In this review we highlighted

two potential innate inflammatory mechanisms that may lead to development of synovitis in OA, the TLR pathway and the complement cascade (Fig. 3). Furthermore, we highlighted the roles of cytokines selleck chemicals and chemokines that play a role in the initiation and perpetuation of synovitis and OA symptoms. These pathways and mediators also may impact cartilage matrix homeostasis and peri-articular bone remodeling. In addition, the products associated with synovial inflammation may serve as surrogate markers of disease activity or responses to therapeutic interventions. Further understanding of mechanisms promoting synovial inflammation in OA may lead to identification of novel therapeutic targets for controlling symptoms and slowing structural progression in this disabling

joint disease. This study was supported by 1K08 AR057859-02, Mentored Clinical Scientist Career Development Award, from the National Institute of Arthritis, Panobinostat clinical trial Musculoskeletal and Skin Diseases (CRS). “
“Linear bone growth involves the replacement of a cartilaginous template by mineralized bone through endochondral ossification. This growth process is orchestrated by various actions at the growth plate, a developmental region consisting of chondrocytes in distinct cellular zones. The proliferation, hypertrophy and apoptosis of these growth plate chondrocytes are regulated by a tight array of factors ensuring effective cartilage Digestive enzyme mineralization and thus longitudinal growth [1]. Hydroxyapatite (HA) crystals form associated with the trilaminar membrane bound matrix vesicles (MV) which in the growth plate are localised to the mineralized longitudinal septae and form from the plasma membrane of the terminal hypertrophic chondrocytes [2]. Mineralization is a biphasic process which is under tight control so as to

ensure levels of calcium (Ca2 +) and inorganic phosphate (Pi) are permissive for effective HA formation [2]. Three molecules have been identified as imperative in controlling levels of the mineralization inhibitors inorganic pyrophosphate (PPi), and osteopontin [2] and [3]. These are alkaline phosphatase (ALP), a nucleotide pyrophosphatase/phosphodiesterase isozyme (NPP1), and the Ankylosis protein (ANK). However, mechanisms beyond the supply and hydrolysis of PPi likely exist to control chondrocyte matrix mineralization. Once such mechanism could involve matrix extracellular phosphoglycoprotein (MEPE, OF45). This was originally isolated and cloned from tumors of oncogenic hypophosphatemic osteomalacia (OHO) as a candidate substrate for phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX) [4]. MEPE is a 56–58 kDa SIBLING (small integrin-binding ligand N-linked glycosylated) protein along with dentin matrix protein 1 (DMP1), osteopontin (OPN), dentin sialophosphoprotein (DSPP) and bone sialoprotein (BSP) [5].

“
“Ovulation is characterized as a sequence of events in a responsive preovulatory follicle after a luteinizing

hormone (LH) surge [12] and [28]. This event is controlled by a complex interaction of factors, including endocrine mechanisms, cellular messengers, proteases, cinases and activating enzymes and has been compared to an inflammatory response [12] and [28]. The kallikrein–kinin system (KKS) is an important mediator of inflammatory responses acting Dinaciclib nmr on vasodilatation, activation and inactivation of proteases, stimulation of prostaglandin biosynthesis as well as induction of smooth muscle contractility [3] and [24]. Kininogen (KNG) is a precursor protein of the KKS; plasma kallikrein uses KNG as a substrate to generate bradykinin while tissue kallikrein liberates kallidin that is cleaved to the bradykinin [3] and [11]. Transmembrane Transporters modulator Bradykinin is a nonapeptide kinin, the main mediator of KKS responses [3] and [8]. This system acts through two types of receptors, type 1 (B1R) and

type 2 receptor (B2R). Therefore, the ovulation resembles an inflammatory process and the KKS is involved in the inflammatory function. This system has been suggested as a possible important mediator of the ovulatory process [5], [16], [17] and [18]. Despite the increasing evidences on the role of the KKS in mammal ovaries, little is known about the regulation of these components at distinct ovarian compartments, mainly in monovulatory species. Additionally, the intrafollicular factors that initiate and control the ovulatory process are not well understood [13]. Thus, the knowledge on this system role during the ovulatory process can allow a better control of physiological functions to be applied to reproduction biotechnology and infertility treatments. The purpose of this study is to characterize the presence and regulation of some of the KKS components during the bovine ovulation process.

Twenty-seven cyclic beef cows were pre-synchronized to obtain a GnRH responsive follicle (≥12 mm; [30]) at the beginning of the experiment according to a previous study [13]. Briefly, females that had ≥12 mm pre-ovulatory follicles on Day 10, were administered GnRH analog (Gonadorelin, 100 μg IM, Profertil®, Tortuga, Brazil) and the ovaries were removed 0, 3, 6, 12 and 24 h after the GnRH, by colpotomy Clomifene in standing position [10]. After the ovariectomy, follicular fluid, granulosa and theca cells were collected and stored conform described first [29]. All procedures involving animals performed in this experiment were approved by the Ethics and Animal Welfare Committee, Universidade Federal de Santa Maria, protocol number 23081.007716/2010-61. Total RNA was extracted using Trizol (theca cells) or silica based protocol (granulosa cells; Qiagen, Mississauga, Canada) according to the manufacturer’s instructions and was quantified by absorbance at 260 nm.

3). Heat-inactivation (to remove complement activity) abolished serum bactericidal activity, consistent with bacterial killing being complement-dependent as previously shown for D23580 ( MacLennan et al., 2008). S. Paratyphi A CVD1901 was highly sensitive to serum killing with all dilutions of human sera tested killing the bacteria. 1/2, 1/4, 1/8 Adriamycin manufacturer dilutions effected a 3 log10 kill and 1/16 dilution a 1 log10 kill by 180 min. The bactericidal activities of the human sera against S. Typhimurium isolates were more affected by serum dilutions, particularly

D23580 — the highest dilution of the human sera that could still kill LT2 was 1/8 for donor 1 and donor 2 sera, and 1/4 for the pooled Malawian serum, while 1/4, but not E7080 in vivo 1/8 dilution of all sera killed D23580. These findings indicate the limitation of using diluted human serum in serum bactericidal assays against S. Typhimurium. Since both antibody and complement are co-diluted, the individual contributions of anti-Salmonella antibody and complement to killing of Salmonella cannot be determined. Hence, it is necessary to provide an exogenous source of complement in S. Typhimurium serum bactericidal assay when serial dilutions of human

serum are used as the source of antibody. BRS is commonly used as an exogenous source of complement in serum bactericidal assays and was used as the exogenous source of complement in this study. We first measured the ability of BRS alone to kill Salmonella by determining the viable bacterial numbers following exposure to different percentages (20%, 50%, 75%, next 100%) of BRS over a 3 h time course. All percentages of BRS tested (both AbD Serotec and Pel-Freez BRSs) did not kill S. Typhimurium D23580 and LT2 ( Fig. 4). The viable

bacterial count of S. Typhimurium D23580 increased by approximately 1 log10 in all percentages of BRS tested, while S. Typhimurium LT2 was bacteriostatic. With S. Paratyphi A CVD1901, higher percentages of both AbD Serotec and Pel-Freez BRS (100% and 75%) could kill the bacteria by 1–2 log10 over 180 min ( Fig. 4). This antibody-independent killing was removed when BRS was heat-inactivated. The difference in susceptibility of the three Salmonella isolates to killing by neat and diluted human serum suggested that there will be differences in the amount of BRS required for bactericidal activity in the presence of antibody. Using AbD Serotec BRS as the exogenous complement source and heat-inactivated diluted pooled Malawian serum for antibody, we investigated the amount of BRS required to kill the three bacterial isolates. With S. Typhimurium D23580 as the target isolate and 1/40 or 1/400 diluted human sera as antibody source, bacterial growth occurred with 20% BRS, and bacteriostasis with 50% BRS ( Fig. 5). Killing of D23580 occurred with 75% BRS. All three percentages of BRS killed S. Typhimurium LT2 at 1/40, 1/400 and 1/4000 diluted human serum, although with limited killing at 1/4000. With S.

In 47 Ländern ist Iodmangel immer noch ein öffentliches Gesundheitsproblem.

Jedoch sind seit 2003 auch einige Erfolge zu verzeichnen: In 12 Ländern wurde ein optimaler Iodstatus erreicht, und der Prozentsatz der Schulkinder mit Risiko Natural Product Library für einen Iodmangel ist um 5% gesunken (Abb. 1). Jedoch ist nun in 34 Ländern die Iodaufnahme mehr als adäquat oder exzessiv, ein Anstieg um 27 seit 2003 [25]. In Australien und den USA, zwei Ländern mit zuvor ausreichender Iodversorgung, nimmt die Iodaufnahme ab. In Australien herrscht nun milder Iodmangel [26], und in den USA liegt die mediane Iodkonzentration im Urin (UI) bei 145 μg/L, ein Wert, der zwar noch adäquat ist, aber nur halb so hoch wie der Median von 321 μg/L aus den 1970er

Jahren [27]. Diese Veränderungen Hydroxychloroquine cost unterstreichen die Notwendigkeit einer regelmäßigen Überwachung des Iodstatus, um zu niedrige wie zu hohe Iodaufnahme gleichermaßen festzustellen. Für diese von der WHO herausgegebenen Daten zur Prävalenz des Iodmangels gelten einige Einschränkungen. Zunächst einmal ist es problematisch, von einem populationsbezogenen Wert (Median der UI) auf die Anzahl der betroffenen Einzelpersonen zu extrapolieren. So würde z. B. ein Land, in dem Kinder eine mediane UI von 100 μg/L aufweisen, als ausreichend mit Iod versorgt gelten, obwohl gleichzeitig 50% der Kinder zuwenig Iod aufnehmen würden. Zweitens repräsentieren nationale Erhebungen nur 60% der in den WHO-Daten berücksichtigten Weltbevölkerung, und in regionalen Daten wird das Ausmaß des Iodmangels möglicherweise unter- oder überschätzt [25]. Drittens gibt es aus nahezu allen Ländern zu wenig Daten, um die Prävalenz des Iodmangels bei schwangeren Frauen zu beurteilen. Empfehlungen zur Iodaufnahme Cetuximab concentration für verschiedene Altersgruppen sind in Tabelle 3 aufgelistet. Im Allgemeinen werden vier Methoden empfohlen, um die Iodversorgung in Populationen

zu untersuchen: die Konzentration von Iod im Urin (UI), die Häufigkeit von Strumen, TSH und Thyreoglobulin (Tg). Diese Werte sind komplementär in dem Sinn, dass die UI ein sensitiver Indikator für die aktuelle Iodaufnahme (Tage) ist und Tg einen mittleren Zeitraum abdeckt (Wochen bis Monate), die Strumahäufigkeit dagegen die langfristige Iodversorgung (Monate bis Jahre) widerspiegelt. Zur Bestimmung des Schilddrüsenvolumens stehen zwei Methoden zur Verfügung: die Untersuchung und das Abtasten des Halses sowie die Ultraschalluntersuchung (Sonographie) der Schilddrüse. Erhebungen zur Häufigkeit von Strumen werden üblicherweise bei Schulkindern durchgeführt. Beim Abtasten wird eine Schilddrüse als Struma eingestuft, wenn jeder Seitenlappen ein Volumen aufweist, das größer ist als das Daumenendglied der untersuchten Person.

, 1996). These structures provided the first insight into T cell antigen recognition and revealed a number of important features of the interface between the TCR and pMHC. Ten years later, only 10 unique human TCR/pMHC complexes had been solved, as reviewed by Rudolph et al. (2006). In recent years, this number has increased to ~ 25 human TCR/pMHC complexes, but progress has still been relatively slow compared with the number

of antibody structures, or unligated pMHC structures that have been reported. This lack of structural information selleck screening library regarding human TCR/pMHC complexes has compromised the determination of a comprehensive and accepted set of rules that govern T cell antigen recognition and a number of conflicting theories still dominate the field (Bridgeman et al., 2012). Difficulties in generating sufficient quantities of soluble TCR and pMHC protein, and in producing high quality TCR/pMHC Selleckchem HKI 272 complex crystals, may explain the low number of these structures. Additionally, TCRs bind to pMHCs with relatively weak affinity (KD = 0.1–300 μM (Cole et al., 2007 and Bridgeman et al., 2012)), which may further impede their ability to form stable complexes for crystallization. A number of approaches have been proposed for the production of stable, soluble recombinant TCRs, including modification of the expression

vectors and optimization of culture conditions. To date, soluble Epothilone B (EPO906, Patupilone) TCRs have been generated using various eukaryotic expression systems such as: Drosophila melanogaster ( Garcia et al., 1996), myeloma cells ( Wang et al., 1998), Chinese hamster ovary cells ( Reiser et al., 2000) and Spodoptera frugiperda cells ( Hahn et al., 2005). However, prokaryotic expression as inclusion bodies using Escherichia coli

strains, followed by artificial refolding, remains the most popular and robust system because it produces high yields of homogenous protein ( Cole et al., 2007, Cole et al., 2008 and Cole et al., 2009). Additionally, four different TCR cloning methods have been designed to improve soluble TCR stability including: (1) expression of the variable domains only in a form of a single chain Fv fragment (scFv) ( Housset et al., 1997); (2) expression of TCR α and β chains carrying c-Jun (α) and c-Fos (β) leucine-zipper heterodimerization motifs at their carboxyl termini ( Garcia et al., 1996); (3) introduction of a carboxy-terminal flanking sequence to the full length V and C ectodomains to promote the formation of an interchain disulphide bridge ( Stewart-Jones et al., 2003); and, (4) introduction of a non-native disulphide bond into the interface between the TCR constant domains ( Boulter et al., 2003). The ‘Boulter-disulphide’ method has been the preferred choice in our laboratory.

Studies have demonstrated that the 80-kDa mature form, but not the 66-kDa one, is predominantly expressed on the cell surface. Incorrect posttranslational modification of 66-kDa immature HER2 inhibitor form may lead to formation of disulfide-bonded aggregates in the endoplasmic reticulum, that ultimately do not proceed to the cell

surface [32], [34] and [35]. Here, we analyzed dental pulp cells from probands carrying both a heterozygous missense mutation (p.R152C) and a heterozygous deletion (p.N432del) in different alleles. Western blotting analysis revealed the presence of both the 66-kDa and ~ 80-kDa forms of TNAP in total protein extracts from probands and control cells (Fig. 4A), however the ~ 80-kDa form predominated in control cells, whereas there was increased ratio of the 66-kDa form (non-glycosylated, immature form of TNAP) to the 80-kDa (glycosylated or mature form of TNAP) in probands compared to control cells (Fig. 4B). Furthermore, immunocytochemistry

revealed that TNAP was localized to the cell surface (and cytoplasm) in control dental pulp cells (with native TNAP), whereas mutated TNAP protein was more predominantly localized to the perinuclear region and cytoplasm in cells from the probands (Fig. 5). We have demonstrated previously that primary periodontal ligament and dental pulp cells

harvested from the same probands exhibited increased ALPL mRNA, whereas residual Selleckchem GSK2126458 ALP activity and ability to promote mineralization in vitro were markedly reduced (40% and 50%, respectively) [18] and [20]. Here, we showed that increased ALPL mRNA concentration in these cells does not result in increased protein Florfenicol expression, suggesting that regulatory mechanisms, such as the ER quality-control system, may be intervening and resulting in defective intracellular transport of mutant TNAP, likely due to retention of a fraction of mutant TNAP molecules in the intracellular compartment. Mutations affecting TNAP trafficking have been described previously. Shibata et al. [35] showed that a homozygous missense mutation in TNAP affecting the 179 residue (p.A179T), associated with a lethal hypophosphatasia, exhibited defective folding that affected trafficking of TNAP molecules, causing only a small fraction of mutated TNAP protein to reach the cell membrane, presumably due to the formation of disulfide-bonded high-molecular mass aggregates. Intriguingly, cells expressing mutant TNAP (p.A179T) exhibited residual TNAP activity, suggesting the mutation did not lead to complete inactivation of the enzyme [35]. Conversely, Numa et al. [34] showed that the TNAP mutation (p.

Even when needs were expressed by relatives, they were not considered as a potential client “How can I put it? Even though I was sad, they did not ask why I was feeling that way…” (R25T2). There was a perception of inequality, of inconsistency in services received by relatives where those who were themselves (or a close one) part of the health care system were favored “I told them that my wife used to be a nurse, so maybe it played in Ion Channel Ligand Library cell line my favor” (S14T2) or “I think it might have helped communication

with the social worker once they knew that she was also a social worker” (S15T1). Communication abilities of health professionals emerged as a key factor to foster respect and confidence toward health professionals “He gave me his hand, and he explained me this and that. I liked it when they introduced themselves” (R2T1) or “They were always available and always smiling all the time, as if we were not disturbing them, you know” (S1T1). Good communication between health professionals was appreciated but was perceived as a challenge in acute care settings “I would repeat in the evening, repeat over the next morning, I would repeat every hour, because I was there on a working shift, you know. You tell yourself ok, at some point,

I have other things to do. Always repeating…” (R4T1). Information-seeking on the part of relatives was perceived as being the norm “I tell you, it’s the same everywhere. Here [in rehabilitation] or in acute care, it’s just the same thing. If you want information, you have to run after it yourself, that’s all” (R23T2). As relatives needed to seek for services, availability RG7422 and attitudes of health professionals emerged as a determinant factor which was perceived as a facilitator when for example doctors would do systematic daily rounds “…we had a doctor who would

come almost every day. He took time to talk with us… he would come early in the morning or in the afternoon at around 3 pm” (S9T2) or when the physical environment was supportive “Yes, and buy Sorafenib of course we would pass by, we would walk around, and they were very close… on the ward, three doors away, and the physiotherapist and occupational therapist were there” (R1T2) or when there was a stability in personnel which was mentioned more frequently in the context of rehabilitation as compared to acute care “So we would walk by, and with time they would recognize us because it was always the same staff. And they would talk to us and ask how we were doing and all that” (R1T2). In contrast, barriers mentioned were high staff turnover “In the first few days, there was a lot of staff turnover, and it was difficult to get new information” (R10T1), scheduling issues such as personnel availability only during day time and weekdays (working hours) “…we did not really speak to the neurologist because he was working days, and we could not be there during the day” (R20T1) or “But you know, treatments were during the day.

However, the specific ease with which particular participants or groups completed the task during scanning is unknown and may be variable. Variations in task difficulty can affect physiological responses, linearly increasing

neuronal firing with increasing difficulty (Chen et al., 2008) and increasing amplitude of electrical activity (Mulert et al., selleck kinase inhibitor 2007). However, using functional transcranial Doppler ultrasound, we have shown that difficulty in both an auditory naming and a word generation task does not affect lateralisation or the intensity of activation (Badcock, Nye, & Bishop, in press). There are a number of limitations of this research that relate to the small sample size and differences between the groups in terms of age ranges and distribution of handedness and sex. Although the group sizes are small, they are comparable with group sizes from other studies of brain structure and function in language-impaired populations

(e.g., Watkins et al., 2002b). To minimise the effects of differences on brain structure relating to factors such E7080 as age, sex and handedness, we implemented the use of a nonlinear registration of the functional images to standard space, which removes gross differences in size and shape among the brains. We also included an image of grey matter volume for each individual subject as a voxel-dependent covariate in the functional analysis; only functional differences over and above structural differences would remain, therefore. Finally, although our groups check details were small, we used a mixed-effects analysis to compare groups rather than a fixed-effects analysis, which is typically used in

small samples of special populations. By using a mixed-effects analysis, which combines between-subject and within-subject variance at the group level, our data are less likely to be influenced by outliers, such as the left-handed SLI subject whose LI is reliably right-lateralised. This approach allows us to generalise our results to the wider population rather than limit their inference to the study-population as with a fixed-effects analysis. In our experience, brain structure is minimally affected by handedness and sex (see Watkins et al., 2001), so the age differences among our participants is likely to be the main confound. It is well described that although white matter continues to increase linearly across the life span, grey matter increases to a peak during childhood or adolescence and then decreases during later years (Giedd et al., 1999 and Gogtay et al., 2004). A longitudinal analysis of grey matter volume collected on the same scanner with the same protocol as used here and analysed with the same tools, revealed reductions in grey matter from in a cohort aged 13 to 19 year olds over a 2–3 year period in mainly right hemisphere regions (Giorgio et al.

Technical replicates for individual miRNAs were averaged using the median signal intensity. Box plots and cluster analyses were used to identify potential outliers (poor quality chips). This quality control check resulted in the elimination of one array from the analysis. Identification of differentially expressed miRNAs was carried out on the probe level as well as the miRNA level. The MAANOVA model included the sample identity as a random effect and the gene specific variance estimate (F1 test)

was used to test for differences between the controls and treated samples. In this analysis, parametric p-values were obtained and were then FDR corrected. All this website data are MIAME compliant and that the raw data have been deposited in a MIAME compliant database (GEO), as detailed on the MGED Society website http://www.mged.org/Workgroups/MIAME/miame.html.

For each sample, 1 μg total RNA (containing the small RNA fraction) was polyadenylated then converted to cDNA using an oligodT primer with a universal tag and miScript Reverse Transcription mix (The Qiagen miScript PCR system, Qiagen). Real-time PCR was performed in duplicate for each sample, using a primer complementary find more to the universal tag and a miScript primer (Qiagen) specific for each miRNA. PCR product was detected using SYBR Green and a CFX real-time detection system (Bio-Rad). Expression levels of miRNAs were normalized to expression levels of U6

snRNA. Statistical analysis of data was done by Student’s t-test. Approximately 800 ng of total RNA per sample (n = 5/group) was reverse transcribed using RT2 first Florfenicol strand kit (SABiosciences™). Reverse transcription and real-time PCRs were carried out using RT2 SYBR Green PCR Master Mix on 96-well PCR arrays designed for the evaluation of mouse T cell and B cell activation (SABiosciences™) and using a CFX real-time Detection System (BioRad). Threshold cycle values were averaged. Relative gene expression was determined according to the comparative Ct method and normalized to the Hprt and β-actin housekeeping genes. Fold changes were calculated using online PCR array data analysis software (SABiosciences™). Statistical significance was calculated using REST method ( Pfaffl et al., 2002). Statistically significant and differentially expressed (by both microarray and RT-PCR analyses) miRNA were further analysed for their functional implications in biological processes as described in Li et al. (2011). First, using TargetScan (Friedman et al., 2009 and Lewis et al., 2005), the predicted target genes of miR-150, miR-29b, miR-142-5p, miR-34c, miR-34b-5p and miR-122 were identified. TargetScan was specifically used because it is suggested to be more accurate than other available prediction software. Next, predicted targets that were also differentially expressed (p-value ≤ 0.05, fold change ± 1.

The properties measured were tensile strength (MPa), elongation at break (%), and Young’s modulus (MPa). The apparent opacity (Yap) of the films was determined using a colorimeter (BYK Gardner, USA) and was calculated based on the ratio between the

luminosity (L*) of the system (CIELab), which was measured with a black background ( LB*) and a white background ( LW*), and the thickness of the film (φ). The results were expressed on an arbitrary scale (0–100% μm−1) according to Equation this website (1): equation(1) Yap=[(LB*/LW*)/φ]×100 The opacity of the films intercalated with fresh pasta was determined after 2 and 37 days of storage at 10 °C. Water vapour permeability (WVP) was determined gravimetrically, according to the ASTM E96-00 (1996) and under a relative

humidity gradient of 33–75%. The tests were conducted in duplicate. The yeast and mould counts in fresh pasta were taken in Dichloran Rose Bengal Chloramphenicol (DRBC) agar incubated at 24 °C for 5–7 days; coliform bacteria, which were grown at 45 °C, were counted using the most probable number method (MPN) (APHA, 2001, p. 676). The water activity of the fresh pasta was determined using an Aqualab CX2T equipment (Decagon Devices, USA) at 25 ± 2 °C, and the moisture content (on a wet basis) was determined according to the procedure described in the AOAC 925.04 (1995). Analyses were performed in duplicate. The colour parameters L*, a* and b* (CIELab system)

of the fresh selleck kinase inhibitor pasta were determined using a colorimeter (BYK Gardner, Germany) with an illuminant D65 (daylight) and a visual angle of 10°. The ΔE values (i.e., the colour difference between two spectrophotometric measurements) were calculated according SPTLC1 to Equation (2): equation(2) ΔE=(Lt∗−L0∗)2+(at∗−a0∗)2+(bt∗−b0∗)2where ‘t’ represents a specific storage period and ‘0’ is the beginning of storage. The reference sample was the pasta in the beginning of storage (t = 0). The sorbic acid content in the fresh pasta was assessed by ultraviolet absorption spectrometry (UV) at 530 nm AOAC 975.31 (1995). The results of mechanical properties, colour parameters, opacity and water vapour permeability were analysed using analysis of variance (ANOVA); treatment means were compared using Tukey’s test and Student’s t-test at a 5% significance level (p < 0.05) using a Statistica 8.0 software (Stat-Soft, Tulsa, OK, USA). The opacity of all films containing potassium sorbate (Fig. 1) was lower than that of the control films (CF), most likely due to the presence of sorbate, which acted as a plasticiser, thereby allowing a higher mobility between the starch molecules, and the passage of electromagnetic radiation. The FS4.5 film became more opaque during storage, most likely due to starch retrogradation.