Data were analysed using the Spearman’s correlation, Wilcoxon signed rank, and Mann–Whitney U-test. Results.  Except group IV, there was a statistically significant decrease in fluorescence after the application of sealants (P < 0.05). The decrease of LFpen readings in the opaque sealant groups was more significant than the clear

sealant groups (P < 0.05). But for both sealants, the difference between phosphoric acid and Clearfil S3 Bond groups was nonsignificant (P > 0.05). Conclusions.  There was a statistically significant decrease in fluorescence for both clear and opaque sealant groups. However, clear sealant with Clearfil S3 Bond does not influence the LFpen readings. “
“Generalized aggressive periodontitis (GAP) is a multifactorial disease that shows a specific microbial profile and a familial Y-27632 manufacturer aggregation. This study evaluated the salivary microbial

profile of families with a history of GAP and compared them with healthy families. Fifteen families with parents presenting periodontal health and 15 with parents with a history of GAP were selected. Each family had a child aged 6–12 years. Stimulated saliva was collected from all subjects, and Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), and Aggregatibacter actinomycetemcomitans (Aa) amounts were determined. Children of GAP families showed higher detection of Aa (90%) Selleck BMS354825 than children of healthy families (45%) (P < 0.05). Parents with GAP showed a Pg salivary concentration statistically higher than that of healthy parents (P < 0.05).Children of GAP families, however, exhibited similar Pg concentration than healthy children (P > 0.05). Tf amounts did not differ either in parents or in children (P > 0.05) The infection risk calculation indicates that children who have one parent who is positive for Aa have 16.3 times (95% CI 3.1–87.2) more risk of being infected with Aa (P < 0.05) than children from an Aa-negative ever family. It may be concluded that children

of parents with aggressive periodontitis have higher levels and higher risk of Aa infection. “
“Background.  With increasing survival rates for childhood cancer, late effects are of growing importance. Oral health is central to general health, level of nutrition, quality of life, and is significant in the holistic care of children during cancer therapy. Hypothesis.  The oral health needs of children treated for solid tumours/lymphoma will be greater than the general population, groups will differ according to tumour and treatment. Design.  One hundred and twenty patients, 0–17 years, under follow-up from 01/07/06 to 07/02/07 were investigated for caries, opacities, microdontia, and gingivitis. Analysis was performed with stratification according to tumour and treatment. Comparisons made with the UK 2003 Child Dental Health Survey. Results.

The work was supported by the Oversight Committee for The Evaluation of Metabolic Complications of HAART, a collaborative committee with representation from academic institutions, the European Agency for the valuation of Medicinal Products, the Food and Drug Administration, the patient community, and all pharmaceutical companies with licensed anti-HIV drugs in the US market:

Abbott, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Merck, Pfizer, and Hoffman-LaRoche. It was also supported by a grant (CURE/97-46486) from the Health Insurance Fund Council, Amstelveen, the Netherlands, to the AIDS Therapy Evaluation Project Netherlands (ATHENA); by a grant from the Agence Nationale http://www.selleckchem.com/products/ABT-263.html de Recherches sur le SIDA (Action Coordonnée no. 7, Cohortes) to the Aquitaine Cohort. The Australian HIV Observational Database is funded as part of the Asia Pacific HIV Observational buy NVP-BKM120 Database, a programme of The Foundation for AIDS Research (amfAR). The work was also supported in part by a grant from the US National Institutes of Health’s National Institute of Allergy and Infectious Diseases (NIAID) (Grant No. U01-AI069907) and by unconditional grants from Merck Sharp & Dohme, Gilead, Bristol-Myers Squibb, Boehringer Ingelheim, Roche, Pfizer, GlaxoSmithKline and Janssen-Cilag. The National Centre in HIV Epidemiology and Clinical Research is funded by The Australian Government

Department of Health and Ageing, learn more and is affiliated with the Faculty of Medicine, The University of New South Wales. In addition, the Barcelona Antiretroviral Surveillance Study (BASS) received grants from the Fondo de Investigación Sanitaria (FIS 99/0887) and Fundación para la Investigación y la Prevención del SIDA en Espanã (FIPSE 3171/00); the Terry Beirn Community Programs for Clinical Research on AIDS (CPCRA) received grants from the National Institute of Allergy and Infectious Diseases, National Institutes of Health (grants 5U01AI042170-10 and

5U01AI046362-03); the EuroSIDA study received grants from the BIOMED 1 (CT94-1637) and BIOMED 2 (CT97-2713) programmes and the fifth framework programme (QLK2-2000-00773) of the European Commission and grants from Bristol-Myers Squibb, GlaxoSmithKline, Boehringer Ingelheim and Roche; the Italian Cohort Naïve to Antiretrovirals (ICONA) Foundation received unrestricted educational grants from Abbott, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead, GSK, Pfizer and Janssen-Cilag; and the Swiss HIV Cohort Study (SHCS) received a grant from the Swiss National Science Foundation. Conflicts of interest: The D:A:D collaboration is supported financially by various institutions including all pharmaceutical companies with licensed anti-HIV drugs in the US market: Abbott, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Merck, Pfizer and Hoffman-LaRoche.

We recommend annual influenza vaccination (level of evidence 1B). We recommend vaccination Afatinib against pneumococcus and hepatitis B virus (level of evidence 1D). We recommend

that patients with antibodies against hepatitis B core antigen (HBcAb) should be treated with prophylactic antivirals in line with BHIVA hepatitis guidelines (level of evidence 1B). Kaposi sarcoma is still the most common tumour in people with HIV infection, is an AIDS-defining illness and is caused by the Kaposi sarcoma herpesvirus (KSHV). The diagnosis is usually based on the characteristic appearance of cutaneous or mucosal lesions and should be confirmed histologically since even experienced clinicians misdiagnose KS [1] (level of evidence 1C). Lesions are graded histopathologically into patch, plaque or nodular grade disease. Visceral disease is uncommon, affecting about 14% at diagnosis [2] and CT scans, bronchoscopy and endoscopy are not warranted in the absence of symptoms (level of evidence 2D). The AIDS Clinical Trial Group (ACTG) staging system for AIDS-related KS was developed in the pre-HAART selleck chemical era to predict survival and includes tumour-related criteria

(T), host immunological status (I) and the presence of systemic illness (S) (see Table 3.1) [3,4]. The ACTG also established uniform criteria for response evaluation many in AIDS KS (see Table 3.2) [3]. In the era of HAART, the prognostic value of this staging system has been questioned and one study suggested that only the T and S stages identify patients with poor survival [5], whilst another study from Nigeria found that I and S stages but not T stage were of prognostic significance [6]. However, a comprehensive evaluation of prognostic factors in 326 patients diagnosed with AIDS KS in the era of HAART, externally validated on 446 patients from the US HIV/AIDS Cancer Match Study, has established

a prognostic scoring scheme [7] and more detailed immune subset analysis does not provide additional prognostic information [8]. Having KS as the first AIDS-defining illness (-3 points) and increasing CD4 cell count (-1 for each complete 100 cells/μL in counts at KS diagnosis) improved prognosis, whereas age at KS ≥50 years old (+2) and S1 stage (+3) conveyed a poorer prognosis. On the basis of this index it was suggested that patients with a poor risk prognostic index (score >12) should be initially treated with HAART and systemic chemotherapy together, whilst those with a good risk (score <5) should be treated initially with HAART alone, even if they have T1 disease. Over time, there has been a rise in the CD4 cell count at diagnosis of KS, and the impact of initiation of treatment may also change [9–12].

Limited or no therapeutic options (following multiple failing selleckchem regimens, including the newer drugs with novel actions). Record in patient’s notes of resistance result at ART initiation (if available) and at first VL >400 copies/mL and/or before switch. Record in patient’s notes of adherence assessment and tolerability/toxicity to ART in patients experiencing virological failure or repeated viral blips. Number of patients experiencing virological failure on current ART regimen. Proportion of patients experiencing virological failure switched to a new suppressive regimen within 6 months. Proportion

of patients on ART with previously documented HIV drug resistance with VL <50 copies/mL. Record of patients with three-class virological failure with or without three-class resistance referred/discussed in multidisciplinary team with expert advice. In patients on ART: A single VL 50–400 copies/mL preceded and followed by an undetectable VL is usually not a cause for clinical concern (GPP). We recommend a single VL >400 copies/mL is investigated further, as it is indicative of virological failure (1C). We recommend in the context of repeated viral blips, resistance Mitomycin C mouse testing is attempted (1D). Optimal HIV control is ordinarily

reflected by complete viral suppression with an undetectable VL. A virological blip is variably defined but for the purposes of these guidelines the definition that has been adopted is a detectable VL <400 copies/mL, which is preceded and followed by an undetectable result without any change of therapy. Blips are frequent and represent random variation around a mean undetectable VL [5-7]. Many patients have at least one at some time [8] when they are not predictive of virological failure or associated with emergent resistance in most studies [5, 9, 10]. VL assay variation and laboratory processing artefacts account for many blips (i.e. no ‘true’ increase in viral replication), which partly explains why blips do not appear to compromise long-term

outcomes [9, 11-13]. However, those with Progesterone sustained low-level increases in VL run a higher risk of virological failure. Most blips are low level [median magnitude 79 copies/mL in one study (range 51–201)] and short lived [median 2.5 days (range 2–11.5)] [7]. In a retrospective study, 28.6% of patients, experienced VL increases from 50 to 500 copies/mL over 8 years; 71% of these were blips [8]. Review and reiteration of the importance of full adherence, as well as looking for any tolerability/toxicity issues, DDIs/food interactions, and archived resistance should take place. However, blips do not appear to be related to intercurrent illness, vaccination, baseline CD4 cell count/VL, duration of preceding suppression or level of adherence [7, 14, 15].

Suppression of the effects of the lack of RpoS by overexpression of SOD or catalase indicated that the damage caused by ROS reduces survival and increases the mutation frequency in a starving P. putida RpoS-deficient strain. Interestingly, although the absence of RpoS in starved P.

putida affected the spectrum of mutations, the spectrum was different from that identified in P. putida lacking the GO repair system (Saumaa et al., 2007). Thus, it is possible that the accumulation of oxidative DNA damage other than GO could elevate the frequency of mutation in these bacteria. There is also another, not exclusive explanation for these differences. It is known that oxidative damage of proteins and membrane components, but not that of INCB018424 solubility dmso DNA, is a major reason for mortality of cells (Nyström, 2004). Oxidative damage to components of protein synthesis selleck chemical increases mistranslation, and

vice versa, mistranslated proteins are more susceptible to oxidative damage (Dukan et al., 2000). Mistranslation is increased 10–100-fold in E. coli due to amino acid starvation (Sørensen, 2001). Importantly, mistranslation of DNA repair and replication proteins has been demonstrated to create a transient mutator phenotype (Humayun, 1998; Balashov & Humayun, 2002, 2003; Al Mamun et al., 2006). For example, hypermutagenesis in E. coli mutA cells mistranslating aspartate as glycine due to a mutation in the glycine tRNA anticodon was mediated by modifications of DNA polymerase Pol III due to elevated mistranslation (Al Mamun et al., 2006). Additionally, oxidative modification of replication proteins and inactivation of the components of repair pathways have been reported in eukaryotic systems (Graziewicz et al., 2002; Men et al., 2007; Montaner et al., 2007; Bae et al., 2008; Jarrett et al., 2008). Hence, because the elevated mutation frequency Tangeritin observed by Tarassova et al. (2009) in starving RpoS-deficient

P. putida was associated with an increased death of bacteria and the spectrum of mutations did not resemble that induced by oxidative damage of DNA, the higher mutation frequency in the surviving populations observed in this study might primarily be caused by a decline in DNA replication and repair fidelity due to the oxidative damage of enzymes and/or the errors occurring during the translation of proteins. So far, the role of oxidative damage to proteins in DNA integrity has been underestimated in stationary-phase mutagenesis. It certainly needs more comprehensive investigations. Bacteria have multiple DNA polymerases, each of those with a specific role. DNA polymerase Pol III is a replicative polymerase, and its inactivation is lethal to bacteria. Pol I is involved in Okazaki fragments’ processing and DNA repair synthesis (Okazaki et al., 1971; Cooper & Hanawalt, 1972). Additionally, E.

After the reaction, samples

were analyzed on a 2% agarose gel, followed by staining with ethidium bromide and photography. The primers used are listed in Table S2. The experimental conditions are given in the NCBI GEO website, and the accession numbers are given in Table 1 and in Table S1. Briefly, crude RNA was extracted from each sample, and then cDNA was synthesized, followed by fragmentation and labeling with biotin–dUTP using DNA-labeling reagents from Affymetrix Inc. (Santa Clara) or ENZO Life Sciences Inc. (Farmingdale) according to the manufacturer’s instructions, as described previously (Shinkai et al., 2007; Agari et al., 2008). The 3′-terminal-labeled cDNA was hybridized to a TTHB8401a520105F GeneChip (Affymetrix Inc.), and then the array was washed, stained, and scanned

as described previously (Agari et al., 2008). selleck inhibitor The raw intensity data were summarized as 2266 ORFs using genechip operating software version 1.4 (Affymetrix Inc.). The datasets were normalized through the following normalization steps using the Subio Platform (Subio Inc.), i.e. shifting of low signals <1.0 to 1.0, check details log-based transformation of the data, and global normalization [normalized as to 75 percentile (third quartile)]. The data for chemically treated cells were normalized using the data for the nontreated cells as a control. The t-test P-value of the observed differences in the normalized intensities was calculated using the Subio Platform, and then from the value, the false discovery rate (q-value), which is useful for measuring statistical significance in multiple-hypothesis testing (Storey & Tibshirani, 2003), was calculated using r (http://www.R-project.org). In this study, we arbitrarily considered the q-value

threshold to be 5%, a well-used significant threshold value, which means that q-values ≤0.05 provide significant genes for differential expression, whereas values >0.05 do not, but still may not be false. Three hundred and six datasets from 117 experimental conditions were used for the analysis (Table S1). Normalization of the datasets was performed as described above except that the normalization to the mean value for each gene was performed after the global normalization. Spearman’s correlation coefficients, between the sdrP gene and each of 2266 genes, were calculated using the Subio Platform. The microarray data used in this study GNE-0877 have been summarized and deposited in the GEO database, and are accessible through GEO series accession number GSE21875. The regions upstream of the TTHA0029, TTHA0557, TTHA1128, TTHA1215, TTHA1625, TTHA1635, TTHA1892, TTHB132, and TTHA0987 genes were amplified by genomic PCR using the primers listed in Table S2. The amplified fragments were digested with BamHI and EcoRI, and then cloned into pUC19 (Merck). Using each plasmid as the template, PCR was performed with primers P21 and P22 (Table S2) to prepare template DNAs for the transcription assay.

DGGE is a technique in which the variability of sequence is used to show the presence of certain types of microorganisms. Thus, any change in the primer sequence attached to the amplified region has the potential to affect the banding pattern of the DGGE. To demonstrate the implication of this, the 16S rRNA gene V3–5 region of B. subtilis 168 was attached to the variety of GC-clamp primers sequenced from F357GC, and their GC percentage and Tm were calculated. The

B. subtilis sequence attached to a correctly constructed F1 GC primer had a GC content of 58.06% and a melting temperature of 81 °C. The deviation DNA Damage inhibitor for an incorrectly assembled GC-clamp primer extended to a GC content of 55.44% and a melting temperature of 79 °C. This large degree of difference would easily translate into multiple bands on a DGGE gel and result in multiple bands for each sequence in the sample. None of the primer sequences in the PCR amplicons had 100% integrity, and each batch displayed a different degree of variation. In the original publication describing a 40-bp GC clamp, suggestions on the design of GC-clamp primers were made (Sheffield et al., 1989). Despite the actual sequence not being crucial, inverted repeats and strings of consecutive G nucleotides should be avoided

(Sheffield et al., 1989). Strings of G nucleotides would be problematic Selleck Z-VAD-FMK in the synthesis process (Sheffield et al., 1989). Avoidance of the recommended rules for GC-clamp construction, with the example as the one we used (F357GC F1) as evidence, shows that increased error occurs in a poorly planned GC clamp. Even when using

a GC clamp that follows the recommended rules of design, errors are still possible. (-)-p-Bromotetramisole Oxalate Purification of GC-clamp primers could eliminate this problem, and it has been recommended in the past (Felske & Osborn, 2005). Others have indicated that it is not necessary (Wu et al., 1998). The decrease in three nucleotides in the primer sequence for three of our primers might allow for an increased amount of amplification among organisms that do not share that sequence as part of their 16S gene, but there is no evidence that this affected the DGGE outcome. Microheterogeneity occurs when there are a small number of nucleotide changes in a gene between two bacteria of the same species. It can also refer to nucleotide differences occurring in various copies of a gene in a pure culture of bacteria. This has been known to cause problems in the comparison of 16S rRNA genes because of the variable copy number occurring among different organisms (Clayton et al., 1995). Any significant difference in the sequence of these genes could lead to the formation of multiple bands on a gel for the same type strain, as has been shown in Paenibacillus polymyxa (Nubel et al., 1996).

Subjects were predominantly male (64%) and from countries of low (<0.5%) HIV prevalence (84%). The median age was 30 years (range 14–87 years). Fifty per cent of subjects did not selleck compound belong to any known risk groups for HIV infection. The other 50% consisted of clients of commercial sex workers (16%), MSM (15%), IDUs (6%) and commercial sex workers (3%). Housekeepers,

who frequently sought care after injuries from needles left in trash bags, and police officers, who were exposed to infectious body fluids during violent arrests, accounted for 2 and 3% of the subjects, respectively. Four per cent were stable partners of HIV-infected persons. Excluded subjects differed from those included in the analysis in the following ways: they were more likely to be older than 40 years, more likely to be exposed through nonsexual routes, and less likely to be IDUs and clients of commercial sex workers but more likely to be exposed as housekeepers. Of 734 sexual exposures, 527 (72%) involved heterosexual contact and 132 (18%) homosexual contact (see

Table check details 1). Proportions of anonymous sexual contacts were similar in heterosexual and homosexual subjects (62 and 61%, respectively). Fifty-eight sexual assaults were also registered. The majority of the 179 nonsexual events were related to needlestick injuries (37%) and IDU equipment sharing (25%). In 208 episodes (23% of 910 eligible requests), the source was reported to be HIV positive, and in 187 episodes the Sitaxentan HIV-positive status could be confirmed. Among those for whom information was available, more than half were not under ART and had a detectable viral load at the time of exposure. In 702 events (77%), the HIV status of the source subjects was unknown. In these cases, 298 (42%) source persons could be tested and 11 new HIV infections were diagnosed (see Table 2). The likelihood of being able to contact and test the source varied significantly across risk categories. Police officers were more likely to have

their source found and tested compared with non-police officer subjects (57 vs. 32%; P<0.001). Conversely, IDUs, MSM and housekeepers were less likely to have their source tested than non-IDUs (4 vs. 34%; P<0.001), non-MSM (24 vs. 34%; P=0.02) and nonhousekeepers (10 vs. 33%; P=0.02), respectively. No difference was seen for commercial sex workers (27% of sources tested) and clients of commercial sex workers (32%). Heterosexual subjects had their contacts tested more often than did MSM (38 vs. 24%; P=0.001). The median time to consultation was 17 h after the exposure. Five hundred and forty-seven participants (60%) sought care within 24 h and 747 (82%) within 48 h. Among 910 eligible events for nPEP, it was received in 710 cases (78%) (Fig. 1). Twenty-six persons received nPEP twice during the study time, while five patients had three nPEP courses.

Subjects were predominantly male (64%) and from countries of low (<0.5%) HIV prevalence (84%). The median age was 30 years (range 14–87 years). Fifty per cent of subjects did not selleck chemical belong to any known risk groups for HIV infection. The other 50% consisted of clients of commercial sex workers (16%), MSM (15%), IDUs (6%) and commercial sex workers (3%). Housekeepers,

who frequently sought care after injuries from needles left in trash bags, and police officers, who were exposed to infectious body fluids during violent arrests, accounted for 2 and 3% of the subjects, respectively. Four per cent were stable partners of HIV-infected persons. Excluded subjects differed from those included in the analysis in the following ways: they were more likely to be older than 40 years, more likely to be exposed through nonsexual routes, and less likely to be IDUs and clients of commercial sex workers but more likely to be exposed as housekeepers. Of 734 sexual exposures, 527 (72%) involved heterosexual contact and 132 (18%) homosexual contact (see

Table buy Trametinib 1). Proportions of anonymous sexual contacts were similar in heterosexual and homosexual subjects (62 and 61%, respectively). Fifty-eight sexual assaults were also registered. The majority of the 179 nonsexual events were related to needlestick injuries (37%) and IDU equipment sharing (25%). In 208 episodes (23% of 910 eligible requests), the source was reported to be HIV positive, and in 187 episodes the G protein-coupled receptor kinase HIV-positive status could be confirmed. Among those for whom information was available, more than half were not under ART and had a detectable viral load at the time of exposure. In 702 events (77%), the HIV status of the source subjects was unknown. In these cases, 298 (42%) source persons could be tested and 11 new HIV infections were diagnosed (see Table 2). The likelihood of being able to contact and test the source varied significantly across risk categories. Police officers were more likely to have

their source found and tested compared with non-police officer subjects (57 vs. 32%; P<0.001). Conversely, IDUs, MSM and housekeepers were less likely to have their source tested than non-IDUs (4 vs. 34%; P<0.001), non-MSM (24 vs. 34%; P=0.02) and nonhousekeepers (10 vs. 33%; P=0.02), respectively. No difference was seen for commercial sex workers (27% of sources tested) and clients of commercial sex workers (32%). Heterosexual subjects had their contacts tested more often than did MSM (38 vs. 24%; P=0.001). The median time to consultation was 17 h after the exposure. Five hundred and forty-seven participants (60%) sought care within 24 h and 747 (82%) within 48 h. Among 910 eligible events for nPEP, it was received in 710 cases (78%) (Fig. 1). Twenty-six persons received nPEP twice during the study time, while five patients had three nPEP courses.

High-frequency stimulation of

the subthalamic nucleus (STN-HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l-DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN-HFS-evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l-DOPA-induced dyskinesias, focusing on the role of NR2B-containing N-methyl-d-aspartate receptors (NR2B/NMDARs). We applied STN-HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN-HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue PF-02341066 research buy Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN-HFS-induced

forelimb dyskinesia was decreased in a dose-dependent manner by systemic injections of CP-101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased Mitomycin C order by the non-selective N-methyl-d-aspartate receptor antagonist, MK-801. “
“A role for endocannabinoid signaling in neuronal morphogenesis as the brain develops has recently been suggested. Here we used the developing somatosensory circuit as a model system to examine the role of endocannabinoid signaling in neural circuit formation. We first show that a deficiency in cannabinoid receptor Progesterone type 1 (CB1R), but not G-protein-coupled receptor 55 (GPR55), leads to aberrant fasciculation and pathfinding in both corticothalamic and thalamocortical axons despite normal target recognition. Next, we localized CB1R expression to developing corticothalamic projections and found little if any expression in thalamocortical axons, using a newly established reporter mouse expressing GFP in thalamocortical projections. A similar thalamocortical projection phenotype was observed following removal of CB1R from cortical principal neurons, clearly demonstrating that CB1R in

corticothalamic axons was required to instruct their complimentary connections, thalamocortical axons. When reciprocal thalamic and cortical connections meet, CB1R-containing corticothalamic axons are intimately associated with elongating thalamocortical projections containing DGLβ, a 2-arachidonoyl glycerol (2-AG) synthesizing enzyme. Thus, 2-AG produced in thalamocortical axons and acting at CB1Rs on corticothalamic axons is likely to modulate axonal patterning. The presence of monoglyceride lipase, a 2-AG degrading enzyme, in both thalamocortical and corticothalamic tracts probably serves to restrict 2-AG availability. In summary, our study provides strong evidence that endocannabinoids are a modulator for the proposed ‘handshake’ interactions between corticothalamic and thalamocortical axons, especially for fasciculation.