We believe such compressive-vacuum

component of friction force do in fact exist in practice. We have called this component as compressive-vacuum friction force (F cv). This additional force consists of compressive component arising at the entry of the contact and a vacuum one acting on the contact exit. Therefore, Equation 1 should be rewritten as (2) Figure 1 A sliding tribosystem model: cylindrical roller rotating over the motionless block. Figure 2 Closed volumes formed by valleys between peaks on contacting surfaces. Vacuumization processes not only add to friction force but also increase wear, because produced suction forces along with contact of the naked surface make easier to damage sliding surfaces. In our opinion, wear of sliding contact could be greatly reduced by searching some methods to reduce friction force. These methods may include GDC0449 formation of micro-roughness of special Regorafenib mouse shape on

the surface. Similar approach was successfully used in [7] to reduce friction force in point-contact friction system. Though we use linear contact which differs significantly in properties, specially formed surface can also be used to reduce friction and wear. According to our compressive-vacuum hypothesis of friction, this can be done by preventing vacuumization. This idea is supported by the experimental data obtained during the friction testing of steel surfaces with specially designed micro-roughness [8, 9]. Methods In the present work, the Timken test [6] is chosen as a physical model of a sliding tribosystem. This model corresponds to a rotating shaft on plane bearing system,

www.selleckchem.com/products/nec-1s-7-cl-o-nec1.html which is the most widespread Erythromycin and also the most often friction-damaged unit in engineering. Boundary lubrication is accompanied by wear, so additional care should be taken in experiments. It is important not to allow wear debris to cause micro-cutting damage of the contact zone on the one hand and not to allow formation of simple elastohydrodynamic (contactless) friction on the other hand. In used experimental system, the evolution of wear scar in time is controlled by microscopy, so these precautions are easily satisfied. On the basis of the compressive-vacuum hypothesis described above, we suppose that it is necessary to create special initial three-dimensional (3D) geometry of a sample’s surface roughness which will allow to reduce compressive and vacuum hydrodynamic components of friction force and as a consequence will also reduce contribution of adhesive interaction of surfaces. For this purpose, creation of test samples with specific channels on the surface is suggested. These channels would provide bypass for the lubricant from areas entering the contact to areas leaving the contact, so reduction of vacuum in the exit region becomes possible. Such channels on a surface of test objects can be formed as parallel grooves, like shown in Figure 3.

aureus. The in vivo relevance of the host cathelicidin response to S. aureus infection is not fully established. It has been demonstrated that exposing keratinocytes to live S. aureus induces production of beta-defensin peptides, hBD1 and 3, but does not induce expression of hBD2 or LL-37. In addition, intracellular S. aureus did not induce LL-37 expression. However, Endocrinology antagonist heat-killed S. aureus or lipotechoic acid (LTA), a component of S. aureus cell wall, were able to induce LL-37 expression in keratinocytes [1]. These studies indicate that the presence of this bacterium in or on the human host may induce the expression of LL-37 in

vivo under the appropriate circumstances. Finally, in addition to direct effects on the bacteria, these peptides can also exert direct effects on host cells (although they do not appear to lyse host cells at these concentrations). LL-37 may have wound-healing properties [43]. The host targets of LL-37 in human cells were found to include GAPDH [44], EGFR [45, 46] and the P2X7 receptor [47]. D-LL-37 has been reported CB-839 datasheet to exhibit powerful immuno-stimulatory activity on the host (more effectively than the L-peptide), such as the induction of IL-8 in keratinocytes and promoting fibroblast proliferation [28], which suggests that it could promote wound healing as

an added effect. The bacterial and host-cell targets of these peptides will be the focus of our continued studies. Conclusions Novel treatments for chronic wound infections are critically needed. These wound infections are characterized by the presence of a polymicrobial population of biofilm-forming bacteria, including S. aureus. The desired characteristics of a novel therapeutic for treating these wounds would include incorporating the peptides in broad-spectrum, anti-biofilm, topical treatments with wound-healing properties. In this work, we

examined the anti-biofilm activity of two synthetic cathelicidin-like synthetic peptides against S. aureus. Overall, our results suggest that novel synthetic peptides can be designed based on naturally occurring cathelicidins, peptides Abiraterone order which demonstrate similar or improved potencies relative to that of the parent full-length AMPs. Exemplifying this proposition, the highly-effective anti-microbial peptide NA-CATH:ATRA1-ATRA1 not only displayed improved anti-biofilm activity relative to parent peptide, but it also exhibited enhanced anti-microbial activity. D-LL-37 represents a protease-resistant peptide mimetic that was as effective as the L-peptide isomer LL-37 at inhibiting biofilm formation. Furthermore, D-LL-37 may possesses wound-healing properties towards the host. These peptides may have potential to be developed as topical treatments against infections 4-Hydroxytamoxifen cell line involving biofilm-forming bacteria, such as S. aureus, reflecting the modern understanding of the role of biofilms in chronic wound infections.

β-galactosidase activity

was measured for evaluating the Selleck Dactolisib sycO-ypkA-yopJ promoter activity in each strain. Since the crp mutation had an effect on the copy number of recombinant or empty pRS551 plasmid [4], a normalized fold change in the activity of each fusion promoter in WT in relative to Δcrp was calculated to avoid the influence of copy number of pRS551 (Table 2). Table 2 Promoter activity determined with the sycO:lacZ reporter Selleckchem Y-27632 fusion   Fold change (Δcrp/WT) Normalized fold change of promoter activity in Δcrp in relative to WT LacZ fusion Plasmid copy number Miller units   PsycO-lacZ 0.006 0.182 30.33 β-Galactosidase activity (miller units) was detected as the promoter activity. An extremely low promoter activity was detected for the Δcrp or WT transformed with empty pRS551 (data not shown). Copy number of recombinant pRS551 (PsycO-lacZ) was determined by real-time quantitative PCR, the detecting fold change of plasmid copy number was set to be 1 to generate a normalization factor that was subsequently used for generating the normalized fold change of promoter activity

(miller units) in the Δcrp in relative to the WT. Each experiment was done in triplicate. Accordingly, the β-galactosidase activity in the Δcrp increased compared to the WT when they grew in the ‘TMH-1mM cAMP’ medium, indicating that CRP greatly repressed the promoter activity of sycO-ypkA-yopJ (Table 2). CRP binds to promoter-proximate PHA-848125 stiripentol region of sycO-ypkA-yopJ A CRP box-like sequence was found in the promoter-proximate region of sycO-ypkA-yopJ [4], indicating the direct association of CRP with the sycO-ypkA-yopJ promoter region. Further EMSA experiments showed that the cAMP-CRP complex bound to the sycO-ypkA-yopJ promoter region in a CRP dose-dependent manner (Fig. 3a). CRP could not bind to the target DNA in the absence of cAMP. To validate the specifiCity of CRP-DNA interaction, YPO0180 and YPO1099 [gene IDs in CO92 [20]] were used as negative controls

(Fig. 3b). The PCR-generated upstream DNA of YPO0180 did not harbor the predicted CRP binding site, while the YPO1099 upstream region gave an extremely low score value of 0.96 during the pattern matching analysis using the CRP consensus (sycO gave a score value of 8.57) [4]. Both of them gave negative EMSA result, even the CRP protein was increased to 4 μg in a single reaction mixture (Fig. 3b). Figure 3 Electrophoretic mobility shift assay. The band of DNA fragment containing the promoter region of sycO disappeared with increasing amounts of CRP protein, and a retarded DNA band with decreased mobility turned up (Fig. 3a), which presumably represented the CRP-DNA complex. But for YPO0180 and YPO1099, the CRP-DNA complex did not appear even His-CRP was increased to 4 μg for each reaction mixture (Fig. 3b). Therefore, CRP specifically bound to the sycO-ypkA-yopJ promoter region and directly repressed the transcription of sycO-ypkA-yopJ.

Photo, 1958 Fig. 10 Fred Crane’s research group picnic. Although this photograph was damaged, it Lenvatinib is shown here for historical purposes. Sitting on the ground: children at the picnic. First standing row 3rd from right is Helen Crane; 5th from right is Rita Barr. On the next standing row (just below the very top row), Ron Berezney (wearing glasses) is on the extreme right; 2nd from right is Linda Funk; 3rd from right is the author Fred Crane (wearing checkered shirt); 4th from right is Frank Sun (wearing glasses). On the very top row is Jack Wilson (right above Linda Funk). All others in the photograph are either members of

Crane laboratory or those related to these members. Photo, 1967 Fig. 11 Fred L. Crane (the author) in his office at Purdue University. Photo, 1972 Q-VD-Oph in vivo Fig. 12 Fred and Marilyn Crane at Purdue University (Marilyn was in the Vision Research Group). Photo, 1983 Acknowledgments David Green (of the Enzyme Institute, University of Wisconsin, Madison)

deserves a lot of credit for encouraging my research into PQ when it was not in the mainstream of heart bioenergetics that he was interested in. Further, Karl Folkers deserves credit for interrupting coenzyme Q research to provide analogs of PQ that advanced research in this area. I express my appreciation to my dedicated colleagues who worked on the PQ story with me: Rita Barr, Larry Kegel, selleck chemicals Barbara Ehrlich, Pat Wood, Melva Henninger and H. N. Bhagavan. I thank Govindjee, the founding Historical Corner editor of Photosynthesis Research, for inviting me to write this personal minireview, for constant interaction,

suggestions and editing from its original draft to the final manuscript. I thank Lilli A Davis for her technical assistance with the manuscript. References Allen JF (2002) Plastoquinone redox control of chloroplast thylakoid protein phosphorylation and distribution of excitation energy between photosystems: new discovery, background, implications. Photosynth Res 73:139–148PubMedCrossRef Ambe KS, Crane FL (1960) Studies on the electron transport system. XXVI. Specificity of coenzyme Q and coenzyme Q derivatives. Biochim Biophys Acta 43:30–40PubMedCrossRef Amesz J (1964) Spectrophotometric evidence for the participation of a quinone in photosynthesis of intact blue-green algae. Biochim Biophys Acta 79:257–265PubMedCrossRef Amesz J (1973) The function of plastoquinone in photosynthetic electron transport. Biochim Biophys Acta 301:35–51PubMed Amesz J (1977) Plastoquinone. In: Trebst A, Avron M (eds) Encyclopedia of plant physiology, vol 5. Springer, Berlin, pp 238–246 Austin JR, Frost E, Vidi PA, Kessler F, Staehelin LA (2006) Plastoglobules are lipoprotein subcompartments of the chloroplast that are permanently coupled to the thylakoid membrane and contain biosynthetic enzymes. Plant Cell 18:1693–1703PubMedCrossRef Barber J, Andersson B (1994) Revealing the blueprint of photosynthesis. Nature 370:31–34CrossRef Barr R, Crane FL (1967) Comparative studies on plastoquinones.

The yellow mealworm, T. molitor, is a freeze-susceptible, stored product pest. When provided with sufficient food supply, T. molitor MM-102 larvae have low humidity tolerance and can survive under FG-4592 purchase relatively xeric conditions because of their ability to metabolize water from ingested food [12]. Clopton et al. [13] sterilized adult and larval T. molitor by incubation at 36°C to 37°C for 5 d to

eliminate the effect of existing gregarine infections on the tests. In the present study, the host insects were cultured and sterilized by generational dilution in sterile wheat bran substrates, and the insects were almost fully sterilized when given enough generation culture. This new method may provide host insects for strict experimental infections. The efficacy of M. anisopliae under desiccation stress was tested in dry wheat bran substrate with initial moisture content of 8%. At this low moisture level, M. anisopliae was difficult

to grow, but the isolate MAX-2 was still active, whereas the other isolates showed very low efficacy. This result suggests that the infection of sterile T. molitor larvae in wheat bran substrates with low moisture content could constitute a valid laboratory bioassay system to study M. anisopliae efficacy under desiccation stress. Efficacy of M. anisopliae isolate MAX-2 This study demonstrated that M. anisopliae isolate MAX-2 had pathogenicity Histone Methyltransferase inhibitor & DOT1 inhibitor against T. molitor larvae in all the tested moisture levels, particularly

lower moisture levels, and showed relatively high tolerance to desiccation stress. Daoust et al. [14] indicated that the efficacy of M. anisopliae against insects depends on conidial germination. Conidial germination of all tested isolates in the present study showed a tendency to decrease with the decrease in substrate moisture content within the tested scope (8% to 35%). The mortality of larvae for the isolates in different moisture levels also showed the same tendency, which indicates the correlation between conidial germination and efficacy of M. anisopliae. However, the mortality for MAX-2 decreased much more slowly than those of the other isolates. At the substrate with 8% moisture, which was too low for M. anisopliae to facilitate germination, MAX-2 still Endonuclease showed medium mortality of 41% versus low mortality < 5% for the other isolates against T. molitor larvae. Howard et al.[15] observed that high virulence of M. anisopliae against mosquitoes is not significantly affected by low viability, and they deduced that the difference is possibly due to the different abilities of the fungal conidia to germinate on mosquito cuticles and the agar. Leger [16] also reported the existence of two diverse sets of selection pressures on Metarhizium spp., one for optimum characteristics for soil survival and another for virulence to insects.

PubMedCrossRef 15. Haverkamp J, Charbonneau B, Ratliff TL: Prostate inflammation and its potential impact on prostate cancer: a current review. J Cell Biochem 2008,103(5):1344–1353.PubMedCrossRef 16. Sutcliffe S, Platz EA: Inflammation in the JNK-IN-8 etiology of prostate cancer: an epidemiologic perspective. Urol Oncol 2007,25(3):242–249.PubMed 17. De Marzo AM, Nakai Y, Nelson WG: Inflammation, atrophy, and prostate carcinogenesis. Urol Oncol 2007,25(5):398–400.PubMed 18. Al-Mously N, Eley A: Interaction of Chlamydia trachomatis serovar E

with male genital tract epithelium results in secretion of proinflammatory cytokines. J Med Microbiol 2007,56(Pt 8):1025–1032.PubMedCrossRef 19. Takeyama K, Mitsuzawa H, Shimizu T, Konishi M, Nishitani C, Sano H, Kunishima Y, Matsukawa M, Takahashi S, Shibata K, et al.: Prostate cell lines secrete IL-8 in response to Mycoplasma hominis through Toll-like receptor 2-mediated mechanism. Prostate 2006,66(4):386–391.PubMedCrossRef 20. Jugeau S, Tenaud I, Knol AC, Jarrousse V, Quereux G, Khammari A, Dreno B: Induction of toll-like receptors by Propionibacterium acnes. Br J Dermatol 2005,153(6):1105–1113.PubMedCrossRef 21. Kundu SD, Lee C, Billips BK, Habermacher GM,

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epithelial cells can act as early sensors of infection by up-regulating TLR4 expression and proinflammatory mediators upon LPS stimulation. J Leukoc Biol 2006,79(5):989–998.PubMedCrossRef Idoxuridine 23. Takeda K, Kaisho T, Akira S: Toll-like receptors. Annu Rev Immunol 2003, 21:335–376.PubMedCrossRef 24. Chen Q, Koga T, Uchi H, Hara H, Terao H, Moroi Y, Urabe K, Furue M: Propionibacterium selleck chemicals acnes-induced IL-8 production may be mediated by NF-kappaB activation in human monocytes. J Dermatol Sci 2002,29(2):97–103.PubMedCrossRef 25. Kishimoto T: Interleukin-6: from basic science to medicine–40 years in immunology. Annu Rev Immunol 2005, 23:1–21.PubMedCrossRef 26. Waugh DJ, Wilson C: The interleukin-8 pathway in cancer. Clin Cancer Res 2008,14(21):6735–6741.PubMedCrossRef 27. Hamilton JA: GM-CSF in inflammation and autoimmunity. Trends Immunol 2002,23(8):403–408.PubMedCrossRef 28. Gillitzer R, Berger R, Mielke V, Muller C, Wolff K, Stingl G: Upper keratinocytes of psoriatic skin lesions express high levels of NAP-1/IL-8 mRNA in situ. J Invest Dermatol 1991,97(1):73–79.PubMedCrossRef 29. Abd El All HS, Shoukry NS, El Maged RA, Ayada MM: Immunohistochemical expression of interleukin 8 in skin biopsies from patients with inflammatory acne vulgaris. Diagn Pathol 2007, 2:4.PubMedCrossRef 30.

Different methods of target DNA detection has been used using FRET QNZ price phenomena. Most of these methods are based on the hybridization between target DNA and QD-tagged probes (QD nanoprobes). These probes are usually double-tagged with QD (in one end) as well as a quencher molecule (in the other end). As mentioned previously, these nanoprobes can be designed to produce signal (signal on) or disappear the signal of tagged QD molecule (signal off) when they recognize target DNA. In the signal-on method the probe

DNA is designed as stem-loop structure. In this state QD is located in the vicinity of quencher molecule, absorbing the fluorescent signal of QD and preventing it from detection. However, when the nanoprobe hybridizes with the target DNA, the stem-loop structure denatures and is converted to the linear conformation. The QD and quencher molecule are thus located away from each other, making it possible to detect the fluorescent signal of tagged QD. In the signal-off method, the nanoprobe is tagged with QD and the target selleck compound is tagged with quencher. In unhybridized state, the tagged QD emits signal and its

signal is detectable. But when the nanoprobe recognizes the target DNA, it hybridizes the target DNA, leading to bringing QD to the vicinity of quencher and prevention of QD emission [52]. QDs can also be used as electroactive labels for detection

of target DNA in the electrochemical biosensors. This property originates from inherent electrochemical properties with ease of miniaturization, low cost, low power requirements, and excellent biocompatibility. In electrochemical detection of target DNA molecules by QDs, they serve as electrochemical catalyst (electroactive molecules), which transports loads of electrons through the reduction of dissolved oxygen, resulting in a significant increase in the reduction peak current. In fact, they show sharp selleck kinase inhibitor voltammetry signals proportional to the concentration of corresponding DNA targets and serve as signal-enhancing agents [53]. In addition to detection of one target, several different-sized Mirabegron QD molecules can be excited by one excitation source simultaneously. This ability is advantageous in detecting more than one target in the same time [54]. It is thus possible to implement multiplex iLAMP assays for detecting multiple proteins in a sample. The application of nanoprobes for detecting iLAMP products is depicted in Figure 2. Figure 2 The principle and possible ways of iLAMP products analysis with different nanoprobes (nanoprobe-iLAMP platform). Integration with liposome Liposomes are spherical micro/nanostructures made of lipid bilayers and can be filled with various molecules.

D. the epidemiology and symptoms of anthrax had been described [1]. A 1995 report from China described the results of an anthrax surveillance and control project in 10 provinces in China between 1990–1994 [2]. Stations in these 10 provinces (Sichuan, Tibet, Inner Mongolia, Xinjiang, Qinghai, Gansu, Guangxi, Guihou, Yunnan and Hunan) reported 72 outbreaks and 8,988 human cases of anthrax. These results, which are indicative of a long history and significant levels of contamination in these Elacridar price specific areas, are the reason for concern by the Chinese Institute of Epidemiology and Microbiology [2]. The population structure of Bacillus anthracis has only recently begun to be resolved

with specific geographical patterns spread 3-deazaneplanocin A ic50 across areas mostly inhabited by man and his animals. Higher genetic resolution within B. anthracis has resulted from two molecular typing approaches: An ongoing comparative, single nucleotide polymorphism BYL719 ic50 (SNP) analysis of diverse isolates that describes a conserved, clonally derived basal tree, [3] and a multiple locus variable

number tandem repeat analysis (MLVA) system that provides improved resolution among individual isolates [4–7]. This process for molecular typing has now been applied to the study of isolates from China. An archival collection of 191 B. anthracis isolates from China [collection dates from 1947–1983, except isolates A0034 (1993) and A0038 (1997)] was obtained and used in this study (see Methods and Additional file 1). This collection contained an unusual subset of 122 B. anthracis isolates recovered from soil, including 107 isolates collected between 1981/1982 in Xinjiang province. This province is located in the western most tip of China and was one of the 10 regions surveyed in the study conducted

from 1990–1994. The remaining isolates originated from many regions across the whole of China. This report focuses on the molecular genotyping of these 191 isolates. Our goal Glutathione peroxidase was to determine the nature and distribution of genotypes found in China and to establish phylogenetic relationships between these isolates and those found elsewhere in the world. Canonical SNP analysis The original comparative analysis of 5 B. anthracis whole genome sequences examined the status of ~1,000 single nucleotide polymorphisms (SNPs) in 26 diverse isolates [3]. This study revealed an extremely conserved phylogenetic tree with only one homoplastic character in ~26,000 measurements. These results prompted the hypothesis that a few strategically placed “”canonical SNPs”" could replace the 1,000 assays and still describe an accurate SNP based tree. This idea was confirmed in a study using 13 canonical SNPs (canSNP) to examine 1,000 world-wide isolates of B. anthracis [5]. Figure 1 illustrates this original canSNP tree and is used here to define important nomenclature and terminology.

SD standard deviation, n.d. not determined To address additive or synergistic effects of AMPs, we performed a model assay using N. farcinica and a combination of LL-37 and HNP 1-3 (Figure 2). Since the combination of the two AMPs exhibited nocardial killing comparable to each peptide alone at twofold higher concentrations, we found

additive activity Cediranib ic50 of the two AMPs. Figure 2 Additive activity of the two AMPs HNP 1-3 and LL-37 in a colony forming unit (CFU) assay against N . farcinica ATCC 3318. A combination of HNP 1-3 and LL-37 exhibited killing comparable to each peptide alone at twofold higher concentrations (i.e. 78.9% CFU reduction by 8 μg/ml HNP 1-3 in combination with 8 μg/ml LL-37 compared to 68.5% CFU reduction by 16 μg/ml LL-37 or 45.6% reduction by 16 μg/ml HNP 1-3 alone). Data are results of a single assay. In Ganetespib contrast to results with N. farcinica and N. nova, hBD-3 and LL-37 did not show

antinocardial activity against N. asteroides ATCC 19247 (Figure 1C). Only human α-defensins HNP 1-3 were found to be active against N. asteroides with LD90 of 32 μg/ml. N. brasiliensis ATCC 19296 proved to be resistant to all human AMPs tested since neither HNP 1-3 nor hBD-3 or LL-37 exhibited killing activity in concentrations up to 64 μg/ml (Figure 1D). Remarkably, stronger growth of N. brasiliensis was observed with all three AMPs investigated. Enhanced growth was not found after incubation with equivalent concentrations of DPY (data not shown). To investigate whether proteolytic degradation of AMPs by N. brasiliensis-derived proteases might play a role, we added a protease inhibitor mix during incubation in CFU assays. Protease inhibitors AZD0156 mw were not able to alter the observed AMP resistance of N. brasiliensis, yet enhanced growth of N. brasiliensis after co-incubation with protease inhibitors could be observed again(data not shown). Activity of bovine AMPs Ribociclib concentration against Nocardia species CFU-assays revealed activity of all tested bovine AMPs against N. farcinica ATCC 3318 (Figure 3A). Neutrophil-derived indolicidin

and bovine β-defensin LAP showed potent killing with LD90 of 16 μg/ml respectively. Bovine TAP was also active, LD90 proved to be 32 μg/ml. All bovine AMPs revealed at least comparable or greater activity at 32 μg/ml against N. farcinica than levofloxacin. Accordingly, bovine indolicidin exhibited killing activity against N. nova (LD90 8 μg/ml) and N. asteroides (LD90 64 μg/ml) (Table 1). Figure 3 Activity of bovine AMPs TAP, LAP indolicidin and levofloxacin (killing control) against A N. farcinca ATCC 3318 (p < 0.05 for all tested substances), B N. brasiliensis ATCC 19296 (indolicidin and levofloxacin p < 0.05) was investigated using a colony forming unit (CFU) assay. Data are means (percent CFU reduction) of at least two independent sets of experiments with each peptide and each Nocardia species. In contrast to human AMPs, bovine indolicidin exhibited activity against N.

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