: Genome-wide association study for crohn’s disease in the quebec

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M, Hardt WD: Role of the salmonella pathogenicity island 1 effector proteins sipa, sopb, sope, and sope2 in salmonella enterica subspecies 1 serovar typhimurium colitis in streptomycin-pretreated mice. Infection and Immunity 2004,72(2):795–809.PubMedCrossRef 35. Liao AP, Petrof EO, Kuppireddi XL184 S, Zhao Y, Xia Y, Claud EC, Sun J: Salmonella type iii effector avra stabilizes cell tight junctions to inhibit inflammation in intestinal epithelial cells. Plos One 2008,3(6):E2369.PubMedCrossRef 36. Wang X, D’Andrea AD: The interplay of fanconi anemia proteins in the dna damage response. Dna Repair (Amst) 2004,3(8–9):1063–1069.CrossRef 37. Meetei AR, Yan Z, Wang W: Fancl replaces brca1 as the likely ubiquitin ligase responsible for fancd2 monoubiquitination. Cell Cycle 2004,3(2):179–181.PubMedCrossRef 38. Fei P, Yin J, Wang W: New advances

in the dna damage response network of fanconi anemia and brca proteins. faap95 replaces brca2 as the true fancb protein. Cell Cycle 2005,4(1):80–86.PubMedCrossRef 39. Dey BR, Spence SL, Nissley P, Furlanetto Sulfite dehydrogenase RW: Interaction of human suppressor of cytokine signaling (socs)-2 with the insulin-like growth factor-i receptor. The Journal of Biological Chemistry 1998,273(37):24095–24101.PubMedCrossRef 40. Hilton DJ, Richardson RT, Alexander WS, Viney EM, Willson TA, Sprigg NS, Starr R, Nicholson SE, Metcalf D, Nicola NA: Twenty proteins containing a c-terminal socs box form five structural classes. Proc Natl Acad Sci USA 1998,95(1):114–119.PubMedCrossRef 41. Chen XP, Losman JA, Rothman P: Socs proteins, regulators of intracellular signaling. Immunity 2000,13(3):287–290.

The nature of these compounds

is still unknown, but dival

The nature of these compounds

is still unknown, but divalent anions such as sulfates are suspected. As seen in previous work with other mutacins, purification yields were low (Table 1) and additional chromatographic steps will be necessary to improve yields and purity. The higher concentration of methanol used to recover mutacin D-123.1 suggests that the peptide is more hydrophobic than mutacin F-59.1. Collected samples of pure mutacin D-123.1 were very viscous because they probably retain part of the polymeric sugars from the agarose. However, with the methods used here, sufficient amounts of the substances were collected to carry out a preliminary characterisation of the peptides but the evaluation of their antibacterial TH-302 in vivo spectrum was somewhat Buparlisib chemical structure Selleck CB-5083 restricted. The sequence of mutacin F-59.1 (25 residues) was shorter than the

generally recognised size for pediocin-like bacteriocins which is between 37 and 48 residues [2, 13]. This may be due to peptidase activity of the strain. Fifty three peptidases or peptidase homologues are found in the genome of S. mutans UA159 using the MEROPS database [17, 18]http://​merops.​sanger.​ac.​uk. The pediocin-like bacteriocin sequence could thus be a substrate in its 25th position for many of these peptidases. MALDI-TOF MS analysis revealed a major peak with an isotopic mass [M+H]+ of 2720 Da for mutacin F-59.1 (Figure 4). This mass represents the lowest reported mass for an active naturally-produced

pediocin-like bacteriocin after the study of Bhunia et al. [19]. The length of mutacin F-59.1 was sufficient to confer antimicrobial activity against several bacterial genera including Bacillus spp., Enterococcus spp., Lactococcus spp., Micrococcus spp., Listeria spp., and Streptococcus spp. (Table 2). Salvucci et al. [20] eltoprazine reported activity of short peptides derived from the NH2-terminus of enterocin CRL35 and other class IIa bacteriocins, suggesting that the C-terminus of pediocin-like bacteriocins is not essential for their inhibitory activity. Also, an active antimicrobial region in the NH2-terminus of this class of bacteriocin was identified by a bioinformatic approach [21]. The C-terminus section is known to confer specificity in the activity spectra of class IIa bacteriocins and to interact with their cognate immunity proteins [22]. Pediocin-like bacteriocins are unstructured in an aqueous solution and become structured when in contact with membrane-mimicking entities [2]. The electrostatic distribution along the molecule is highly polarized with most of the cationic residues concentrated in the N-terminal region.

The results proved that miR-19a acted as an oncogenic miRNA in bl

The results proved that miR-19a acted as an oncogenic miRNA in bladder cancer and the up-regulation of miR-19a in bladder tissues would lead to unlimited cell proliferation. Figure 2 Enforced expression of miR-19a promotes bladder cancer cell growth and colony formation. (A) Overexpression of miR-19a in RT4 cells was confirmed by qRT-PCR. (B) The cell growth of RT4 cells at 0, 1, 2, 3, 4 days post transfection which was detected by CCK-8 assay. (C) Overexpression of miR-19a in TCCSUP cells was confirmed by qRT-PCR. (D) The cell growth of

Salubrinal TCCSUP cells at 0, 1, 2, 3, 4 days post transfection which was detected by CCK-8 assay. (E) The colony number of RT4 cells per well in 6-well Veliparib mw plates cultured for 7 days. (F) The colony number of TCCSUP cells per well in 6-well plates cultured for 7 days. Data are shown as mean + s.d. (n = 3); * indicates P-value < 0.05; ** indicates P-value < 0.01; *** indicates P-value < 0.001. Attenuated expression of miR-19a in bladder cancer cells can inhibit cell growth and colony formation To further confirm the oncogenic role of miR-19a in bladder carcinogenesis, we suppressed the expression of miR-19a in the two bladder cancer cell lines J82 and HT1376 which had higher expression of miR-19a than the other bladder cancer cell lines. Successful repression of miR-19a Selleck Ro 61-8048 in the two bladder cancer cell lines was

confirmed by q-PCR (Figure 3A, C). As demonstrated by CCK-8 growth assays, repression of miR-19a reduced cell proliferation in both the two cell lines, whereas the scramble control had no effect on cell proliferation compared with the untreated cells (Figure 3B, D). As demonstrated by the colony formation assay, repression of miR-19a also significantly decreased the colony number of J82 and HT1376 cells, whereas the scramble control had little effect on the colony number compared with the untreated cells (Figure 3E, F). The results proved that miR-19a might Bay 11-7085 act as an oncogenic miRNA in bladder cancer again. Figure 3 Attenuated expression of miR-19a in bladder cancer

cells can inhibit cell growth and colony formation. (A) Repression of miR-19a in J82 cells was confirmed by qRT-PCR. (B) The cell growth of J82 cells at 0, 1, 2, 3, 4 days post transfection which was detected by CCK-8 assay. (C) Repression of miR-19a in HT1376 cells was confirmed by qRT-PCR. (D) The cell growth of HT1376 cells at 0, 1, 2, 3, 4 days post transfection which was detected by CCK-8 assay. (E) The colony number of J82 cells per well in 6-well plates cultured for 7 days. (F) The colony number of HT1376 cells per well in 6-well plates cultured for 7 days. Data are shown as mean + s.d. (n = 3); * indicates P-value < 0.05; ** indicates P-value < 0.01; *** indicates P-value < 0.001. miR-19a plays its oncogenic role in bladder cancer through targeting PTEN We further dissected the mechanism of miR-19a functioning as an oncogenic miRNA in bladder cancer.

Blood was withdrawn for determination of TNFα after 1 and 2 weeks

Blood was withdrawn for determination of TNFα after 1 and 2 weeks of treatments. Animals were sacrificed after 2 weeks and a 10 % W/V liver homogenate was assayed for both parameters. Data represent the mean ± SEM of each group; n = 8. Symbols indicate significance against VPA-treated group (asterisks) and normal control group (dollar symbols), DHA docosahexaenoic

acid, TNFα tumor necrosis factor alpha, VPA valproate Figure 4 represents necropsies of the liver to assess the pathological changes in the studied Androgen Receptor signaling pathway Antagonists animals. The negative control group showed average size and color of the liver with no detected histopathologic abnormalities (photos 1, 2). Conversely, the VPA-treated group showed grossly enlarged pale livers with significantly increased weights over control values. Besides, multiple foci of focal lytic necrosis were detected in which replacement by both inflammatory cells and cellular degeneration had occurred (photo 3). Moreover, combined macrovesicular and AG-881 microvesicular steatosis were evident in the periportal zone of four animals (out of six) of this group (photo 4). Concurrent treatment with DHA significantly alleviated the hepatic cellular

and molecular anomalies entailed by VPA treatment. This was manifested as reduced serum liver enzymes (better PRIMA-1MET chemical structure after 1 than 2 weeks), lipid peroxide generation, and increased levels of hepatic GSH and serum albumin, consonant with promoted liver defensive mechanisms and enhanced protein synthesis. Furthermore, when combined with VPA, DHA showed only minimal small focal necrosis/apoptosis (single cell death) with no evidence of degeneration or steatosis (photo 5); consistent with amelioration of pathologic anomalies by DHA. Fig. 4 Necropsies of the liver of studied animals from each group selleck products to assess the pathologic changes. Photos 1, 2 are for the negative control group, showing average size/color of the liver with no detected histopathologic abnormalities. Photo 3: VPA control group showing grossly enlarged pale livers with multiple foci of focal lytic necrosis with replacement by inflammatory cells and hepatocyte degeneration. Also, combined macrovesicular

and microvesicular steatosis occurring in the periportal zone were evident in four animals in this group (photo 4). DHA when combined with VPA showed only minimal small focal necrosis with no evidence of degeneration (photo 5). DHA docosahexaenoic acid, VPA valproate Because DHA recently demonstrated some neuroinhibitory effects on its own [18], it was of current interest to also seek possible synergy with anticonvulsant effects of VPA. Figure 5 shows that DHA elicited a dose-responsive increase in latency (onset) of mouse tonic convulsions, with significance from control value elicited at (250 mg/kg, p < 0.05), a response that was also comparable to that evoked by VPA at its ED50 dose (13.8 vs 14.9 min). Combining the two FAs at such lower doses triggered a notable synergy in the latency of convulsion (32.8 min, p < 0.05).

Biochem Biophys Res Commun 2001, 284:57–64 PubMedCrossRef 37 Gao

Biochem Biophys Res Commun 2001, 284:57–64.PubMedCrossRef 37. Gao H, Wang Y, Liu X, Yan T, Wu L, Alm E, Arkin A, Thompson DK, Zhou J: Global transcriptome analysis of the heat shock response

of Shewanella oneidensis . J Bacteriol 2004,186(22):7796–7803.PubMedCrossRef 38. Ingram VM: Gene evolution and the haemoglobins. Nature 1961,4(189):704–708.CrossRef 39. #Autophagy Compound Library cell line randurls[1|1|,|CHEM1|]# Graf PCF, Jakob U: Redox-regulated molecular chaperones. Cell Mol Life Sci 2002, 59:1624–1631.PubMedCrossRef 40. Gustavsson N, Kokke BP, Anzeilius AB, Boelens WC, Sundby C: Substitution of conserved methionines by leucines in chloroplast small heat shock protein results in loss of redox-response but retained chaperone-like PCI-34051 activity. Protein Sci 2001, 10:1785–1793.PubMedCrossRef 41. Fu X, Zhang H, Zhang X, Cao Y, Jião W, Liu C, Song Y, Abulimiti A, Chang Z: A dual role for the N-terminal region of Mycobacterium tuberculosis Hsp 16.3 in self-oligomerization and binding denaturing substrate proteins. J Biol Chem 2005, 280:6337–6384.PubMedCrossRef 42. Usui K, Hatipoglu OF, Ishii N, Yohda M: Role of the N-terminal

region of the crenarchaeal sHSP, Sthsp14.0, in thermal-induced disassembly of the complex and molecular chaperone activity. Biochem Biophys Res Commun 2004, 315:113–118.PubMedCrossRef 43. Goldenberg O, Erez E, Nimrod G, Ben-Tal N: The ConSurf-DB: pre-calculated evolutionary conservation profiles of protein structures. Nucleic Acids Res 2009, 37:D323-D327.PubMedCrossRef STK38 Authors’ contributions All authors have read and approved the final manuscript. DAR and LMMO conceived the idea and designed the experiments. DAR and LFCF executed the RTq-PCR experiments. DAR wrote the manuscript. RV performed the bioinformatics analysis; LEVDB, the phylogenetic analysis; and MTM, the molecular modeling.”
“Background Bacteria, especially pathogenic bacteria, must deal with a very hostile environment on a nearly continuous basis. How pathogenic bacteria first respond to this environment

and lethal environmental stressors is a key element in their survival. Based on their initial response, either the pathogen may succumb and die, or it can respond and live despite its hostile surroundings. Long-term adaptive bacterial responses to antimicrobials include well-characterized mechanisms of expressing an altered version of the antibiotic target, enzymes to degrade the antibiotic, and transporters to remove the antibiotic [1]. Here, we consider the time immediately after the first exposure to a threat and before activation of long-term adaptive resistance to stressors. Understanding how bacteria mount this initial defense against stresses is critical to understanding how bacteria respond to, and survive, hostile environments.

α-IPMS-14CR, with the additional 12 copies of the repeat units, i

α-IPMS-14CR, with the additional 12 copies of the repeat units, is ~30% larger than α-IPMS-2CR. The lower Km (higher affinity for substrates) of α-IPMS-14CR is more difficult to understand. A report on the cystine protease CPB isoforms of Leishmania mexicana showed that variation in a few charged amino acid residues located outside of but close to the active site may influence

SB525334 cost the electrostatic potential on the surface of the proteins, resulting in different Km values [22]. In the case of α-IPMS-14CR, although the segment of the protein that includes the 14 copies of the repeat units is located in the C-terminal domain, it may come into close proximity with the active site due to its huge size. The amino acid composition of the repeat units may also be important. Since seven of the 19 residues in the repeat unit are hydrophilic and charged (Figure 5), they could affect

the electrostatic potential on the surface of the enzyme and, therefore, the enzyme’s affinity for its substrates. Figure 5 Amino acid sequence of α-IPMS containing two copies of the VNTR. The N-terminal domain (catalytic domain), residues 51–368, is colored red. Residues involved in substrate (α-KIV) binding are underlined: D81, H285, H287, N321, E309 and G320. The conserved GxGERxG motif (residues 314–320, H379 and Y410), which forms a groove possible for acetyl CoA binding, is this website underlined. Linker domain: subdomain I (residues 369–424) is colored blue; subdomain II (residues 434–490) is colored magenta. The C-terminal regulatory Thiazovivin in vitro domain (residues 491–644) is colored green. The two copies (one copy contains 19 amino acids, vtiaspaqpgeagrhasdp, at residues 575–612) of the repeat sequence are underlined. The hydrophilic and charged residues

are in bold. Residues involved in leucine binding are indicated in bold italics: L535, A536, V551, Y554, A565 and A567. 6-phosphogluconolactonase Mutation of residues G531, G533 and A536 (underlined) abolished feedback inhibition of α-IPMS in S. cerevisiae. The Y410F mutant form of M. tuberculosis α-IPMS was insensitive to feedback inhibition. The mechanism of l-leucine inhibition was suggested to be a slow-onset inhibition (time-dependent) [19]. After a rapid formation of an initial inhibitory complex (leucine binds to the regulatory domain), isomerization of the complex occurs, leading to a tightly bound complex. Evidence confirmed that an inhibitory signal is transmitted through the linker domain to the catalytic domain, as the Tyr410Phe mutant form of M. tuberculosis α-IPMS is insensitive to l-leucine feedback inhibition [23]. Mutations that abolish l-leucine feedback inhibition in S. cerevisiae α-IPMS are clustered around residues surrounding the l-leucine binding site (amino acids Leu-535, Ala-536, Val-551, Tyr-554, Ala-558, Ala565 and Ala-567; Figure 5) [9].

J Clin Endocrinol Metab 95:134–142CrossRef 22 Burt-Pichat B, Laf

J Clin Endocrinol Metab 95:134–142CrossRef 22. Burt-Pichat B, Lafage-Proust

MH, Duboeuf F, Laroche N, GSK3235025 Itzstein C, Vico L, Delmas PD, Chenu C (2005) Dramatic decrease of innervation density in bone after ovariectomy. Endocrinology 146:503–510PubMedCrossRef 23. Jeyabalan J, Shah M, Viollet B, Roux JP, Chavassieux P, Korbonits M, Chenu C (2012) Mice lacking AMP-activated protein kinase (AMPK)-alpha 1 catalytic subunit have increased bone remodeling and modified skeletal responses to hormonal challenges induced by ovariectomy and intermittent PTH treatment. J Endocrinol 214:349–358PubMedCrossRef 24. Harrison LJ, Cunningham JL, Stromberg L, Goodship AE (2003) Controlled induction of a pseudarthrosis: a study using a rodent model. J Orthop Trauma 17:11–21PubMedCrossRef 25. Amanat N, McDonald M, Godfrey C, Bilston L, Little D (2007) Optimal timing of a single dose of selleck chemicals zoledronic acid to increase strength in rat fracture

repair. J Bone Miner Res 22:867–876PubMedCrossRef 26. Chappard D, Palle S, Alexandre C, Vico L, Riffat G (1987) Bone embedding in pure methyl methacrylate at low temperature preserves enzyme activities. Acta Histochem 81:183–190PubMedCrossRef 27. Chavassieux selleck products PM, Arlot ME, Reda C, Wei L, Yates AJ, Meunier PJ (1997) Histomorphometric assessment of the long-term effects of alendronate Rapamycin on bone quality and remodeling in patients with osteoporosis. J Clin Invest 100:1475–1480PubMedCrossRef 28. Parfitt AM, Drezner MK, Glorieux FH, Kanis JA, Malluche H, Meunier PJ, Ott SM, Recker RR (1987) Bone histomorphometry: standardization of nomenclature, symbols, and units. Report of the ASBMR Histomorphometry Nomenclature Committee. J Bone Miner Res 2:595–610PubMedCrossRef 29. Zaman G, Sunters A, Galea GL, Javaheri B, Saxon LK, Moustafa A, Armstrong VJ, Price JS, Lanyon LE (2012) Loading-related regulation of transcription factor EGR2/Krox-20 in bone cells is ERK1/2 protein-mediated and prostaglandin, Wnt

signaling pathway-, and insulin-like growth factor-1 axis-dependent. J Biol Chem 287:3946–3962PubMedCrossRef 30. Amini H, Ahmadiani A, Gazerani P (2005) Determination of metformin in human plasma by high-performance liquid chromatography. J Chromatogr B Analyt Technol Biomed Life Sci 824:319–322PubMedCrossRef 31. Kaneb HM, Sharp PS, Rahmani-Kondori N, Wells DJ (2011) Metformin treatment has no beneficial effect in a dose–response survival study in the SOD1(G93A) mouse model of ALS and is harmful in female mice. PLoS One 6:e24189PubMedCrossRef 32. Fryer LG, Parbu-Patel A, Carling D (2002) The anti-diabetic drugs rosiglitazone and metformin stimulate AMP-activated protein kinase through distinct signaling pathways. J Biol Chem 277:25226–25232PubMedCrossRef 33.

Activation of Par6 or overexpression of aPKC regulates formation

Activation of Par6 or overexpression of aPKC regulates formation of tight junctions. On the other hand, cell polarity regulates diverse biological events such as localization of embryonic determinants and establishment of check details tissue and organ architecture [17]. Epithelial cell polarity is known to be regulated by the polarity complex Par6/Par3/aPKC [15]. Polarized epithelial cells maintain an asymmetric composition of their apical and basolateral membrane domains by at least two different

processes [18]. These include I-BET151 in vivo regulated trafficking of macromolecules from the biosynthetic and endocytic pathway to the appropriate membrane domain and prevention of free mixing of membrane domain-specific proteins and lipids by the tight junction. Cdc42, a Rho family GTPase, is known to govern cellular polarity and membrane traffic in several cell types [19, 20]. Expression of dominant-active Cdc42V12 or dominant-negative Cdc42N17 in MDCK cells was found to alter tight junction

function, indicating that Cdc42 may modulate the multiple cellular pathways required for maintenance of epithelial cell polarity [20]. Nucleotide exchange factor ECT2 stimulates guanine nucleotide exchange on RhoA, Rac1, or Cdc42 in vitro [21]. Another study disclosed that ECT2 also associates with this polarity-related complex and regulates aPKC activity. MDCK cells expressing a dominant-negative form of ECT2 are unable to form normal cystic structures with central lumens in three-dimensional collagen gels [22]. Thus, lack of ECT2 ZD1839 manufacturer molecules in renal epithelial cells could disturb normal development in organs including renal tubulogenesis as well as regeneration of renal tubules after injury. However, since genetically engineered animals lacking ECT2 have not been established, the crucial role of

ECT2 for renal tubular function or architecture except for tight junction function remains uncertain. Even before the appearance AZD9291 research buy of glomerular lesions, FSGS shows greater glomerular diameters than does minimal change nephrotic syndrome (MCNS). Also, a tubulointerstitial disorder develops early in FSGS, but generally does not develop in MCNS [22]. In our patients, the number of glomeruli per unit area was normal in early specimens, but glomerular diameter was greater than in age-matched normal specimens. Glomerular enlargement progressed and the number of glomeruli decreased together with the progression of tubulointerstitial lesions in later biopsy specimens. Possibly, deletion of ECT2, which is essential for embryonic development and maintenance of the function of uriniferous tubules, caused tubular dysplasia, and when the tubulointerstitial disorder progressed postnatally after an infection, the renal circulation was disturbed. As the number of glomeruli decreased, hyperfiltration by residual glomeruli induced FSGS lesions [23].

On CMD after 72 h 3–5 mm at 15°C, 0 2–1 5 mm at

25°C; aft

On CMD after 72 h 3–5 mm at 15°C, 0.2–1.5 mm at

25°C; after 2 weeks 7–11 mm at 6–10°C in the dark and 21–25 Epigenetics Compound Library price mm at 15°C; mycelium typically covering the plate after more than a month at 15°C. Colony at 15°C hyaline, thin, indistinctly concentrically zonate, hardly visible; mycelium loose, hyphae hyaline, becoming moniliform and turning reddish brown. Aerial hyphae scant, short, more frequent along the distal margin. Autolytic activity low at 15°C, conspicuous at 25°C; coilings inconspicuous. Diffusing pigment turning the agar yellow, pale or greyish orange to yellow-brown, 4–5A3–5, 6B5–6, beginning in the centre. No distinct odour noted. No chlamydospores noted within a month. Conidiation noted after a month or later at 15°C, gliocladium-like in small white pustules. At 6–10°C colony colourless, sterile, margin becoming downy by long aerial hyphae. On PDA after 72 h 3–4 mm at 15°C, <1 mm at 25°C; after 2 weeks 3–9 mm at 6–10°C in the dark and 9–24 mm at 15°C; mycelium not covering the plate within a month at 15°C. Colony at 15°C first hyaline, thin, dense; becoming downy by long stout aerial hyphae; marginal hyphae sinuous or helical. Autolytic activity moderate at 15°C, conspicuous at 6–10°C; no coilings observed. No distinct odour noted. Plug and colony centre turning bright yellow to orange, 3–4A4–7, 6AB6–7, after a week, changing

to orange-brown to reddish brown, 6–8CD6–8; 9C7–8; hyphae turning red. Conidiation lacking or noted after ca 1 weeks, scant, around the plug,

effuse, spreading, Selleck Poziotinib gliocladium-like, soon degenerating. On SNA after 72 h 1–2 mm at 15°C; after 2 weeks 2–4 mm at 6–10°C in the dark and 10–16 mm at 15°C; mycelium not covering the plate within a month at 15°C. Colony at 15°C hyaline, thin, dense, zonate; margin downy; hyphae with irregular thickenings. Aerial hyphae typically abundant and long in downy distal areas of the colony. Autolytic activity inconspicuous to moderate at 15°C; coilings inconspicuous or frequent. No diffusing pigment, no distinct odour noted. No chlamydospores seen. Conidiation seen after (1–)2–3 weeks at 15°C, first scant and effuse in L-NAME HCl mostly central minute shrubs, becoming visible at the beginning of a broad concentric downy zone as white floccules or tufts 0.5–1.5 mm diam, confluent to 5 mm, and on long branched aerial hyphae, gliocladium-like. Sometimes tufts evenly or irregularly disposed on the colony surface. Tufts fluffy or compact, typically transparent, of a loosely branched reticulum with long main axes and a minutely granular surface caused by whorls of phialides and conidial heads. p38 MAPK signaling Primary branches often paired, terminal branches paired or not. Main axes mostly erect, branched 2–3 fold, with side branches mostly unpaired and inclined upwards in steep angles. Terminal branches emerging in right angles or steeply inclined upwards, at the highest levels often paired, also often in clusters of 2–3.

China Statistics Press, Beijing National Bureau of Statistics (20

China Statistics Press, Beijing National Bureau of Statistics (2004) China statistical yearbook. China Statistics Press, Blasticidin S clinical trial Beijing National Bureau of Statistics (2005) China statistical yearbook. China Statistics Press, Beijing National Bureau of Statistics (2006) China statistical yearbook. China Statistics Press, Beijing

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