The sampling interval in the X-Y axis was adjusted so that at lea

The sampling interval in the X-Y axis was adjusted so that at least 100 cells were counted for each region of interest. Coefficient of error attributed to the sampling was calculated according to Gundersen & Jensen (1987). Errors = 0.10 were accepted. In Figs 4

and 6 data are expressed as percentage surviving cells and in Table 1 as percentage lost, with the intact hemisphere corresponding to 100% for each check details individual mouse. The average number of TH+ cells counted in the intact SN was 2698 ± 699.57 and the average in the VTA was 2645 ± 782.94. All data are expressed as mean ± SEM unless stated otherwise. All statistical analyses were conducted using the Statistical Package

learn more for the Social Sciences 17 (SPSS Inc.). A paired Student’s t-test was used to compare the number of midbrain TH+ neurons on the intact and 6-OHDA-injected side. Linear regression was performed on the densitometric values and cell counting in Fig. 4, the correlations between the performances in the different behavioural tests in Fig. 5 and the correlations between behavioural impairments and densitometric values and cell counts in Fig. 6. A one-way anova with a Tukey post hoc was performed on the behavioural data comparing subgroups of lesioned mice in Fig. 7. The long-term deficits observed in lesioned and intact animals (Fig. 8) were compared using a two-way anova using the generalised linear model and the Wald chi-square test, with main effects of group and time. A one-way anova with a Student–Newman–Keuls post hoc was performed ever for all of the parameters described in Table 1, with all contrasts at least P < 0.05. The 6-OHDA injection was targeted at the mediolateral/anterior–posterior mid-point of the SN pars compacta, as illustrated

in a composite, horizontal TH-immunostained section in Fig. 2. The lesion caused in most cases a substantial loss of the A9 cells in the SN, while the A10 cells in the VTA were less affected. In the 40 mice included in the present study the total TH+ cell loss, in SN and VTA combined, ranged from −12 to −82% (mean, −58.5 ± 15.9%), which was highly significant compared to the intact hemisphere (t35 = −21.5; P < 0.0001). The loss of TH+ cells in the SN (−85.8 ± 15.7%; t35 = −31.2, P < 0.0001) was more severe than in VTA (−31.6 ± 18.6%; t35 = −9.8, P < 0.0001) when compared to the respective structures in the intact hemisphere. Representative examples of the extent of TH+ cell loss in animals with varying degrees of degeneration are illustrated in Fig. 3. As illustrated in the TH-stained sections in Fig. 3, the loss of TH+ cell bodies was accompanied by a substantial loss of TH+ innervation in the striatum.

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Chest radiographs may reveal interstitial lesions, cavities, fibr

Chest radiographs may reveal interstitial lesions, cavities, fibrotic lesions and mass lesions [101,102]. The diagnosis can be made by direct microscopic Selleck FK866 examination of smears from skin or other lesions that reveal septate yeast forms. Culture of

specimens from the bone marrow, lymph nodes, skin, and other infected sites shows a characteristic red colour on plates and diamorphism, which means that the fungus changes to a hyphal form at a lower temperature. Culture of these lesions is important, because other fungal infections, such as histoplasmosis and cryptococcus, may have similar clinical manifestations [90,103]. There are no widely available serological tests for this disease although antigen can be easily detected in the urine [104]. Penicilliosis should be treated with amphotericin B induction therapy for 2 weeks, followed by itraconazole 200 mg bd orally for 10 weeks and then maintenance therapy 200 mg once a day (category IV recommendation). Penicillium marneffei is sensitive to commonly used antifungals [105]. In Thailand, the greatest

treatment experience has been with intravenous amphotericin B 0.6 mg/kg per day for 2 weeks followed by oral itraconazole 200 mg bd po for a further 10 weeks. This regimen has a response rate of up to 95% and is well tolerated [106]. As discussed for other dimorphic fungi induction therapy with liposomal amphotericin B, 3 mg/kg/day intravenously, for the first 2 weeks should be considered in the UK (category IV recommendation). Itraconazole has been recommended as lifelong Selleck Pirfenidone suppressive therapy in patients infected with HIV who have completed successful treatment of P. marneffei infection [107]; however, there are some recent small case series suggesting that prophylaxis may be safely discontinued when immune reconstitution occurs on ART and individuals have sustained CD4 counts >100 cells/μL [108,109]. Prophylaxis with itraconazole may be considered for

travellers to endemic areas with CD4 counts <100 cells/μL. It has been suggested, based on studies in other systemic mycoses [110] and a small trial in Thailand [111], that itraconazole 200 mg once a day orally be given as prophylaxis to travellers to the Progesterone endemic areas who have CD4 counts <100 cells/μL [112]. There is little information on the impact of HAART on penicilliosis, but in Thailand the incidence appears low in individuals receiving HAART [113]. Most cases of penicilliosis occur at very low CD4 cell counts where HAART is indicated by current guidance. However, HAART should be commenced in all patients diagnosed with penicilliosis as soon as a clinical response is noted to treatment of penicilliosis. There is little information on IRIS due to penicilliosis but as with other dimorphic fungi it is a possible presentation. "
“Atazanavir (ATV) has demonstrated high efficacy and safety in both treatment-naïve and treatment-experienced patients.

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Our results suggest that practicing specialists and fellowship pr

Our results suggest that practicing specialists and fellowship programs should

avail themselves of opportunities for further education. Options mentioned by survey respondents included participating in the International Society of Travel Medicine (ISTM) courses and meetings as well as those of the American Society of Tropical Medicine and Hygiene, by obtaining a LBH589 Certificate in Travel Health (CTH) through the ISTM, and through accessing the CDC Travelers’ Health website training ( and informational tools. Malaria and travelers’ diarrhea were the travel-related diagnoses reported by the greatest number of respondents. Travel-related skin ailments and parasitic infections were also encountered by a high percentage of respondents. These are consistent with diagnoses reported through GeoSentinel.9,10 The number of respondents reporting travel-associated STIs was alarming. This problem has been recognized previously12 and consideration should be given to further investigation to explore better prevention strategies. Our results suggest that infectious disease experts should take detailed exposure histories and keep STIs in the differential diagnosis for ill-returning travelers. Our study

has several limitations. First, although our response rate was relatively high and the results represent physician responses from 48 different states, our results are not population-based and thus may not be generalizable to the entire US population and are not directly comparable to the results of GeoSentinal. Infectious disease physician members of the EIN may not be representative of all infectious click here disease clinicians practicing travel medicine. EIN membership represents about 15% of IDSA membership. Respondents with a greater interest in travel medicine may have been more likely to participate in the survey, potentially introducing a form of responder

and selection bias. Our survey method, which is not an audit, introduces the possibility of recall bias. Additionally, limiting our survey to infectious disease experts may introduce referral bias for both pre-travel and post-travel PRKD3 queries, as more severe or recalcitrant illness may have been encountered by these practitioners. Finally, the length of our survey was constrained by EIN policy and thus we were unable to explore many interesting topics including: diagnostic testing approaches, detailed traveler destination information, vaccination practices, and detailed background demographics concerning responding infection diseases specialists. Infectious disease clinicians are a valuable population to engage further in the study and practice of the unique specialty of travel medicine. The relatively recent requirements for travel medicine training during fellowship may need to be enhanced in light of more than one third of recent program graduates reporting inadequate training.

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[43] While a number of pharmacists

expressed negative per

[43] While a number of pharmacists

expressed negative personal attitudes towards CPD, the majority of the research participants within the various studies seemed beset by the compound interaction of barriers apparently outside of their control, such as time and resource issues. A number of theories have been developed to examine the process by which people attribute behaviour (including their own) to internal or external causes and there is now a large body of Belnacasan mouse evidence showing that people’s judgements about the causes of behaviour are not completely rational but biased.[44] A common observation is that people attribute successes internally, as within their control, whereas failures are attributed externally to others or to the circumstances, GKT137831 a concept captured by the term ‘self-serving attribution bias’.[44] A self-serving bias is therefore said to exist where an individual’s assignment of responsibility affects his or her beliefs in an optimistic way, a way that

makes things appear better than they are from the individual’s point of view. We believe there may be an element of self-serving attribution bias at play in terms of pharmacy professionals’ stated barriers to CPD. That is, pharmacy professionals’ own explanations for lack of participation in CPD could stem from their erroneous perception that it is mainly factors external to their control that pose the real barriers, and that ultimately external factors are helping to drive participation in CPD. This would indicate that making CPD a statutory requirement could compel pharmacy professionals to engage with the process at some level, and indeed the personal correspondence referred to above seems to indicate the same. Nonetheless, if CPD is to Dolutegravir be truly successful and useful for revalidation, it seems that people’s beliefs and attitudes must be addressed through the modification

of the various other external barriers perceived to be impacting on CPD behaviour. The implications of the current findings can be considered as follows. If CPD is to succeed and be useful as part of revalidation, pharmacy professionals’ beliefs and attitudes must be addressed by recognising and modifying barriers through a combination of four main categories of regulatory, professional, work-related and personal channels (see Figure 2). We believe it is possible to draw on the current findings to suggest a number of remedial steps in relation to these categories so as to ultimately impact on pharmacy professionals’ personal motivations and therefore participation in CPD.

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Treatment was commenced with oral levofloxacin (500 mg once daily

Treatment was commenced with oral levofloxacin (500 mg once daily), rifampicin

(600 mg once daily), and co-trimoxazole (sulfamethoxazole 1600 mg/trimethoprim 320 mg, three times a day) for 3 months, followed by levofloxacin (500 mg once daily) and co-trimoxazole (sulfamethoxazole 800 mg/trimethoprim 160 mg, three times a day) for 9 months. His clinical course was followed up at monthly intervals in the outpatient department. Repeat MRI scans at 8 and 11 months showed a decrease in LY2109761 ic50 the diameter of the granuloma implying favorable response to therapy (Figure 3). Rhinoscleroma is endemic to many countries but this chronic granulomatous disease occurs sporadically in Western Europe usually in immigrant populations arriving from countries where the disease is endemic. This disease is transmitted by air and humans are the only identified host. Our patient had lived in Italy for 8 years without traveling back to Egypt; we had hypothesized that he might have contracted the disease in Italy living in close contact with other immigrants from Egypt. Moreover, we cannot exclude the possibility the patient might have acquired the infection in his country of origin with a

delay in diagnosis because of the slow progression of the disease. Rhinoscleroma usually Talazoparib mw involves the nasal cavity and nasopharynx, but it may also affect the larynx, trachea, bronchi, the middle ear, oral cavity, paranasal sinuses, orbit, soft tissues of the lips, and nose. Rhinoscleroma is divided into three stages: catarrhal, granulomatous, and fibrotic.[4, 5] The catarrhal stage causes symptoms

of non-specific rhinitis that can last for weeks or months and often evolves into purulent and fetid rhinorrhea with crusting. The second granulomatous stage is characterized by development of a bluish red nasal mucosa and intranasal rubbery nodules or polyps, and manifests with epistaxis and nasal deformity; destruction Interleukin-3 receptor of the nasal cartilage and bony destruction are also features. The third sclerotic stage is characterized by extensive fibrosis leading to extensive scarring and possible nasal/laryngeal stenosis.[2, 5] The lack of awareness when disease presents in developed countries may lead to a delay in diagnosis and can cause nasal deformities, airway obstruction, and symptoms mimicking allergic rhinitis or prolonged sinusitis. Rhinoscleroma may mimic granulomatous, neoplastic or systemic infectious diseases including tuberculosis, actinomycosis, syphilis, leprosy, histoplasmosis, blastomycosis, paracoccidioidomycosis, sporotrichosis, mucocutaneous leishmaniasis, lymphomas, verrucous carcinoma, sarcoidosis, and Wegener’s granulomatosis.

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However, at face value, it seems that the IDF predictions for dia

However, at face value, it seems that the IDF predictions for diabetes in China in 2010 failed to take account of the true prevalences measured in 2000–2001. That subsequent diabetes prevalence measured by glucose SB431542 research buy estimates in a large representative sample in 2007–20085 would be greater than the IDF prediction was perhaps entirely predictable, given that diabetes prevalence has been increasing, rather than reducing, everywhere else. Indeed, published data available in 1997 suggest that China had already experienced a three-fold rise in diabetes prevalence in the

preceding decade.8 It seems implausible to think that with increasing Westernisation in China, a factor known to influence increased diabetes prevalence, subsequent diabetes prevalence would fall as predicted by the IDF in 2010. It is possible that in setting the 2010 estimate there were concerns that the prevalence found in the 2000–2001 study was exaggerated. This seems improbable, however, given that another large prevalence study in 1995 of 29 859 subjects aged 30–64 years in Beijing found a measured diabetes prevalence of 3.63%,9,10 and is thus entirely consistent with the 5.2–5.8% prevalence found in the InterASIA study some five

to six years later given the rising diabetes rates in China at that time. Is there evidence that the apparent underestimate for China was repeated for other countries and regions? Unfortunately, the answer appears Ruxolitinib to be yes. In Sri Lanka, for example, the IDF predicted an 11.5% prevalence

in 2010. This was despite a publication which showed in 2005 that true measured prevalence in 6447 subjects was 14.2% for men and 13.5% for women,11 and a rather ironic comment in the Ceylon Medical Journal in 2006 that ‘The Nintedanib (BIBF 1120) World Health Organization and International Diabetes Federation estimates and forecasts are much lower than the available local prevalence rates’.12 In the United Kingdom, the introduction of incentive payments in general practice led to the development of reasonably robust data on, among other things, diabetes prevalence. Thus, whilst the IDF Atlas was predicting a 4.9% prevalence in 2010, the data published annually by the NHS Information Centre, and freely available on the internet, showed that in 2008/09 the diabetes prevalence was 5.1% whereas in 2009/10 it had increased to 5.4%.13 In the Middle East, the gap between the IDF prediction and published actual prevalences may be greater. For instance in Iran, the IDF prediction for 2010 was a 6.1% prevalence,14 whereas meta-analysis of available data between 1996 and 2004 suggests that the figure in those aged >40 years was already 24% at least six years before the IDF prediction of only a quarter of that value.

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subtilis and Escherichia coli; however, the precise manner of Spo

subtilis and Escherichia coli; however, the precise manner of SpoIISA toxicity remains unknown. In this work, we focused on the N-terminal, transmembrane domain of SpoIISA and verified the prediction of its topology. Using truncated SpoIISA constructs, we show that the entire transmembrane domain is required for its toxicity. Moreover, we propose that

the oligomerization of this transmembrane domain is crucial for activity of SpoIISA, possibly by forming a pore-like structure. “
“The pHW126-like plasmids are a recently discovered small group of cryptic plasmids replicating by the rolling circle mode. The replication origin of pHW126 consists of a conserved stretch, four perfect Avasimibe order direct repeats and a so-called accessory region. The latter increases plasmid stability but is not absolutely necessary for replication. Here, we report that

deletion of the accessory region causes rapid multimerization of pHW126. While the number RO4929097 of pHW126-units per cell remains constant, the number of physically independent plasmid molecules is reduced by approximately 40%, rendering random distribution to daughter cells less effective. A conserved inverted repeat within the accessory region could be identified as a sequence necessary for maintaining pHW126 in its monomeric form. A mutant version of pHW126 lacking this inverted repeat could be rescued by placing the single-strand initiation site (ssi) of pHW15 on the plus strand, while including the ssi in the opposite direction had no effect. Thus, our data provide evidence that multimer formation is, besides copy number

reduction and ssDNA accumulation, an additional means how loss of a mechanism ensuring efficient lagging strand synthesis may cause destabilization of rolling circle plasmids. Plasmids of bacteria appear in a wide variety of sizes, have different Sulfite dehydrogenase copy numbers and may encode various functions. Accordingly, plasmids have evolved different strategies for their maintenance. Huge circular plasmids usually replicate by the theta mechanism, are frequently self-transmissible and have a low copy number of just a few molecules per cell. Consequently, these plasmids depend on systems mediating partitioning, multimer resolution and postsegregational killing to ensure distribution to daughter cells. Small plasmids may also use the theta mode, but many of them replicate by the rolling circle mechanism or by strand displacement (del Solar et al., 1998; Rawlings & Tietze, 2001; Khan, 2005). Small plasmids are nonself-transmissible but may possess systems mediating mobilization in the presence of a conjugative plasmid (Francia et al., 2004; Garcillan-Barcia et al., 2009). Owing to their high copy number, small plasmids can rely on random distribution.

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norvegicum and S halorespirans; and some that might remove toxic

norvegicum and S. halorespirans; and some that might remove toxic material Trametinib chemical structure from the water, such as bacteria in genera Beggiatoa, Desulfobacterium and Sulfurospirillum. In addition, a few of the genera detected might have the ability to utilize organic phosphorus, such as those in genus Enterobacter. In short, most of the endophytic bacteria in reed roots might have a strong potential to enhance phytoremediation, especially with regard to the nitrogen and sulfur cycles and removal

of some organic matter during water purification by the reed-constructed wetland. However, no ammonia-oxidizing bacteria (AOB), such as Nitrosomonas and Nitrosospira, and no anammox bacteria, such as Candidatus‘Brocadia’, ‘Kuenenia’, ‘Scalindua’, and ‘Jettenia,’ which are often detected in certain soil types and at particular depths (Humbert et al., 2010), were detected in our clone library. This suggests that the endophytic buy Avasimibe bacteria in reed roots are probably not involved in the first step of nitrification during which ammonia is converted to nitrite, and anaerobic oxidation of ammonium, but could carry out the other steps of nitrification as well as denitrification and nitrogen fixation. However, some AOB and Bacillus bacteria have been found in the rhizosphere of P. australis (Xing et al., 2008; Xie et al., 2009), indicating that bacteria in the rhizosphere and endophytic

bacteria may play different roles in nutrient metabolism in wetland ecosystems. However, because the cloning sequences cannot provide direct information on the function of the individual community members, further work is necessary to improve our understanding of the mechanisms through which endophytic bacteria of reed roots mediate water purification. We would like to thank

Daniel Keck at UC Santa Cruz for his assistance with English language and grammatical editing of the manuscript. This work was funded by the Scientific Research Program of Beijing Municipal Commission of Education. Y.H.L. and J.N.Z. contributed equally to this work. Nucleotide Dipeptidyl peptidase sequence data reported are available in the GenBank databases under the accession numbers from GU178822 to GU178836, from GU178838 to GU178862 and from GU178864 to GU178880. “
“Subtilisin-like proteases are widely distributed and reported to be required for virulence in pathogenic fungi. In chestnut blight fungus Cryphonectria parasitica, prb1, encoding a putative subtilisin-like protease, was expressed and recombinant Prb1 protein was shown to have a protease activity in vitro. prb1-deleted mutants exhibited reduced total protease activity by 60%. The Δprb1 mutants showed a phenotype of reduced aerial hyphae, lower level of sporulation, and a significant reduction in virulence. Additionally, site-directed mutagenesis of Prb1 protein revealed that D195, H227, and S393 are critical for C. parasitica Prb1 function in vivo.

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[6-9] Thus far, these efforts have been marginally effective Fur

[6-9] Thus far, these efforts have been marginally effective. Further, the French Health Authorities

have forced the hospitals to follow very strict mandatory guidelines when admitting patients from abroad; these hospitals have isolated these patients upon repatriation and admission followed by rapid attempts to detect MRB—in fact, the guidelines employed include travelers who have been hospitalized for more than 24 hours in a foreign country within the last year.[10] While these measures aim to limit MRB exposure to the greater French population, they also dramatically complicate the procedure of repatriation of patients; hospitals are reluctant to offer admission to these individuals immediately after repatriation. Medical repatriation and evacuation services must deal

with this new challenge. In this study, we attempted to evaluate the incidence of MRB this website occurrence among patients treated in foreign hospitals and repatriated by international inter-hospital air transport; obviously, the determination of the incidence of this important and complex medical issue will allow hospitals to better manage these patients and adjust admission procedures in an appropriate fashion. This descriptive, retrospective study was carried out in Mondial Assistance France (MAF, French branch of Allianz Global Assistance Group), which provides worldwide medical assistance and aeromedical repatriations and evacuations. GDC-0449 datasheet As previously described, the company has a medical coordination platform (MCP) in Paris with a number of physicians, including emergency physicians and critical care specialists.[11] MAF has medical teams involved in the evacuations and repatriations; members of this team include emergency physicians, nurses, and nurse anesthetists. International transfers are performed using air ambulance aircraft or commercial airlines, depending on the severity and

needs of the patient during the transfer. In most cases, the MAF MCP attempts to directly contact the physician in charge of the patient prior to transfer so as to obtain detailed and accurate medical information. If this contact cannot be established, the intervention of a local MAF agent, termed the medical correspondent, is required. The medical correspondent then provides a written medical report. The actual movement second of the patient is determined entirely by the MAF MCP physician, including the decision to repatriate the patient, the time period in which to perform the repatriation, and the method of transfer. The identification of an accepting hospital and specific bed assignment is also the responsibility of the MAF MCP. The records from all consecutive aeromedical evacuations and overseas repatriations executed by MAF from December 2010 to November 2011 were reviewed for this study by a single investigator, an MCP physician at MAF. All inter-hospital transfers from a foreign to a French hospital and escorted by one of the MAF teams were included.

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4a and b) The TSP of hutHUI is located 70 nucleotides upstream o

4a and b). The TSP of hutHUI is located 70 nucleotides upstream of the translational start of hutH. For the divergent genes hutG and hutR, TSPs were mapped 24 bp upstream of the start codon of hutG, whereas the TSP of hutR was identical to the first guanine residue of the GTG start codon, indicating the presence of a leaderless transcript (Pátek

et al., 2003). The TSPs were used to deduce the Selleck GSI-IX associated promoter regions according to corynebacterial consensus sequences for −10 and −35 regions (Pátek et al., 2003). The transcription of the hut genes is most likely driven by the housekeeping sigma factor SigA. The predicted −10 regions of the hut promoters (TAttgT, TAggaT, TAgggT) contain the typical leading TA and trailing T residues, whereas the predicted −35 regions (TgGtgA, gTGcCA, ccGcgc) showed varying matches to the corynebacterial consensus sequence. To demonstrate the direct interaction of HutR with the upstream regions of the

hut genes, DNA band FK506 in vivo shift assays were performed with Cy3-labeled PCR fragments. For this purpose, the HutR protein was tagged with streptavidin, expressed in E. coli DH5αMCR, and purified by means of Strep-Tactin sepharose-packed columns (data not shown). First, the upstream region of hutH and the intergenic region of hutR-hutG were amplified by PCR (Fig. 4a and b). Retardation of the respective DNA fragments 1 and 4 was observed, as the HutR protein apparently bound to the DNA in vitro (Fig. 4c). A DNA sequence containing a LexA binding site of C. glutamicum (Jochmann et al., 2009) served as a negative control. Subsequently, the DNA fragments were shortened to yield Fossariinae smaller candidate HutR binding regions upstream of hutH (fragments 2 and 3) and in the hutR-hutG gene region (fragments 5 – 7). The results of the respective DNA band shift assays revealed a candidate HutR binding region of 41 bp upstream of

the hutH coding region (Fig. 4a) and a 34-bp region between hutR and hutG (Fig. 4b). In both cases, the deduced HutR binding region is located upstream of the −35 promoter region, suggesting that the HutR regulator might function as an activator (Madan Babu & Teichmann, 2003). To identify the DNA-binding motif of HutR, both DNA regions were aligned, thereby revealing the presence of a common 14-bp motif with the consensus sequence TCTGwwATwCCAGA in front of hutH and in the hutR-hutG gene region (Fig. 5c). This DNA motif contains the 4-bp terminal palindrome TCTG/CAGA. To elucidate whether the 14-bp DNA motif is required for the specific binding of the HutR protein, fluorescein-labeled 40-mers carrying this sequence in the center were used for DNA band shift assays (Fig. 5a and b). Furthermore, mutated versions of the 14-bp motifs were generated by introducing transitions in the four palindromic bases. In these cases, the purified HutR protein failed to shift the mutated 40-mers (Fig. 5a and b).

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