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In the title mol-ecule, C(15)H(17)IO(4)S, the O atom and the methyl group of the methyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran fragment. In the crystal structure, inter-molecular I⋯O [2.994 (3) Å] halogen bonding links the mol-ecules into centrosymmetric dimers, which are further packed into ribbons along the c axis by inter-molecular sulfin-yl-sulfinyl inter-actions [S⋯O 3.128 (3) Å].

In the title compound, C(14)H(15)IO(4)S, the O atom and the methyl group of the methyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran fragment. The crystal structure is stabilized by C-H⋯π inter-actions between a methyl H atom and the benzene ring of an adjacent mol-ecule, and by weak inter-molecular C-H⋯O hydrogen bonds.

The title compound, C(12)H(11)BrO(4)S, was synthesized by the oxidation of methyl 2-(5-bromo-3-methyl-sulfanyl-1-benzofuran-2-yl)acetate with 3-chloro-peroxy-benzoic acid. The O atom and the methyl group of the methyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran ring system. The crystal structure is stabilized by C-H⋯π inter-actions, involving a methyl H atom and the benzene ring of a neighbouring mol-ecule, and by weak inter-molecular C-H⋯O hydrogen bonds.

In the title compound, C(14)H(15)BrO(4)S, the O atom and the methyl group of the methyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran fragment. The crystal structure is stabilized by C-H⋯π inter-actions between a methyl H atom and the benzene ring of a neighbouring mol-ecule, and by weak inter-molecular C-H⋯O hydrogen bonds.

Background: The wild grass species Brachypodium distachyon (Brachypodium hereafter) is emerging as a new model system for grass crop genomics research and biofuel grass biology. A draft nuclear genome sequence is expected to be publicly available in the near future; an explosion of gene expression studies will undoubtedly follow. Therefore, stable reference genes are necessary to normalize the gene expression data., Results: A systematic exploration of suitable reference genes in Brachypodium is presented here. Nine reference gene candidates were chosen, and their gene sequences were obtained from the Brachypodium expressed sequence tag (EST) databases. Their expression levels were examined by quantitative real-time PCR (qRT-PCR) using 21 different Brachypodium plant samples, including those from different plant tissues and grown under various growth conditions. Effects of plant growth hormones were also visualized in the assays. The expression stability of the candidate genes was evaluated using two analysis software packages, geNorm and NormFinder. In conclusion, the ubiquitin-conjugating enzyme 18 gene (UBC18) was validated as a suitable reference gene across all the plant samples examined. While the expression of the polyubiquitin genes (Ubi4 and Ubi10) was most stable in different plant tissues and growth hormone-treated plant samples, the expression of the S-adenosylmethionine decarboxylase gene (SamDC) ranked was most stable in plants grown under various environmental stresses., Conclusion: This study identified the reference genes that are most suitable for normalizing the gene expression data in Brachypodium. These reference genes will be particularly useful when stress-responsive genes are analyzed in order to produce transgenic plants that exhibit enhanced stress resistance.

Mol-ecules of title compound, C(16)H(20)O(4)S, which was synthesized by the oxidation of isopropyl 2-(4,6-dimethyl-3-methyl-sulfanyl-1-benzofuran-2-yl)acetate, inter-act through C-H⋯π inter-actions between a methyl-ene H atom and the aromatic carbon ring of the benzofuran ring system, and by C-H⋯O hydrogen bonds. Adjacent stacked mol-ecules exhibit a carbon-yl-carbonyl inter-action [3.295 (2) Å]. The O atom of the methyl-sulfinyl group is disordered over two positions with site-occupancy factors of 0.9 and 0.1.

The title compound, C(12)H(11)ClO(4)S, was prepared by the oxidation of methyl 2-(5-chloro-3-methyl-sulfanyl-1-benzofuran-2-yl)acetate with 3-chloro-peroxy-benzoic acid. The O atom and the methyl group of the methyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran fragment. The crystal structure is stabilized by aromatic π-π inter-actions between the benzene rings of neighbouring mol-ecules [centroid-to-centroid distance = 3.809 (2) Å], and by C-H⋯π inter-actions between a methyl H atom and the furan ring of an adjacent mol-ecule. In addition, the crystal structure exhibits inter-molecular C-H⋯O hydrogen bonds.

In the title compound, C(12)H(13)BrO(2)S, there are two symmetry-independent mol-ecules, A and B, in the asymmetric unit. The crystal studied was an inversion twin with a 0.70 (2):0.30 (2) domain ratio. The methyl-sulfinyl group in mol-ecule B is disordered over two positions with site-occupancy factors fixed at 0.6 and 0.4. The crystal structure is stabilized by C-H⋯O hydrogen bonds and inter-molecular C-H⋯π inter-actions. In addition, the crystal structure exhibits C-Br⋯π inter-actions, with C-Br⋯Cg1 = 3.646 (8) Å where Cg1 is the centroid of the furan ring.

The title compound, C(15)H(18)O(4)S, was prepared by the oxidation of isopropyl 2-(5-methyl-3-methyl-sulfanyl-1-benzofuran-2-yl)acetate with 3-chloro-peroxy-benzoic acid. The crystal structure is stabilized by inter-molecular π-π inter-actions between the benzene rings; the centroid-centroid distance between the adjacent benzene rings (symmetry code: ) is 3.713 (2) Å. In addition, C-H⋯π and weak inter-molecular C-H⋯O inter-actions are present in the structure.

The ability to activate dormant transcription factors is an important molecular feature of the transcriptional regulatory networks that govern diverse cellular functions. An intriguing example is the controlled proteolytic activation of membrane-bound transcription factors (MTFs). Most MTFs are activated either by intramembrane proteases or by the ubiquitin-proteasome pathway. Recent studies have shown that several members of the bZIP and NAC families in Arabidopsis are membrane-associated and are activated by membrane-associated proteases during stress responses in the endoplasmic reticulum and when the plants experience environmental stresses. A genome-scale analysis shows that over 10% of all transcription factors are membrane bound, indicating that activation of MTFs occurs at the genomic level, allowing transcription to be regulated rapidly under stressful conditions.

The title compound, C(17)H(15)BrO(2)S, which was synthesized by the oxidation of 5-bromo-2,4,6-trimethyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid, features a trigonally-coordinated S atom. The phenyl ring is approximately perpendicular to the plane of the benzofuran fragment [dihedral angle 75.11 (7)°]. The crystal structure is stabilized by non-classical C-H⋯O and Br⋯Br inter-actions [3.7169 (6) Å].

The title compound, C(18)H(18)O(3)S, was prepared by the oxidation of 2-methyl-3-phenyl-sulfanyl-5-propyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 81.74 (6)° with the plane of the benzofuran fragment. The crystal structure is stabilized by C-H⋯π inter-actions between a methyl H atom and the phenyl ring of the phenyl-sulfonyl substituent from a neighbouring mol-ecule, and by inter-molecular C-H⋯O inter-actions.

The title compound, C(13)H(14)O(4)S, was prepared by oxidation of methyl 2-(5-methyl-3-methyl-sulfanyl-1-benzofuran-2-yl)acetate with 3-chloro-peroxy-benzoic acid. The O atom and methyl group of the methyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran system. The crystal structure is stabilized by inter-molecular aromatic π-π inter-actions between the benzene rings of neighbouring mol-ecules, with a centroid-centroid separation of 3.841 (3) Å.

The title compound, C(15)H(12)O(2)S, was prepared by the oxidation of 3-methyl-sulfanyl-2-phenyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 37.65 (8)° with the plane of the benzofuran fragment. The O atom and the methyl group of the methyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran ring system. The crystal structure is stabilized by aromatic π-π inter-actions between the benzene rings of neighbouring mol-ecules [centroid-centroid distance = 3.549 (2) Å] and by inter-molecular C-H⋯O inter-actions.

In the title compound, C(13)H(14)O(3)S, the methyl group of the methyl-sulfanyl substituent is almost perpendicular to the plane of the benzofuran fragment [80.5 (9)°]. The carboxylic acid groups are involved in inter-molecular O-H⋯O hydrogen bonds, which link the mol-ecules into centrosymmetric dimers. These dimers are further packed into stacks along the a axis by C-H⋯π inter-actions.

The title compound, C(13)H(14)O(3)S, was prepared by alkaline hydrolysis of ethyl 2-(5,7-dimethyl-3-methyl-sulfanyl-1-benzofuran-2-yl)acetate. In the crystal structure, the carboxyl groups are involved in inter-molecular O-H⋯O hydrogen bonds, which link the mol-ecules into centrosymmetric dimers. These dimers are further packed into stacks along the a axis by weak C-H⋯π inter-actions.

The title compound, C(17)H(16)O(2)S, was prepared by the oxidation of 2,4,6-trimethyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The O atom and the phenyl group of the phenyl-sulfinyl substituent lie on opposite sides of the planar benzofuran fragment. The phenyl ring is nearly perpendicular to the plane of the benzofuran unit [89.88 (8)°] and is tilted slightly towards it. The crystal structure is stabilized by C-H⋯π inter-actions between a phenyl H atoms and the phenyl and furan rings of neighbouring mol-ecules. In addition, the crystal structure exhibits inter-molecular C-H⋯O inter-actions.

The title compound, C(15)H(12)O(2)S, was prepared by the oxidation of 2-methyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The O atom and the phenyl group of the phenyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran system. The phenyl ring makes a dihedral angle of 78.76 (4)° with the benzofuran mean plane. The crystal structure is stabilized by π-π inter-actions between the furan and benzene rings of neighbouring mol-ecules [centroid-centroid distance = 4.017 (3) Å]. In addition, the crystal structure exhibits inter-molecular C-H⋯π and C-H⋯O inter-actions.

The title compound, C(17)H(16)O(2)S, was prepared by the oxidation of 2,5,7-trimethyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The O atom and the phenyl group of the phenyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran fragment. The phenyl ring is nearly perpendicular to the plane of the benzofuran unit [88.30 (9)°] and is tilted slightly towards it. No π-π or C-H⋯π inter-actions are observed between neighbouring mol-ecules in the crystal structure because of steric hindrance induced by the three methyl groups.

The title compound, C(18)H(18)O(3)S, was prepared by the oxidation of 5-isopropyl-2-methyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 79.37 (6)° with the plane of the benzofuran fragment. The crystal structure is stabilized by aromatic π-π stacking inter-actions between the benzene and furan rings of neighbouring mol-ecules [centroid-centroid distance = 3.762 (3) Å]. In addition, the stacked mol-ecules exhibit C-H⋯π and intra-molecular C-H⋯O inter-actions.

The title compound, C(15)H(11)ClO(3)S, was prepared by the oxidation of 5-chloro-2-methyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. There are two symmetry-independent mol-ecules in the asymmetric unit. The dihedral angles formed by the phenyl ring and the plane of the benzofuran system are 77.80 (8) and 78.34 (8)°. The crystal structure is stabilized by aromatic π-π stacking inter-actions between the furan ring and the benzene rings of neighbouring benzofuran fragments from two symmetry-independent mol-ecules; the centroid-centroid distances within the stacks are 3.689 (4), 3.702 (4), 3.825 (4) and 3.826 (4) Å. Additionally, the stacked mol-ecules exhibit inter- and intra-molecular C-H⋯O inter-actions.

In the title compound, C(18)H(18)O(2)S, the O atom and the phenyl group of the phenyl-sulfinyl substituent lie on opposite sides of the planar benzofuran fragment. The phenyl ring is nearly perpendicular to the benzofuran system [88.56 (7)°] and is tilted slightly towards it. Molecules form pseudo-helices along the a axis. The crystal structure is stabilized by a C-H⋯π inter-action between a methyl H atom and the phenyl ring of the phenyl-sulfinyl substituent, and by intra- and inter-molecular C-H⋯O inter-actions.

The title compound, C(20)H(15)BrO(3)S, was prepared by the oxidation of 7-bromo-2-methyl-1-(4-tolyl-sulfan-yl)naph-tho[2,1-b]furan with 3-chloro-peroxy-benzoic acid. The 4-tolyl ring makes a dihedral angle of 70.96 (6)° with the plane of the naphthofuran fragment. The crystal structure is stabilized by aromatic π-π stacking inter-actions, with centroid-centroid distances of 3.672 (3) and 3.858 (3) Å between the central benzene and furan rings, and between the brominated benzene and central benzene rings of the naphthofuran system of neighbouring mol-ecules, respectively. In addition, the stacked mol-ecules exhibit C-H⋯π and inter- and intra-molecular C-H⋯O inter-actions.

The title compound, C(16)H(13)IO(2)S, was prepared by the oxidation of 5-iodo-7-methyl-3-methyl-sulfanyl-2-phenyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 27.17 (9)° with the plane of the benzofuran fragment, with the O atom and the methyl group of the methyl-sulfinyl substituent lying on opposite sides of this plane. The crystal structure exhibits inter-molecular C-H⋯I inter-actions, and an I⋯O halogen bond of 3.107 (2) Å with a nearly linear C-I⋯O angle of 173.73 (6)°.

The title compound, C(17)H(15)IO(2)S, was prepared by the oxidation of 2-(4-iodo-phen-yl)-5,7-dimethyl-3-methyl-sulfanyl-1-benzofuran using 3-chloro-peroxy-benzoic acid. The 4-iodo-phenyl ring makes a dihedral angle of 26.0 (1)° with the plane of the benzofuran fragment, and the O atom and the methyl group of the methyl-sulfinyl substituent lie on opposite sides of this plane. The crystal structure is stabilized by inter- and intra-molecular C-H⋯O hydrogen bonds, and by an I⋯O halogen bond with an I⋯O distance of 3.145 (2) Å and a nearly linear C-I⋯O angle of 164.01 (9)°.

The title compound, C(16)H(13)IO(2)S, was prepared by the oxidation of 2-(4-iodo-phen-yl)-5-methyl-3-methyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The 4-iodo-phenyl ring makes a dihedral angle of 37.97 (9)° with the plane of the benzofuran fragment, and the O atom and the methyl group of the methyl-sulfinyl substituent lie on opposite sides of this plane. The mol-ecular packing is stabilized by C-H⋯π inter-actions between H atoms on the 4-iodo-phenyl ring and the benzofuran rings, and by an I⋯O halogen bond of 3.252 (2) Å with a nearly linear C-I⋯O angle of 163.06 (8)°. In addition, the stacked mol-ecules exhibit inversion-related S⋯O contacts [3.209 (2) Å] involving the sulfinyl groups.

The title compound, C(17)H(16)O(3)S, was prepared by the oxidation of 5-ethyl-2-methyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 75.94 (8)° with the plane of the benzofuran fragment. The crystal structure is stabilized by π-π inter-actions between the furan rings of neighbouring mol-ecules [centroid-centroid distance = 3.620 (4) Å]. In addition, the crystal structure exhibits C-H⋯π inter-actions.

The title compound, C(19)H(13)BrO(3)S, was prepared by the oxidation of 7-bromo-2-methyl-1-(phenyl-sulfan-yl)naph-tho[2,1-b]furan with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 80.4 (2)° with the plane of the naphthofuran fragment. The crystal structure is stabilized by aromatic π-π stacking inter-actions between the brominated benzene ring and the central benzene ring of the naphthofuran system of neighbouring mol-ecules; the centroid-centroid distances within the stack are 3.889 (3) and 3.981 (3) Å. In addition, the stacked mol-ecules exhibit C-H⋯π, inter- and intra-molecular C-H⋯O inter-actions.

The title compound, C(16)H(13)IO(3)S, was prepared by the oxidation of 5-iodo-2,7-dimethyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 76.31 (8)° with the plane of the benzofuran fragment. The crystal structure is stabilized by aromatic π-π inter-actions between the furan and benzene rings of neighbouring mol-ecules, and between the benzene rings of neighbouring mol-ecules; the centroid-centroid distances within the stack are 3.700 (4) and 3.788 (4) Å. In addition, the crystal structure exhibits inter- and intra-molecular C-H⋯O inter-actions, and an I⋯O halogen bond with an I⋯O distance of 3.282 (2) Å and a nearly linear C-I⋯O angle of 165.69 (8)°.

The title compound, C(16)H(12)O(5)S, was prepared by oxidation of 2-methyl-5,6-methyl-ene-di-oxy-3-phenyl-sulfanyl-1-benzo-furan with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 83.64 (4)° with the mean plane of the 5,6-(methyl-ene-di-oxy)-benzo-furan fragment. The crystal structure is stabilized by C-H⋯π inter-actions between a benzene H atom of the 5,6-(methyl-ene-di-oxy)-benzo-furan unit and the phenyl ring of the phenyl-sulfonyl substituent. Additionally, the crystal structure exhibits inter- and intra-molecular C-H⋯O inter-actions.

The title compound, C(16)H(14)O(3)S, was prepared by the oxidation of 2,5-dimethyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 76.98 (9)° with the plane of the benzofuran fragment. The crystal structure is stabilized by π-π inter-actions between furan and benzene rings of neighbouring mol-ecules [centroid-centroid distance = 3.775 (4) Å]. In addition, the crystal structure exhibits intra- and inter-molecular C-H⋯O inter-actions.

The title compound, C(19)H(13)ClO(3)S, was prepared by the oxidation of 3-(4-chloro-phenyl-sulfan-yl)-2-methyl-naphtho[1,2-b]furan with 3-chloro-peroxy-benzoic acid. The 4-chloro-phenyl ring makes a dihedral angle of 68.59 (5)° with the plane of the naphthofuran fragment. The crystal structure is stabilized by π-π inter-actions between the benzene rings of neighbouring mol-ecules [centroid-centroid distance = 3.635 (3) Å], and by C-H⋯π inter-actions between a methyl H atom and the furan ring of an adjacent mol-ecule. In addition, the crystal structure exhibits inter-molecular C-H⋯O inter-actions.

The title compound, C(17)H(16)O(3)S, was prepared by the oxidation of 2,5,7-trimethyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring exhibits a dihedral angle of 81.16 (4)° with the plane of the benzofuran fragment. The crystal structure is stabilized by π-π inter-actions between the furan and benzene rings of neighbouring mol-ecules [centroid-centroid distance = 3.874 (2) Å] and by C-H⋯π inter-actions between a phenyl H atom of the phenyl-sulfonyl substituent and the furan ring of adjacent mol-ecules. In addition, the crystal structure exhibits intra- and inter-molecular C-H⋯O inter-actions.

The title compound, C(15)H(11)BrO(3)S, was prepared by the oxidation of 5-bromo-2-methyl-3-phenyl-sulfanyl-1-benzofuran with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 78.99 (8)° with the plane of the benzofuran fragment. The crystal structure is stabilized by C-H⋯π inter-actions between a benzene H atom of the benzofuran unit and the phenyl ring of the phenyl-sulfonyl substituent from a neighbouring mol-ecule. In addition, the crystal structure exhibits intra- and inter-molecular C-H⋯O inter-actions.

Shoot apical meristem (SAM) development is coordinately regulated by two interdependent signaling events: one maintaining stem cell identity and the other governing the initiation of lateral organs from the flanks of the SAM. The signaling networks involved in this process are interconnected and are regulated by multiple molecular mechanisms. Class III homeodomain-leucine zipper (HD-ZIP III) proteins are the most extensively studied transcription factors involved in this regulation. However, how different signals are integrated to maintain stem cell identity and to pattern lateral organ polarity remains unclear. Here, we demonstrated that a small ZIP protein, ZPR3, and its functionally redundant homolog, ZPR4, negatively regulate the HD-ZIP III activity in SAM development. ZPR3 directly interacts with PHABULOSA (PHB) and other HD-ZIP III proteins via the ZIP motifs and forms nonfunctional heterodimers. Accordingly, a double mutant, zpr3-2 zpr4-2, exhibits an altered SAM activity with abnormal stem cell maintenance. However, the mutant displays normal patterning of leaf polarity. In addition, we show that PHB positively regulates ZPR3 expression. We therefore propose that HD-ZIP III activity in regulating SAM development is modulated by, among other things, a feedback loop involving the competitive inhibitors ZPR3 and ZPR4.

The title compound, C(19)H(14)O(3)S, was prepared by the oxidation of 2-methyl-1-(phenyl-sulfan-yl)naphtho[2,1-b]furan with 3-chloro-peroxy-benzoic acid. The phenyl ring makes a dihedral angle of 87.13 (4)° with the plane of the naphthofuran fragment. The crystal structure is stabilized by π-π inter-actions between the furan and benzene rings of neighbouring mol-ecules [centroid-centroid distance = 3.850 (2) Å] and weak C-H⋯π inter-actions. In addition, there are also intra-molecular C-H⋯O inter-actions.

Pathogenesis-related (PR) proteins are a group of heterogeneous proteins encoded by genes that are rapidly induced by pathogenic infections and by salicylic acid (SA), jasmonic acid (JA) and ethylene (ET). They are widely used as molecular markers for resistance response to pathogens and systemic acquired response (SAR). However, recent studies have shown that the PR genes are also regulated by environmental factors, including light and abiotic stresses, and by developmental cues, suggesting that they also play a role in certain stress responses and developmental processes. In this work, we systematically examined the expression patterns of Arabidopsis PR genes. We also investigated the effects of environmental stresses and growth hormones on the expression of PR genes. We found that individual PR genes are temporally and spatially regulated in distinct patterns. In addition, they are differentially regulated by plant growth hormones, including SA, ABA, JA, ET and brassinosteroid (BR), and by diverse abiotic stresses, supporting the contention that the PR proteins play a role in plant developmental processes other than disease resistance response. Interestingly, PR-3 was induced significantly by high salt in an ABA-dependent manner. Consistent with this, a T-DNA insertional knockout plant with disruption of the PR-3 gene showed a significantly reduced rate of seed germination in the presence of high salt. It is thus proposed that PR-3 mediates ABA-dependent salt stress signals that affect seed germination in Arabidopsis. PR-4 and PR-5 also contributed to salt regulation of seed germination, although their effects were not as evident as those of PR-3.

The title compound, C(16)H(13)IO(2)S, was prepared by the oxidation of 5-iodo-2,7-dimethyl-3-phenyl-sulfanyl-1-benzofuran using 3-chloro-perbenzoic acid. The O atom and the phenyl group of the phenyl-sulfinyl substituent lie on opposite sides of the plane of the benzofuran system. The phenyl ring is nearly perpendicular to the plane of the benzofuran fragment [89.15 (5)°]. The crystal structure is stabilized by an I⋯O halogen bond [I⋯O = 3.177 (2) Å and C-I⋯O = 175.68 (6)°] linking mol-ecules into centrosymmetric dimers and by a weak C-H⋯π inter-action between a phenyl H atom and the furan ring of the benzofuran system.

The title compound, C(15)H(12)O(3)S, was prepared by alkaline hydrolysis of ethyl 2-{1-(methyl-sulfan-yl)naphtho[2,1-b]furan-2-yl}acetate. The crystal structure is stabilized by CH(2)-H⋯π inter-actions between the methyl H atoms of the methyl-sulfanyl substituent and the central benzene ring of the naphthofuran system, and by inversion-related inter-molecular O-H⋯O hydrogen bonds between the carboxyl groups.

In the title mol-ecule, C(19)H(14)O(3)S, the phenyl ring forms a dihedral angle of 69.13 (6)° with the plane of the naphthofuran fragment, being slightly tilted towards it. The crystal packing exhibits π-π inter-actions between the benzene rings from neighbouring mol-ecules [centroid-centroid distance = 3.616 (4) Å] and weak C-H⋯O and C-H⋯π inter-actions.

The title compound, C(17)H(15)BrOS, was prepared by the Lewis acid-catalysed reaction of 2,4-dimethyl-phenol with 4'-bromo-2-chloro-2-(methyl-sulfan-yl)acetophenone. The 4-bromo-phenyl ring is rotated slightly out of the benzofuran plane, making a dihedral angle of 8.4 (1)°. The crystal structure is stabilized by a CH(2)-H⋯π inter-action between the 5-methyl group and the benzene ring of the benzofuran system.

Regulated RNA metabolism appears to be a critical component of molecular mechanisms directing flowering initiation in plants. A group of RNA binding proteins exerts their roles through the autonomous flowering pathway. Posttranscriptional mechanisms regulated by microRNAs (miRNAs) also play a key role in flowering-time control. Here, we demonstrate that the GIGANTEA (GI)-regulated miR172 defines a unique genetic pathway that regulates photoperiodic flowering by inducing FLOWERING LOCUS T (FT) independent of CONSTANS (CO). A late-flowering mutant in which a miR172 target gene, TARGET OF EAT1, is constitutively activated by the nearby insertion of the cauliflower mosaic virus 35S enhancer normally responded to vernalization and gibberellic acid treatments. By contrast, its response to daylength changes was severely disrupted. In the mutant, FT was significantly repressed, but other flowering genes were unaffected. Notably, miR172 abundance is regulated by photoperiod via GI-mediated miRNA processing. Accordingly, miR172-overproducing plants exhibit early flowering under both long days and short days, even in the absence of functional CO, indicating that miR172 promotes photoperiodic flowering through a CO-independent genetic pathway. Therefore, it appears that GI-mediated photoperiodic flowering is governed by the coordinated interaction of two distinct genetic pathways: one mediated via CO and the other mediated via miR172 and its targets.

An Arabidopsis GH3 gene WES1 encodes an auxin-conjugating enzyme that plays a role in stress responses by modulating endogenous levels of active auxin through a negative feedback regulation. Here, we report a photomorphogenic role for WES1 in hypocotyl growth. Hypocotyls of the WES1-overexpressing wes1-D and the knockout wes1 mutants were similar to control hypocotyls in darkness. However, the wes1-D hypocotyls were significantly shorter but the wes1 hypocotyls were longer than control hypocotyls under red light. Accordingly, WES1 transcription was up-regulated in a phytochrome B mutant. These results provide support for WES1 regulating hypocotyl growth by mediating phytochrome B-perceived light signals.

Controlled proteolytic cleavage of membrane-associated transcription factors (MTFs) is an intriguing activation strategy that ensures rapid transcriptional responses to incoming stimuli. Several MTFs are known to regulate diverse cellular functions in prokaryotes, yeast, and animals. In Arabidopsis, a few NAC MTFs mediate either cytokinin signaling during cell division or endoplasmic reticulum (ER) stress responses. Through genome-wide analysis, it was found that at least 13 members of the NAC family in Arabidopsis contain strong alpha-helical transmembrane motifs (TMs) in their C-terminal regions and are predicted to be membrane-associated. Interestingly, most of the putative NAC MTF genes are up-regulated by stress conditions, suggesting that they may be involved in stress responses. Notably, transgenic studies revealed that membrane release is essential for the function of NAC MTFs. Transgenic plants overexpressing partial-size NAC constructs devoid of the TMs, but not those overexpressing full-size constructs, showed distinct phenotypic changes, including dwarfed growth and delayed flowering. The rice genome also contains more than six NAC MTFs. Furthermore, the presence of numerous MTFs is predicted in the whole transcription factors in plants. We thus propose that proteolytic activation of MTFs is a genome-wide mechanism regulating plant genomes.

Lamivudine is widely used for the treatment of chronic hepatitis B infection because of it's remarkable antiviral efficacy and safety. We report a case of severe skin eruption caused by lamivudine. A 47-year-old female was admitted because of jaundice and itching sensation. She was diagnosed as chronic hepatitis B infection a few years ago but did not receive any specific treatment. Laboratory data showed acute deterioration of chronic hepatitis B infection. We prescribed lamivudine as a rescue therapy. Her general condition improved and lab data showed improvement in liver function test thereafter. However, she complained of severe skin eruption and itching sensation a few days after the discharge. We stopped lamivudine because the symptoms did not improve despite the use of anti-histamine. Skin biopsy showed interface dermatitis. After stopping lamivudine, her symptoms improved. However, the skin eruption developed again after lamivudine was restarted. Adefovir was used instead, and the patient did not experience any further skin problems since then.

Background/aims: Protein induced by vitamin K absence or antagonist-II (PIVKA-II), also known as des-carboxyprothrombin (DCP), can be used as an alternative tool to alpha-fetoprotein (AFP) for surveillance of hepatocellular carcinoma (HCC). The aims of the present study were to compare PIVKA-II levels between the patients with HCC and patients with non-HCC chronic liver disease, to evaluate the correlation of PIVKA-II and AFP in HCC patients, and finally to estimate the optimal cut-off value for PIVKA-II for the diagnosis of HCC with using the receiver operating characteristic (ROC) curve., Methods: A total of 227 consecutive patients with HCC (n=42) or chronic liver disease (n=185) were enrolled in this study. HCC was diagnosed histologically or by imaging such as computed tomography, magnetic resonance imaging or angiography. The serum PIVKA-II and AFP levels were measured by electrochemiluminoimmunoassay with using the Haicatch PIVKA-II kit and by immunoradiometric assay, respectively., Results: The PIVKA-II level in the HCC patients was significantly higher than the non-HCC chronic liver disease patients (903.0+/-1156.7 vs. 111.7+/-211.0 mAU/ mL, respectively, P<0.01). PIVKA-II and AFP showed a statistical correlation in HCC patients (r=0.46, P<0.01). The sensitivity and specificity of PIVKA-II for the diagnosis of HCC were 66.7% and 74.1%, respectively, and when tasted together with AFP, the sensitivity was increased by 85.7%. For the ROC curve of PIVKA-II in HCC patients, the specificity of a 250 mAU/mL level of PIVKA-II was 95%., Conclusions: PIVKA-II was as useful surveillance tool for differentiating HCC from chronic liver disease, and a PIVKA-II value of 250 mAU/ mL was proposed as a significant cut-off value for diagnosis of hepatocellular carcinoma.

Pancreatic metastases are found in up to 40% of patients with small cell lung cancer, but metastasis-induced acute pancreatitis is rare. Treatment of metastasis-induced acute pancreatitis is initially supportive, but failure of conservative management are common. There are few reports on aggressive treatment with chemotherapy which lead to rapid clinical improvement and prolongation of survival in patients with metastasis-induced acute pancreatitis. We experienced a case of metastasis-induced acute pancreatitis in a patient with small cell lung cancer. Despite conservative treatment with dietary restriction and intravenous fluid supply, serum amylase levels increased persistently with severe abdominal pain. After chemotherapy with irinotecan and carboplatin, abdominal pain and serum amylase levels resolved dramatically.

The total synthesis of nomeolignans isolated from Krameria species, 2-aryl-5-(E)-propenylbenzofurans (5, 11), is described. The key step involves the one-pot reaction for 2-arylbenzofurans (2, 7) from 4-hydroxyphenylacetone with 4'-acetoxy-2-chloro-2-(methylthio)acetophenone (1) and 2-chloro-2-methylthio-(2',4',6'-trimethoxy)acetophenone (6) under Friedel-Crafts reactionconditions.

The facile synthesis of a series of 2-(4-hydroxyphenyl)benzofurans (4a-e) is described. The one-pot reaction of 4-substituted phenols with the chloride 1 in the presence of zinc chloride afforded 3-methylthio-2-(4-acetoxyphenyl)benzofurans (2a-e). The compounds 4a-e were obtained from the hydrolysis of 2a-e followed by the desulfurization of the resulting 3-methylthio-2-(4-hydroxyphenyl)benzofurans (3a-e). 5-Methyl-3-p-toluoyl-2-[4-(3-diethylaminopropoxy)phenyl]benzofuran (7), a beta-amyloid aggregation inhibitor, was synthesized by three steps starting from 4a.

An efficient synthesis of 5-chloro-3-[4-(3-diethylaminopropoxy)benzoyl]-2-(4-methoxyphenyl)benzofuran (8), a potent beta-amyloid aggregation inhibitor, is described. 5-Chloro-2-(4-methoxyphenyl)benzofuran (3) was obtained by the one-pot synthesis of 4-chlorophenol with omega-(methylsulfinyl)-p-methoxyacetophenone (1) under Pummerer reaction conditions, and it was followed by the desulfurization of the resultant 5-chloro-3-methylthio-2-(4-methoxyphenyl)benzofuran (2e). Acylation of benzofuran 3 with 4-(3-bromopropoxy)benzoyl chloride (6) gave the ketone 7, which was converted into compound 8 by the treatment of diethylamine.