All seal isolates included in the current study (n = 6) had serotype Ia, suggesting buy Target Selective Inhibitor Library a human origin. In humans, ST23 is common as vaginal-rectal carrier strain in adults although it may also cause neonatal invasive disease [1, 13]. Given the predominant niche of ST23 in humans, it is conceivable that its presence in seals is due to microbial contamination of surface water. ST23 probably has the broadest known host range of all S. agalactiae STs. Both homeothermic and poikilothermic

species can be affected, including humans, cattle, dogs, crocodiles and seals [6, 14, 15]. Despite the high prevalence of ST23 in humans, its wide host range and its ability to affect aquatic mammals and semi-aquatic reptiles, there are no reports on occurrence of ST23 in fish. This may reflect the relatively www.selleckchem.com/products/Trichostatin-A.html small number of fish isolates characterized to date or it may indicate true biological differences, e.g. an inability to infect fish. Challenge studies using ST23 are required to assess its ability to cause disease in fish. If ST-associated differences in virulence are confirmed, comparative genomic analysis of human,

fish, seal and bovine isolates may help to identify molecular correlates of virulence. S. agalactiae ST260 and ST261 are associated with fish but not with humans The final subpopulation in our collection consisted of non-haemolytic strains of S. agalactiae. Non-haemolytic S. agalactiae may cause invasive disease such as endocarditis in adult humans [42] but no MLST data on non-haemolytic human isolates could be found. The prevalence of non-haemolytic S. agalactiae among carriage isolates has been estimated at 5 to 8%, although this

value may be underestimated in studies that use β-haemolyis as a diagnostic criterion for identification of the organism [43]. All 4��8C non-haemolytic isolates in our collection belonged to serotype Ib, a serotype that has been associated with β-haemolytic and non-haemolytic human isolates [1, 37]. The subpopulation of non-haemolytic serotype Ib isolates in our study encompassed all fish isolates that did not originate from Southeast Asia, suggesting an association between geographic origin and strain. The association with host species and geographic origin is not absolute, as β-haemolytic serotype Ib isolates and ST261 have also been reported from frogs [37, 44] and ST261 has been reported in fish from Indonesia [45]. This is the first report of ST261 in aquarium fish, which originated from Australia. Outbreaks of streptococcosis in wild fish have occurred repeatedly in Australia in the past few years [21]. The isolates causing disease in Queensland grouper and other reef fish were non-haemolytic with serotype Ib, suggesting that they belong to the fish-associated subpopulation of S. agalactiae.

Reddy’s Laboratories Ltd., Hyderabad, India) cRisperdal® tablet (Xian-Janssen Pharmaceutical Ltd., Xi-an, China) On ANOVA, using logarithmic-transformed data, no significant sequence effects, treatment effects, or period effects were observed for any pharmacokinetic property

of risperidone or its active metabolite, 9-hydroxy-risperidone. The 90% CIs of the relative values (test vs. reference) of the ln-transformed Cmax, AUCt, and AUC∞ values are shown in Table 3. For the parent drug, risperidone, these values were 97.0–124.0%, 92.7–115.1%, and 92.8–114.2%, respectively. For the active metabolite, 9-hydroxy-risperidone, these values were 104.4–117.7%, 101.0–113.7%, and 100.4–113.4%, respectively. The two formulations met the predetermined criteria for bioequivalence. In the nonparametric analysis, selleck chemical differences between the formulations did not reach the level of statistical significance in the Wilcoxon signed-rank test with regard to the tmax values for

the two compounds. Table 3 Comparison of the 90% confidence intervals of natural log-transformed pharmacokinetic parameters of the parent drug, risperidone, and its active metabolite, 9-hydroxy-risperidone, following administration of two formulations (testa/referenceb) of risperidone tablets in healthy male Chinese volunteers (n = 24) Compound and parameter Relative value [testa vs. referenceb] (%) 90% CI (%) p values <80% >125% Risperidone  ln Selleck 5-Fluoracil Cmax 111.0 97.0–124.0 0.00001 0.00001  ln AUCt 103.3 92.7–115.1

0.00002 0.003  ln AUC∞ 102.9 92.8–114.2 0.00002 0.002 9-hydroxy-risperidone  ln Cmax 109.8 104.4–117.7 0.00001 0.00002  ln AUCt 107.1 101.0–113.7 0.00001 0.00003  ln AUC∞ 106.7 100.4–113.4 0.00002 0.00001 AUC area under the plasma concentration–time curve, AUC t AUC from time zero to time t, AUC ∞ AUC from time zero to infinity, Thiamet G CI confidence interval, C max maximum plasma drug concentration, ln natural log-transformed aRisperidone tablet (Dr. Reddy’s Laboratories Ltd., Hyderabad, India) bRisperdal® tablet (Xian-Janssen Pharmaceutical Ltd., Xi-an, China) 4 Discussion This study examined the pharmacokinetic properties and bioequivalence of two formulations of risperidone tablets in healthy adult male Chinese subjects. As shown in Fig. 1, we found nearly overlapping concentration–time curves for the two risperidone formulations. Moreover, the mean AUC∞ and Cmax values were not significantly different, and the 90% CIs of both the parent drug, risperidone, and the active metabolite, 9-hydroxy-risperidone, were completely contained within the predefined bioequivalence criteria of 80–125% for the primary endpoints of the AUC and Cmax [20]. There are few reports in the literature regarding the pharmacokinetics of risperidone, and the existing reports appear to differ [10, 11].

For these two strains we re-measured the persister fractions in single antibiotics, as well as in all pairwise combinations of the three antibiotics. We found that the killing dynamics were qualitatively similar to those when using a single antibiotic: all kill curves exhibited biphasic behavior, indicating that at least two subpopulations Birinapant of cells were present (Figure 4). Figure 4 Kill curves in combinations of antibiotics are biphasic and vary between treatments. We used combinations of antibiotics to examine the dynamics of cell killing. These dynamics are

similar to those observed in single antibiotics. A–C: Killing dynamics of all replicate cultures upon treatment of strains SC552 with all pairwise combinations of the three antibiotics. D-F: Killing dynamics of strain SC649. The precise dynamics of this killing in combinations of antibiotics may yield additional insight into how persisters are formed. We briefly outline three general possibilities. BMN 673 order (1) No cells persist when a population is simultaneously treated with antibiotics. This implies that the mechanisms underlying persistence to the two antibiotics are exclusive, and cannot occur within the same cell. (2) The fraction of persistent cells under the combination of antibiotics is approximately multiplicative relative

to the fraction in the two single antibiotics. Although this observation would be consistent with several explanations, the simplest is that the mechanisms of persister formation are independently induced, and occur randomly within the same cell. (3) The fraction of persistent cells under a combination of antibiotics is similar to the fraction observed under treatment with the more lethal antibiotic. 5-Fluoracil mouse Again, although several explanations would be consistent with this, the simplest is that cells that are persistent to the more lethal antibiotic are also persistent to the second. We refer to these

three hypotheses as exclusive, independent, and coincident, respectively. We found that for these two strains, there were no cases in which persister fractions were exclusive. Instead, the persister populations were largely coincident, with the fraction of cells in combinations of antibiotics being similar to the fraction observed in the more lethal antibiotic (Figures 4 and 5). This is consistent with this subset of cells being multidrug tolerant. Thus, although not all persisters are multi-drug tolerant, there appears to be a subset that is. Figure 5 A subset of persister cells is multidrug tolerant. The persister fractions estimated from the killing dynamics are shown for single or combinations of antibiotics. A: strain SC552; B: SC649. For both strains, there is a subset of persisters that appear to be resistant to both antibiotics. Toxin-antitoxin pairs are frequently gained and lost in E.

Results and

Discussion Due to the very limited number of completely sequenced rotavirus genomes, studies on reassortments have been limited to a few gene segments. Recently, the increased availability of complete rotavirus genome sequences, and the introduction of an extended classification and nomenclature system, comprising all 11 rotavirus gene segments, has prompted many investigators to start complete rotavirus genome sequencing projects. Both reassortments between strains belonging to the same host species, and between strains belonging to different host species have been documented several times in the Wnt inhibitor past [10–12]. The new classification system creates a necessary framework to thoroughly analyze possible interspecies transmissions of whole rotaviruses from one host to another, and Selleck Y 27632 to study the effect of reassortments on the generation of genetic rotavirus diversity, host range restriction, co-segregation of certain gene segments, and adaptation to a new host species [5]. A Rotavirus Classification Work Group was setup to evaluate potentially new genotypes that will be discovered when more and more complete

rotavirus genomes from multiple host species will be sequenced [6]. The analyses of complete rotavirus genomes, and the assignment to the appropriate genotypes will be highly facilitated by the use of the free online RotaC-tool. The RotaC-tool will be updated regularly, an will work closely together with the RCWG in order to update the tool with new genotypes, to reflect all established and new genotypes. Conclusion There are several useful web-based tools and database resources for the genotyping analysis of viral sequences, based

on phylogenetic trees, or sequence similarities of whole/partial sequences for the genotyping of HIV-1/HIV-2, HTLV-1/HTLV-2, hepatitis B virus, hepatitis C virus and poliovirus sequences [13–17]. Here we have introduced a reliable and easy-to-use automated classification tool for group A rotaviruses. Our RotaC TCL classification tool is in agreement with the rotavirus classification strategy and guidelines as proposed by the Rotavirus Classification Working Group. The web-based RotaC tool can be freely accessed at http://​rotac.​regatools.​be. Availability and requirements Project name: RotaC, Rotavirus Classification Tool v1.0 Project home page: http://​rotac.​regatools.​be Operating system: platform independent Programming language: java, perl and PHP License: none Restrictions to use by non-academics: none Acknowledgements PM is supported by a postdoctoral grant from the ‘Fonds voor Wetenschappelijk Onderzoek (FWO)-Vlaanderen’. JM is supported by the Institute for the Promotion and Innovation through Science and Technology in Flanders (IWT Vlaanderen). References 1. Parashar UD, Hummelman EG, Bresee JS, Miller MA, Glass RI: Global illness and deaths caused by rotavirus disease in children. Emerg Infect Dis 2003, 9:565–572.

Cell 2006, 127:1109–1122.PubMedCrossRef 8. Alexander SP: Flavonoids learn more as antagonists at A1 adenosine receptors. Phytother Res 2006, 20:1009–1012.PubMedCrossRef 9. Ferré S: An update on the mechanisms

of the psychostimulant effects of caffeine. J Neurochem 2008, 105:1067–1079.PubMedCrossRef 10. Cheuvront SN, Ely BR, Kenefick RW, Michniak-Kohn BB, Rood JC, Sawka MN: No effect of nutritional adenosine receptor antagonists on exercise performance in the heat. Am J Physiol Regul Integr Comp Physiol 2009, 296:R394-R401.PubMedCrossRef 11. Nieman DC, Henson DA, Davis JM, Angela Murphy E, Jenkins DP, Gross SJ, Carmichael MD, Quindry JC, Dumke CL, Utter AC, McAnulty SR, McAnulty LS, Tripplett NT, Mayer EP: Quercetin´s influence on exercise-induced changes in plasma cytokines and muscle and leukocyte cytokine mRNA. J Appl Physiol 2007, 103:1728–1735.PubMedCrossRef 12. Davis JM, Murphy EA, McClellan JL, Carmichael MD, Gangemi JD: Quercetin reduces susceptibility to influenza infection following stressful exercise. Am J Physiol Regul Integr Comp Physiol 2008, 295:R505-R509.PubMedCrossRef 13. Vlachodimitropoulou E, Naftalin RJ, Sharp PA: Quercetin is a substrate for the transmembrane

oxidoreductase Dcytb. Free Radic Biol Med 2010, 48:1366–1369.PubMedCrossRef 14. McAnulty SR, McAnulty LS, Nieman DC, Quindry JC, Hosick PA, Hudson MH, Still L, Henson DA, Milne GL, Morrow JD, Dumke CL, Utter AC, Triplett NT, Dibarnardi A: Chronic quercetin ingestion and exercise-induced oxidative damage and inflammation.

PD-332991 Appl Physiol Nutr Metab 2008, 33:254–262.PubMedCrossRef 15. Quindry JC, McAnulty SR, Hudson MB, Hosick P, Dumke C, McAnulty LS, Henson D, Morrow JD, Nieman D: Oral quercetin supplementation and blood oxidative capacity in response to ultramarathon Mirabegron competition. Int J Sport Nutr Exerc Metab 2008, 18:601–616.PubMed 16. Nieman DC, Henson DA, Maxwell KR, Williams AS, McAnulty SR, Jin F, Shanely RA, Lines TC: Effects of quercetin and EGCG on mitochondrial biogenesis and immunity. Med Sci Sports Exerc 2009, 41:1467–1475.PubMedCrossRef 17. Cureton JK, Tomporowski PD, Sinhal A, Pasley JD, Bigelman KA, Lambourne K, Trilk JL, McCully KK, Arnaud MJ, Zhao Q: Dietary quercetin supplementation is not ergogenic in untrained men. J Appl Physiol 2009, 107:1095–1104.PubMedCrossRef 18. Nieman DC, Williams AS, Shanely RA, jin F, McAnuty SR, Triplett NT, Austin MD, Henson DA: Quercetin´s influence on exercise performance and muscle mitochondrial biogenesis. Med Sci Sports Exerc 2010, 42:338–345.PubMed 19. Davis JM, Carlstedt CJ, Chen S, carmichael MD, Murphy EA: The dietary flavonoid quercetin increases VO2max and endurance capacity. Int J Sport Nutr Exerc Metab 2010, 20:56–62.PubMed 20.

Each ces gene displays 90 ~ 95% identity

between B. cereus and B. weihenstephanensis, and 95 ~ 100% identity within B. weihenstephanensis learn more isolates. Similar but slightly lower identity levels were observed for the corresponding proteins. Thus, based on the concatenated ces genes and protein sequences, two main clusters, namely “”cereus”" and “”weihenstephanensis”", could be distinguished, and within “”weihenstephanensis”" cluster, two subsequent clades were identified (Figure  1B). Genomic location of the ces gene clusters IS075 harbors a larger plasmid pool than AH187. The cereulide gene cluster of IS075 was observed to be located on a large plasmid with a size similar to that of pCER270 (270 kb) in AH187 (Figure  2A). Like pCER270, IS075 was PCR-positive to the pXO1 backbone genes pXO1-11, pXO1-14, pXO1-45, pXO1-50 and pXO1-55, which all encode hypothetical proteins (data not shown). It was also observed that the IS075 contig containing the ces gene cluster is ca. 180.7 kb with 146 predicted CDSs, of which 85.6% matched to those of pCER270, with a good synteny (Figure  2B). This indicated that the emetic plasmid in IS075 is pXO1-like with high similarity to pCER270. The deduced proteins from 21 predicted CDSs not matching those of pCER270 were blasted with

databases (Nr and Swissprot). The result showed that two matched putative transposases, one was related to putative DNA topoisomerases I, one to putative transcriptional repressors, see more and the others to

hypothetical proteins, all with homologs in other B. cereus group plasmids. Figure 2 Genomic location of the cereulide gene cluster. (A) Genomic location of the cereulide gene cluster of emetic B. cereus group isolates determined by plasmid profiling (L) and hybridization (R). Lane 1: IS075, lane 2: MC118, lane 3: MC67, lane 4: CER057, lane 5: BtB2-4, lane 6: non cereulide-producing B. cereus isolate CER071, lane 7: AH187. The probe used was cesB internal fragment amplified with EmF and EmR primers from the reference strain AH187. pMC118 and pMC67, displaying a larger size than pCER270, are indicated by a dark triangle. (B) Linear arrangement of the contig containing the ces gene cluster of (L) CER057 with the chromosome of KBAB4 and (R) Sclareol IS075 with the plasmid pCER270. Aligned segments are represented as dots (20 ~ 65 bp) and lines (>65 bp), with red and blue colors refer to forward and reverse matching substrings, respectively. For BtB2-4 and CER057, although large plasmid with smaller size to pCER270 was observed in the profile, no hybridization signal was detected (Figure  2A). It was observed that the contig containing the ces gene cluster in CER057 is about 245.4 kb with 215 predicted CDSs, of which 80% and 85% matched those of the chromosomes of AH187 and KBAB4, respectively.

Thalidomide does not require dose control depending on renal dysfunction, but it has not been reported in large studies that thalidomide is effective on the improvement of renal function. In any case, early diagnosis and timing of initiation of treatment are important. In addition, full understanding of efficacy and safety selleck chemicals llc profiles of novel agents and using them in combination with existing drugs appropriate for individual patients are the basis of treatment strategy. Diagnosis of AL amyloidosis and renal dysfunction AL amyloidosis is a disease with poor progression

in which deposition of amyloid causes multiple organ failure. Amyloid consists of immunoglobulin light chains secreted from monoclonal proliferated plasma cells. Its relative disease MM is often complicated with AL amyloidosis. In spite of the fact that it has the

same chromosome translocation such as t (11:14) to MM, it shows different pathological condition (Fig. 10). This may be due to slight difference of translocation breakpoint between AL amyloidosis and MM. However, the C646 manufacturer disease mechanism remains unknown. Fig. 10 Correlation of pathogenesis between MM, AL amyloidosis and Mantle cell lymphoma by the up-regulated cyclin D1 function. Mantle cell lymphoma is high tumor growth with 100 % t (11:14), MM have 10–20 % t (11:14) with moderate growth and secretary Ig functions. Some strange and rear MM patients (i.e. IgM-type, IgE-type, non-secretary-type) showed translocation 11:14 over 80 %. Otherwise, AL amyloidosis showed 30–50 % t (11:14). There may be the differences of break points on the translocation foci It is classified to cardiac, renal, gastrointestinal, and pulmonary amyloidosis depending on the main organ with amyloid deposition. The symptoms vary and the most common Levetiracetam cause of death is cardiac failure. The diagnosis is based on confirmation of amyloid deposition in the involved organs. When AL amyloidosis is suspected in patients with clinical findings such as general malaise, edema, heart failure, tubercle in margin of

tongue, and skin nodule with stigma, biopsy of organs should be first conducted to confirm deposit of amyloid (Fig. 11). Amyloid is positive with Congo red stain and has positive signal under polarized light with the polarizing filters. AL amyloidosis is definitely diagnosed by confirming monoclonal proliferation of plasma cells through identification of M protein and/or staining pattern of cell surface antigens in addition to deposition of amyloid. Low detection sensitivity of M protein even in immunofixation in AL amyloidosis has been a problem so far. However, the free light chain (FLC) assay that has listed itself in insurance coverage in 2011 in Japan, allows over 90 % detection and is reported to be effective in diagnosis. Amyloid deposits are predominantly composed of amyloid fibrils which are very stable structures with a common cross core fold.

The cure MK-1775 purchase algorithm for patients with BMs is extremely variable and depends on several factors such as primary histology and other clinical characteristics of patients. Moreover, though a multidisciplinary strategy is needed when approaching such complex patients, the lack of technical resources may influence the therapeutic decision of the treating physician. In fact, in clinical practice, the treatment of BMs is often planned on the basis of the resources available at each treating center. The incidence of BMs reported in our series of

patients for each tumor was similar to that reported in other studies [2]. In our analysis, breast cancer was the tumor with the longest time to brain recurrence (46 months), probably reflecting the advantages of an early diagnosis and the availability of effective treatments. In fact, anthracycline- and taxanes-including regimens as well as new hormonal and biologic agents have significantly increased disease-free and overall survival in early breast cancer patients potentially leading to a higher incidence of BMs [15–17]. Regardless CH5424802 purchase of

the treatment used for BMs, breast cancer showed the highest 2-year survival rate (36%). The dramatic reduction of survival at 2 years observed for NSCLC and melanoma might be due to poor control of either cranial and extracranial disease usually achieved in both malignancies, thus reflecting the intrinsic radio-resistance of their BMs [18] and Evodiamine the low systemic efficacy of medical therapies [19, 20]. Similarly to breast cancer, a long time to brain recurrence (42 months) was observed also for colorectal cancer. Nevertheless, only 18% of patients with BMs from colorectal cancer survived at 1 year (in contrast with a 1-year survival of 58% for breast cancer patients with BMs), indicating that in colorectal cancer brain spread probably represents a final event in the course

of the disease. In our series of patients, WBRT was the most used up-front therapy for BMs (about 50% of patients) followed by chemotherapy which was delivered in approximately one fourth of cases. The reason why many patients received chemotherapy as up-front treatment for BMs despite the fact that only 41% of patients suffered from multiple (> 3) brain lesions, can be explained by several reasons. Firstly, nearly all patients of our series had active systemic disease at the time of diagnosis of brain metastases. Secondly, about half of patients had no neurological symptoms, which might have favored physicians’ choice of using chemotherapy as up-front treatment for BMs along with the fact that an oncology unit was available in each institution.

J Biol Chem 1998,273(29):18268–18272.PubMedCrossRef 14. Webb DJ, Nguyen DH, Sankovic M, Gonias SL: The very low density lipoprotein receptor regulates urokinase receptor catabolism and breast cancer cell motility in vitro. J Biol Chem 1999,274(11):7412–7420.PubMedCrossRef selleck 15. Webb DJ, Nguyen DH, Gonias SL: Extracellular signal-regulated kinase

functions in the urokinase receptor-dependent pathway by which neutralization of low density lipoprotein receptor-related protein promotes fibrosarcoma cell migration and matrigel invasion. J Cell Sci 2000,113(Pt 1):123–134.PubMed 16. Yu W, Kim J, Ossowski L: Reduction in surface urokinase receptor forces malignant cells into a protracted state of dormancy. J Cell Biol 1997,137(3):767–777.PubMedCrossRef 17. Seddighzadeh M, Zhou JN, Kronenwett U, Shoshan MC, Auer G, Sten-Linder M, et al.: ERK signalling in metastatic

human MDA-MB-231 breast carcinoma cells is adapted to obtain high urokinase expression and rapid cell proliferation. Clin Exp Metastasis 1999,17(8):649–654.PubMedCrossRef 18. Holst-Hansen C, Johannessen B, Hoyer-Hansen G, Romer J, Ellis V, Brunner N: Urokinase-type plasminogen activation in three human breast cancer cell lines correlates with their in vitro invasiveness. Clin Exp Metastasis 1996,14(3):297–307.PubMed 19. Mhaidat NM, Thorne RF, Zhang XD, Hersey P: Regulation of docetaxel-induced apoptosis of human melanoma cells by different isoforms of protein kinase C. Mol Cancer Res 2007,5(10):1073–1081.PubMedCrossRef 20. Yacoub A, Han SI, Caron R, Gilfor D, Mooberry S, Grant selleck chemicals llc S, et al.: Sequence dependent exposure of mammary carcinoma cells to Docetaxel and the MEK1/2 inhibitor U0126 causes enhanced cell killing in vitro. Cancer Biol Ther 2003,2(6):670–676.PubMed 21. Davies BR, Logie A, Mckay JS, Martin P, Steele S, Jenkins R, et al.: AZD6244 (ARRY-142886), a potent inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 kinases:

mechanism of action in vivo, pharmacokinetic/pharmacodynamic relationship, and potential for combination in preclinical models. Mol N-acetylglucosamine-1-phosphate transferase Cancer Ther 2007,6(8):2209–2219.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions JL did the cell invasion essay and immunohistochemistry, XS did the Cell-culturing, submitted paper and revised the paper, FG did the medical statistics, XZ cultured the cell and did PCR, BZ tested the cells in PCR, HW detected the cells in western blot, ZS designed this experiment and wrote this paper. All authors read and approved this final draft.”
“1. Introduction Human gliomas are the most common primary intracranial tumors in adults. A grading scheme proposed by the WHO distinguishes four different grades of gliomas, of which glioblastoma multiforme (GBM) WHO grade IV is the most malignant variant with a median survival time of 1 year [1].

Fig. 3 Mean percentage of species found in a single subsamples, forest- or habitat type relative to the total number of species found in the study region The Mantel test of Sørensen’s indices among taxonomic groups showed significant positive correlations for nearly all groups (lichens excluded) in the terrestrial habitat, whereas only very low correlations were found in the epiphytic habitat (Table 3). The only significant correlation of lichens was with epiphytic ferns. Table 3

Correlations (R values) between similarity matrices of Sørensen’s (Bray Curtis) index of epiphytic (E) and terrestrial (T) species compositions per plot between the four study groups BGJ398 in vitro   Lichens Liverworts Mosses E T E T E T Ferns 0.15* – 0.13* 0.25** 0.18** 0.37***

Lichens     −0.13 – −0.01 – Liverworts         0.12 0.50*** * P < 0.05, ** P < 0.01, *** P < 0.001 Discussion phosphatase inhibitor library Forest structure and microclimate have been identified as principal drivers of diversity of ferns, bryophytes and lichens in tropical forests (Richards 1984; Sipman and Harris 1989; Wolseley and Aguirre-Hudson 1997; Holz and Gradstein 2005; Sporn et al. 2009) For terrestrial ferns, in addition, soil characters play an important role (Kluge et al. 2006). This is the first study that compares patterns of alpha and beta diversity among mosses, liverworts, ferns, and lichens in a tropical montane forest. We also separated epiphytic and terrestrial assemblages as well as forests occurring on ridge and slope because of the different environmental conditions of these habitats. Alpha diversity The epiphytic habitat was significantly richer in species than the terrestrial habitat. The taxonomic groups varied in their occurrence in the different habitat types. Whereas mosses were most species-rich in the terrestrial habitat, liverworts, Alectinib chemical structure ferns and lichens were most diverse in the epiphytic habitat. Slope forests were generally richer in species than ridges forests. We presume that this pattern is linked to differences in structure between the two forest types. Probably, the higher trees

in slope forests provide more varied and more favorable microhabitat conditions as well as more space for different species to coexist (Mandl et al. 2008), (unpubl.data). Overall, on average only 5% (±31% SD) of the variance in species richness of one taxonomic group could be predicted by species richness of another. Considering only the epiphytic habitat, this value increased to 15% (±20%). However, these mean values conceal a high level of variation. Patterns of alpha diversity were highly congruent for ferns, liverworts, and mosses in the epiphytic habitat (R² = 0.28–0.41), and for ferns and liverworts to a lesser degree in the terrestrial habitat (R² = 0.28). Thirty two percentage of variance in epiphytic species richness of a given group was explained by other taxa (lichens omitted).