The results indicated that H. parasuisOmpP2 from SC096 strain is an important surface protein involved in serum resistance. Haemophilus parasuis is the causative agent of Glässer’s disease, which is characterized by fibrinous polyserositis, polyarthritis

and meningitis. Haemophilus Selleck PD0325901 parasuis infection produces significant mortality and morbidity in pig farms, giving rise to important economic losses in the pig industry (Oliveira & Pijoan, 2004). To date, 15 serovars have been described, with apparent differences in virulence (Kielstein & Rapp-Gabrielson, 1992); the virulent serovars 5 and 4 are the most prevalent serovars in China (Cai et al., 2005). Serum-resistance in H. parasuis is frequently associated with systemic disease in swine, suggesting that it is a potential pathogenic mechanism of this bacterium (Cerda-Cuellar & Aragon, 2008). However, the major determinants of serum resistance in this pathogen are largely unknown. Natural transformation is a process by which bacteria take up extracellular DNA and incorporate it into the host genome learn more by homologous recombination (Wang et al., 2006). Haemophilus parasuis has a cyclic AMP (cAMP)-dependent natural transformation system that enables the uptake of DNA in which the ACCGAACTC sequence signal must be present (Bigas et al., 2005). Using this system, a thy-deficient mutant of H. parasuis has been obtained previously (Bigas et al., 2005). Therefore,

natural transformation provides a method for the construction of mutants to study the function of H. parasuis genes. Haemophilus parasuis outer membrane protein P2 (OmpP2), a member of the porin family, is the most abundant protein in the outer membrane (Zhou et al., 2009). Mullins et al. (2009) reported that H. parasuis OmpP2 proteins exhibit a high level of sequence heterogeneity and that two distinct protein structures exist in this bacterium, suggesting that OmpP2 has experienced high selective pressure which may contribute to virulence. Furthermore, H. parasuis OmpP2 has been identified as a target for protective antibodies

and OmpP2 vaccines provide partial protection to mice against this bacterial infection (Zhou et al., 2009). In this study, we constructed a H. parasuis ompP2-deficient mutant (ΔompP2) by a modified natural transformation Inositol oxygenase method to investigate the role of the OmpP2 in serum resistance. Bacterial strains and plasmids used in this study are listed in Table 1. Escherichia coli plasmids were propagated in E. coli DH5α and grown in Luria–Bertani medium. Haemophilus parasuis strains were used and cultivated in trypticase soy agar (TSA) and trypticase soy broth (TSB) (Oxoid, Hampshire, UK) supplemented with 0.002% nicotinamide adenine dinucleotide (NAD) (Sigma, St. Louis, MO) and 5% inactivated bovine serum at 37 °C in a 5% CO2-enriched atmosphere for 36 h. When required, the media were supplemented with kanamycin (30 mg mL−1) or gentamicin (20 mg mL−1).

, 2003), as well as its homologus gene vraDE, which was highly induced by vancomycin treatment in

Staphylococcus aureus (Kuroda et al., 2003). In the present study, lmo1431, which encodes a protein similar to the ABC transporter, was identified as a possibly σB-dependent gene. Thus, these results suggest that the ABC transporter is involved in cell wall stress tolerance under the regulation of σB in several Gram-positive bacteria including L. monocytogenes. Beside transporters, cell envelope biogenesis-related proteins such as Pbp2 and MurZ were upregulated by vancomycin treatment in S. aureus (Kuroda et al., 2003). Accordingly, our proteomic analysis showed that Pbp2 and MurZ were also highly upregulated in wild-type L. monocytogenes. Lmo2085, a cell wall-associated protein containing an LPXTG motif, was also upregulated Hydroxychloroquine in vitro in wild-type L. monocytogenes. Vancomycin acts by inhibiting cell wall synthesis in Gram-positive bacteria. The proteomic analysis found that cell wall-associated

proteins showed the largest changes in accumulation, suggesting that cell wall biogenesis is activated to maintain inherent cell wall integrity when cells are exposed to vancomycin stress. The internalins are the largest family of surface proteins in L. monocytogenes. These proteins function in the attachment and invasion of host cells (InlA and InlB) or virulence (InlC, InlD, InlH) (Lingnau see more et al., 1996; Dramsi et al., 1997). Two σB-dependent proteins, internalin-like protein Lmo2085 and InlD, were upregulated in our proteomic

analyses. However, there is no knowledge on whether internalins are directly or indirectly involved in monitoring cell wall integrity. Additionally, proteins related to metabolism, general stress and Dichloromethane dehalogenase cell division were upregulated in wild-type L. monocytogenes. In conclusion, a total of 18 vancomycin-inducible σB-dependent proteins were identified in our proteomic analyses. Interestingly, we newly detected eight possibly σB-dependent proteins that had not previously appeared to be under the control of σB. These proteins may be indirectly regulated by σB depending on specific circumstances. Taken together, σB may contribute to monitoring and maintaining cell wall integrity by regulating certain genes and factors important to stress response. We thank Chester Price for providing pLJH4 and E. coli SM10, and Martin Wiemann for L. monocytogenes 10403S and the isogenic ΔsigB mutant. This study was supported by a grant from the Korea Healthcare technology R&D Project, Ministry for Health, Welfare & Family Affairs, Korea (A084798). “
“Acinetobacter baumannii continues to be a major health problem especially in hospital settings. Herein, features that may play a role in persistence and disease potential were investigated in a collection of clinical A. baumannii strains from Australia. Twitching motility was found to be a common trait in A.

, 2003), as well as its homologus gene vraDE, which was highly induced by vancomycin treatment in

Staphylococcus aureus (Kuroda et al., 2003). In the present study, lmo1431, which encodes a protein similar to the ABC transporter, was identified as a possibly σB-dependent gene. Thus, these results suggest that the ABC transporter is involved in cell wall stress tolerance under the regulation of σB in several Gram-positive bacteria including L. monocytogenes. Beside transporters, cell envelope biogenesis-related proteins such as Pbp2 and MurZ were upregulated by vancomycin treatment in S. aureus (Kuroda et al., 2003). Accordingly, our proteomic analysis showed that Pbp2 and MurZ were also highly upregulated in wild-type L. monocytogenes. Lmo2085, a cell wall-associated protein containing an LPXTG motif, was also upregulated BVD-523 research buy in wild-type L. monocytogenes. Vancomycin acts by inhibiting cell wall synthesis in Gram-positive bacteria. The proteomic analysis found that cell wall-associated

proteins showed the largest changes in accumulation, suggesting that cell wall biogenesis is activated to maintain inherent cell wall integrity when cells are exposed to vancomycin stress. The internalins are the largest family of surface proteins in L. monocytogenes. These proteins function in the attachment and invasion of host cells (InlA and InlB) or virulence (InlC, InlD, InlH) (Lingnau check details et al., 1996; Dramsi et al., 1997). Two σB-dependent proteins, internalin-like protein Lmo2085 and InlD, were upregulated in our proteomic

analyses. However, there is no knowledge on whether internalins are directly or indirectly involved in monitoring cell wall integrity. Additionally, proteins related to metabolism, general stress and Lonafarnib order cell division were upregulated in wild-type L. monocytogenes. In conclusion, a total of 18 vancomycin-inducible σB-dependent proteins were identified in our proteomic analyses. Interestingly, we newly detected eight possibly σB-dependent proteins that had not previously appeared to be under the control of σB. These proteins may be indirectly regulated by σB depending on specific circumstances. Taken together, σB may contribute to monitoring and maintaining cell wall integrity by regulating certain genes and factors important to stress response. We thank Chester Price for providing pLJH4 and E. coli SM10, and Martin Wiemann for L. monocytogenes 10403S and the isogenic ΔsigB mutant. This study was supported by a grant from the Korea Healthcare technology R&D Project, Ministry for Health, Welfare & Family Affairs, Korea (A084798). “
“Acinetobacter baumannii continues to be a major health problem especially in hospital settings. Herein, features that may play a role in persistence and disease potential were investigated in a collection of clinical A. baumannii strains from Australia. Twitching motility was found to be a common trait in A.

kernoviae were more acidic tolerant (pH 3–9). These tolerant germinants formed compact hyphae or secondary sporangia to RG7204 price allow longer survival of these pathogens. Long-term survival at a broad pH range suggests that these pathogens, especially P. ramorum, are adapted to an aquatic environment and pose a threat to new production areas through water dispersal. Phytophthora alni (Brasier et al., 2004), Phytophthora kernoviae (Brasier et al.,

2005), and Phytophthora ramorum (Werres et al., 2001) are three pathogens of forests and ornamental production areas. Phytophthora ramorum, known for Sudden Oak Death (Rizzo et al., 2002), has been found in Europe and United States since the late 1990s. Phytophthora alni, causing alder mortality in Britain (Brasier et al., 1995) is widespread across Europe (Brasier et al., 2004; Cerny et al., 2008; Solla et al., 2010) and has recently been found in the USA (Schwingle et al., 2007; Adams et al., 2008). Phytophthora kernoviae has been reported in the United Kingdom and shares symptoms and hosts with P. ramorum (Brasier et al., 2005; Ramsfield et al., 2009). The identification and spread of these pathogens has led to increasing concern about their threat to plant biosecurity and natural ecosystems. The horticultural trade has been identified as a major route for

pathogen introduction to new areas, as was demonstrated in the case of P. ramorum (Lane et al., 2003). However, some

pathogens could also spread through wind, runoff, O-methylated flavonoid and irrigation water (Campbell, 1999; Hong & Moorman, 2005). Phytophthora ramorum has been detected in streams Lapatinib mw and effluents of irrigation systems and demonstrated to be spread through an artificial irrigation system (Werres et al., 2007; Tjosvold et al., 2008; Chastagner et al., 2009). Phytophthora alni also has been shown to be able to grow and sporulate in river water (Chandelier et al., 2006). Phytophthora kernoviae is biologically and ecologically similar to P. ramorum (Brasier et al., 2005), thus it may be capable of dispersal by water splash or by irrigation water recycling. Zoospores are believed to be relatively short-lived but how they manage to disperse in irrigation water and natural water ways within their life span is not clear. In fact, some Phytophthora species are continuously recovered from aquatic environments despite the fact that their populations decline with increasing distance from the entrance of runoff water in irrigation reservoirs (Hong et al., 2003; Hong & Moorman, 2005; Werres et al., 2007; Tjosvold et al., 2008; Chastagner et al., 2009). It has been found that there are diurnal and seasonal fluctuations in pH from 6.5 to 10.3 in irrigation water reservoirs (Hong et al., 2009). Apparently, zoospores or other life stages have to adapt to a wide range of pH in order to survive in and be dispersed by water.

1b). The secretion of type III secreted proteins – BteA, BopB, BopD, BopN, and Bsp22 – into bacterial culture supernatant was detected. Interestingly, the band corresponding to Bsp22 had completely disappeared in ∆BB1618, although bands for other type III secreted proteins – BteA, BopB, BopD, and BopN – were detected selleck inhibitor at levels similar to

those for the wild type. Again, Bsp22 was detected in a complemented strain, ∆BB1618/pBB1618. To further confirm these phenotypes, the secreted proteins and the bacterial whole cell lysates were subjected to immunoblot analysis using anti-BopB and anti-Bsp22 antibodies (Fig. 1b). The amounts of BopB translocator in the bacterial supernatants and the whole cell lysate were not affected by the deletion of BB1618. In contrast, the signal of Bsp22 disappeared in

the bacterial supernatant and the whole cell lysate in ∆BB1618, indicating that BB1618 is required for the stability of Bsp22. In order to further investigate the role of BB1618 in the secretion of Bsp22, a plasmid containing bsp22 driven by the fhaB promoter (pBsp22) was introduced into B. bronchiseptica wild type, ∆Bsp22 or ∆BB1618 to allow overexpression of Bsp22 and the amount of Bsp22 secreted into the culture supernatants was analyzed by immunoblot RG-7388 in vivo analysis (Fig. 1c). We confirmed that the Bsp22-deficient strain (∆Bsp22) could be complemented

by introduction of pBsp22. By contrast, the amount of Bsp22 in the culture supernatants was not fully restored in ∆BB1618 overexpressing Bsp22 (∆BB1618/pBsp22), indicating that BB1618 is involved in the effective secretion of Bsp22. Furthermore, a quantitative real-time PCR analysis showed that the amount of bsp22 mRNA in ∆BB1618 was similar to that of wild-type B. bronchiseptica (data not shown), indicating that BB1618 does not affect transcription of the bsp22 gene. Collectively, these results strongly suggest that BB1618 is required for the secretion and the stability of Bsp22. Bordetella bronchiseptica induces hemolysis on rabbit RBCs in an adenylate cyclase toxin- or T3SS-dependent manner. In particular, the T3SS-dependent hemolysis is caused by formation of pore complexes, BopB and BopD, in the RBC plasma membrane, resulting selleck products in membrane disruption (Kuwae et al., 2003; Nogawa et al., 2004; Medhekar et al., 2009). In a previous report, we established a measurement system for the T3SS-dependent hemolytic activity (Kuwae et al., 2003). To investigate whether BB1618 is involved in the T3SS-dependent hemolytic activity, rabbit RBCs were exposed to the B. bronchiseptica wild type, ∆T3SS, ∆Bsp22, ∆BB1618 or ∆BB1618/pBB1618 strains (Fig. 2). The hemolytic activity of the wild type was 35.0% that of the Triton X-100-treated RBC employed as a positive control.

The global burden of infectious diseases caused by mycobacteria highlights the importance of developing effective

tools for the diagnosis and prevention of mycobacterial infections (Wilson, 2008; First WHO Report on Neglected Tropical Diseases, 2010; WHO, 2012). The application MK-2206 supplier of molecular biological techniques provided a huge step forward in the identification of mycobacterial antigens for use in potential diagnostics and vaccines (Wilson, 2008; First WHO Report on Neglected Tropical Diseases, 2010). One of the first mycobacterial antigens to be identified using these techniques was the major 65-kDa antigen of M. tuberculosis (Young et al., 1987), which was initially discovered as an immunodominant antigen in both humoral and cell-mediated immune responses in TB and leprosy (Young et al., 1987, 1988). The subsequent demonstration that the 65-kDa antigen was homologous to

the heat shock protein GroEL of Escherichia coli led to its common nomenclature as Hsp65 in TB studies (Shinnick et al., 1988; Young et al., 1988) and numerous studies on the protein and encoding gene as potential diagnostics and vaccines (Silva, 1999). However, the demonstration of the function of E. coli GroEL as an essential molecular chaperone responsible for the correct folding of key housekeeping genes suggested that Hsp65 is a member of the family of protein chaperonins (Hemmingsen et al., Protease Inhibitor Library concentration 1988). The chaperonins are a group of molecular chaperones related by homology to the GroEL proteins of E. coli (Hemmingsen et al., 1988; Hartl & Hayer-Hartl, 2002). They usually form oligomers of c. 800 kDa, made up of two heptameric rings of 60-kDa subunits, each with an apical, an intermediate and an equatorial domain that together enclose a central cavity in which client proteins fold (Hemmingsen et al., 1988; Hartl & Hayer-Hartl, 2002). Client proteins bind to the apical domains and chaperonin

function requires a heptameric cochaperonin (GroES in E. coli) which binds the same regions of the chaperonin as the client proteins and displaces these into the cavity, IMP dehydrogenase where they fold without interacting with other proteins with which they might aggregate (Hartl & Hayer-Hartl, 2002). The chaperonin folding cycle requires binding and hydrolysis of ATP, and networks of allosteric interactions within and between the two rings are needed to complete the cycle (Hartl & Hayer-Hartl, 2002). In E. coli, the groEL and groES genes form part of a single operon and homologous groEL/S operons have now been described as essential genes in all phyla and kingdoms; these genes have been ascribed the names cpn60 and cpn10 (Coates et al., 1993; Lund, 2001). However, c.

The global burden of infectious diseases caused by mycobacteria highlights the importance of developing effective

tools for the diagnosis and prevention of mycobacterial infections (Wilson, 2008; First WHO Report on Neglected Tropical Diseases, 2010; WHO, 2012). The application MI-503 of molecular biological techniques provided a huge step forward in the identification of mycobacterial antigens for use in potential diagnostics and vaccines (Wilson, 2008; First WHO Report on Neglected Tropical Diseases, 2010). One of the first mycobacterial antigens to be identified using these techniques was the major 65-kDa antigen of M. tuberculosis (Young et al., 1987), which was initially discovered as an immunodominant antigen in both humoral and cell-mediated immune responses in TB and leprosy (Young et al., 1987, 1988). The subsequent demonstration that the 65-kDa antigen was homologous to

the heat shock protein GroEL of Escherichia coli led to its common nomenclature as Hsp65 in TB studies (Shinnick et al., 1988; Young et al., 1988) and numerous studies on the protein and encoding gene as potential diagnostics and vaccines (Silva, 1999). However, the demonstration of the function of E. coli GroEL as an essential molecular chaperone responsible for the correct folding of key housekeeping genes suggested that Hsp65 is a member of the family of protein chaperonins (Hemmingsen et al., Trichostatin A ic50 1988). The chaperonins are a group of molecular chaperones related by homology to the GroEL proteins of E. coli (Hemmingsen et al., 1988; Hartl & Hayer-Hartl, 2002). They usually form oligomers of c. 800 kDa, made up of two heptameric rings of 60-kDa subunits, each with an apical, an intermediate and an equatorial domain that together enclose a central cavity in which client proteins fold (Hemmingsen et al., 1988; Hartl & Hayer-Hartl, 2002). Client proteins bind to the apical domains and chaperonin

function requires a heptameric cochaperonin (GroES in E. coli) which binds the same regions of the chaperonin as the client proteins and displaces these into the cavity, Interleukin-3 receptor where they fold without interacting with other proteins with which they might aggregate (Hartl & Hayer-Hartl, 2002). The chaperonin folding cycle requires binding and hydrolysis of ATP, and networks of allosteric interactions within and between the two rings are needed to complete the cycle (Hartl & Hayer-Hartl, 2002). In E. coli, the groEL and groES genes form part of a single operon and homologous groEL/S operons have now been described as essential genes in all phyla and kingdoms; these genes have been ascribed the names cpn60 and cpn10 (Coates et al., 1993; Lund, 2001). However, c.

The results from our model match qualitatively with those from Herrero et al. (2008) as can be seen in comparing Fig. 7 with fig. 1A from Herrero et al. That is, the strongest response of the layer 2/3 neurons in RF1 comes when both top-down attention and ACh are applied to the column and the weakest response is when ACh is not applied and attention is directed

into RF2. As was Selleck Stem Cell Compound Library speculated in Hasselmo & Sarter (2011), the attentional mechanism in our model was facilitated by the local release of ACh as a result of GluACh interactions between top-down attention signals from prefrontal cortex (PFC)/V4, cholinergic fibers, and V1 neurons, as shown in Fig. 6. As explained in the Discussion and the Results below, this mAChR-mediated increase in firing rate with attention is primarily mediated by mAChR increases in the excitability of excitatory neurons, whereas the mAChR-mediated increase in excitability of inhibitory neurons, which also occurs with top-down attention, helps to maintain low levels of excitatory–excitatory correlations. Note that the absolute changes in firing rate shown in Fig. 7 are greater than those seen in Herrero et al., although this is a function of the rate

that was chosen for the Poisson spike generator driving the top-down attention signal and should therefore not influence our result that mAChRs modulate attention. In the Herrero et al. experiments, they found that attentional modulation was enhanced only at low doses of see more ACh application. Higher doses of ACh, by contrast, could reduce attentional modulation. We ran additional simulations (data not shown) showing that selleck chemicals these results could be replicated if the excitability of inhibitory neurons increases at a faster rate than the excitability of excitatory neurons. This suggests that the number and distribution of mAChRs on excitatory and inhibitory neurons could play an important role in shaping these dose-dependent effects. We investigated the change in between-cell correlations that resulted from attentional

and BF-related signals in comparison with control conditions. To achieve this, we periodically either stimulated top-down attentional areas, mAChRs in RF1, or the BF, as described in the Methods. This led to the six conditions shown in Figs 8 and 9: (i) no attention, no mAChR stimulation and no BF stimulation (Fig. 8, top); (ii) no attention and mAChRs in RF1 stimulated (Fig. 8, middle); (iii) no attention and BF stimulated (Fig. 8, bottom); (iv) attention signal in RF1 only (Fig. 9, top); (v) attention signal in RF1 and mAChRs in RF1 stimulated (Fig. 9, middle); and (vi) attention signal in RF1 and the BF stimulated (Fig. 9, bottom). We refer to these six cases as the ‘non-control’ conditions. Control conditions, by contrast, refer to times in the experiment when there was no top-down attention, no mAChR stimulation and no BF stimulation was applied to the network.

Details are shown in Table 3. Fulvestrant datasheet (Fisher’s exact test) Our results did not confirm our hypothesis that an ADMA-induced inhibition of NOS leads to an increase in PAP and to an increased susceptibility to AMS. On the contrary, our tests suggested the exact opposite as described above. The increase in PAP thus may not be caused by an increase in ADMA. Against our assumptions, ADMA was not confirmed as a potential trigger to generate

a PAP value of higher than 40 mmHg, which is considered to be the critical threshold for the development of HAPE. In summary, the reported results show a statistically significant negative correlation of Δ-ADMA and PAP (ρ: −0.74; p ≤ 0.01) and altitude symptoms (ρ: −0.8; p ≤ 0.01). In addition, the measurement of Δ-ADMA under conditions

of acute hypoxia (at 4000 m) is also a suitable method for identifying individuals who are likely to develop critical PAP of more than 40 mmHg (ϕ: 0.69; p ≤ 0.05) and who are susceptible to AMS (LLS ≥ 5) (ϕ: 0.82; p ≤ 0.02). Those at risk can be identified as early as 2 hours after the start of exposure to hypoxia (at an altitude of 4000 m). It is not the absolute ADMA level but rather the change (increase or decrease) in ADMA against the baseline level that plays a key role GSK126 mouse in this context. In our collective results, the Δ-ADMA value after 2 hours of hypoxia can predict the development of AMS with a sensitivity of 80% and a specificity of 100%. If PAP increases to more than 40 mmHg within 2 hours of exposure, the occurrence of AMS is likely to be expected in 100% of the cases. In their study on the course of PAP during altitude exposure, Dorrington and colleagues[15] indirectly confirmed that prognostic information can be obtained after such a short period of exposure. Using right-heart catheterization, these authors showed that a maximum PAP level was reached as early as 2 hours after the onset of exposure to hypoxic conditions. Our results confirmed the findings reported by Song and colleagues.[16] These authors exposed mice to previously lethal conditions—a why fraction of oxygen (FO2)

of 0.046%—and expected that NOS inhibition (eg, by ADMA) would decrease hypoxic tolerance. Contrary to their original hypothesis, they found that hypoxic tolerance improved greatly and some of the mice that were treated with ADMA even survived. As synthetic NOS inhibitors such as Nω-nitro- l-arginine (l-NNA) also improved hypoxic tolerance, these unexpected results confirmed that it was this NOS-mediated function in the systemic response to acute hypoxia rather than a nonspecific effect of ADMA that was responsible for the improvement in hypoxic tolerance. The administration of the NO donor 3-morpholinosydnoeimine (SIN-1) attenuated the increase in hypoxic tolerance produced by l-NNA. This, too, was contrary to the initial hypothesis.

This can be accomplished using solid media (e.g. agar or uncompacted soil). For soil studies, Ljungholm et al. (1979) have demonstrated that the problem can be readily solved. They closed their ampoules with a 1-mm-thick porous silicone rubber seal because the material readily transmits simple gases. This procedure was shown to allow sufficient gas exchange (O2 and CO2), without significant loss of water, between the calorimetric ampoule and the atmosphere. Similarly, addition of glucose as a powder and not as LY2606368 mw a solution to soil samples combined with

the use of a flow-through cell is also a simple means to achieve calorimetric measurements in soil samples (Sparling, 1983) without reaching oxygen depletion. Finally, it is also possible to calculate the amount of oxygen present in the headspace of the calorimetric ampoule and calculate the amount of substrate that can be consumed using this oxygen. Using such simple calculations, Vor et al. (2002) were able to estimate when the transition from oxic to anoxic conditions in soil samples occurred and study changes in the metabolic heat production associated with this transition. Similarly, the use of agar medium or other solid growth substrates allows microorganisms to grow on top of the medium and therefore remain in contact with oxygen http://www.selleckchem.com/products/r428.html present in the headspace (Wadsöet al., 2004).

Furthermore, a closed environment can also be analytically advantageous – for mass balance calculations for example. Finally, it must be noted that the heat flow signal is a nonspecific, net signal related to the sum of all chemical and physical processes taking place in an IMC Cyclic nucleotide phosphodiesterase ampoule. As a consequence, unknown phenomena may produce some of the heat measured, and there may be simultaneous exothermic and endothermic processes taking place (Lewis & Daniels, 2003). However, well-described phenomena can be studied

under controlled conditions with a high accuracy [see the ‘diauxie’ (Monod, 1949) example in Fig. 1, Table 2]. Careful planning of IMC experiments is of great importance. Logical experimental designs must be devised and used that ensure that the observed heat flows are directly related to the processes of interest. IMC has been used in many different fields of microbiology. Medical and environmental applications provide an indication of the possibilities. One noteworthy medical application is rapid isothermal microcalorimetric detection of bacterial infection or contamination, which is of critical importance in quickly implementing the correct treatment. Recent studies have shown that with IMC, it is possible to detect bacterial contamination of donated blood platelets within a few hours (Trampuz et al., 2007). Similarly, it is also possible to determine inhibitory effects and/or the minimal inhibitory concentration for different antimicrobial compounds and microorganisms within hours using IMC (Xi et al., 2002; Yang et al., 2008; von Ah et al., 2009).