A pharmacokinetic study in healthy volunteers was reminiscent of the saquinavir study, and was terminated early because of high rates of severe transaminitis [101]. Recent data suggest that atazanavir with or without ritonavir boosting had unfavourable pharmacokinetics when administered with rifampicin [102–104]. Trough atazanavir ZD1839 molecular weight concentrations were reduced by >80% [103]. Tipranavir concentrations were reduced by 80% by rifampicin [105]. The interaction between darunavir and rifampicin has not yet been investigated. In line with other PIs, it is currently recommended that darunavir should not be coadministered with rifampicin. The use of

rifabutin in treating TB in HIV-positive patients is discussed above (see ‘Use of rifapentine’ [EII]). Rifabutin can be administered Veliparib order with unboosted PIs except saquinavir [106], although they will rarely be used in practice. The balance between rifabutin induction and PI inhibition of CYP3A4 means that the dose of rifabutin should be decreased from 300 to 150 mg daily to avoid toxicity [48,70]. If PIs are used with low-dose ritonavir boosting then the dose of rifabutin should be reduced to 150 mg three times per week [49,105]. This recommendation

is derived from pharmacokinetic studies and modelling. There are no clinical outcome data for either HIV or TB using this strategy. Adherence should be monitored closely as the dose of rifabutin would become inadequate if the boosted PI is not taken concomitantly. Where available, drug levels of the PI should be measured. There have been reports of acquired rifabutin resistance occurring even in patients taking rifabutin 150 mg three

times a week with boosted PIs. No rifabutin drug levels were available in those patients and, although there may have been other reasons for these failures, physicians may consider measuring the levels of rifabutin and its active metabolite 25-0-desacetyl rifabutin if results are available in a timely manner [107]. Complex Cell press interactions may occur when a rifamycin is given with salvage regimens such as an integrase, boosted PI and an NNRTI. Rifabutin is safer than rifampicin, but there are few data to guide the clinician regarding dose modification. TDM is recommended. We recommend that PI/ritonavir combinations should not be given with rifampicin. [EII] If possible, the HAART regimen should be changed to avoid PIs. If effective HAART necessitates the use of PIs then rifabutin should be used instead of rifampicin. [AII] Raltegravir is metabolized by UGT1A1 glucuronidation. Rifampicin is an inducer of UGT1A1, and reduces trough levels of raltegravir by approximately 60% [108]. Because the antiviral activity of raltegravir 200 mg twice daily was very similar to that of the licensed dose (400 mg twice daily), an earlier recommendation was that standard doses of raltegravir should be used with rifampicin. There is at least one report of raltegravir failure when given like this with rifampicin (S.

5 log from 3.2 × 105 to 3.7 × 105 CFU mL−1. Only slight changes in the pH of the fermentation were observed during the first 18 h, followed by a sharp decrease to a pH of 4.5 within 24 h. These data are in agreement with previous analyses using Tibetan and Bulgarian kefirs that demonstrated that lactic streptococci, specifically Lactococcus spp., are the dominant microorganisms during the first 24 h of fermentation (Simova et al., 2002; Chen et al., 2008). Furthermore, lacticin 3147 production by L. lactis was detected >8 h into the kefir fermentation and persisted thereafter (Fig. 2b). Indeed, a random sampling of 100

presumptive lactococci isolated from kefir milk (24 h) confirmed that approximately 90% of the colonies analysed were able to inhibit L. lactis HP but not L. lactis HP (pMRC01) indicating them to be producers of lacticin 3147 (data not shown). These results establish that lacticin CDK inhibitor 3147-producing lactococci are the dominant lactococci present

within the kefir-fermented milk. Of particular note with regard to presumptive Lactobacillus populations is the fact that previous culture-dependent analysis of a Turkish kefir found that lactobacilli increased from undetectable levels to 108 CFU mL−1 over the course of a fermentation (22 h) in milk and that similar findings have also been reported with respect to the use of a Brazilian surgary kefir, i.e. lactobacilli increased from 6.6 × 106 to 2 × 108 CFU mL−1 (Magalhaes et al., 2010). GSK1120212 chemical structure As lacticin 3147 has previously been shown to inhibit a number of Lactobacillus species, it is possible that the production of lacticin 3147 may negatively influence cultivable Lactobacillus populations within the kefir community (Ryan et al., 1996). Future work is required to fully elucidate the activity of lacticin 3147 against these populations in this environment. The taxonomic assignments from kefir check details milk and its

corresponding starter grain (interior and exterior) are summarized in Fig. 3. A total of 17 416 unique V4 variable regions of the 16S rRNA gene were amplified from the interior kefir starter grain (4883 reads), exterior starter grain (3455 reads), and the corresponding kefir milk fermentate (9078 reads). Diversity richness, coverage, and evenness estimations were calculated for each data set (Table 1). The Chao1 estimator of species richness at the 98% similarity level was 609.3 for the kefir milk, 170 for the exterior starter grain, and 358 for the interior starter grain. For each sample, the Good’s coverage at the 98% similarity level was approximately 98%. A lower level of microbial diversity was observed on the exterior surface of the starter grain with a Shannon diversity index of 1.04 at the 98% similarity level, while the Shannon diversity indices for kefir milk and the interior starter grain were both over 2.0. Rarefaction curve analysis revealed that the overall bacterial diversity present is well represented (Fig. 4).

For traumatic deaths, Europe contributed to 68% (81) of deaths followed by the Americas (12, 10%), and the Mediterranean region (10, 8%). Similarly, of the 341 deaths due to failure of the circulatory system, 74% (254) occurred in Europe, followed by the Americas (38, 11%), and the Mediterranean region (21, 6%). The five countries Galunisertib where most deaths occurred were all EU: being Spain (195, 33%), France (34, 6%), Greece (28, 5%), Portugal (28, 5%), and Netherlands (25, 4%). The most common non-EU countries where deaths occurred were the

Americas (21, 5%), United Arab Emirates (15, 3%), Canada (13, 2%), Australia (9, 2%), and Iraq (7, 1%). Comparison of the age distribution of death from failure of the circulatory system between the deaths abroad (Figure 1A and B) and the Scottish population (Figure 1C and D) suggested that a higher proportion of deaths were occurring in lower age groups among those who died abroad. It was

decided to test for any association between age at death and location of death (abroad/not abroad) across the age range 25 to 64. Using Method A, a significant association was found between death abroad and age at death for all (χ2 = 26.9, df = 3, p < 0.001) and for males (χ2 = 20.7, df = 3, p < 0.001), but not for females (χ2 = 2.7, df = 1, p = 0.099); numbers of females were too low for analysis across four age groups. For Method B, which sought to estimate an expected age distribution of death among travelers by using data from the International Passenger Survey (IPS2002), a significant association was found between Selleck Belnacasan death abroad and age at death for all (χ2 = 21.3, df = 3, p < 0.001). There is a great deal of literature in travel medicine on deaths among travelers relating to travel to remote areas,15 deaths during the journey,16,17 and deaths due to specific causes, eg, infectious diseases,18 accidents,19–21,22 cardiovascular disease,19,20 and envenomation.23 This analysis was carried out to estimate the causes of death among travelers Thiamet G from Scotland abroad and to test whether travel altered the risk of dying from circulatory disease among Scots

abroad. The data highlighted the low proportion of infection-related deaths and the high proportion of deaths due to failures in the circulatory system and to accidents. For the 5-year period 2000 to 2004, there were 572 reports on the cause of death compared to 952 deaths reported in a similar study published in 199124 for the 15-year period 1973 to 1988. This observed increase in average number of cremations among travelers per year (114.4 per year in this study compared with 63.5 previously24) may reflect either increased numbers of deaths abroad as observed elsewhere22 and/or an increase in preference for cremation observed in the UK population.14 If the former then this may merely reflect the increase in travel observed among the UK population.12 That being said the UK Office of National Statistics estimated 8.

Many of these partake in aquatic activities such as swimming, snorkelling, scuba diving, and water skiing. As dangerous box jellyfish are present in Malaysian waters, this exposes participants to the risk of severe envenomation, especially if personal protective precautions are not undertaken. Travelers to this region need to have these aquatic risks and their mitigation addressed as

part of pre-travel health education. It is imperative that government authorities, aquatic resorts, and aquatic operators warn clients of the potential threat so that they can make an informed decision prior to entering the sea in such areas. These warnings should ideally be included in pre-trip information from travel agents and travel medicine GSK126 order advisors. However, it is also essential that adequate and appropriate warning signs are present in affected areas and multi-lingual brochures are provided to tourists by resorts and operators. Figure 6 shows a suitable sign, as well as vinegar access. Neither scraping the skin nor flushing with fresh water should

be used on the sting site as both can trigger discharge of further nematocysts. Sea water can be used to wash off tentacles, or preferably vinegar, LDE225 purchase if available, which rapidly and effectively neutralizes cubozoan nematocysts.24

Vinegar should be readily accessible to locals and tourists alike for prompt access in the event of a sting. Lifeguards trained in CPR should be provided by coastal tourist resorts to increase the likelihood Parvulin of survival from a severe chirodropid sting. Potentially lethal chirodropid and Irukandji jellyfish are present in Malaysian waters with an associated incidence of morbidity and mortality in both tourists and Malay Nationals. It is essential that adequate preventative treatment and management strategies are implemented to minimize harm from these species. DAN AP provides one method to address the historic lack of knowledge about such stings to improve sting prevention. Preventative strategies must include education of travel medicine specialists, travel agents, local medical and ambulance personnel; government-initiated policies for education of tourist bodies and tourism operators; multi-lingual resources of educational literature; and signage with clear, accurate warnings for visitors to these areas; fenced walkways for entry to beaches with multi-lingual signs at their start and entrance to the beach; and vinegar bottles of up to 5 L quickly and easily accessible.

A diagnosis is identified in around one-third to one-half of all patients. Whilst the ultimate diagnosis was frequently obtained at other sites, BME was the only site in a minority of cases in most studies [21–24]. Diagnosis by BME may be achieved through bone marrow culture, visualization of granulomas and/or histologically apparent organisms. Special stains for mycobacteria and fungus, and immunohistostaining for lymphoma

should be requested. If other HIF-1 activation diagnoses such as Castleman disease, visceral leishmaniasis and Penicillium marneffei are under consideration then discuss with a histopathologist and, if the patient is not under the care of an HIV or infectious disease specialist, then contact your local HIV or Infectious disease department for advice. FNA is a worthwhile procedure in patients Pifithrin-�� supplier with adenopathy and fever. Sampling is quick and easy to perform and may

obviate the need for more invasive sampling and enable immediate treatment of specific infections [25,26]. In one large reported series, which included more than 650 samples, a diagnosis was reached in 80% of cases with malignancy accounting for 13% and infection 14% (mainly mycobacterial). A definitive diagnosis was associated with deep aspirate location and lesion size >2 cm [27]. The procedure is associated with a low rate of uninterpretable slides/inadequate sample or false-negative results. In these situations consideration should be given to either

lymph node sampling or surgical excision of the lymph node. Lymph node biopsy is a useful alternative to FNA. It has been shown to have a good diagnostic yield in patients with smear-negative TB [28]. If Castleman disease is suspected biopsy or excision of the lymph node may be preferable to FNA due to the focal nature of Castleman disease within lymph nodes. The presence of hepatomegaly or splenomegaly have been reported to be the most important factors in predicting the usefulness of the PLB, with a positive predictive value (PPV) of 86.1% and negative predictive value (NPV) of 68.2%. In patients with tuberculosis, an increased alkaline phosphatase and hepatomegaly had a PPV of 86.4% Vildagliptin and NPV of 71.4% [29]. Imaging plays a key role in the diagnostic work up in PUO. It assists in identification of focal pathology that may be amenable to biopsy in order to get a tissue diagnosis. A chest X-ray film should be part of the routine investigations. More detailed investigations should be based on clinical symptoms and signs and may include CT/MRI of chest, abdomen and pelvis. There is emerging evidence that 18-fluorodeoxyglucose positron emission tomography (FDG-PET)/CT scanning can help identify the source of disease when earlier investigations have been unsuccessful [30,31]. “
“Our objectives were to assess trends in late presentation and advanced HIV disease (AHD) and determine associated risk factors.

Participants were clinically evaluated and interviewed regarding their adherence to ART pre-travel and post-travel, international border passage with selleck kinase inhibitor medications and reasons for missing ART doses. Post-travel change in CD4 counts and RNA-PCR viral load were measured. Outcomes were proportion who missed ≥1 dose of ART during Hajj compared with pre-travel or post-travel and failure of ART, defined as decline in CD4 cell counts or high viral load or both. Results. Thirty-one HP and 27 NP had similar characteristics and were away for (median [range]) 36 days (28–43

days) and 84 days (28–84 days), respectively (p < 0.0001). Those who missed ≥ 1 ART doses among HP and NP while away were 16/31 (51.6%) and 5/27 (18.5%), respectively with risk ratio (95% confidence interval [CI]) 2.79 (1.18–6.60). Among HP, the proportions who missed ≥ 1 ART doses pre-travel and post-travel were lower than those who missed it during Hajj. Those who failed ART among HP compared with NP were 15/31 (48.4%) and 5/27 (18.5%), respectively with odds ratio (95% CI) 4.13 (1.10–17.21). Reasons for missing ART included forgetfulness, exhaustion of supplies, stigma, spiritual alternatives, or disinclination; ZD1839 chemical structure five patients were unable to cross airports with medications. Conclusions. Patients who went on Hajj were more likely to miss medications and to have ART failure due to several reasons including inability

to cross borders with medications. Annual Hajj pilgrimage to Mecca in Saudi-Arabia is a fundamental

religious rite in Islam that is observed by Muslims throughout the world at least once in a lifetime. It is an annual mass gathering with a congregation of over 2.5 million people that takes days to weeks during the 11th to 12th months of the Islamic lunar calendar.1,2 Many countries with considerable burden of human immunodeficiency virus (HIV) infection in Africa and Asia also have substantial Muslim populations. With massive and rapid anti-retroviral therapy (ART) expansion,3,4 infected patients on ART might be able to go for the Hajj. But to succeed, its provision and expansion should adapt to cultural and religious practices like Hajj.5 Its sustained effectiveness depends on long-term, regular, fixed interval, and time-specific dosing schedules Thalidomide that ensure drug concentrations are consistently high.6,7 However, infected Hajj-pilgrims (HP) encounter some challenges regarding adherence to ART. Firstly, they travel from their countries crossing national boundaries to another country where passage with medications might prove difficult. Secondly, the circumstances, mobility, and overcrowding with strong potential for stigma, and the rigorous rites might compromise adherence to ART.1,2 Thus, consequent suboptimal adherence might lead to reduced effectiveness, therapeutic failure, emergence of resistance, and potential transmission of drug-resistant virus strains within the global community.

D70847), and Rba. azotoformans S3 (GenBank accession no. DQ402051). Based on these results, CGMCC 6086 was identified as Rba. azotoformans. Two DNA fragments containing carotenogenesis genes were amplified via PCR from the genomic DNA of Rba. azotoformans CGMCC 6086. The GenBank accession number was JF723980. A 4.9 kb fragment containing four carotenogenesis genes (crtA, crtI,

crtB, and tspO) was amplified with primers Ra-Ad and Ra-Od (Table 1). The other 5.3 kb fragment containing four carotenogenesis genes (crtC, crtD, crtE, Talazoparib in vitro and crtF) was amplified with primers Ra-Fd and Ra-Cd (Table 1). The putative gene products showed a higher identity to their counterparts in Rba. sphaeroides (83–97%) than in Rba. capsulatus (48–68%), Rvi. gelatinosus (33–53%), and Rhodopseudomonas palustris (42–53%) by protein-to-protein alignment AZD2281 datasheet (Table S2). The neighboring genes on both sides of the crtAIB-tspO fragment were bchI and the ferredoxin gene. Those on both sides of the crtCDEF fragment were the dihydrodipicolinate synthase gene and bchC (Fig. 2). According to the acquired sequence of carotenogenesis gene cluster from Rba. azotoformans CGMCC 6086 (GenBank

accession no. JF723980), four primers (Ra-Af, Ra-Of, Ra-Ff, and Ra-Cf) were designed to amplify the sequence between the crtAIB-tspO and crtCDEF fragments. However, no fragments could be amplified by those primers. The result meant that the eight carotenogenesis genes were located in two separate regions within the genome and were clustered Neratinib purchase as crtAIB-tspO and crtCDEF. Several organizations of the carotenogenesis gene cluster in purple photosynthetic bacteria have been reported (Fig. 2). In Rba. sphaeroides and Rba. capsulatus, eight carotenogenesis genes were successively clustered in the sequence crtAIB-tspO-crtCDEF (Armstrong et al., 1989; Lang et al., 1995). In Rvi. gelatinosus, seven carotenogenesis genes are separated into three parts (crtBCDA, crtFE, and crtI fragments) by genes involved in the biosynthesis of bacteriochlorophyll and photosynthetic

reaction center (Igarashi et al., 2001). In Tca. roseopersicina, a partial carotenogenesis gene cluster has been cloned. A crtCDEF fragment and a separated crtI gene were determined (Kovacs et al., 2003). In Rps. palustris, the crtBCDA and crtFE fragments were separated by a 21.9 kb fragment containing genes involved in phosphonate metabolism (Larimer et al., 2004). In Rhodospirillum rubrum, the crtBCDA and crtFE fragments are widely dispersed in the chromosome (Reslewic et al., 2005). In this study, the eight carotenogenesis genes from Rba. azotoformans CGMCC 6086 were located in two separate regions, although each region had the same gene order as that of Rba. sphaeroides and Rba. capsulatus. The genes located downstream of tspO and crtC were not involved in the photosynthetic gene cluster. The organization of the carotenogenesis gene cluster was unusual for purple photosynthetic bacteria.

, 2010). Although integrons are transposition defective, they can be mobilized in association with functional transposons and/or conjugative plasmids (Cambray et al., 2010). Despite their relevance in HGT processes, the association of integrons with conjugative plasmids has been poorly addressed in aquatic environments. Wastewater treatment plants (WWTPs) are important reservoirs of resistance determinants and favourable places for HGT, due to high microbial abundance, high nutrient concentrations and intense selective pressures imposed by antibiotics, detergents and other pollutants

(Schlüter et al., 2007). Moreover, it has been shown that natural conjugative plasmids may induce the development of biofilms, which might also increase the chances of cell-to-cell contact and the occurrence of HGT events (Ghigo, 2001). As a result, WWTPs may favour the ATR cancer persistence of plasmids through the treatment Venetoclax cell line process, contributing to the dissemination

of integrons and undesirable genetic traits, such as those coding for antibiotic resistance and virulence determinants, to natural waters, soils and eventually the food chain. Previously, the presence and distribution of integron-carrying bacteria was investigated at different stages of the treatment process in two WWTPs, one treating urban discharges and the other treating wastewaters from a slaughterhouse (Moura et al., 2007, 2012). The present study was performed Rucaparib to investigate the diversity of plasmids in integron-positive strains retrieved from wastewaters, providing data pertaining to the contribution of these environments to the spread of integrons and antibiotic resistance determinants through HGT. Sixty-six integron-positive (intI+) strains belonging to Aeromonas sp. (n = 48) and Enterobacteriaceae (n = 18) previously isolated from urban and slaughterhouse wastewaters (Moura et al., 2007, 2012) were included as donors in mating assays using rifampicin- and kanamycin-resistant Escherichia coli CV601-GFP

and Pseudomonas putida KT2442-GFP as recipient strains (Smalla et al., 2006). Liquid cultures of donor and recipient strains were prepared separately in 10 mL Luria–Bertani broth (LB) and grown overnight with gentle shaking at 28 °C. Recipient and donor strains were mixed (ratio 1 : 1) and centrifuged for 5 min at 6700 g to precipitate cells. Supernatants were discarded and replaced by 1 mL fresh LB. Mixtures were incubated overnight at 28 °C without shaking. Cells were then precipitated by centrifugation (5 min, 6700 g) and washed in 0.9% NaCl solution. Serial dilutions were prepared in 0.9% NaCl and aliquots of 100 μL were spread on Plate Count Agar plates supplemented with rifampicin (50 mg L−1) and streptomycin (50 mg L−1) or with rifampicin (50 mg L−1) and tetracycline (50 mg L−1). Putative transconjugants were grown at 28 °C for 48 h. Assays were run in duplicate.

“
“All methane-producing Archaea (methanogens) are strict anaerobes, but the majority of species are tolerant to oxidants. Methanosarcina species are important

environmental and industrial methanogens as they are one of only two genera capable of producing methane with acetate. Importantly, Methanosarcina species appear to be the most oxidant-tolerant; however, the mechanisms underlying this tolerance are poorly understood. We report herein two similar methods (spot-plating and microtiter plate) developed to examine the oxidant tolerance of Methanosarcina acetivorans by viability see more assessment. Both methods revealed that M. acetivorans can tolerate exposure to millimolar levels of hydrogen peroxide

(H2O2) without a complete loss of viability. The exogenous addition of catalase was also shown to protect M. acetivorans from H2O2 toxicity, indicating catalase can serve as an antioxidant enzyme in methanogens even though oxygen is a byproduct. Of the two methods, the microtiter plate method provided this website a simple, reliable, and inexpensive method to assess viability of M. acetivorans. Combined with recent advances in the genetic manipulation of methanogens, methods in assessment of methanogen oxidant tolerance will aid in the identification of components of the antioxidant defense systems. “
“The aims of this work were to characterize the 16S–23S internal spacer region of the fish pathogen Tenacibaculum soleae and to develop a PCR assay for its identification and detection. All T. soleae strains tested displayed a single internal spacer region class, containing tRNAIle and tRNAAla genes; nevertheless, a considerable intraspecific heterogeneity was observed. However, this region proved to be useful for differentiation of T. soleae from related and non-related species. Species-specific primers were designed targeting the 16S rRNA gene and

the internal spacer region Celecoxib region, yielding a 1555-bp fragment. Detection limit was of 1 pg DNA per reaction (< 30 bacterial cells) when using pure cultures. The detection level in the presence of DNA from fish or other bacteria was lower; however, 10 pg were detected at a target/background ratio of 1 : 105. The PCR assay proved to be more sensitive than agar cultivation for the detection of T. soleae from naturally diseased fish, offering a useful tool for diagnosis and for understanding the epidemiology of this pathogen. Tenacibaculosis caused by bacteria belonging to the genus Tenacibaculum is one of the more devastating infectious diseases of farmed marine finfish worldwide (Hansen et al., 1992; Toranzo et al., 2005).

, 1992). Interestingly, the tatA genes of some cyanobacteria appear to be localized selleck compound in a cluster with genes involved

in cyanate transport (Fig. 1), and this co-localization perhaps suggests a similar role for the Tat-dependent carbonic anhydrase in preventing the loss of bicarbonate in some cyanobacteria. The Tat motifs of many of the cyanobacterial strains examined herein, appear to differ somewhat from the previously described Ser/Thr-Arg-Arg-x-Phe-Leu-Lys consensus sequence of bacteria (Berks, 1996). Thus, the usually well-conserved Phe residue is commonly replaced by an additional Leu residue, whereas the Lys and Ser/Thr residues are not conserved at all. In this respect they resemble chloroplast Tat signals of eukaryotic cells, which contain the twin-arginine motif but usually lack the Phe and Lys residues

of the bacterial consensus motif. A complete list of the predicted Tat motifs is given in Table S1. A minimal Tat system has been described in Gram-positive bacteria where just two membrane protein components (TatA and TatC) are required for translocation activity (Yen et al., 2002; Dilks et al., 2003). The only exception to this is in the actinomycetes (Schaerlaekens et al., 2001), which in common with Gram-negative bacteria have an additional TatB component. TatA and TatB are closely related proteins and the TatA XL184 ic50 proteins found in Gram-positive bacteria are bifunctional, sharing features common to both proteins (Jongbloed et al., 2006; Barnett et al., 2008, 2009, 2011). Synechocystis has RNA Synthesis inhibitor a single tatC gene (sll0194) whilst two separate genes encode TatA/B homologues (slr1046 and ssl2823) (Aldridge et al., 2008). This suggested that cyanobacteria, like other Gram-negative bacteria and also plant chloroplasts, possess TatABC-type translocation systems. The similarity in primary sequence between TatA and TatB proteins makes assigning function difficult. In an attempt to address this problem, the slr1046 and ssl2823 genes of Synechocystis were expressed in E. coli mutant strains and the ability

of each protein to complement the function of TatA or TatB in the translocation of the E. coli Tat substrate, Trimethyl N-oxide-reductase, was examined. Both the slr1046 and ssl2823 genes can complement both tatA and tatB mutant strains (Aldridge et al., 2008) indicating that at least in E. coli, these proteins have a bifunctional capability, similar to the TatA proteins of Gram-positive bacteria. Despite this study, it still remains unclear whether Synechocystis has a single TatABC system that is operating in both the thylakoid and cytoplasmic membranes or two minimal TatAC pathways operating independently in the two membrane locations. This is an important question that must be addressed, if we are to understand how Tat substrates are correctly targeted in cyanobacteria.