was induced by administration of paraquat. After 24 hours oral administration of paraquat, three drugs (SST, Octreotide and dexamethasone at dosage of 1 mg/kg, 0.1 mg/kg and 1 mg/kg respectively) were infused into the tail veins of rats so as to form three treatment groups. The rats given only paraquat were subjects in the ARDS group. PaO2 level and pulmonary coefficient were detected, and the morphological changes of lungs were examined. In addition, TNF-alpha and IL-6 levels in plasma, Bronchoalveolar lavage fluids (BALF) and intestine homogenate were measured respectively. RESULTS: The ARDS rats treated with SST, Octreotide and dexamethasone showed mitigation of inflammatory response in the lungs, improvement in lung ventilation, reduction of pulmonary coefficient (-13%-15%), increase in PaO2 level (+75%-84%), decrease in PaCO2 level (-17%-22%), and restoration of pH value to normal in plasma, when compared with the rats of ARDS group. TNF-alpha level in plasma tended to decline (P>0.05); it significantly lowered in BALF and intestine homogenate in the ARDS rats treated (P< 0.05). IL-6 level in BALF tended to be lower in treatment group (P>0.05), but the IL-6 level in plasma and intestine homogenate displayed no significant difference between the treatment group and ARDS group. CONCLUSIONS: These results suggest that SST and its analog Octreotide assume a role in improving the clinical manifestation of ARDS, alleviating the inflammatory condition of the lungs, and reducing the TNF-alpha level in the BALF and intestine homogenate, therefore they may be useful adjuvants in the treatment of ARDS.

Inhibitory actions of genistein in human breast cancer (MCF-7) cells.

Genistein, a natural isoflavanoid phytoestrogen, is thought to be the active ingredient in soy that possesses breast cancer preventive properties. The molecular mechanisms that are involved in its cancer preventive properties have not been completely understood. The present study is designed to investigate the mechanism involved in the inhibitory action of genistein in MCF-7 cells. Genistein at 50 and 100 microM significantly arrested the growth of MCF-7 cells at G2/M phase (P<0.05) and decreased at the proliferative S phase (P<0.05). Using cDNA microarray technology, genes differentially regulated by genistein were identified. In particular, as confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR), genistein up-regulated heat shock protein 105 (HSP) mRNA and down-regulated mRNA expression of serum response factor (SRF), estrogen receptor (ER) alpha, disabled homolog 2 (DOC 2) and recombination activation gene 1 (RAG-1). Using real time RT-PCR, we have shown that HSP and SRF mRNA were both regulated by genistein in a time- and dose-dependent manner; however, it appears that only the effect of genistein on SRF mRNA, but not HSP mRNA expression, can be partially abolished by cotreatment with estrogen antagonist ICI 182,780. Western blotting analysis showed that the expressions of the ERalpha and SRF protein decreased significantly with genistein treatment (P<0.05). These results suggest that the inhibitory action of genistein on human breast cancer cells appears to be complex and is only partially mediated by the alteration of estrogen receptor-dependent pathways.

[Changes of somatostatin and expression of somatostatin receptor in small intestine and liver tissues during macaque development].

Intestinal tract, which produces more than fifty kinds of gut peptides, is regarded as the largest endocrine organ. With regard to the gut peptides, a number of studies were focused on their structure, function and the roles in some diseases. The changes in output or distribution of gut peptides in the intestinal tract during development have been largely unknown. This study was aimed to investigate the changes of somatostatin (SST) and somatostatin receptor 2 (SSTR2) in small intestinal and hepatic tissues during the development of macaque. The tissue samples of small intestine, liver or blood samples from peripheral and portal vein of 4 macaques in 6-month fetus, 2-day neonate, 45-day neonate and adult were obtained after anesthetization. The concentrations of SST in blood or tissues of macaques were measured by radioimmunoassay. The distributions of SST in small intestinal or hepatic tissues were visualized by immunohistochemical staining. The expression of SSTR2 was detected by in situ hybridization. SST concentration of intestinal tissue in 6-month-old macaque was (27.3+/-16.6) ng /mg protein and light positive staining of SST was localized in mucosal crypts but negative in muscle layer. The intestinal concentration of SST increased gradually with macaque development and reached to the peak [(120.1+/-35.3) ng /mg protein] in adult. It was significantly higher than that in fetus (P<0.01). Strong positive staining of SST was found in both mucosal crypts and myenteric nerve plexus of adult animal. SSTR2 was obviously expressed in intestinal epithelium of fetus but its expression was greatly reduced in epithelium and was shifted to mucosal crypts when grown to adult. Negative staining of SSTR2 in muscle layer of fetal or neonatal macaque turned to be positive in myenteric nerve plexus of adult. The levels of SST or SSTR2 in liver decreased gradually during development. SST concentrations of small intestinal tissue kept significantly higher than those of hepatic tissues in the macaque developing stages. SST levels of portal vein were also maintained significantly higher than those of peripheral blood in the macaque developing stages. In conclusion, the level of SST and expression of SSTR2 in mucosal crypt increased gradually with macaque development. SST from intestinal tract was quickly degraded in portal vein before entering into liver. SST positive myenteric nerve plexus was visualized only in mature macaque.

[Gene expression profiles in early stage of BALB/c 3T3 cells' transformation promoted with 12-O-tetradecanoylphorbol-13-acetate].

OBJECTIVE: To elucidate the potential molecular mechanism responsible for the early time of tumor promotion, gene expression profile was studied in the transformed BALB/c 3T3 cells induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). METHODS: The two-stage cell transformation model was established by using the initiator of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promoter of TPA. Cell proliferation was measured by trypan blue staining and cell cycle analysis was carried out by flow cytometry assay. A cDNA microarray representing 1 152 genes was used to investigate the gene expression profiles of BALB/c 3T3 cells exposed to TPA at 4 h and 24 h respectively. RESULTS: TPA could effectively inhibit cell proliferation and induce the G1 and S cell cycle arrested in the early time. Moreover 19 genes were found differentially expressed at least twofold in the TPA treated cells as compared with the control cells, 9 of them were upregulated and 10 downregulated. Most of the differentially expressed genes were involved in cell proliferation, differentiation or apoptosis, and related to ras or p53 signal transduction pathway. CONCLUSION: TPA could influence the transcriptional expression of some genes related to cell cycle modulation and ultimately result in the cell growth arrest.