e CD25+ cells) were depleted before activation (Fig  2a; compare

e. CD25+ cells) were depleted before activation (Fig. 2a; compare whole versus CD25-depleted populations on day 0). In contrast to control PBMC, depletion of CD25+ cells resulted in loss of CD4+ FoxP3HI cells at day 3 post-activation (Fig. 2a; DAPT solubility dmso compare whole versus CD25-depleted populations on day 3). Moreover, if carboxyfluorescein succinimidyl ester (CFSE)-labelled CD25Neg cells were reintroduced

into these polyclonally activated PBMC, there was significantly greater Teff proliferation in PBMC depleted of Tregs (Fig. 2b). Together, these data provide evidence to support the conclusion that aTregs derive from a starting pool of rTregs within PBMC. To study the effect of IFN-I on the generation of aTregs, freshly isolated PBMC were stimulated with anti-CD3 in the absence or presence of human leucocyte IFN (predominantly IFN-α) at 100 or 1000 U/ml or purified recombinant human IFN-β. Then, the total number of CD4 T cells and the generation of aTregs (CD4+ FoxP3HI IFN-γNeg)

and aTeffs (CD4+ FoxP3Low/Neg IFN-γPos) were analysed for separate normal donors after 3 days of polyclonal activation without or with added IFN-α (Fig. 3) or IFN-β (Fig. S1). While there was no consistent inhibitory p38 MAPK inhibitor review or stimulatory effect of IFN-α on total CD4 cell numbers (Fig. 3a,b), there was an average of 42% (P = 0·03) and 50% (P = 0·005) inhibition of aTreg generation in the presence of 100 and 1000 U/ml of IFN-α, respectively (Fig. 3c,d). In contrast, the presence of IFN-α tended

to increased the number of aTeff cells with an average of 53% increase in the number of aTeff cells using 1000 Units IFN-α (P = 0·06) (Fig. 3e,f). In contrast, although IFN-β significantly suppressed Treg activation, this cytokine also tended to decrease Teff activation at the higher concentration (Fig. S1). Although the number of donor PBMC tested with IFN-β was limited, the results may suggest that IFNs α and β may exert distinct effects on lymphocyte homeostasis during cell activation. As a result of the opposite effects of IFN-α on aTreg and aTeff, there was an alteration in the balance Flavopiridol (Alvocidib) between regulatory and effector cells as represented by the aTreg:aTeff ratio. Across all seven donors, this balance tended to favour aTregs in the absence of IFN-α (average aTreg:aTeff ratio = 1·4). However, the substantial suppression of aTreg generation induced by IFN-α caused a statistically significant shift in the mean aTreg:aTeff ratio for all seven donors [ratio = 0·7 for 100 U IFN-α (P = 0·05) and 0·5 for 1000 U IFN-α (P = 0·01)] such that aTeffs outnumbered aTregs on average by 2:1. Together, these data suggest that IFN-α significantly suppresses generation of activated Tregs in polyclonally activated PBMC, and at the same time promotes an increase in IFNγ-producing aTeffs.

Plasmid curing was used to examine the function of plasmids Five

Plasmid curing was used to examine the function of plasmids. Five plasmids of A. Protein Tyrosine Kinase inhibitor baumannii A3 were cured but no differences were observed between wild-type and plasmid-cured strains with respect to the biofilm formation capabilities. The prevalence of A. baumannii strains with biofilm mode of growth could explain their ability to persist in clinical environments and their role in device-related infections. The genus Acinetobacter includes a group of bacteria that are nonmotile, Gram-negative coccobacilli, displaying strict aerobic metabolism.

Acinetobacter spp. have evolved as important nosocomial pathogens. They are found in diverse environments such as soil, water, food products and are often isolated from medical devices (Bergogne-Bérézin & Towner, 1996). They cause severe infections in immune-compromised patients by colonizing on different medical

devices and surviving on these surfaces (Tomaras et al., 2003). A large number of reports describe the outbreaks of Acinetobacter-associated nosocomial infections such as secondary meningitis, pneumonia, wound, burn and urinary tract infections (UTI) (Bergogne-Berenzin et al., 1993; Patwardhan et al., 2008). Biofilm formation Autophagy activity is an important feature of most clinical isolates of Acinetobacter spp. Biofilms are assemblages of surface microbial cells that are enclosed in an extracellular polymeric matrix (Donlan, 2002). It is clear from the epidemiologic evidence that Acinetobacter biofilms play a role in infectious diseases such Thiamet G as cystic fibrosis, periodontitis, in bloodstream and UTI because of their ability to indwell

medical devices (Struelens et al., 1993; Donlan & Costerton, 2002; Gaddy et al., 2009). Acinetobacter is known to show resistance to a majority of commercially available antibiotics (penicillins, aminoglycosides, cephalosporins, quinolones) and therefore raises an important therapeutic problem (Smolyakov et al., 2004; Shin et al., 2009). A control of the spread of these infections thus demands the removal of Acinetobacter spp. from medical settings (Zavascki et al., 2010). Antibiotic resistance markers are often plasmid borne and plasmids present in Acinetobacter strains can be transferred to other pathogenic bacteria (Chopade et al., 1985; Patwardhan et al., 2008). The ability of Acinetobacter species to adhere to the surfaces, form biofilms, display antibiotic resistance and gene transfer means that there is an urgent need to study the factors responsible for their spread. In the present study, biofilm formation on different abiotic surfaces by six clinical isolates of Acinetobacter baumannii obtained from UTI, as well as catheter surfaces, and the effects of physical parameters (temperature, pH and NaCl) on biofilm formation, was investigated. Factors such as cell surface hydrophobicity (CSH) and production of lectins, important in biofilm formation, were also evaluated.

With the growing awareness that bacterial biofilms play a signifi

With the growing awareness that bacterial biofilms play a significant role in prosthetic joint infection, surgeons and investigators are increasingly looking to molecular technologies to enhance their diagnostic capabilities, but no clear consensus has yet selleck chemicals formed as to their reliability. Interrogation of joint aspirates with PCR-based assays has yielded conflicting opinion, having been interpreted as both encouraging (Mariani et al., 1996) and ineffective (Hoeffel et al., 1999). There are multiple factors that can lead to both false-positive (e.g. imprecise assay conditions)

and false-negative (e.g. contaminating inhibitors) results in PCR studies. One of the potential limiting factors of any given PCR protocol is that it should be able to survey and discriminate between the entire range of organisms known to be involved in prosthetic joint infections; although S. aureus and S. epidermidis are thought to comprise the bulk of causative organisms in infected arthroplasties, Gram-negative bacteria, anaerobes, and rare organisms have all been found as well (Fulkerson et al., 2006; Rafiq et al., 2006). The Ibis technology reported herein offers multiple significant advantages over any previously described PCR-based assay. It

simultaneously surveys a broad range of organisms (>3000), but is capable Kinase Inhibitor Library of discriminating to the species level. It is rapid, with results potentially available as soon as 6 h after sample presentation, and it is largely automated. It provides semi-quantitative information as to the numbers of genome copies per well, providing an indication of the abundance of the organism(s)

in the sample, and it provides a confidence value for its results, essentially internally analyzing its own potential for error. It can provide information on antibiotic sensitivities, reducing the time necessary to direct adjunctive antibiotic therapy from ∼3 days to <1 day. The Ibis PCR-MS technology either has been used to detect and characterize both bacterial (Whitehouse et al., 2010) and viral organisms (Grant-Klein et al., 2010), from both medical and environmental sources. It has multiple characteristics suggesting an excellent applicability to the diagnostic challenge frequently posed by prosthetic joint infection; in this case, it provided the first evidence of a multispecies infection, an observation subsequently confirmed by expanded culture, species-specific PCR, RT-PCR, and confocal microscopy using viability and FISH staining for targeted pathogens. We therefore submit that, pending a wider experience with the technology, the use of the Ibis T5000 system to evaluate clinical samples in suspected prosthetic joint infections may prove to be a superior means of diagnosis. A prospective clinical study is now underway to rigorously evaluate this hypothesis.

Left unchecked, this residual islet cell function/mass is general

Left unchecked, this residual islet cell function/mass is generally short-lived due to continued immune-mediated Talazoparib manufacturer β cell death [3]. However, the preservation of even this reduced β cell mass has clear therapeutic benefits by enabling tighter control of blood glucose, reducing exogenous insulin requirements and thus reducing the risk of diabetes-related complications [4–6]. As was apparent in a recent study

of a monoclonal anti-CD3 antibody [6], individuals with higher pretreatment levels of stimulated C-peptide (i.e. greater remaining endogenous insulin production) benefit most from intervention at this stage. Thus, clinical trials conducted in patients recruited shortly after diagnosis and with significant residual β cell function (often termed ‘tertiary prevention’ or ‘intervention trials’) have become a critical starting-point for assessing immunological therapies.

This approach forms part of a wider strategy that would subsequently see efficacious agents investigated for prophylaxis in high-risk individuals. selleck chemical Trials in new-onset patients have several advantages over prevention trials – potential risks are justified more easily when disease is present and studies can be completed in a shorter, 12–24-month time-period using a well-defined end-point, such as maintenance of stimulated C-peptide secretion. As a consequence, there are savings of both cost and time compared to true T1D prevention trials, which may take 5–10 years to complete and require the screening of large numbers of subjects to identify those at the highest risk. During the past 20 years, several immune interventions for new-onset T1D have been tested clinically. Early attempts involving broadly immunosuppressive agents with proven track records in solid organ transplantation, such as cyclosporin A, azathioprine and prednisolone, failed

to produce lasting remission and beneficial effects were limited only to the duration of treatment [4,7–9]. While highlighting the role of immune-mediated islet injury, these studies also demonstrated the inherent Mannose-binding protein-associated serine protease tendency of the autoimmune effector response in humans to recur, an issue that is also evident in islet graft failures 4–5 years post-transplantation. However, because of multiple long-term side effects, including secondary cancers and infections [10], continuous immunosuppression is not a viable option for the management of T1D. Therefore, it is critical that immunomodulatory therapies induce tolerance to β cell antigens while minimizing detrimental effects on host defence. Few treatments, such as monoclonal anti-CD3 antibodies [6,11] and anti-CD20 antibodies [12], in addition to islet antigen-specific therapies, have demonstrated this property to date and these will be central to novel combination therapies discussed herein.

1A) Both immunization protocols generated NP118-specific memory

1A). Both immunization protocols generated NP118-specific memory CD8+ T cells with similar frequency, phenotype (CD127hi, KLRG-1lo, CD27hi, CD43lo), and functionality (IFN-γ, TNF, and granzyme B expression; Fig. 1B–D). Mice from both vaccinated groups and nonimmunized controls were then challenged with LCMV-Arm. Consistent with our previous results [[16]], the NP118-specific CD8+ T cells in the att LM-NP118-vaccinated PKO mice underwent massive expansion, constituting ∼75% of all CD8+ T cells in the spleen (∼ 6–7×107 per spleen), at day 5 after LCMV challenge (Fig. 1C and D). One hundred percent

of these mice succumbed to the infection based https://www.selleckchem.com/products/hydroxychloroquine-sulfate.html on morbidity criteria by day 11 post-LCMV challenge (Fig. 1E). In sharp contrast, nonimmunized PKO mice exhibited relatively modest expansion of NP118-specific CD8+ T cells at day 5 post-LCMV infection and none of these mice succumbed (Fig. 1C–E). Interestingly, massive expansion of NP118-specific CD8+ T cells was also observed in DC-NP118-vaccinated mice and all of those mice succumbed to LCMV infection (Fig. 1C–E). Finally, the NP118-specific secondary effector CD8+

T cells at day 5 post-LCMV challenge exhibited similar phenotypes in the two vaccinated groups (Fig. 1F). These results suggest that mortality in vaccinated PKO mice following LCMV-Arm challenge is independent of immunization modalities. Immune system Current literature suggests that the magnitude of CD8+ T-cell expansion after primary infection is related to the number of precursors recruited into the response [[32, 33]]. However, Metabolism inhibitor it remains unclear whether the number of LCMV-specific memory CD8+ T cells at the time of LCMV infection determines the magnitude of secondary expansion and subsequent mortality in PKO mice. To address this question, we generated different levels of memory CD8+ T cells either by varying

the dose of att LM-NP118 used for immunization or by adoptive transfer of different numbers NP118-specific memory CD8+ T cells into naïve PKO mice. Naïve PKO mice were immunized with 5 × 106 CFU (high dose) or 5 × 102 CFU (low dose) of att LM-NP118. In order to control the extent of inflammation elicited by two different doses of infection used, mice that received a low dose of att LM-NP118 were coinfected with 5 × 106 CFU of the att LM strain that does not express the NP118 epitope (Fig. 2A). Approximately fourfold fewer NP118-specific memory CD8+ T cells (detected in PBL) were present in “low dose” compared with “high dose” immunized groups of mice (Fig. 2B). At day 70 post infection (p.i.) mice from both experimental groups and an additional control (nonimmunized) group were challenged with LCMV-Arm. Despite having fourfold difference in starting memory numbers (Fig.

In the absent reference comprehension literature, there is growin

In the absent reference comprehension literature, there is growing evidence that infants’ ability to locate the absent referent depends on various spatial factors. Some of the factors are the accessibility of the hiding location (Ganea, 2005), its proximity to the infant (Ganea & Saylor, 2013; Saylor & Baldwin, 2004) and, most central

to the present discussion, the stability of object location (Huttenlocher, 1974; Saylor & Ganea, 2007). The current study shows that location information may affect infants’ absent reference comprehension indirectly through affecting their object representation. Encountering an object several times across different locations affects infants’ understanding of the object identity, and this impairs their ability to locate the hidden object upon the experimenter’s verbal request. An interesting question Depsipeptide research buy for

future research is whether this effect can be extended to other types of referents that are less likely to have duplicates, for example to people or objects that infants know are unique. Another question is whether highly salient features that naturally help infants identify objects can release them from the location LEE011 ic50 change effect. Finally, it would be interesting to know when in development such type of location change stops interfering with infants’ performance and to understand what cognitive factors lead to such improvement. Previous research has shown that infants are able to individuate objects based on featural information before 12 months, at 4.5–10 months depending on the procedure (McCurry, Wilcox, & Woods, 2009; Wilcox, 1999; Wilcox & Baillargeon, 1998; Wilcox & Woods, 2009; Xu & Carey, 1996). In the current study, 12-month-old infants were confused about the number of objects when not given consistent spatiotemporal information and when their attention was not deliberately drawn to surface features. Several

aspects of the current study design might have contributed to CHIR-99021 cost this. First, the time lag between the two object presentations was much larger (10 min) in this study than in object individuation studies (a few seconds). Second, infants in this research had not only to individuate an object (establish its representation as a distinct solid entity in space), but also to identify it (that is, bind different object features together that define its identity and hold them in memory throughout occlusion for future retrieval). It is known that object identification is a more challenging task than object individuation (Tremoulet et al., 2000). Third, in the current study, infants’ object recognition was assessed in response to a verbal request for the object when it was absent. Presumably this is a more demanding test situation.

The degree and pattern of staining and inflammation was then eval

The degree and pattern of staining and inflammation was then evaluated. Furthermore, secreted Ro52 protein was measured in saliva and serum samples from the same individuals through a catch-enzyme-linked immunosorbent assay (ELISA). Ro52 was highly expressed in all the focal infiltrates in pSS patients. Interestingly, a significantly higher degree of Ro52 expression

in ductal epithelium was observed in the patients compared to the non-pSS controls (P < 0·03). Moreover, the degree of ductal epithelial expression of Ro52 correlated with the level of inflammation (Spearman's r = 0·48, P < 0·0120). However, no secreted Ro52 protein MG-132 cost could be detected in serum and saliva samples of these subjects. Ro52 expression in ductal epithelium coincides with degree of inflammation and is up-regulated in pSS patients. High expression of Ro52 might result in the breakage of tolerance and generation of Ro52 autoantibodies in genetically susceptible individuals. We conclude that the up-regulation of Ro52 in ductal epithelium might be a triggering factor for disease progression in SS. “
“The initiation of CD8+ T cell (CTL) immune responses can occur via cross-priming. Recent data suggested a relationship between cross-presentation

and immunodominance of epitope-specific T cells. To test this association, Selumetinib concentration we evaluated the efficacy of cross-presentation for several virus epitopes Doxorubicin research buy in vitro and examined if this can be extrapolated in vivo. Employing lymphocytic choriomeningitis virus (LCMV), we demonstrate that the cross-presentation and cross-priming of LCMV antigens were dominated by NP396, but not NP205 when analyzing the LCMV-NP. Although with LCMV-GP, cross-presentation was dominated by GP276, and cross-priming was dominated by GP33. Importantly, although NP396 was significantly more efficient

than GP33 in cross-presentation, cross-priming of their specific CTL was comparable. In a subsequent virus challenge after cross-priming, GP33-specific CTL dominated the response. Accordingly, based on our data, the ability of viral epitopes to be cross-presented in vitro does not entirely reflect what would occur in cross-priming. Thus, weak cross-presenting antigens may still cross-prime an efficient CTL response depending on other in vivo elements such as the naïve T-cell precursor frequencies. The priming of CTL is initiated by BM-derived professional APC (pAPC) 1–3, and is achieved via endogenous “direct-presentation” and exogenous “cross-presentation” 4–6. The contribution of multiple epitopes from viral proteins to the cross-presentation pathway after infections is not well understood.

The duration of hospitalization was significantly shorter in the

The duration of hospitalization was significantly shorter in the F group compared to the NF group. Conclusion: Our findings demonstrated

that clinical characteristics other than CKD-MBD at hemodialysis initiation were similar between very elderly patients and younger patients with ESRD. Furthermore, Venetoclax appropriate management by nephrologists may lead the improvement of quality of life for very elderly patients with ESRD. WANG JI-WEI1, ZHANG LING2, LI MINGZI3, CHEN JIN-BOR4, CHENG BEN-CHUNG5, CHEN TUN-LING6, TSENG TA-CHUAN7 1Division of Nephrology, Jilin City Central Hospital, Yanbian University Medical College; 2Division of Nephrology, China-Japan Friendship Hospital, China; 3Division of Nephrology, Jilin City Central Hospital, Yanbian University

Medical College, China; 4Division of Nephrology, Dabrafenib solubility dmso Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan; 5Division of Nephrology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan; 6Bo Da Ling Zheng (Bj) Hospital Investment Management Consulting Limited Inc. China; 7Bo Da Ling Zheng (Bj) Hospital Investment Management Consulting Limited Inc. China Introduction: Hyperparathyroidism is an impact factor for cardiovascular disease in dialysis patients. However, there are limited data pertaining the severity of hyperparathyroidism and cardiac function in dialysis patients. The purpose of present study was to explore the influence of severity of hyperparathyroidism on cardiac function in dialysis patients. Methods: The study design

was a retrospective, parallel-group, cross-sectional cohort study. The enrolled patients were chronic dialysis patients either on hemodialysis or peritoneal dialysis in two hospitals. A total 106 subjects were recruited, men: women were 53:53. The comparable variables included blood levels of Ca, P, Ca-P product, iPTH and parameters of cardiac echography. http://www.selleck.co.jp/products/Abiraterone.html The study subjects were stratified into two groups according to cutoff iPTH level 800 pg/mL. Results: In severe group, the mean age was 48.8 years, dialysis duration was 105.2 months, mean iPTH level was 1552.2 pg/mL. In mild group, the mean age was 50.4 years, dialysis duration was 33.0 months (P < 0.0001), and mean iPTH level was 353 pg/mL (P < 0.0001). The Ca/P profiles were Ca 2.6: 2.2 mmol/L (P < 0.0001), P 2.1: 1.5 mmol/L (P < 0.0001), Ca-P product 5.4: 3.4 (P < 0.0001). The significant variables in cardiac echography were left atrium diameter 43.1: 34.3 mm (P < 0.0001), ejection fraction 64.6: 59.3% (P = 0.031). The other variables including left ventricle end-systolic volume, end-diastolic volume, aortic root diameters, interventricular septum thickness were not statistical significance between two groups.

The MDP give rise to monocytes and common DC progenitors (CDPs)

The MDP give rise to monocytes and common DC progenitors (CDPs). Although monocytes can directly participate in immune responses or differentiate into macrophages or DCs, the differentiation potential of CDPs is restricted to the DC lineage. Common DPs give rise to cDCs and pre-classical DCs (pre-cDCs), which subsequently give rise to DCs.[8] In these differentiation steps, several cytokines and transcription factors have been identified as key molecules in regulating mononuclear

phagocyte development. Several reports have demonstrated that granulocyte–macrophage colony-stimulating factor (GM-CSF) drives inflammatory DC development from monocytes, and FMS-like tyrosine kinase 3 ligand (Flt3L) plays a critical

role in the development of cDCs and pDCs in the AZD1208 steady state.[4, 5, 9] The use of knockout mouse models revealed key roles of several transcription factors in DC development. Many transcription factors – including interferon regulatory factors, signal transducers and activators of transcription proteins (STATs), and Ets gene family members (SpiB, PU.1) –participate in DC differentiation and homeostasis.[4, 5, 9-11] The Fli-1 gene is a member of the Ets gene family of transcription factors.[12, 13] Members of the Ets gene family are found in genomes of diverse organisms, including Drosophila, Xenopus, sea urchin, chicken, mouse and human.[14-16] Like selleck chemicals other Ets gene family members, Fli-1 has the conserved DNA binding sequence, the Ets domain. Ets proteins bind to DNA sequences that contain a consensus GGA(A/T) core motif (Ets binding site) and function as either transcriptional activators or repressors.[15, 16] It has also been demonstrated that the 17-DMAG (Alvespimycin) HCl Fli-1 transcription factor plays an important role in megakaryocytic

differentiation and B-cell development.[17-22] Targeted disruption of the Fli-1 gene resulted in haemorrhage into the neural tube and embryonic death, due in part to thrombocytopenia.[23] We have reported that the number of platelets in the peripheral blood was reduced, and platelet aggregation and activation were also impaired in homozygous mutant Fli-1 mice that express Fli-1 protein (Fli-1∆CTA) with a truncated C-terminal regulatory (CTA) domain.[24] Expression of Fli-1 has been implicated in systemic lupus erythematosus in both human patients and murine models.[25-27] In this report, we investigated the role of Fli-1 in development of monocytes, macrophages and DCs. We found that populations of monocytes, macrophages and DCs were significantly increased in Fli-1∆CTA/∆CTA mice compared with wild-type littermates, and expression of Fli-1 in both haematopoietic cells and stromal cells has an effect on mononuclear phagocyte development. Expression of Flt3L was statistically higher in multipotent progenitors from Fli-1∆CTA/∆CTA mice compared with wild-type controls, and Fli-1 directly binds to the promoter of the Flt3L gene.

047 ± 0 004 (newborn), 0 046 ± 0 004 (10 days),

047 ± 0.004 (newborn), 0.046 ± 0.004 (10 days), ABT-263 cell line 0.051 ± 0.004 (20 days) and 0.049 ± 0.004 (30 days). No statistically significant difference was detected between the groups (F = 1.68, P > 0.05, Fig. 7A, Table 1). Mean inverse difference moment of MDC chromatin structures was: 0.458 ± 0.007 (newborn), 0.453 ± 0.012 (10 days), 0.457 ± 0.009 (20 days) and 0.448 ± 0.010

(30 days). Similarly as with ASM, no statistically significant difference was detected between the groups (F = 1.78, P > 0.05, Fig. 7B, Table 1). The results for GLCM parameters indicate that textural properties of MCD chromatin structure does not change in postnatal development and is not related to complexity loss determined by reduction of chromatin fractal dimensions. The results of our study indicate that chromatin of macula densa cells undergoes age-related loss of structural complexity that is most pronounced immediately after birth and remains during the first month of mouse postnatal life. The detected

complexity reduction is not followed by similar changes in chromatin textural homogeneity (measured primarily by the values of inverse difference moment) suggesting that in MDC, chromatin textural patterns are not related with fractal features. These findings also indicate that intrinsic nuclear click here factors, such as changes in chromatin epigenetic regulation, may have an important role in development and aging of macula densa. One of the possible explanations

for the detected reduction of chromatin complexity may be the relationship between the fractal dimension and lacunarity within nuclear structures. In contrast to fractal dimension, lacunarity significantly increased in mice aged 10 days compared with newborns and remained increased in older animals. Also, in all age groups fractal dimension was strongly correlated (negative correlation) with lacunarity. Although simple correlation does not necessarily implicate causal relationship, we may speculate that the increase of number and size of gaps in chromatin structure (measured by lacunarity) led to the reduction of chromatin complexity in our Tangeritin experiment. Fractal analysis is a commonly used method for evaluation of structural and organizational complexity in biological systems. It has so far been successfully applied in various biological and medical research areas, including cell biology[17, 25] and clinical practice.[26] In this study, we demonstrate age-related decrease of chromatin complexity of macula densa cells measured by fractal dimension. This result is in accordance with findings of other authors, which show generalized and sustained loss of both tissue and cell complexity during aging.[27-30] Our study, however, is the first to demonstrate this loss of complexity on kidney macula densa cells, as well as to combine fractal and GLCM approach in quantification of chromatin structure in kidney.