g., chondrogenesis is predominantly a prenatal event in skeletogenesis, while adipogenesis is entirely postnatal [41]. Furthermore, a wealth of evidence, albeit circumstantial in large part, highlights the ability of individual cell types regarded as differentiated to modulate into different phenotypes.

For example, chondrocytes can revert to fibroblasts [42] and [43] or osteoblast-like cells in vitro and in vivo [44] and [45], or even to bone marrow stromal cells in vivo [46]; bone marrow stromal cells can convert into adipocytes in vivo [47]. This “plasticity” of the stromal system (not to be confused with the once claimed, and now luckily find more dispelled, “trans-differentiation” ability of any cell to generate any cell, “turning blood into brain” [48], “brain into blood” [49], “blood into muscle” [50], “muscle into blood” [51], and water into wine [52]) remains to be understood mechanistically, but may be seen as one defining feature of the system and of its unique nature. Nonetheless, the differentiation potential of skeletal stem cells E7080 chemical structure is strictly limited to phenotypes that belong to the skeleton: cartilage, bone, fat, fibroblasts and the bone marrow stroma itself are

the only progenies of the marrow stromal stem cells. Skeletal stem cells, like all other kinds of postnatal stem cells, are committed and system-specific, and are not pluripotent. Finally, all cell types in the stromal system exist within an extracellular matrix. This is another noted peculiarity of the stromal system compared to other stem cell-dependent tissues such as blood or epithelial tissues. As the extracellular matrix embodies differentiation cues, maintenance of an individual phenotype within the stromal system is partly regulated “in trans”; constant remodeling of the extracellular matrix makes the “in trans” determination of phenotype inherently unstable. This instability may have been conserved as a specific adaptive function, other than constant and fast

cell replacement such as in blood or epithelial tissues. These adaptive responses include the integrated remodeling of DOCK10 hard tissues with that of soft and fluid tissues. Following the disruption of soft tissue remodeling by ablation of the pivotal protease for collagen degradation, MT1-MMP, vicarious remodeling of bone disrupts skeletal integrity [53]. The adaptive co-regulation of skeletal and hematopoietic physiology involves remodeling of the bone marrow (e.g., timed generation of yellow (adipose) marrow during postnatal growth and aging, and local vascular remodeling) [54]. In a way, one of the notions that come from the existence of skeletal stem cells and the stromal system is that remodeling of bone is part of a much broader adaptive response, which involves the coordinated remodeling of other connective tissues.

Workers aged 2 and 100 days had no positive reactions for the anti-vitellogenin antibody (Fig. 4). Neither the 120 kDa protein found in workers aged 2 and 5 days nor the protein of 135 kDa from samples of workers aged 20–100 days reacted positively to the vg2 antibody (Fig. 4). The native vitellins from queens and workers were compared and their eggs showed one main protein with the same size (Fig. 5). In the haemolymph from 30 days old workers a similar protein was also identified (Fig.

5). In eggs from queens of ant species in the families Myrmicinae, Ponerinae and Ectatomminae the vitellin is formed by two or more proteins (Lewis et al., 2001 and Wheeler et al., 1999). Our results show that the eggs of E. tuberculatum queens have vitellins that consist of four major proteins, Depsipeptide order while in the eggs of workers only two of them are the vitellins. In queens, these four proteins join

to form an oligomeric protein which PD0332991 chemical structure in its native form has a molecular weight between 400 and 500 kDa estimated based on data from Wheeler et al. (1999). In the eggs of workers, the 156 and 31 kDa vitellins form an oligomeric protein with the same molecular weight of the native vitellin found in queens. The two proteins found in the greatest amounts in the egg extracts of E. tuberculatum were used for antibody production because the vitellins make up the largest fraction of proteins found in the eggs of insects ( Raikhel and Dhadialla, 1992 and Tufail and Takeda, 2008). The immunolocalization tests showed that these proteins occur in fat body cells, the main production site of vitellogenins. Since vitellogenins are the precursors of vitellins ( Chapman, 1998), our results confirm that these two proteins are actually vitellin compounds. Comparing the vitellins of the queen and worker eggs with the vitellogenins from their haemolymph revealed that only the proteins of 31 and 156 kDa were shared, suggesting

that the vitellogenin circulating in the haemolymph of E. tuberculatum consists GBA3 of only these two proteins. Also, the presence of a native protein in worker’s haemolymph with similar size of the native vitellins found in queen and worker eggs indicates that the vitellogenin forms a protein complex in the haemolymph similar to the vitellins found in the eggs. The proteins of 36 and 123 kDa present in the eggs of queens may be products of additional cleavage of the 156 kDa protein, which is supported by the occurrence of cross-reactivity between antibodies vg1 and vg2 to the proteins of 123 and 156 kDa. Moreover, the haemolymph of the queens shows only the proteins of 31 and 156 kDa. In B. germanica, vitellogenins of 160 kDa are cleaved into subunits of 50 and 95 kDa after internalization in the oocyte ( Wojchowski et al., 1986). The difference in vitellin processing found between queen and worker eggs of E.

Autopsy reports described prevalent white matter abnormalities and brainstem pathology [36]. The presence of numerous spiny neurons dispersed in the white matter has also been reported, which is suggestive of impaired neuronal migration and apoptosis [20]. Using functional neuroimaging selleck compound library techniques in a patient with early myoclonic encephalopathy, Hirose et al. [46] demonstrated hypoperfusion and hypometabolism

in the basal ganglia and thalami interictally, with ictal hyperperfusion of the basal ganglia, thalami, brainstem, and deep front-parietal cortex. This finding was indicative of dysfunction in these regions, and was thought to suggest a functional deafferentation of the cortex from subcortical structures [46]. A number of familial cases of early myoclonic encephalopathy have been reported [14] and [40], raising the question of whether the disease involves a genetic component. A likely genetically mediated case was reported in association with Schinzel-Giedion syndrome,

a rare genetic multiple malformation disorder [47]. In 2009, early myoclonic encephalopathy was reported in association with CT99021 clinical trial a mutation of the v-erb-a erythroblastic leukemia viral oncogene homologue 4 (ErbB4 gene), which is involved in the migration of interneurons to the cortex [48]. This genetic abnormality is consistent with the persistence of spiny neurons in the white matter on pathologic examination, and of the functional deafferentation described by Hirose et al. [46], both of which seem to indicate impaired neuronal migration to the cortex, suggesting a degree of “cortical isolation” in the brains of these patients [20], [46] and [48]. The diagnosis of both Ohtahara syndrome and early myoclonic Tacrolimus (FK506) encephalopathy is based on a typical clinical picture and associated electroencephalographic findings,

as already described. The prognosis is universally poor. Neuroimaging to assess for structural brain abnormalities is generally recommended in cases of Ohtahara syndrome. Brainstem evoked potentials are occasionally abnormal in both conditions, but normal studies do not exclude the possibility of disease [36]. Only anecdotal evidence supports the use of specific antiepileptic drugs in these conditions. Phenobarbital, valproate, pyridoxine, zonisamide, and benzodiazepines have all demonstrated limited effectiveness in seizure control in Ohtahara syndrome [10] and [49]. Adrenocorticotropic hormone therapy also exerts limited efficacy, and may be particularly beneficial in cases of Ohtahara syndrome that progress to West syndrome [3] and [9]. None of the antiepileptic medications has been effective in treating early myoclonic encephalopathy, nor have alternative methods of seizure management such as adrenocorticotropic hormone therapy, corticosteroids, and pyridoxine.

In many regions aerosol-cloud interactions are perturbed by increasing amounts of anthropogenic aerosol particles.

In this respect, changes in cloud albedo, cloud lifetime and the amount of precipitation exert the greatest influence. For Europe knowledge about the emissions and concentrations of air pollutants, and in particular information on aerosols and their precursor gases, is quite comprehensive. In addition, measurements and model calculations indicate the strong variability of this pollution plume owing to changing emissions, chemical transformations, deposition and long-range transport of manifold species, all depending on season and weather type (see e.g. Eliassen and Saltbones, 1983, Krüger and Tuovinen, 1997, EMEP – The European Monitoring and Programme, selleck compound 2004, Schaap et al., 2004, Van Dingenen et al., 2004 and Putaud et al., 2004). During the late 1980s, enormous amounts of particulate matter and aerosol precursor gas emissions, such check details as sulphur dioxide, nitrogen oxides and ammonia, made a strong contribution to the aerosol load over Europe. The extraordinarily

high sulphur dioxide emissions in the former German Democratic Republic (GDR), which amounted to even more than 5 Tg per year, were of major importance to secondary aerosol particle formation. The sizeable contributions from elevated point sources around Halle, Leipzig and Cottbus resulted in pronounced spatial differences of sulphur dioxide (SO2) and particulate matter (PM) concentrations in air. Such an increase in air pollution lead to reduced extinction and altered cloud optics. In Germany Liepert & Kukla (1997) found a statistically significant decrease in the mean annual surface global solar radiation between 1964 and 1990 under completely overcast skies. selleckchem This result can be potentially explained by an increase in cloud optical thickness, changing cloud types, or by human impact on aerosol cloud-mediated processes. The collapse of the Eastern Bloc in 1989 led to significant reductions in industrial activities and thus atmospheric pollution.

A pronounced declining trend was observed in the so-called ‘Black Triangle’; this name refers to the enormous damage to human health and ecosystems caused by soot. This area, covering the southern part of Saxony (Germany), northern Bohemia (Czech Republic) and south-western Lower Silesia (Poland), is a prominent example of the extensive use of lignite deposits in Europe. Stjern et al. (2011) analysed the visibility changes in the ‘Black Triangle’ between 1983 and 2008. They confirmed that the strong reductions in SO2 and PM emissions in central Europe, i.e. a 90% decrease of SO2 emissions and a 72% decrease of measured sulphate concentrations, improved the mean horizontal visibility in the ‘Black Triangle’ from 11 to 27 km between 1983 and 2008.

3% vs 9.2 ± 1.7%, P = .001; Figure 3B). The average number of cells with caspase-3 expression in the treatment group increased significantly compared to that of the control one [(82.6 ± 3.5) × 103 and (21.4 ± 2.3) × 103, respectively; Figure 3A]. All mice were alive during the whole experiment. In the preparatory Venetoclax study, we observed the tumor slices under the TEM and calculated the mean sizes of gaps between vascular endothelial cells (865 ± 5.2 nm; range, 630-1325 nm) for 20 xenograft tumors. This result indicated that average gap sizes between tumor vascular endothelial cells were larger than our NB mean sizes (586 ± 6.0 nm) in our mouse model.

As the time line in Figure 2 showed, we processed the following experiment and observed that there were no statistical differences in the average weights of mice within four groups on day 0 (P = .76) and day 7 (P = .79). As for tumor sizes, the data indicated no differences among four groups

from day 0 to day 7 during the whole treatment process (P = .98; Figure 4A). Histologic analysis showed that there were no significant differences in the percentage of necrotic areas of samples between treatment (TI and T2) and control groups (C1 and C2; P = .21). At the end of treatment, anti–Her-2 therapy response was investigated by IHC analyses of Her-2 and caspase-3 expression in excised tumors. The data showed that the percentages of Her-2–positive expression in mouse tumors in the two treatment groups

(TI and T2; 54.5% click here and 66.7%) were lower than the control ones (91.2% and 80%, respectively; Progesterone Figure 6B). This indicated that there was effective treatment in mouse xenograft models (T1 and T2 groups) and the trastuzumab treatment also induced apoptosis cells in these tumors. Thus, the percentages of caspase-3–positive expression in mouse samples in the two treatment groups (TI and T2) were higher than those of the control groups (C1 and C2; 90.0% and 83.3% vs 66.7% and 70%, respectively; Figure 6A). The ultrasound contrast imaging detected NB signals in in vivo models after 60 minutes from the injection of NB through the mouse tail vein, and this process was carried out under different time points (days 0, 3, 5, and 8; Figure 5A). Then, ultrasound imaging software analyses indicated that the average mean intensities of targeted bubbles in ROIs ( Figure 5B) in the T1 group were significantly higher than those in the other three groups (T2, C1, and C2; P = .001; Figure 4C). However, there were no differences within the three groups (T2, C1, and C2 groups), when one group was compared to other three groups (T2 vs T1 + C1 + C2, P = .74; C1 vs T1 + T2 + C2, P = .51, and C2 vs T1 + T2 + C1, P = .33, respectively). As for peak intensities of intratumor microbubble perfusion, they were also higher in the T1 group than those in the other groups (T2, C1, and C2; P = .00), but there were no differences within T2, C1, and C2 groups (P = .43, .96, and .42, respectively; Figure 4B).

3 Therefore, inflammation has emerged as an integrative cardiovascular disease factor,4 and novel risk factors such as fibrinogen and inflammatory markers have been introduced.5 Interestingly, individuals with severe chronic periodontitis have been reported to have a significantly increased risk of developing cardiovascular disease, after adjusting for many traditional risk factors.6 Although the mechanisms accounting for such a relationship have not been fully defined, it has been proposed that bacteria can access systemic circulation, leading to the invasion of vascular cells and increased levels of circulating cytokines.7 and 8 selleckchem The endothelium

is the active inner monolayer of the blood vessels, forming an interface between circulating blood in the lumen and the rest of the vessel wall. It

is well established that systemic inflammatory factors activate the endothelium, see more leading to its dysfunction.9, 10 and 11 One of the hallmarks of endothelial dysfunction is an altered response to endothelial-dependent stimuli, such as acetylcholine.12 Acetylcholine stimulates endothelial nitric oxide synthase (NOS-3) to generate NO, that diffusing to the underlying smooth muscle cell and induces relaxation by increasing the production of cGMP. On the other hand, response to the endothelium-independent vasodilator sodium nitroprusside, a nitric oxide donor, remains intact during endothelial dysfunction. Additionally, it has been shown that endothelial dysfunction enhances vasoconstriction response to agents like phenylephrine by reduction of endothelial nitric oxide buffering capacity.13 Endothelial dysfunction is an early event

in the development of cardiovascular disease.14 and 15 A number of studies have shown that patients with cardiovascular risk factors but no clinical signs of atherosclerosis have endothelial dysfunction.16 and 17 Emerging evidence has shown an association between periodontitis and endothelial dysfunction in humans.18, 19 and 20 These findings suggest that periodontitis is associated Chlormezanone with endothelial dysfunction through decreased nitric oxide (NO) bioavailability and that systemic inflammation may be, at least in part, a cause of endothelial dysfunction. Despite the link between periodontitis and endothelial dysfunction in humans, more knowledge of this association is needed. The studies that show this relationship use flow-mediated dilation of brachial artery as a clinical marker of endothelial function18, 19 and 20, a method that is reproducible and closely correlated with invasively measured endothelial function21, but that fail to provide more detailed information about the vascular changes. Thus, the objective of the present work was to evaluate the vascular reactivity changes in isolated vessels and specific vascular beds as well as the systemic inflammatory response induced by periodontitis in rats.

g., no instructions to strategically recode 19•• and 26]), MVPA typically reveals a stable set of regions to represent MLN0128 in vitro memoranda across the duration of a delay-period. However, the activity patterns within these regions can be dynamic. For example, with auditory STM, the frequency-specific pattern of elevated stimulus-evoked activity transitions to become a pattern of negative activity during the delay period [30]. For visual STM, a classifier trained on a time point early in the trial will often perform progressively worse as it is slid forward across the remainder of the delay period, the converse being true for a classifier trained on a late-in-the-delay time point and slid backwards (Figure 1b). This suggests

a temporal evolution of the neural code underlying the short-term retention of a subjectively ‘stable’ mental representation 11•• and 31•]. It remains to be determined whether these observations from fMRI relate in a meaningful way to the finding of dynamic coding in populations of neurons in monkeys performing tasks requiring sustained attention to an object 32 and 33]. Another neural effect that has influenced models of visual STM capacity limitation is the contralateral delay activity (CDA), an ERP component that scales monotonically with STM load, but asymptotes at the psychophysically estimated capacity of an individual [34]. The

CDA is AZD8055 manufacturer widely interpreted as an index of the short-term retention of information (e.g., [35]), such that, for example, the presence of a CDA during visual search has been taken as evidence for ‘memory in search’ 36 and 37], and the

diminution of the CDA across consecutive trials requiring search for the same target as evidence for the ‘handoff’ of the mnemonic representation of the search template from STM to LTM [38]. Not unlike with univariate analyses of fMRI data, however, there can be problems with equating a 1-D, signal intensity-based measure like the CDA with a single psychological construct (in this case, the short-term retention of information). For example, empirically, the CDA can be observed during tasks for which it is unclear that the short-term retention of information is required, such as during multiple object tracking [39], or during change detection ‘even when the observers know that the objects will not disappear from the visual field’ [40] (p. Osimertinib solubility dmso 8257). Further, the CDA during STM and during visual search is markedly reduced after intensive visual working memory training, despite the fact that STM capacity is increased and search performance improves with training [41•]. Under these conditions, a physiological marker specific to the short-term retention of information would be expected to increase in intensity. An additional challenge to the idea that the CDA is specific to the short-term retention of information comes from the proposal that it may, in fact, be the consequence of averaging across trials containing asymmetric amplitude modulation of alpha-band oscillations [42].

5 mM EGTA-supplemented, 20 mM HEPES-buffered Hank’s balanced AZD8055 nmr salt solution (5.36 mM of KCl, 0.44 mM of KH2PO4, 137 mM of NaCl, 4.2 mM of NaHCO3, 0.34 mM of Na2HPO4, and 5.55 mM of d-glucose). This was followed by a 12 min perfusion with 25 mM NaHCO3-supplemented Hank’s solution containing 5 mM

CaCl2 and 0.2 U/mL collagenase. Flow rate was maintained at 28 mL/min and all solutions were kept at 37 °C. After in situ perfusion, the liver was excised and mechanically disrupted. The cells were suspended in William’s medium E without phenol red and filtered through a set of tissue sieves (30-, 50-, and 80-mesh). Dead cells were removed by a sedimentation step (1 ×g, for 15 min at 4 °C) followed by a Percoll centrifugation step (Percoll density: 1.06 g/mL, 50 ×g, 10 min) and an additional centrifugation in William’s medium E (50 ×g, 3 min). Around (100–300) × 106 cells were obtained from one rat liver. Cell viability was assessed by trypan blue exclusion and ranged between 85% and 95%. Cells were seeded into collagen-coated 24-well Falcon Primaria plates (Fisher Scientific AG, Wohlen, Switzerland), at a density of 3 × 105 cells/well in 0.5 mL of William’s medium E supplemented with 10% FCS, penicillin (100 U/mL), streptomycin

(0.1 mg/mL), insulin (100 nM), and dexamethasone (100 nM). Different batches of human platetable hepatocytes isolated from several male non-smoking donors 30–50 years-old were obtained from Celsis and seeded on collagen-coated 24-well plates at density of 3 × 105 cells/well in 0.5 ml of William’s medium E containing 10% FCS and

the same BI 6727 mw supplements like the medium for the rat hepatocytes. After an attachment period of 3 h, the hepatocyte medium was replaced with serum-free medium and the cells were further kept for a maximum of 3 days at 37 °C in an atmosphere of 5% CO2/95% air. The media of the hepatocytes was replaced daily. The cells were exposed to drugs in serum-free medium the next day after seeding. We compared the performance of 3D liver cells with the standard hepatocyte monolayer culture, because this is the most common in vitro model used in the pharmaceutical industry for drug hepatocyte toxicity screenings, Adenylyl cyclase mechanistic studies as well as metabolism experiments ( Guillouzo, 1998, Hewitt et al., 2007, Roth et al., 2011 and Sivaraman et al., 2005). Culture medium from rat and human 3D liver cells was collected at the indicated time points and stored at − 80 °C for albumin, transferrin, fibrinogen and urea measurements. Human and rat transferrin and fibrinogen concentrations were determined using an enzyme-linked immunosorbent assay (ELISA) kit from GenWay Biothech, Inc. (cat #: 40-288-20009F; 40-288-22856; 40-374-130022 and 40-374-130015) as described in the manufacturer’s instructions. Human and rat albumin concentrations were determined using an ELISA kit from Bethyl Laboratories, Inc (cat #: E80-129 and E101) or from GenWay Biotech, Inc. (cat #: 40-374-130010).

Patients were randomized to receive oral enobosarm at a dosage of 1 (n = 53) or 3 mg (n = 54) or placebo (n = 52) once daily for up to 113 days at centers in the United States or Argentina. The primary end point was defined as the change in total lean body mass from baseline as assessed by dual-energy X-ray absorptiometry (DEXA). After study termination, significant increases in total lean mass were noted in both enobosarm groups (enobosarm 1 mg: median 1.5 kg, range –2.1 to 12.6, P = .001 vs baseline, enobosarm 3 mg: 1.0 kg, –4.8 to 11.5, P = .046). The study drug was well

tolerated. POWER (Prevention and treatment Of muscle Wasting in patients with cancER) was a double-blind, randomized, placebo-controlled phase III trial of enobosarm 3 mg once daily that aimed to assess lean body mass and physical

function after treatment. Preliminary results were recently presented in abstract form. 75 A total Vincristine molecular weight of 641 patients MAPK inhibitor with stage 3 or 4 non–small cell lung cancer were randomized into 1 of 2 trials at initiation of first-line chemotherapy (platinum plus taxane or platinum plus nontaxane) plus add-on, consisting of either enobosarm or placebo for 5 months. The study’s coprimary end points, as assessed after 84 days of treatment, were physical function response assessed by stair-climb power and lean body mass as measured by DEXA. Compared with placebo, enobosarm treatment was associated with an increase in the stair-climb power and the lean body mass in the platinum plus taxane treatment arm, whereas in the platinum plus nontaxane arm, there was only a significant increase in the patients’ lean body mass (all P < .02). Using intramuscular testosterone replacement, Del Fabbro et al76 performed a randomized, double-blind, placebo-controlled trial in 29 patients with advanced cancer,

low bioavailable testosterone, and a fatigue score higher than 3 of 10 on the ESAS. Unfortunately, 4 weeks of treatment did not change patients’ FACIT score values in the testosterone group (n = 13, administered every 2 weeks) as compared with the placebo group (n = 16). Improvements were noted in the testosterone group with regard to the Sexual Desire Inventory score (P = .05) and the patients’ performance status (P = .02). The authors therefore concluded Lonafarnib research buy that “four weeks of intramuscular testosterone replacement in hypogonadal male patients with advanced cancer did not significantly improve quality of life.” 76 Another novel anabolic agent has recently been tested in a randomized, double-blind, controlled trial. MT-102, also known as espindolol, is a novel anabolic/catabolic transforming agent that appears to possess 3 potential pharmacological targets in cancer cachexia: (1) reduced catabolism through nonselective β-blockade, (2) reduced fatigue and thermogenesis through central 5-HT1a antagonism, and (3) increased anabolism through partial β-2 receptor agonism.

Several bands can be viewed in the range of 1700–600 cm−1. The wavenumber range of 1400–900 cm−1 is characterized by vibrations of several types of bonds, including C–H, C–O, C–N and P–O (Sablinskas et al., 2003 and Wang et al., 2009). Other studies on FTIR analysis of roasted coffees (Briandet et al., 1996 and Kemsley et al., 1995) have reported that carbohydrates exhibit several absorption bands in this region, so it is expected

that this class of compounds will contribute to several of the observed bands. According to Kemsley et al., 1995 and Briandet et al., 1996, and Lyman et al. (2003), chlorogenic acids also present absorption in the region of 1450–1000 cm−1. Chlorogenic acids represent a family of esters formed between quinic acid

and one to four residues Dasatinib cell line of certain trans-cinnamic acids, most commonly caffeic, p-coumaric and ferulic ( Clifford, Kirkpatrick, Kuhnert, Roozendaal, & Salgado, BKM120 in vitro 2008). Axial C–O deformation of the quinic acid occurs in the range of 1085–1050 cm−1, and O–H angular deformation occurs between 1420 and 1330 cm−1. The C–O–C ester bond also absorbs in the 1300–1000 cm−1 range ( Silverstein, Webster, & Kiemle, 2005) and therefore the bands located in the range of 1450–1050 cm−1 could be partially due to chlorogenic acids. Hashimoto et al. (2009) studied the influences of coffee varieties, geographical origin and of roasting degree on the mid-infrared spectral characteristics of brewed coffee, and also developed a fast and reliable procedure to determine the Hydroxychloroquine caffeine and chlorogenic acid contents in brewed coffee using the ATR-FTIR method. In their method, developed based on the spiking of the coffee brew with different amounts of caffeine, they identified the band at 1242 cm−1

as the most relevant absorption band for characterization of the caffeine content in the brew. In the roasted and ground coffee IR spectra herein obtained for defective and non-defective coffee beans this peak appears shifted to a slightly lower band (1238 cm−1), but it is present in all spectra. Another substance that can be associated to peaks in the 1600–1300 cm−1 range is trigonelline, a pyridine derivative that has been reported to present four bands in this range, due to axial deformation of C C and C N bonds ( Silverstein et al., 2005). A comparison of the average spectra of green and roasted coffees presented in Fig. 2b shows a decrease in the relative absorbance of several bands in the 1700–600 cm−1 region after roasting. Several literature reports confirm that the levels of carbohydrates, trigonelline and chlorogenic acids diminish upon roasting ( Farah et al., 2006 and Franca et al., 2005), so such variations in chemical composition are expected to affect the spectra in the 1700–600 cm−1 range.