Three-Dimensional Polyoxometalate Organic Frameworks with One-Dimensional Channels Constructed by Multiple Helical Chains Based on 22-Core Ln/Mn/Mo Clusters for Proton Conduction.

Two unique 22-core sandwich {[Mn6Mo6O37]Ln3[MnMo6O24]} (Ln = La or Pr) units have been assembled, featuring an undisclosed {Mn6Mo6} cluster. This assembly is subsequently integrated into two three-dimensional polyoxometalate organic frameworks, which exhibit one-dimensional hydrophilic hexagonal channels formed by six intertwined 63 helical chains, leading to effective proton conduction primarily facilitated by an abundance of water molecules within the channels.

Three New Constituents with Anti-Inflammatory and Antimicrobial Activities in Vitro from the Roots of Capsicum annuum L.

Three new compounds, including two new sesquiterpenes (1-2), named Annuumine E-F, and one new natural product, 3-hydroxy-2,6-dimethylbenzenemethanol (3), together with seventeen known compounds (4-20) were isolated from the ethanol extract of the roots of Capsicum annuum L. Among them, five compounds (4, 5, 9, 10 and 20) were isolated from this plant for the first time. The structures of new compounds (1-3) were determined via detailed analysis of the IR, HR-ESI-MS and 1D and 2D NMR spectra. The anti-inflammatory activities of the isolated compounds were evaluated by their ability to reduce NO release by LPS-induced RAW 264.7 cells. Notably, compound 11 exhibited moderate anti-inflammatory activity (IC50 =21.11 µM). Moreover, the antibacterial activities of the isolated compounds were also evaluated.

Two three-dimensional Fe(II) frameworks based on {P4Mo6} tetrameric clusters exhibiting efficient visible-light photocatalytic properties for the degradation of Cr(VI) and methylene blue.

Two three-dimensional frameworks based on the {P4Mo6} unit, H(4,4'-bipy)2[Fe4(PO4)(H2O)4Na6][Fe6(H2O)4][(Mo6O12)(HPO4)3(PO4)(OH)3]4·5H2O (4,4'-bipy = 4,4'-bipyridine) (1) and H3(C12H14N2)4[Fe4(PO4)(H2O)4Na4][Fe2(Mo6O12(HPO4)3(PO4)(OH)3)4]·6H2O (2) were successfully synthesized by varying the solvent. The extended structures of the two compounds were formed by transition metal Fe(II) ions bridging the {P4Mo6}-based tetrameric clusters around [NaXFe4(PO4)] (X = 6 (1), or X = 4 (2)) core. The 4,4'-bipy molecules and in situ generated methyl viologen cations as templates induce the formation of two three-dimensional structures, an 8-connected bcu topology framework for 1 and a 4-connected 2-fold interpenetrating diamond-like topological network for 2, respectively. Additionally, multiform hydrogen bonds are found in the framework and also play an important role in stabilizing the structure. The proton conduction mechanism of the two compounds can be mainly classified as the Grotthuss mechanism; the proton conductivity values are 1.06 × 10-3 S cm-1 for 1 and 3.13 × 10-3 S cm-1 for 2 at 75 °C under 98% relative humidity. The visible-light photocatalytic activity was evaluated by photocatalytic decomposition of Cr(VI) and MB dye, and the removal ratios can reach 95.6% (1) and 82% (2) for Cr(VI), and 98% (1) and 99% (2) for MB.

Construction of Water-Stable Rare-Earth Organic Frameworks with Ambient High Proton Conductivity Based on Zirconium Sandwiched Heteropolytungstate.

Water-stable proton-conducting materials owning excellent performances at ambient temperatures are currently one of the crucial challenges. Herein, four water-stable three-dimensional polyoxometalate-based rare-earth organic frameworks have been successfully synthesized and formulated as H{Ln4(L)2(H2O)21[Zr3(OH)3(PW9O34)2]}·15H2O (1-3) (Ln = La (1), Ce (2), Pr (3); L = 3,5-pyridine dicarboxylic acid), which are the first examples of MOFs constructed by a zirconium sandwiched polyoxoanion. There are abundant coordinated water molecules functionalizing the PrIII centers, and simultaneously, plenty of lattice water molecules are fitted into the channel of the framework. A continuous H-bonding network is found between the architectures and plays an important role in stabilizing the structure. Benefiting from the consecutive H-bonding networks, compounds 1-3 showed high proton conductivities at ambient temperature (up to 1.05 × 10-3 S·cm-1 under 98% RH) by a synergistic effect of the combined components.

Effect and Safety of Helicobacter pylori Eradication Treatment Based on Molecular Pathologic Antibiotic Resistance in Chinese Elderly People.

Background: The elderly people generally have poor tolerance to drugs and an increased risk of adverse effects. Our study was designed to determine the effect and safety of Helicobacter pylori (H. pylori) eradication treatment based on molecular pathologic antibiotic resistance in Chinese elderly people over the age of 60 years. Methods: A total of 364 people were retrospectively analyzed, including 113 older people over 60 and 251 young and middle-aged people in the age of 20-59 years. Real-time PCR detection and conventional PCR and sequencing method were used for drug susceptibility testing. As the main outcome measure, the eradication rates (ERs) with their 95% confidence intervals (CIs) were analyzed by intention to treat (ITT) and per protocol (PP). For the safety of therapy, adverse events were analyzed. Results: For the total people, the resistance rates to clarithromycin (CLR), amoxicillin (AMX), fluoroquinolone (FLQ) and tetracycline (TET) were 65.06%, 7.54%, 61.39% and 20.37%, respectively. After they were divided into two groups, the resistance rates were 62.39% (CLR), 9.09% (AMX), 69.64% (FLQ) and 22.45% (TET) in the 113 older people over 60, and 66.26%, 6.85%, 57.66% and 19.47% in the 251 young and middle-aged people in 20-59. By the ITT analysis, the ERs were 92.04% (95% CI, 86.97-97.10%, n=113) in the older people and 92.43% (95% CI, 89.14-95.73%, n=251) in the young and middle-aged people. By the PP analysis, the ERs were 96.30% (95% CI, 92.68-99.92%, n=108) and 94.69% (95% CI, 91.87-97.52%, n=245), respectively. No significant differences were shown both in the ITT analysis (P=0.896) and in the PP analysis (P=0.517). The three most common adverse events were black stool, dysgeusia and diarrhea, and no serious adverse event was reported. Conclusion: H. pylori eradication treatment based on molecular pathologic antibiotic resistance showed good effect and safety in Chinese elderly people.

The Zinc Finger Transcription Factor BbCmr1 Regulates Conidium Maturation in Beauveria bassiana.

The entomopathogenic fungus Beauveria bassiana is a typical filamentous fungus and has been used for pest biocontrol. Conidia are the main active agents of fungal pesticides; however, we know little about conidial developmental mechanisms and less about maturation mechanisms. We found that a Zn2Cys6 transcription factor of B. bassiana (named BbCmr1) was mainly expressed in late-stage conidia and was involved in conidium maturation regulation. Deletion of Bbcmr1 impaired the conidial cell wall and resulted in a lower conidial germination rate under UV (UV), heat shock, H2O2, Congo red (CR) and SDS stresses compared to the wild type. Transcription levels of the genes associated with conidial wall components and trehalose synthase were significantly reduced in the ΔBbcmr1 mutant. Further analysis found that BbCmr1 functions by upregulating BbWetA, a well-known transcription factor in the central development of BrlA-AbaA-WetA. The expression of Bbcmr1 was positively regulated by BbBrlA. These results indicated that BbCmr1 played important roles in conidium maturation by interacting with the central development pathway, which provided insight into the conidial development networks in B. bassiana. IMPORTANCE Conidium maturation is a pivotal event in conidial development and affects fungal survival ability under various biotic/abiotic stresses. Although many transcription factors have been reported to regulate conidial development, we know little about the molecular mechanism of conidium maturation. Here, we demonstrated that the transcription factor BbCmr1 of B. bassiana was involved in conidium maturation, regulating cell wall structure, the expression of cell wall-related proteins, and trehalose synthesis. BbCmr1 orchestrated conidium maturation by interplaying with the central development pathway BrlA-AbaA-WetA. BbBrlA positively regulated the expression of Bbcmr1, and the latter positively regulated BbwetA expression, which forms a regulatory network mediating conidial development. This finding was critical to understand the molecular regulatory networks of conidial development in B. bassiana and provided avenues to engineer insect fungal pathogens with high-quality conidia.

Characterizing the voltage fluctuations driven by a cluster of ligand-gated channels.

In this paper we present the properties of the voltage fluctuations driven by a cluster of ligand-gated channels. First, the second-order moment of the voltage is expressed in form of the integrated resistance and the random force. Then the power spectrum of the voltage noise is obtained analytically, and it is proved to have the 1/ω^{4}-form. Its mechanism lies in that the randomness of the voltage fluctuation is weaker than channel (conductance) noise, which can be approximately described by the Ornstein-Ulenbeck process.

The secondary metabolite regulator, BbSmr1, is a central regulator of conidiation via the BrlA-AbaA-WetA pathway in Beauveria bassiana.

The filamentous fungus Beauveria bassiana, an insect fungal pathogen, is widely used for pest biocontrol. Aerial conidia are infectious propagules, and their yield and viability greatly affect the field application of this fungus; however, little is known about the molecular regulatory mechanism of the triggered conidiation. In the present study, we find that the secondary metabolite regulator BbSmr1 is involved in the regulation of asexual conidiation development and stress response in B. bassiana. A deficiency in Bbsmr1 results in a prominent fluffy-like phenotype on solid medium, decreased conidial yield, accelerated conidial germination, as well as increased tolerance to H2 O2 stress and cell wall inhibitors. The deletion of Bbsmr1 also leads to thickened conidial cell walls and changed cell epitopes. Overexpressing either BbbrlA or BbabaA in the ∆Bbsmr1 strain can rescue the phenotypes of conidial development and stress response. BbSmr1 activates BbbrlA transcription by directly binding to the A4GA3 sequence of the BbbrlA promoter. BbBrlA in turn binds to the promoter of Bbsmr1 and negatively regulates the expression of Bbsmr1. These results indicate that BbSmr1 positively regulates conidial development in B. bassiana by activating the central development pathway BrlA-AbaA-WetA and provides insights into the developmental regulatory mechanism of entomopathogenic fungi.

The PI3Kα inhibitor DFX24 suppresses tumor growth and metastasis in non-small cell lung cancer via ERK inhibition and EPHB6 reactivation.

EPHB6 is a metastasis inhibitory gene that is frequently decreased or deficiency in non-small cell lung cancer (NSCLC), which contributed to the subsequent development of distant metastasis. These suggested the possibility that reactivation of EPHB6 might prevent the metastasis of NSCLC. Nevertheless, EPHB6 expression might also promote cancer cell growth and inhibit cell apoptosis by activating Akt and ERK pathway, apart from inhibition of migration and invasion. In the present study, we developed a novel quinazolin-4(3H)-one analog (DFX24) as a potential PI3Kα inhibitor, which inhibited both cell proliferation and metastasis of NSCLC cell lines. Investigation to the molecular mechanisms revealed DFX24 inhibited the cell growth and metastasis via inhibition of PI3Kα and ERK activity, as well as the increase in EPHB6 expression. In addition, DFX24 also induced cell cycle arrest and tumor cell apoptosis by inhibiting PI3K/Akt pathway and activating mitochondria-dependent pathway, respectively. These findings suggested that DFX24 might be considered as a novel drug candidate and may provide a potential therapy for NSCLC.

Ionothermal Synthesis of an Antimonomolybdate Cluster, [Sb8MoVI13MoV5O66]5-, and Its Catalytic Behavior to the Reduction of Nitrobenzene.

The largest antimonomolybdate monomer, [Sb8MoVI13MoV5O66]5- (1-Sb8Mo18), has been isolated and displays a new breakthrough of polyoxometalates (POMs) with an ionothermal synthesis strategy. 1-Sb8Mo18 features the first hexanuclear sandwich-type polymolybdate (POMo) with an unexpected metal ring {Sb6O12} to make its debut in Sb clusters. Furthermore, 1-Sb8Mo18 exhibits a prominent catalytic activity for reducing nitrobenzene to aniline with excellent sustainability.

Eradication Treatment of Helicobacter pylori Infection Based on Molecular Pathologic Antibiotic Resistance.

BACKGROUND: Unfortunately, the eradication rate of Helicobacter pylori (H. pylori) treatment is markedly decreasing in recent years and the major reason is antibiotic resistance. Our study was designed to determine the effect and safety of H. pylori eradication treatment based on the molecular pathologic antibiotic resistance. METHODS: 261 patients were analyzed retrospectively, including 111 patients who were treated for the first time (one group as First-treated) and 150 patients who failed at least once in bismuth quadruple therapy (another group as Re-treatment). Antibiotic resistance was examined by Real-time PCR detection and conventional PCR and sequencing method. The eradication rate (ER) was compared per intention to treat (ITT) and per protocol (PP) between the two groups. RESULTS: The resistance rates to amoxicillin, clarithromycin, fluoroquinolone and tetracycline were 5.5%, 42.1%, 41.7% and 12.9% in the 111 first-treated patients, and 11.7%, 79.7%, 70.7% and 30.0% in the 150 re-treatment patients. The ERs in the ITT and PP analyses were 92.79% (95% CI, 87.98-97.60%, n=111) and 98.10% (95% CI, 95.48-100%, n=105), respectively, in the first-treated patients and 90.67% (95% CI, 86.01-95.32%, n=150) and 95.10% (95% CI, 91.57-98.64%, n=143), respectively, in the re-treatment patients. No significant differences were shown in the ERs between two group patients, and no serious adverse events were found. CONCLUSION: H. pylori eradication treatment based on molecular pathologic antibiotic resistance showed good effect and safety in both first and re-treated patients.

Non-adiabatic membrane voltage fluctuations driven by two ligand-gated ion channels.

In this paper, we construct a piecewise deterministic Markov process to model the membrane voltage fluctuations driven by two ligand-gated channels. The series-solution method is applied to the third-order ordinary differential equations to get its general solutions. Also, the stationary probability density function (PDF) is just the special solution that satisfies certain boundary conditions. The bifurcation conditions of the PDF at the boundary are obtained analytically. As an application, the PDF is used to calculate the power dissipation of the ionic currents in the (nonequilibrium) steady states.

AXL degradation in combination with EGFR-TKI can delay and overcome acquired resistance in human non-small cell lung cancer cells.

Acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) has been a major obstacle in the treatment of non-small cell lung cancer (NSCLC) patients. AXL has been reported to mediate EGFR-TKIs. Recently, third generation EGFR-TKI osimertinib has been approved and yet its acquired resistance mechanism is not clearly understood. We found that AXL is involved in both gefitinib and osimertinib resistance using in vitro and in vivo model. In addition, AXL overexpression was correlated with extended protein degradation rate. We demonstrate targeting AXL degradation is an alternative route to restore EGFR-TKIs sensitivity. We confirmed that the combination effect of YD, an AXL degrader, and EGFR-TKIs can delay or overcome EGFR-TKIs-driven resistance in EGFR-mutant NSCLC cells, xenograft tumors, and patient-derived xenograft (PDX) models. Therefore, combination of EGFR-TKI and AXL degrader is a potentially effective treatment strategy for overcoming and delaying acquired resistance in NSCLC.

Novel 4-aminoquinazoline derivatives induce growth inhibition, cell cycle arrest and apoptosis via PI3Kα inhibition.

Phosphatidylinositol 3-kinase (PI3K) signaling pathway has diverse functions, including the regulation of cellular survival, proliferation, cell cycle, migration, angiogenesis and apoptosis. Among class I PI3Ks (PI3Kα, ß, γ, δ), the PIK3CA gene encoding PI3K p110α is frequently mutated and overexpressed in a large portion of human cancers. Therefore, the inhibition of PI3Kα has been considered as a promising target for the development of a therapeutic treatment of cancer. In this study, we designed and synthesized a series of 4-aminoquinazoline derivatives and evaluated their antiproliferative activities against six cancer cell lines, including HCT-116, SK-HEP-1, MDA-MB-231, SNU638, A549 and MCF-7. Compound 6b with the most potent antiproliferative activity and without obvious cytotoxicity to human normal cells was selected for further biological evaluation. PI3K kinase assay showed that 6b has selectivity for PI3Kα distinguished from other isoforms. The western blot assay and PI3K kinase assay indicated that 6b effectively inhibited cell proliferation via suppression of PI3Kα kinase activity with an IC50 of 13.6 nM and subsequently blocked PI3K/Akt pathway activation in HCT116 cells. In addition, 6b caused G1 cell cycle arrest owing to the inhibition of PI3K signaling and induced apoptosis via mitochondrial dependent apoptotic pathway. Our findings suggested that 6b has a therapeutic value as an anticancer agent via PI3Kα inhibition.

Primary intrahepatic bile duct adenocarcinoma complicating with nonalcoholic fatty liver disease in an elderly woman: independent risk factor or a mere coincidence? A case report.

Our report detailes an eldly woman with multiple liver space-occupying lesions (SOLs). Abdominal ultrasonography revealed multiple hypoechoic masses of different sizes, and enhanced computed tomography showed multiple nodules and masses in the liver parenchyma. Ultrasound-guided liver biopsy was performed because the radiological and endoscopic examinations could not determine the diagnosis. Pathological diagnosis indicated poorly differentiated adenocarcinoma. Immunohistochemical staining showed that the expression of CK7, CK8/18, CK19, mammaglobin, ER/SP1, PR/1E2 and GS were positive whereas the expression of Hepatocyte, AFP, GPC-3, WT-1, CK20, CD34, Syn, CgA, CD56, TTF-1, NapsinA, CDX-2, GCDFP 15 and CA125 were negative. Combined with pathological and immunohistochemical results, the diagnosis was determined as the primary intrahepatic bile duct adenocarcinoma. However, no definite risk factor had been found for this patient, and we found that the patient had a medical history of fatty liver for 20 years. She was obese, with a body weight of 92 kilograms (BMI, 32.86 Kg/m2), and radiological examinations showed the typical imaging characteristics for fatty liver. According to our current knowledge, we deduce that nonalcoholic fatty liver disease may be the possible risk factor for this patient with intrahepatic bile duct adenocarcinoma, but a mere coincidence cannot be ruled out. In this report, we detail the case and discuss the relationship between nonalcoholic fatty liver disease and primary intrahepatic bile duct adenocarcinoma.

Design, synthesis, and biological evaluation of novel 3-substituted imidazo[1,2-a]pyridine and quinazolin-4(3H)-one derivatives as PI3Kα inhibitors.

Phosphatidylinositol 3-kinase (PI3K) is a pivotal regulator of intracellular signaling pathways and considered as a promising target in the development of a therapeutic treatment of cancer. Among the different PI3K subtypes, the PIK3CA gene encoding PI3K p110α is frequently mutated and overexpressed in majority of human cancers. Therefore, the inhibition of PI3Kα has been considered to be an efficient approach for the treatment of cancer. In this study, two series compounds containing hydrophilic group in imidazo[1,2-a]pyridine and quinazolin-4(3H)-one were synthesized and their antiproliferative activities against five cancer cell lines, including HCT-116, SK-HEP-1, MDA-MB-231, SNU638 and A549, were evaluated. Compound 1i with most potent antiproliferative activity was selected for further biological evaluation. PI3K kinase assay showed that 1i has selectivity for PI3Kα distinguished from other isoforms. The western blot assay indicated that 1i is more effective than HS-173, an imidazopyridine-based PI3Ka inhibitor, in reducing the levels of phospho-Akt. All these results suggested that 1i is a potent PI3Kα inhibitor and could be considered as a potential candidate for the development of anticancer agents.

Terfenadine combined with epirubicin impedes the chemo-resistant human non-small cell lung cancer both in vitro and in vivo through EMT and Notch reversal.

The acquired resistance of non-small cell lung cancer (NSCLC) to taxanes eventually leads to the recurrence and metastasis of tumours. Thus, the development of therapeutic strategies based on the mechanisms by which cells acquire resistance to prolong their survival rate in chemotherapy drug treatment failure patients are warranted. In this study, we found that the resistant cells acquired increased migratory and invasive capabilities, and this transformation was correlated with epithelial-mesenchymal transition (EMT) and Notch pathway deregulation in the resistant cells. Finally, we reported for the first time that terfenadine augmented the effect of epirubicin (EPI) better than Taxol and cisplatin (DDP) by inhibiting migration, invasion, and the EMT phenotype, and the combination therapy also reversed Notch signalling pathway and enhanced the accumulation of fluorescent P-gp substrate rhodamine 123 (Rh123). Similar activities of terfenadine on EPI were observed in xenografts. All of our results confirmed that terfenadine combined with EPI synergistically inhibits the growth and metastatic processes of resistant cells both in vitro and in vivo. Therefore, terfenadine or its derivatives are a promising approach for the clinical challenge of resistance in patients with advanced NSCLC.

Anti-proliferative and pro-apoptotic activities of Alpinia oxyphylla on HepG2 cells through ROS-mediated signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Fructus Alpiniae oxyphyllae (A. oxyphylla) is a traditional herb which is widely used in East Asian for the treatment of dyspepsia, diarrhea, abdominal pain, poor memory, inflammatory conditions and cancer. MATERIALS AND METHODS: The cytotoxic activities of ethanol extract (EE) and five extract layers including petroleum ether (PE), dichloromethane (DCLM), acetoacetate (EtOAc), n-Butanol (n-Bu) and water fractions (WF) of A. oxyphylla were tested on HepG2, SW480, MCF-7, K562 and HUVEC cell lines using MTT assay and LDH release assay. The component analysis was performed on HPLC with gradient elution. Hoechst 33342 staining, DCFH-DA fluorescence microscopy, flow cytometry analysis, western blot and migration assays were carried out to determine the anti-cancer mechanisms of PE. RESULTS: MTT analysis showed that EE, PE and DCLM could inhibit cell proliferation on HepG2, SW480, MCF-7, K562 and HUVEC cell lines, especially PE fraction. HPLC analysis pointed out five main components which may contribute to the anti-proliferative activity of PE. Further study showed that PE increased LDH release, induced apoptosis, disrupted mitochondrial membrane potential and elevated intracellular reactive oxygen species (ROS) in HepG2 cells, whereas the antioxidant N-acetyl-l-cysteine (NAC) prevented PE-induced ROS generation. The results of western blot revealed that PE induced apoptosis in HepG2 cells by enhancing Bax/Bcl-2 ratio, increasing cytochrome c in cytosol and activating caspase-3/9. Meanwhile, high levels of ROS could induce DNA damage-mediated protein expression, AKT, ERK inactivation and SAPKs activation. Furthermore, PE conspicuously blocked the migration of HUVEC cells. CONCLUSION: The present results demonstrated that PE induced apoptosis in HepG2 cells may be via a ROS-mediated signaling pathway.

Protective effects of Arctium lappa L. roots against hydrogen peroxide-induced cell injury and potential mechanisms in SH-SY5Y cells.

Accumulated evidence has shown that excessive reactive oxygen species (ROS) have been implicated in neuronal cell death related with various chronic neurodegenerative disorders. This study was designed to explore neuroprotective effects of ethyl acetate extract of Arctium lappa L. roots (EAL) on hydrogen peroxide (H2O2)-induced cell injury in human SH-SY5Y neuroblastoma cells. The cell viability was significantly decreased after exposure to 200 µM H2O2, whereas pretreatment with different concentrations of EAL attenuated the H2O2-induced cytotoxicity. Hoechst 33342 staining indicated that EAL reversed nuclear condensation in H2O2-treated cells. Meanwhile, TUNEL assay with DAPI staining showed that EAL attenuated apoptosis was induced by H2O2. Pretreatment with EAL also markedly elevated activities of antioxidant enzyme (GSH-Px and SOD), reduced lipid peroxidation (MDA) production, prevented ROS formation, and the decrease of mitochondrial membrane potential. In addition, EAL showed strong radical scavenging ability in 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) assays. Furthermore, EAL inhibited H2O2-induced apoptosis by increases in the Bcl-2/Bax ratio, decreases in cytochrome c release, and attenuation of caspase-3, caspase-9 activities, and expressions. These findings suggest that EAL may be regarded as a potential antioxidant agent and possess potent neuroprotective activity against H2O2-induced injury.

Expression and promoter characterization of BbPacC, a pH response transcription factor gene of the entomopathogenic fungus Beauveria bassiana.

To survive, the entomopathogenic fungus Beauveria bassiana, which shows promise as a biocontrol agent for a variety of pests, including agricultural and forestry pests and vectors of human pathogens, must tailor gene expression to the particular pH of its environment. The pH response transcription factor gene BbPacC and its flanking sequence were cloned from this fungus. Quantitative reverse transcription (RT)-PCR revealed that it is highly induced by alkaline pH and salt stress, and the expression level achieved twice that of the housekeeping gene γ-actin. A microfluorometric assay indicated that the 1479 bp promoter region could activate the expression of enhanced green fluorescent protein (EGFP) under the same conditions. Truncation analysis showed that the 1479, 1274, 1040, 888 and 742 bp promoters have similar efficiencies in activating expression of ß-glucuronidase (GUS). The GUS activities of corresponding transformants reached approximately 50 % that of those containing the strong constitutive promoter PtrpC. A truncation upstream at the -572 bp position (referenced to the translation start codon ATG), however, resulted in a significant loss of GUS activity. Both the upstream absences of the -502 and -387 bp positions caused almost complete loss of GUS activity. These results suggest that PPacC is an efficient, alkaline, and salt-inducible promoter, the core cis-elements are mainly located within the -742 to -502 bp region, and promoters equal to or longer than 742 bp may be feasible for regulating gene expression in response to an ambient pH or salt stress.