Flow cytometry permitted discrimination of macrophages from microglia based on levels of CD45 expression; both microglia and macrophages express CD11b, but macrophages express a higher level of CD45 [30, 31]. In our analyses of macrophages and microglia, neutrophils

(which also express CD45 and CD11b) were consistently excluded by using an antibody against Ly6G (Clone 1A8). Blood leukocytes were excluded by perfusing the brain prior to cell recovery. Flow cytometry plots of cell preparations from brain tissues 4 days following TBI of WT mice showed that macrophages are a major part of the inflammatory response to TBI primarily on the side of injury (Fig. 1C); macrophages comprised 40 ± 2% of all CD45+ leukocytes in the ipsilateral TBI hemisphere compared with 5.7 ± 1.5% of CD45+ cells in sham control tissues

(p < 0.001). Quantification of the RXDX-106 cost kinetics of macrophage numbers that accumulate in brain hemispheres after TBI revealed that macrophage infiltration in ipsilateral hemispheres of TBI mice increased Fostamatinib in vitro by 21-fold on day 1 (mean ± SEM, 22 115 ± 1732), and by 77-fold on day 4 (46 968 ± 5918) compared with sham controls (1081±151 and 613± 205, respectively) (Fig. 1D). On day 7, WT ipsilateral TBI macrophage numbers declined but were still 25-fold higher than levels in sham controls, and on day 14 macrophage numbers were fourfold higher (Fig. 1D). On the first day following TBI, there was also a substantial increase in neutrophils (CD45hiCD11b+Ly6G+) in the brain (41 520 ± 4533 compared with 1419 ± 94 in sham controls), with a decline Racecadotril thereafter (Fig. 1D). These

findings are similar to the recent findings of Jin et al. [32], although our results add quantification of absolute cell numbers as well as proportions, and we find that macrophage levels are higher on day 4 than on day 1. To examine macrophage polarization post-TBI, we first sought to trace the genetic expression of Arg1, which is highly expressed during M2 polarization, or of Il12b, the gene for IL-12p40, a signature of M1 polarization. To do this, we took advantage of two reporter mouse strains, YARG (YFP-Arginase-1) and Yet40 (YFP-enhanced transcript for IL-12p40) [28, 33]. TBI was performed in YARG and Yet40 mice, and YFP expression in brain and peripheral blood leukocytes was compared by flow cytometry to WT animals, which lack YFP expression. One day after TBI, 21 ± 1.5% (mean ± SEM, n = 6) of ipsilateral hemisphere brain macrophages in YARG mice expressed YFP (Fig. 2A), but brain macrophages in the contralateral hemisphere and from either hemisphere of sham animals uniformly lacked YFP (data not shown). YFP expression in YARG brain macrophages peaked on day 1 after TBI, fell to 4–7% of the macrophage population by day 4, and was undetectable on days 7 and 14 (data not shown).

We report a case of a 24-year-old woman who presented with calcaneal methicillin-resistant Staphylococcus aureus osteomyelitis after open comminuted fracture due to a fall. PLX4032 molecular weight Radical debridement of bone and soft tissue was repeated six times in combination with negative pressure wound therapy, followed by hindfoot reconstruction with pedicled

vascularized fibula and subtalar arthrodesis. Good functional restoration had been achieved by the final follow-up 18 months after surgery. © 2013 Wiley Periodicals, Inc. Microsurgery, 2013. “
“This study addresses the “pre-expanded perforator flap concept” by demonstrating a case series of relevant reconstructive procedures and evaluate the perforator vessel diameter changes that happen during the pre-expansion procedure. Fourteen patients were treated with 15 flaps. One patient was treated with two pre-expanded internal mammary artery perforator flaps. In other cases, thoracodorsal, circumflex scapular,

lumbar, intercostal, lateral circumflex femoral, and deep inferior epigastric artery perforator flaps were used. Technical details and rate of complications were noted. Evaluations of the flap pedicles were done both by hand held Doppler and by color Doppler ultrasound (CDU). Flaps successfully www.selleckchem.com/products/torin-1.html served to resurface and release thick and rigid broad scar tissues and contractures in 11 of relevant 12 patients (in one patient with 50% flap loss, adequate contracture release could only be obtained with addition of a secondary split thickness skin graft to the residual flap) and provided a good source of tissue for anterior neck reconstruction of one patient and penis reconstruction of another patient. Reverse transcriptase In six patients, perforator artery diameters were measured by CDU both before and after the expansion process and a significant increase secondary to the pre-expansion procedure was detected (Pre-expansion mean: 0.48 ± 0.08 mm; post-expansion mean: 0.65 ± 0.10 mm; P < 0.05). Flaps as large as 30 × 20 cm were harvested. Totally three partial flap necroses were experienced in 15 flap procedures. Suprafascial pre-expansion of the perforator flaps seems to provide a solution

to achieve broader and thinner perforator flaps with larger perforator arteries. © 2013 Wiley Periodicals, Inc. Microsurgery 34:188–196, 2014. “
“Resections of oromandibular squamous cell carcinoma involving anterior mandible, floor of the mouth, and the skin, lead to composite oromandibular defects that can be approached in several ways depending on the extension of the bone defect, of the soft tissue and cutaneous resection, the patient’s general status, and the prognosis. A retrospective evaluation of 27 patients has been performed. The techniques described included single osseous or soft tissues free flap reconstruction, two free flaps or free and locoregional flap association. Postoperative follow-up ranged from 12 to 120 months.

The laboratory of O. Neyrolles is supported by the Centre National de la Recherche Scientifique, the Fondation pour la Recherche Médicale

(FRM), the Agence Nationale de la Recherche, the European Union, and the Fondation Mérieux. G. Lugo-Villarino holds a fellowship from FRM. The funders had no role in the decision to publish this article or in its preparation. The authors declare no financial or commercial conflict of interest. “
“Insulin-dependent (type 1) diabetes is a prototypic organ-specific autoimmune disease resulting from the selective destruction of insulin-secreting β cells within pancreatic islets of Langerhans by an immune-mediated inflammation involving autoreactive CD4+ and CD8+ T lymphocytes which infiltrate pancreatic islets. Current treatment is substitutive, i.e. chronic use of exogenous insulin which, in spite of significant advances, is still associated with major constraints PLX3397 mw (multiple daily injections, risks of hypoglycaemia) and lack of effectiveness over the long term in preventing severe degenerative complications. Finding a cure for autoimmune diabetes by establishing effective immune-based therapies is a real medical health challenge, as the disease incidence increases steadily in industrialized countries. As the disease affects mainly children and young adults, any candidate immune therapy must therefore be safe and

avoid a sustained depression of immune responses with the attendant problems of recurrent infection and drug selleck chemicals toxicity. Thus, inducing or restoring immune tolerance to target autoantigens, controlling the pathogenic response while preserving the host reactivity to exogenous/unrelated antigens, appears to be the ideal approach. Our objective is to review the major progress accomplished over the last 20 years towards that aim. In addition, we would like to present another interesting possibility to access new preventive strategies O-methylated flavonoid based on the ‘hygiene hypothesis’, which proposes a causal link between the increasing incidence

of autoimmune diseases, including diabetes, and the decrease of the infectious burden. The underlying rationale is to identify microbial-derived compounds mediating the protective activity of infections which could be developed therapeutically. Identifying insulin-dependent or type 1 diabetes (T1D) as a polygenic autoimmune inflammatory disease is a relatively recent finding which occurred by the end of the 1970s. The academic diabetes community reacted rapidly to this important discovery, concentrating efforts to approach, first, the major issue of the early diagnosis of the immunological disease and secondly, to devise immune-based therapeutic strategies to delay and/or prevent disease progression. Compared to other autoimmune diseases, approaching the pathophysiology of T1D was problematic because of the difficulties in having direct access to the target organ in patients.

J Am Soc Nephrol. 2008; 19:2384–2395. 5. Kajiyama T, Suzuki Y, Kihara M, et al. Different pathological roles of toll-like receptor 9 on mucosal B cells and dendritic cells

in murine IgA nephropathy. Clin Dev Immunol. 2011; 2011:819646. 6. Maiguma TSA HDAC manufacturer M, Suzuki Y, Suzuki H, et al. Dietary zinc is a key environmental modifier in the progression of IgA nephropathy. PLoS One. 2014; 28;9:e90558. 7. Moldoveanu Z, Wyatt RJ, Lee JY, et al. Patients with IgA nephropathy have increased serum galactose-deficient IgA1 levels. Kidney Int. 2007;71:1148–1154. 8. Suzuki H, Kiryluk K, Novak J, et al. The pathophysiology of IgA nephropathy. J Am Soc Nephrol. 2011; 22:1795–1803. 9. Nakata J, Suzuki Y, Suzuki H, et al. Changes in Nephritogenic Serum

Galactose-Deficient IgA1 in IgA Nephropathy following Tonsillectomy and Steroid Therapy. PLoS One. 2014; 21;9:e89707. WANG JI-GUANG Centre for Epidemiological Studies and Clinical Trials, The Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, China Excessive sodium in the human body, as a consequence of either increased dietary intake or decreased urinary excretion, is a well-established risk factor of hypertension. However, the blood pressure response to dietary sodium intake varies substantially between individuals. For instance, even within a population of a similar modern lifestyle, people may have quite different levels of blood pressure and different risks of hypertension. either If the blood pressure response to a certain amount of sodium intake is typically greater, this

phenomenon is called “salt-sensitive”. The opposite is called “salt-insensitive” ITF2357 or “salt-resistant”. Salt-sensitive hypertension is more likely to be seen in Asians than other populations and often shows a non-dipping pattern. The mechanism of salt-sensitive phenomenon is complex and influenced by many factors, such as renal function, functions of the neuronal and hormonal regulatory system, and the structure and function of the vascular system. Salt-sensitive can be inherited genetically or acquired in the lifetime. Among the complex mechanisms for salt-sensitive, renal sodium handling must play a major role in the determination of the inter-individual variability in the blood pressure response to dietary sodium intake, because the kidney determines whether sodium is reabsorbed back to the blood or excreted into the urine. Our recent data has indicated that proximal renal tubular reabsorption of sodium impacts the relationship between dietary sodium intake and blood pressure, especially during sleeping night-time hours. When the proximal tubular reabsorption is high, blood pressure is high at the current usual range of dietary sodium intake. However, when the proximal tubular reabsorption is low, blood pressure is positively associated with dietary sodium intake. Renal tubular dysfunction might be a cause of salt-sensitive volume expansion hypertension.

The virus suspension was diluted in α-MEM containing 2% FCS to give a concentration of 2 × 107 plaque-forming units/mL, and a volume of 1.6 μL of inoculum was infused over a period of 3 min by means of a microinjector (Narishige) fitted to the syringe. Alternatively, 1.6 μL of diluent (α-MEM

containing 2% FCS) was injected as a control. After the infusion, the CHIR-99021 cell line cannula was removed, and the burr hole was sealed with dental cement (Unifast III; GC, Tokyo, Japan). The incision was sutured with surgical silk (Natsume Seisakusho, Tokyo, Japan), and the mice were subjected to the following analyses. To accurately examine the mode of MPyV infection in mice after stereotaxic inoculation into the brain, the amounts of viral genomic DNA in the respective tissues were determined using quantitative real-time

PCR. The virus inoculum was infused into the brain parenchyma, as described above, and the mice were deeply anesthetized Ridaforolimus clinical trial with an intraperitoneal injection of sodium pentobarbital (100 mg/kg body weight). After the blood was collected, the mice were perfused transcardially with 50 mL of chilled PBS to remove intravascular blood, and then the brain, kidney, liver, and spleen were harvested and homogenized. Total DNA was extracted from the homogenates and blood by using a High Pure PCR Template Preparation Kit (Roche, Penzberg, Germany) following the manufacturer’s instructions. Two sets of primers and Taqman probes were designed

to detect the DNA sequences of MPyV VP2 and mouse β-actin genes (Table 1). The plasmid pPy-1 was used as a standard DNA for real-time PCR. For quantification of mouse β-actin DNA as an internal control, the standard DNA was amplified Dipeptidyl peptidase by conventional PCR from the mouse brain DNA using a specific primer set and Ex Taq (Takara) (Table 1). Real-time PCR was performed on each DNA sample using a LightCycler 480 Probe Master (Roche) and LightCycler (Roche) according to the manufacturer’s protocol. The copy numbers of MPyV DNA were normalized with reference to those of mouse β-actin DNA. In BALB/c mice, the amount of viral DNA in the brain peaked at 4 days p.i. and declined gradually at later time points (Fig. 1a). The MPyV DNA levels in the blood, kidney, and liver of BALB/c mice peaked at 6 days p.i. and were lower than those in the brain, while a marked and temporal elevation of viral DNA was seen in the spleen at 6 days p.i. (Fig. 1a). When KSN nude mice were inoculated with MPyV, the amount of viral DNA in the brain increased up to 4 days p.i. and remained unchanged during the observation period of 14 days (Fig. 1b). The viral DNA levels in the blood, kidney, and liver of KSN mice were similar to those of BALB/c mice (Fig. 1b). In contrast, the viral DNA in the spleen of KSN mice notably increased from 8 days p.i. and remained at a similar level up to 14 days p.i. (Fig. 1b).

In 1988, it was discovered that misfolded forms of influenza virus haemagglutinin triggered the synthesis of two glucose-regulated proteins, GRP78 and GRP94 [4]. As opposed to other

members of the heat shock protein (HSP) family, thermal shock does not induce GRP78 and GRP94. The best-characterized chaperone involved in folding of immunity-related proteins is the GRP78 (or BiP) (Table 1). Initially, GRP78/BiP was found as a fraction associated with the heavy chain of immunoglobulins in pre-B cells, KU-57788 cost B cells, and at highly augmented levels in plasma cells [5, 6]. Later on, it was demonstrated that BiP/GRP78 associated directly with nascent chains of immunoglobulins [4, 7], binding to hydrophobic residues of unfolded chains [8]. Munro and Pelham suggested that all members of the HSP70 family are involved with protein folding, where different members are involved with different proteins according to their intracellular localization [6]. Absence of GRP78/BiP expression results in embrionic lethality by day 3.5 in the mouse [9]. SIL1/BAP (BiP-associated protein) Erlotinib in vitro is a nucleotide exchange factor for GRP78 [10] expressed in several adult tissues (Table 1). SIL1-deficient

mouse develops progressive Purkinje cell degeneration and ataxia, but there are evidences that suggest that the UPR pathway might be activated in absence of SIL1, besides the impairment of BiP function [11]. GRP170/ORP150 is also a nucleotide exchange factor for GRP78/BiP [12] (Table 1). Another chaperone that has clear implications with the functioning

of the immune system is the chaperone GRP94/gp96 (Table 1). Although the expression of this ER chaperone is not required for cell viability, it is necessary for folding and exporting of Toll-like receptors (TLR) and integrins to the cell surface [13]. This chaperone Abiraterone nmr has also been implicated in autoimmune responses and tumour immunity [14]. Calnexin is also an important ER chaperone for immunity molecules. This protein has been shown to participate in folding/exporting of several complexes, including MHC class I and II, CD1b, and TCR [15–19]. ERdJ3 and ERdJ4 are DnaJ proteins that bind to unfolded proteins and recruit chaperones of the HSP70 family. They are co-chaperone for BiP/GRP78, and it has been shown that ERdJ3 binds to the complex BiP-IgH [2, 20–23]. The UPR pathway, as we know it today, was originally described in 1998 in Saccharomyces cerevisae [24]. However, there are previous descriptions in the literature indicating that alterations on protein folding are associated with transcription of ER chaperones [4, 25].

The GenBank accession number for the J1 region sequence, determined

in this study, is AB627957. Based on the J1 region sequence, we designed a PCR primer set, L2F (5′-GATTAAAACAACTCTCCCAA-3′) and L1R (5′-ATAACCGATTGACCATACAA-3′), thus generating a 363-bp PCR product, for detection of SCCmecIV of ST8 CA-MRSA (tentatively designated SCCmecIVl). We performed PCR detection of 45 staphylococcal Everolimus virulence genes using previously described methods (16); the target genes included three leukocidin genes, five hemolysin genes, 19 SE or related genes, three exfoliative toxin genes, epidermal cell differentiation inhibitor Edin gene, and 14 adhesin genes. When required, we determined the gene sequences; we determined the entire seb gene sequence as described previously

(21). The GenBank accession number for the seb2 gene sequence, determined in this study, is AB630021. We performed PFGE analysis as described previously (14). We performed susceptibility testing of bacterial strains for 36 drugs by the agar dilution method according to previously described procedures (4). Breakpoints for drug resistance were those described by the CLSI (4). Of 349 trains examined, eight (2.3%) were positive for MRSA. The MRSA strains were all isolated from different EPZ015666 mw surfaces or subway train lines and at different times; although three cars per train were

swabbed, there were no cases of multiple cars in the same train positive for MRSA. Isolation place/year, molecular characteristics, and identities of the isolated MRSA are summarized in Table 1. PFGE patterns and computer-assisted comparison are shown in Figure from 1. Two strains (PT1 and PT2) belonged to ST5. PT1 resembles the pandemic New York/Japan clone (Japanese type) having the following typical characteristics (11, 14, 16, 24): (i) it was positive for the pathogenicity island (SaPIm1/n1), which carries three superantigen genes, tst (encodes for toxic shock syndrome toxin 1), sec (encodes for SEC), and sel (encodes for SEL); (ii) it expressed a high degree of oxacillin and imipenem resistance (MICs, ≥  256 and 64  μg/mL, respectively); and (iii) it was resistant to multiple drugs, including levofloxacin and fosfomycin. The other ST5 strain (PT2) was a variant of the New York/Japan clone (Table 1 and Fig. 1): (i) it exhibited spa14 (t214); (ii) it lacked SaPIm1/n1, like the USA type (16, 24); and (iii) it was unusually positive for seb (encodes for SEB). SEB suppresses the mobility of polymorphonuclear neutrophils by inhibiting expression of staphylococcal exoproteins, allowing MRSA to invade and damage tissues (22).

, 2006a; Bragonzi et al., 2009; Hoboth et al., 2009; Rau et al., 2010). Thus, the propensity for genetic change appears to be important for the adaptation of P. aeruginosa CP-673451 datasheet isolates for chronic infection. We have previously shown that clinical isolates of P. aeruginosa indeed generate higher morphotypic and phenotypic diversity when grown as biofilms than does the laboratory strain of P. aeruginosa PAO1 (Kirov et al., 2007; data not shown). We now report that variants derived from in vitro grown biofilms have regained hallmarks of acute infection isolates, suggesting a mechanism by which biofilm growth may contribute to acute exacerbations associated with chronic

infection in the CF airway. We compared the dispersal response of a panel of clinical isolates from patients with CF and showed that all strains exhibited cell death and seeding dispersal from biofilms, high morphotypic diversity and the production of superinfective phage during dispersal (Kirov et al., 2007). Pseudomonas aeruginosa strain 18A was selected from that panel of clinical isolates as a representative strain for further study here. The phenotypes tested in this study included metabolic capacity, virulence factor production and colonisation traits. In comparison with strain PAO1, functional diversification was greatest in the dispersal progeny

of the chronic infection CF isolate, strain 18A. For both strains, the development of stable genetic variants was a feature of biofilm dispersal and was not observed in planktonic cultures. JQ1 supplier The diversification in metabolic capacity may play a crucial role in the establishment of chronic, persistent pulmonary infections of P. aeruginosa in patients with CF. For example, the ability of P. aeruginosa to catabolise alanine is known to provide a competitive advantage over other bacterial strains in vivo (Boulette HSP90 et al.,

2009) and could therefore explain why the clinical strain 18A is able to utilise alanine while the laboratory strain PAO1 cannot. Additionally, Hoboth et al. (2009) reported that clinical CF P. aeruginosa isolates that are hypermutators have increased amino acid uptake. These authors further suggested that ornithine metabolism may play a pivotal role in adaptation within the patient’s lungs. Hence, the higher mutation frequency of strain 18A compared to strain PAO1 may be linked to the increased substrate utilisation by the clinical strain and its biofilm variants. The ability to grow on d-alanine, l-alaninamide and l-ornithine was consistently lost in the dispersal population of the clinical isolate strain 18A. This may be a consequence of biofilm development on a glucose medium in contrast to sputum that contains a range of amino acids, including ornithine and alanine (Palmer et al., 2005, 2007).

1). Its role in atherosclerosis is essentially unaddressed to date. MDSCs and their monocyte components often increase in numbers in humans and mice that have cancer

Fulvestrant order or other chronic inflammatory conditions 45–47. The tumor-induced mechanisms that drive this expansion need further investigation, yet interesting studies already indicate that growth factors produced by tumor cells are important. As discussed in What can cardiovascular disease teach us about cancer?, experimental atherosclerosis also leads to great proliferation of Ly6Chigh monocytes in the host 21 and leukocytosis is a risk factor for cardiovascular disease in humans 48. These findings indicate that both diseases trigger systemic monocyte responses, but they also prompt a number of questions. Does atherosclerosis elicit PI3K inhibitor the production

of bona fide MDSCs? Which factors drive the Ly6Chigh monocyte/MDSC response in atherosclerosis and do these factors overlap with those involved in cancer? How do Ly6Chigh monocytes/MDSCs produced in cancer and atherosclerosis compare qualitatively? We propose that investigations of MDSC-like responses at the cellular and molecular levels in atherosclerosis will be valuable. The growth of a tumor and an atherosclerotic lesion are two phenomena where monocyte accumulation and chronic inflammation converge. In this Viewpoint, we have focused on the recent observations in atherosclerosis and cancer. These observations, together with others not discussed here, such as the role of genetics, may serve as useful think tanks for defining future experimental research and for understanding the two diseases better. Conflict of interest: The authors declare no fonancial or commercial conflict of interest. See accompanying Viewpoints: http://dx.doi.org/10.1002/eji.201141719http://dx.doi.org/10.1002/eji.201141894 The complete Macrophage Viewpoint series is available at: http://onlinelibrary.wiley.com/doi/10.1002/eji.v41.9/issuetoc “
“The impact of gestation and fetal–maternal interactions on Methamphetamine pre-existent autoimmune beta cell destruction is

widely unknown. The aim of this study was to investigate the influence of gestation per se and fetal mismatching on the onset of autoimmune diabetes in female non-obese diabetic (NOD) mice. We examined cumulative diabetes frequencies of NOD dams mated to syngeneic NOD, haploidentical CByB6F1/J and fully mismatched C57BL/6J male mice. Pregnancy from NOD males neither increased nor accelerated the diabetes onset of NOD dams (71% by age 28 weeks) compared to unmated female NOD mice (81% by age 28 weeks; P = 0·38). In contrast, delayed diabetes onset was observed when NOD dams were mated at 10 weeks of age with major histocompatibility complex (MHC) haploidentical CByB6F1/J male mice (38% at age 28 weeks; P = 0·01).

[25] that determines:

(1) relative excess risk due to interaction (RERI); (2) attributable proportion due to interaction Inhibitor Library cost (AP) and (3) synergy index (S). RERI is the excess risk due to an interaction relative to the risk without exposure. AP refers to the attributable proportion of disease among individuals exposed to both factors that is due to the factors’ interaction. S is the excess risk from both exposures when there is an additive interaction, relative to the risk from both exposures without an interaction. RERI = 0, AP = 0 or S = 1 means no interaction or strict additivity; RERI > 0, AP > 0 or S > 1 means positive interaction or more than additivity; and RERI < 0,

AP < 0 or S < 1 means negative interaction or less www.selleckchem.com/products/BIBW2992.html than additivity [26]. If any of the null values (0 in RERI and AP or 1 in S) falls outside the 95% CI of its respective measurement, then, the additive interaction is considered statistically significant. Excluding the calculation of linkage disequilibrium and statistical power, all statistical analyses were performed using STATA/SE software version 12.0 (StataCorp, College Station, TX, USA). The characteristics of cases and controls are shown in Table 1. Compared with control subjects, cases were more likely to live in a prefecture other than Fukuoka in Kyushu. There were no differences between cases and control subjects with regard to age at oral examination, education, smoking, toothbrushing frequency or use of an interdental brush. Among our control subjects, the genetic distributions of VDR SNPs rs731236, rs7975232, rs1544410 and rs2228570 did not deviate from the Hardy–Weinberg equilibrium (P = 0.76, 0.11, 0.54 and 0.42, respectively). Of the six SNP pairs, three pairs were in strong linkage disequilibrium: D’ between rs731236 and rs7975232, D’ between rs731236 and rs1544410 and D’ between rs7975232 and

rs1544410 Mirabegron were 0.99, 0.98 and 0.97, respectively (Table 2). In the multivariate model, compared with a reference group of women with the AA genotype of SNP rs731236, those with the GG genotype had a significantly increased risk of periodontal disease, while the AG genotype was not significantly associated with the risk of periodontal disease: the adjusted OR for the GG genotype was 3.68 (95% CI: 1.06–12.78) (Table 3). No evident relationships were observed between SNP rs7975232, rs1544410 or rs2228570 and periodontal disease. With respect to SNP rs1544410, the statistical power calculation revealed that using our sample size, we could detect the gene–disease association for an OR of 1.697 with an accuracy of more than 80% at a significance level of 0.05 with a two-side alternative hypothesis under the log-additive model.