They were then used as viral baits against human cDNA libraries. Viral ORFs coding for NS3 and NS5 proteins were isolated from distinct human pathogens belonging to major flavivirus evolutionary lineages: Saracatinib order (i) aedes-borne pathogen: DENV; (ii) culex-borne pathogens: WNV (including the Kunjin Australian variant

(KUNV)) and JEV; (iii) tick-borne pathogens: Tick-borne encephalitis (TBEV) and Alkhurma (ALKV) viruses. Protein sequence comparison study revealed that the functional enzymatic domains of NS3 are highly conserved amongst these viruses (Additional file 2). At least three independent screenings against human cDNA libraries were performed for each viral bait. Eighty-five percent of the identified cellular targets of each bait were then tested pairwise against all the viral proteins baits including the original bait using an array-based Y2H strategy which confirmed 90% of the interactions identified in the initial screens. Furthermore, the bait panel versus selected targets strategy used in the array cross experiment enabled us to identify 69 additional, novel virus-host Idasanutlin cost interactions not detected in the first screen. Repetition and confirmation of our Y2H experiment by the array strategy allowed us to be very stringent in obtaining a high quality set of 108 human proteins that interacted with one

or more of the viral protein baits (Additional file 3). In one of our previously published studies using the same Y2H screening settings, the the validation rate obtained by co-affinity purification reached 85% [12]. We conducted GST-pull down assays to further validate our Y2H data (Additional file 4). An extensive literature curation allowed us to finally complete our set of data by 16 previously published interactions, 15 of which not identified by our screen (Additional file 3). Analysis of the

flavivirus-human protein-protein interaction network Based on our high-throughput Y2H screen and literature search, we created the flavivirus NS3 and NS5 proteins interaction network composed of 186 interactions involving 120 distinct human proteins, 108 from our screen and 13 from the literature (Table 1, Figure 1, additional files 3 and 5). We emphasize that among the 186 interactions, 171 were obtained from our Y2H screen and only 16 from previously published work. Despite the conserved amino acid patterns within the different viral ORFs that we used as viral baits, only one third of the cellular targeted proteins identified in our study interacted with two or more flaviviruses (Table 2). Moreover, only five cellular proteins (CAMTA2, CEP250, SSB, ENO1, and FAM184A) were found to interact with both NS3 and NS5 proteins (Figure 1, additional file 5).

It has been suggested that delays in presentation are responsible for the majority of perforated appendices or the other complications. Malignancy and appendiceal inflammation frequently form SB431542 molecular weight masses which are virtually indistinguishable and surgeons are often challenged to determine

the pathologic origin of masses [5]. There are many reports in the literature that have addressed this promiscuousness, and right hemicolectomy has been recommended because of the concern of possible malignancy [5–8]. The studies were carried out to evaluate the pathologies and surgical management of the inflammatory cecal masses in patients with suspected appendicitis. In this study, we aim to present the diversity of the inflammatory cecal masses mimicking acute appendicitis. Methods and results A series of 3032 patients from suburban who underwent emergency surgery for clinical diagnosis of acute appendicitis at Bagcılar Training and Research Hospital and Okmeydanı Training and Research Hospital between January 2009 and June 2011 were evaluated retrospectively. 48 patients who had right-hemicolectomy

or ileocecal resection for inflammatory cecal masses of uncertain etiology were included in our study. Right-hemicolctomy was performed as formal resection of the right colon including lymphatic drainage along the ileocolic and right colic arteries. The relevant case notes were subsequently retrieved from the medical records and the following data were obtained for each patient: age, gender, time duration between the onset of symptoms and admission BKM120 concentration to hospital, the history and the symptoms of the patient, signs at presentation, results of the imaging methods, type of surgery, pathology results, length of hospital stay and the outcomes. The present study was approval by Okmeydani Training and Research Hospital Ethics Committee.

28 men and 20 women between ages 16–73 years (mean age 43.1) presented with right iliac fossa pain (Table 1). All patients had localized tenderness leading to a preoperative diagnosis of acute appendicitis. None of the patients applied to the surgery department at the onset of symptoms. They generally preferred self-medication and initial consultation with quacks. Based on our experience in this community, it wasn’t surprising VAV2 for us to find out at least 4 days between the onset of symptoms and admission to hospital (Table 2). Table 1 Age range of patients (mean 43,1 years) Age Number of cases % 10-20 4 8,3 20-30 8 16,6 30-40 4 8,3 40-50 12 24,9 50-60 12 24,9 >60 8 16,6 Total 48 100 Table 2 The time between onset of symptoms and admission to hospital Day Number of cases % 0-1 0 0 1-2 0 0 2-3 0 0 3-4 0 0 4-5 6 12,5 5-6 10 20,8 6-7 18 37,5 >7 14 29,2 The major presenting symptoms were pain in the right iliac fossa in 48 (100%), anorexia in 42 (87,5%), nausea and vomiting in 30 (62,5%), fever in 26 patients (54,2%) (Table 3).

Oncol Rep 2004, 12:259–267.PubMed 78. Giaginis C, Davides

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83. Friedman E, Gold LI, Klimstra D, Zeng ZS, Winawer S, Cohen A: High levels of transforming growth factor beta 1 www.selleckchem.com/screening/chemical-library.html correlate with disease progression in human colon cancer. Cancer Epidemiol Biomarkers Prev 1995, 4:549–554.PubMed 84. Mitropoulos D, Kiroudi A, Christelli E, Serafetinidis E, Zervas A, Anastasiou I, Dimopoulos C: Expression of transforming growth factor beta in renal cell carcinoma and matched non-involved renal tissue. Urol Res 2004, 32:317–322.PubMed

85. Santin AD, Hermonat PL, Hiserodt JC, Fruehauf J, Schranz V, Barclay D, Pecorelli S, Parham GP: Differential transforming growth factor-beta secretion in adenocarcinoma and squamous cell carcinoma of the uterine cervix. Gynecol Oncol 1997, 64:477–480.PubMed 86. Walker through RA, Dearing SJ: Transforming growth factor beta 1 in ductal carcinoma in situ and invasive carcinomas of the breast. Eur J Cancer 1992, 28:641–644.PubMed 87. Steiner MS, Zhou ZZ, Tonb DC, Barrack ER: Expression of transforming growth factor-beta 1 in prostate cancer. Endocrinology 1994, 135:2240–2247.PubMed 88. Hazelbag S, Gorter A, Kenter GG, van den Broek L, Fleuren G: Transforming growth factor-beta1 induces tumor stroma and reduces tumor infiltrate in cervical cancer. Hum Pathol 2002, 33:1193–1199.PubMed 89. Halliday GM, Le S: Transforming growth factor-beta produced by progressor tumors inhibits, while IL-10 produced by regressor tumors enhances, Langerhans cell migration from skin. Int Immunol 2001, 13:1147–1154.PubMed 90.

Time to introduce proliferation markers in clinical routine. Lakartidningen 2010, 107:672–675.PubMed 11. Wesierska-Gadek J, Hackl S, Zulehner N, Maurer M, Komina O: Reconstitution of human MCF-7 breast cancer cells with caspase-3 does not sensitize them to action of CDK inhibitors. J Cell Biochem 2011, 112:273–288.PubMedCrossRef 12. Mingo-Sion

AM, Marietta PM, Koller E, Wolf DM, Van Den Berg CL: Inhibition of JNK reduces G2/M transit independent of p53, leading to endoreduplication, FK228 decreased proliferation, and apoptosis in breast cancer cells. Oncogene 2004, 23:596–604.PubMedCrossRef 13. Sachdev D, Zhang X, Matise I, Matise I, Gaillard-Kelly M, Yee D: The type I insulin-like growth factor receptor regulates cancer metastasis independently of primary tumor growth by promoting invasion and survival. Oncogene 2010, 29:251–262.PubMedCrossRef 14. Zeng X, Sachdev D, Zhang H, Gaillard-Kelly M, Yee D: Sequencing of type I insulin-like growth factor

receptor inhibition affects chemotherapy response in vitro and in vivo. Clin Cancer Res 2009, 15:2840–2849.PubMedCrossRef 15. Yanochko GM, Eckhart W: Type I insulin-like growth factor receptor over-expression induces proliferation and anti-apoptotic signaling in a three-dimensional culture model of breast epithelial cells. Breast Cancer Res 2006,8(2):R18.PubMedCrossRef 16. Carvalho I, Milanezi F, Martins A, Reis RM, Schmitt F: Overexpression of platelet-derived growth factor receptor α in breast cancer is associated with tumour progression. Breast Cancer Res 2005, 7:788–795.CrossRef 17. Pasanisi P, Venturelli E, Morelli D, DMXAA order Morelli D Fontana L, Secreto G, Berrino F: Serum insulin-like growth factor-I and platelet-derived (-)-p-Bromotetramisole Oxalate growth factor as biomarkers of breast cancer prognosis. Cancer Epidemiol Biomarkers Prev 2008, 17:1719–1722.PubMedCrossRef 18. Lev DC, Kim SJ,

Onn A, Stone V, Nam DH, Yazici S, Fidler IJ, Price JE: Inhibition of platelet-derived growth factor receptor signaling restricts the growth of human breast cancer in the bone of nude mice. Clin Cancer Res 2005, 11:306–314.PubMed 19. Kang DW, Min do S: Platelet derived growth factor increases phospholipase D1 but not phospholipase D2 expression via NFkappaB signaling pathway and enhances invasion of breast cancer cell. Cancer Lett 2010, 294:125–133.PubMedCrossRef 20. Chiarenza A, Lazarovici P, Lempereur L, Cantarella G, Bianchi A, Bernardini R: Tamoxifen inhibits nerve growth factor-induced proliferation of the human breast cancerous cell line MCF-7. Cancer Res 2001, 61:3002–3008.PubMed 21. Adriaenssens E, Vanhecke E, Saule P, Mougel A, Page A, Romon R, Nurcombe V, Le Bourhis X, Hondermarck H: Nerve growth factor is a potential therapeutic target in breast cancer. Cancer Res 2008, 68:346–351.PubMedCrossRef 22. Dollé L, El Yazidi-Belkoura I, Adriaenssens E, Nurcombe V, Hondermarck H: Nerve growth factor overexpression and autocrine loop in breast cancer cells. Oncogene 2003, 22:5592–5601.PubMedCrossRef 23.

To this end, Vero monolayers were first infected with Chlamydia and later with ca-PEDV, thus the suspected inducer of persistence would be introduced after chlamydial infection and differentiation into RBs. Simultaneous infection of Chlamydia and ca-PEDV has been performed earlier [12], but did not result in persistent infection in our preliminary experiments (data not shown) and was not considered further as interference https://www.selleckchem.com/products/Y-27632.html of chlamydial infection and concurrent viral uptake could have influenced the results. Viral infection and subsequent development of syncytia was not affected by co-infection with Chlamydia abortus as demonstrated by

unaltered numbers of syncytia observed in the co-infection experiments. In contrast, viral syncytia formation was dramatically decreased in Vero cells double infected with ca-PEDV and Chlamydia pecorum. If Chlamydia pecorum infection might induce a down regulation of the Selleckchem Antiinfection Compound Library host PEDV receptor needed for syncytium

formation at 14-15 hours post-chlamydial infection, this could produce a reduction in syncytium formation without reducing viral entry or replication – the possible persistence inducer mechanism. Interestingly, chlamydial persistence was more prominent in co-infection with Chlamydia pecorum than with Chlamydia abortus, indicating possible species-specific differences. Limited reports are available for in vitro models of chlamydial persistence from non-Chlamydia trachomatis and Chlamydia pneumoniae strains. Kaltenboeck and Storz (1992) [17] suggested that strain 1710S of Chlamydia PtdIns(3,4)P2 pecorum is highly nutrient dependent and this could elicit aberrant forms. Indeed, aberrant forms of this strain were significantly present in our study. Previously, only limited data have been published on

persistent infection of L cells with an ovine abortion strain of Chlamydia psittaci (current classification: Chlamydia abortus) [18]. It should be noted, that in the latter study, chlamydial persistence was not demonstrated using the characteristic features now associated with the morphology of persistent chlamydial infections. Detailed description of electron microscopic observations on the effects of penicillin on the morphology of Chlamydia psittaci Cal10 in L cells showing aberrant chlamydial stages were published by Matsumoto and Manire [13]. The different occurence of persistent forms in co-infection with Chlamydia abortus and Chlamydia pecorum, respectively, has not been described before. Differences between persistence behaviour are already known (reviewed by Hogan et al., 2004) [1] not only between different chlamydial species but also between different serovars and strains of Chlamydia pneumoniae and Chlamydia trachomatis, respectively. The fact that Chlamydia pecorum strain 1710S is an original swine isolate whereas Chlamydia abortus strain S26/3 originates from a sheep abortion and, thus, from another animal species could have an impact but needs further investigation.

Trib., Middle Cypress Creek at power line, Pigg rd., Wayne Co., TN, −87.75489N, 35.04084W 2/2/07   22. Trib., Middle Cypress Creek, E Gilchrest rd. and Pigg rd., Wayne Co., TN, −87.76449N, 35.04931W 3/11/07   23. Trib., Middle Cypress Creek, Dodd rd. and Gilchrest rd., Wayne Co., TN, −87.86627N, 35.05294W

3/11/07, 8/4/08   24. Trib., Middle Cypress Creek, Dodd rd., Wayne Co., TN, −87.77062N, 35.0555W 3/10/07   *25. Trib., Middle Cypress Creek, Wayne Co., TN, −87.77153N, 35.06171W 133 Slackwater Darters collected, 3/3/01 141 Slackwater Darters collected, Pifithrin-�� purchase 3/10/01 41 Slackwater Darters collected, 3/13/01 37 Slackwater Darters collected, 3/9/02 42 Slackwater Darters collected, 3/16/02 20 Slackwater Darters collected, 2/2/07 17 Slackwater Darters collected, 2/28/08 25 Slackwater Darters collected, 8/5/08 6 Slackwater Darters collected, 7/11/12 5 Slackwater Darters collected, 1/25/13   26. Cypress Creek, co rd. 16, Lauderdale Co., AL, −87.73547N, 34.86030W 8/1/07, 8/4/08   27. Cypress Creek, co rd. 10, Lauderdale

co., AL −87.814652N, 34.990676W 6/27/12   28. Middle Cypress Creek, co rd. 8, Lauderdale Co., AL, −87.75691N, 34.94247W 8/1/07   29. Greenbrier Branch, co rd. 8, Lauderdale Co., AL, −87.76386N, 34.942530W 3/17/02, 8/1/07   30. Greenbrier Branch at co rd. 10 Lauderdale Co., AL, −87.79357N, selleck screening library 34.59002W 1/26/13   31. Trib., Cypress Creek, Natchez Trace Parkway, Wayne Co., TN, −87.8207N, 35.0158W 8/4/08   *32. Trib., Middle see more Cypress Creek, Dodd rd., Wayne Co., TN, −87.772N, 35.0592W 1 Slackwater Darter collected, 8/4/08   33. Spain Branch, Gilchrest rd., Wayne Co., TN −87.74900N, 35.06041W 1/26/13   *34. Little Shoal Creek, Dooley rd., Lawrence Co., TN, −87.28507N, 35.32787W 5 E. boschungi, 3/9/02 2/2/07, 8/1/07. 2/28/08, 8/5/08, 7/10/12   35. Little Shoal Creek, Beasley rd., Lawrence Co., TN, −87.32202N, 35.28657W 8/1/07, 8/5/08   36. Little Shoal Creek at Hwy 43, Lawerence Co., TN −87.296021N, 35.32.0327W 7/10/12

  37. Chief Creek at Hwy 240, Lawrence Co., TN −87.425400N, 35.372783W 3/9/02, 1/26/13   38. Round Island Creek, 2.0 mi N Athens, Limestone Co., AL, −87.00705N, 34.81326W 2/23/07   39. Collier Branch, Bean rd. just E I65, Limestone Co., AL, −86.93085N, 34.84381W 2/23/07, 3/27/08, 2/8/13   40. Swan Creek, Piney Chapel rd., Limestone Co., AL, −86.96057N, 34.84842NW 1/26/01, 3/4/01, 3/17/02, 2/23/07, 8/2/07, 8/6/08, 7/10/12   41. Swan Creek, Huber rd., Limestone Co., AL, −86.9697N, 34.86986W 2/23/07, 8/5/08, 7/10/12, 2/8/13   42. Roadside ditch (Swan Creek drainage), co rd. 55, Limestone Co., AL, −86.97186N, 34.8786W 2/23/07   43. Roadside seep (Swan Creek drainage), co rd. 80, Limestone Co., AL, −86.95825N, 34.88084W 2/23/07   44. Trib., Swan Creek at Linton drive Limestone Co., AL −86.92570N, 34.8130W 2/8/13   *45.

Recently, while this manuscript FK866 nmr was in review, a closed E. faecium genome was published by Lam et al. using the ST17 isolate Aus0004, which was isolated from the bloodstream of a patient in Melbourne, Australia [37]. In this study, we report the closed genome of the US E. faecium endocarditis isolate TX16 (DO), and a comparative analysis of this strain’s genome with 21 other available E. faecium draft genomes [32, 38], as well as the recently published

Aus0004 [37]. Due to the fact the TX16 genome has been used in multiple pathogenesis studies and is a part of the clonal group representing the majority of clinical strains globally [2, 5, 30, 36], the complete genome sequence of E. faecium TX16 will facilitate future research by providing a critical starting point for genome-wide functional studies to determine the molecular basis of pathogenesis and to EPZ-6438 concentration further understand the evolution and molecular epidemiology of E. faecium infective strains. Results E. faecium TX16 general genome features The E. faecium TX16 genome consists of one chromosome and three plasmids. The chromosome (Figure 1) contains 2,698,137 bp with 2,703 protein-coding ORFs,

62 tRNAs, 6 copies of ribosomal rRNA and 32 other non-coding RNAs (Table 1). The chromosome has a GC content of 38.15%, and it shows a clear GC skew at the origin of replication (Figure 1). The sizes of the three plasmids (pDO1, pDO2, and pDO3) are 36,262, 66,247 and 251,926 bp, encoding 43, 85, and 283 ORFs, respectively (Table 1). Figure 1 Circular map of the E. faecium TX16 genome. Tracks from inside to outside

are as follows: GC skew (G-C)/(G + C), GC mafosfamide content, forward and reverse RNA, reverse genes, and forward genes. Table 1 General features of E. faecium TX16 genome Features Chromosome Plasmid pDO1 Plasmid pDO2 Plasmid pDO3 Size (bp) 2698137 36262 66247 251926 G + C % 38.15 36.51 34.38 35.97 ORFs 2703 43 85 283 rRNA operons 6 0 0 0 tRNAs 62 0 2 0 ncRNAs 32 1 0 0 To investigate the conservation of the gene order of E. faecium compared to its close relative E. faecalis, a BLASTP alignment of all the predicted proteins from the TX16 and V583 genomes was performed followed by ORF synteny analysis using DAGchainer [39]. The result showed that E. faecium TX16 gene order is very different from that of E. faecalis strain V583 (and therefore OG1RF, which has a very similar synteny to V583 [40, 41]) and all ORF synteny blocks were relatively short (Additional file 1: Figure S1). Interestingly, when comparing TX16 to the closed genome Aus0004, which was published while this paper was in review, Mauve genome alignment analysis resulted in 5 locally collinear blocks for both TX16 and Aus0004 ranging from 33,563–836,291 bp for TX16 and 32,326–905,025 bp for Aus0004 (Additional file 2: Figure S2). The two isolates had very similar synteny, although two regions found in TX16 were inverted in Aus0004.

Figure 4 Representation of COG categories among the core genome. Relative representation of COG categories in the whole genome (hatched bars) compared to the core genome (black bars) of S.

suis strain P1/7. Representation is calculated as the percentage of genes per COG category compared to the total number of genes in the genome. COG categories: J translation, ribosomal structure and biogenesis; K transcription; L replication, recombination and repair; D cell cycle control, cell division, chromosome partitioning; V defense mechanisms; O posttranslational GPCR Compound Library cell assay modification, protein turnover, chaperones; M cell wall/membrane/envelope biogenesis; N cell motility; U intracellular trafficking, secretion, and vesicular transport; T signal transduction mechanisms; C energy production and conversion; P inorganic ion transport and metabolism; G carbohydrate transport and metabolism; E amino acid Trichostatin A research buy transport and metabolism; F nucleotide transport and metabolism; H coenzyme transport and metabolism; I lipid transport and metabolism; Q secondary metabolites biosynthesis, transport and catabolism; R general function prediction only; S function unknown; ‘other’ no COG category attached. Discussion Comparative genome hybridization (CGH) was used to study genetic heterogeneity among a collection of 55 S. suis isolates. S. suis isolates were assigned to two clusters (A

and B). CGH data was compared with MLST and pulse field gel electrophoresis (PFGE) [6] and amplified fragment length polymorphism (AFLP)[25]. In general there was a lot of congruence between typing methods. The discriminatory power of CGH is larger than that of MLST analysis, since isolates that belong to MLST CC1 can be divided into subclusters using CGH. Moreover, Vietnamese isolates that belong to different pulse field types, were assigned to the same CGH subcluster [6]. This could be explained by genomic inversions and substitutions, that were observed in the genome of the Vietnamese reference strain BM407 in comparison to P1/7 [7]. Sitaxentan These changes can be discriminated by PFGE,

but not by CGH. To correlate virulence of isolates to CGH results, virulence of serotype 1 and serotype 9 isolates was determined in an experimental infection. For serotype 1, our animal experiment showed that in contrast to the field isolates, the reference strain was not highly virulent. Since serotype 9 only induced clinical symptoms at very high doses, we concluded that serotype 9 isolates were avirulent under experimental conditions. This was confirmed by other studies [32, 33]. To correlate virulence to CGH data, distribution of 25 putative virulence genes among S. suis isolates was studied. Each CGH cluster was shown to be associated with a specific profile of putative virulence genes. Cluster A isolates contained all 25 putative virulence genes.

Conclusions We demonstrate that immunization with Daporinad a replication-defective

and dominant-negative HSV-1 recombinant CJ9-gD expressing high levels of gD can induce strong cross-protective immunity against primary and recurrent HSV-2 genital infection and disease in guinea pigs. We show further that the latent viral load of challenge wild-type HSV-2 is significantly reduced in immunized guinea pigs compared with the mock-immunized controls. Collectively, CJ9-gD represents a new class of HSV-1 recombinant, which is avirulent, unable to establish detectable latent infection in vivo, and serves as an effective vaccine against genital HSV infection and disease in both mice and guinea pigs. Methods Animals Female Hartley guinea pigs (300-350 g) were obtained from Charles River Breeding Laboratories (Wilmington, MA). The described animal experiments were conducted according to the protocols approved by the Harvard Medical Area Standing Committee on Animals and the American Veterinary Medical Association. The Harvard Medical School animal management program is accredited www.selleckchem.com/products/AZD6244.html by the Association for Assessment and Accreditation

of Laboratory Animal Care (AAALAC) and meets National Institutes of Health standards as set forth in “”The Guide for the Care and Use of Laboratory Animals”" (National Academy Press, 1996). Cells and viruses African Green Monkey Kidney (Vero) cells and RUL9-8 cells, a cell line derived from U2OS cells expressing UL9 and the tetracycline repressor (tetR), were grown and maintained in DMEM growth medium as previously described [33]. Wild-type HSV-2 MS strain (ATCC, Manassas, VA) was propagated and plaque assayed on Vero cells. CJ9-gD was derived from CJ83193 by replacing the essential UL9 gene with the HSV-1 gD gene driven by the tetO-containing hCMV major immediate-early promoter [27]. CJ83193 is a replication-defective virus, in which both copies of the HSV-1 ICP0 gene were replaced by DNA sequences encoding the dominant-negative HSV-1 polypeptide UL9-C535C

under control of the tetO-bearing hCMV major immediate-early promoter [25]. CJ9-gD was propagated and plaque assayed in RUL9-8 cells. Immunization and challenge Amisulpride One set of 8 guinea pigs and one set of 10 guinea pigs were randomly assigned to 2 groups. Animals were either mock-immunized with DMEM (n = 10) or immunized with 5 × 106 PFU of CJ9-gD (n = 8) in a volume of 50 μl s.c. in the right and left upper flank per guinea pig. On day 21 after primary immunization, animals were boosted. At the same time and one day prior to viral challenge, serum was obtained from saphenous veins and stored at -80°C. Six weeks after the initial immunization, the animals were preswabbed with a moist sterile calcium alginate swab (Fisher Scientific, Waltham, MA) and inoculated intravaginally with 100 μl of culture medium containing 5 × 105 PFU of HSV-2 strain MS.

Coelogyne rochussenii √ √ √ 48. Coelogyne septemcostata**     √ 49. Coelogyne

trinervis   √ √ 50. Coelogyne velutina √   √ 51. Corymborkis veratrifolia √ √ √ 52. Crepidium calophyllum   √   53. Cryptostylis arachnites √ √ √ 54. Cymbidium finlaysonianum √ √ √ 55. Cymbidium haematodes**     √ 56. Dendrobium aloifolium √ √ √ 57. Dendrobium anosmum   √ √ 58. Dendrobium bancana   √ √ 59. Dendrobium Nutlin3a bifarium √ √ √ 60. Dendrobium concinnum   √ √ 61. Dendrobium convexum**     √ 62. Dendrobium crumenatum √ √ √ 63. Dendrobium excavatum   √   64. Dendrobium farmeri   √   65. Dendrobium grande √ √ √ 66. Dendrobium leonis √ √ √ 67. Dendrobium metrium   √   68. Dendrobium pachyphyllum √ √   69. Dendrobium plicatile   √ √ 70. Dendrobium sanguinolentum √ √ √ 71.

Dendrobium secundum √ √ √ 72. Dendrobium singaporense   √   73. Dendrobium sinuatum √ √ √ 74. Dendrobium subulatum √ √   75. Dendrobium villosulum √ √   76. Dendrobium xantholeucum √ √   77. Dienia ophrydis √ √ √ 78. Dipodium pictum   √ √ 79. Dipodium scandens   √ √ 80. Eria neglecta √ √ √ 81. Eria nutans √ √ √ 82. Eria ornata   √ √ 83. Erythrorchis altissima √ √   84. Eulophia andamanensis   √ √ 85. Eulophia spectabilis √ √ √ 86. Galeola nudifolia √ √   87. Geodorum citrinum √ √ √ 88. Geodorum densiflorum √ √   89. Goodyera https://www.selleckchem.com/pharmacological_MAPK.html viridiflora   √ √ 90. Grammatophyllum speciosum √ √ √ 91. Habenaria rhodocheila   √ √ 92. Hetaeria nitida   √   93. Hetaeria obliqua √ √   94. Hetaeria oblongifolia   √ √ 95. Lepidogyne longifolia**     √ 96. Liparis barbata**     √ 97. Liparis maingayi √ √ √ Mannose-binding protein-associated serine protease 98. Ludisia discolor √ √   99. Luisia curtisii √ √   100. Macodes petola   √   101. Nervilia plicata   √   102. Nervilia punctata √ √   103. Neuwiedia veratrifolia √ √ √ 104. Neuwiedia zollingeri var. singapureana √ √   105. Oberonia lycopodioides √ √ √ 106. Oberonia pumilio   √   107. Odontochilus uniflorus √ √   108. Paphiopedilum callosum var. sublaeve √ √   109. Peristylus lacertifer √ √   110. Pinalia maingayi √ √   111. Podochilus tenuis √ √

√ 112. Polystachya concreta √ √ √ 113. Renanthera elongata √ √ √ 114. Robiquetia spathulata √ √ √ 115. Spathoglottis plicata √ √ √ 116. Stichorkis elegans √ √ √ 117. Stichorkis viridiflora √ √   118. Taeniophyllum pusillum √ √   119. Tainia maingayi √ √   120. Tainia wrayana   √ √ 121. Thelasis micrantha √ √   122. Thrixspermum amplexicaule √ √ √ 123. Thrixspermum centipeda √ √ √ 124. Thrixspermum duplocallosum**     √ 125. Thrixspermum trichoglottis √ √ √ 126. Thrixspermum.calceolus √ √ √ 127. Trichoglottis cirrhifera √ √ √ 128. Trichotosia ferox √ √ √ 129. Trichotosia gracilis √ √ √ 130. Trichotosia rotundifolia   √   131. Trichotosia velutina √ √   132. Vanilla griffithii √ √ √ 133. Ventricularia tenuicaulis √ √ √ 134. Zeuxine affinis √ √ √ 135. Zeuxine parvifolia   √   136.