However, the RLB assays are relatively laborious, are limited to a maximum of about 40 samples per assay, and depend on visual read-out of the hybridization signal. To overcome these drawbacks, HPV genotyping using Luminex® suspension array technology has

been developed (11–14). The Luminex®-based genotyping coupled with GP5+/6+ PCR allowed sensitive GPCR Compound Library and specific genotyping of 27 mucosal HPV types in a 96-well plate format with a digital read-out (13). Moreover, a modified version of GP5+/6+ PCR was successfully introduced into the Luminex®-based assay, and showed improved sensitivity (15). A VeraCode-ASPE method was first developed for the detection of SNP in the human genome (16) and has

been applied to multiplex SNP genotyping on the Illumina BeadXpress® platform (17, 18). The ASPE primer is composed of two check details distinct regions: the 5′ region that contains the capture sequence, which is used in a subsequent hybridization reaction, and the 3′ region that contains the genomic target region with a SNP nucleotide at the extreme 3′ end. For SNP genotyping, the ASPE primer that matches the SNP nucleotide to the genome is extended by the primer extension reaction and is thus labeled with biotinylated nucleotides. After the primer extension, the products are mixed with VeraCode beads, so that the capture sequence on the primer hybridizes to its complementary sequence attached to the VeraCode beads. Labeling is then carried out with a streptavidin-fluorophore conjugate, followed by scanning and detection of the fluorescent signal using an Illumina

BeadXpress® reader (Illumina Inc., San Diego, CA, USA). In this work, the VeraCode-ASPE method on the Illumina BeadXpress® platform was evaluated for its suitability as a method to detect and genotype HPV-DNA (Fig. 1). The HPV-DNA amplified by PGMY-PCR was selected as a target for the VeraCode-ASPE genotyping, as PGMY-PCR 2-hydroxyphytanoyl-CoA lyase has been validated as a sensitive and specific means for HPV-DNA amplification (19, 20). HPV-type-specific ASPE primers were designed to target the PCR amplicons of 16 HPV types (HPV6, 11, 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66 and 68) in the 3′ region (Table 1), and with type-specific capture sequences in the 5′ region. The Tm values of the HPV-type-specific sequences, the lengths of which ranged from 19 to 28 bases, were adjusted to be between 54°C and 66°C using Primer3Plus software (http://www.bioinformatics.nl/cgi-bin/primer3plus/primer3plus.cgi) thus allowing similar annealing profiles. HPV-DNA, which was provided by the HPV laboratory network in the WHO as a quality-assured authentic panel for validation of HPV genotyping, was used to assess the sensitivity and specificity of the VeraCode-ASPE HPV genotyping.

In the presence of DDMS, vasodilatation to reduced PO2 was eliminated by indomethacin and unaffected by l-NAME in rats fed LS diet, and eliminated by l-NAME and unaffected by indomethacin in rats fed HS diet. The 20-HETE agonist WIT003 restored norepinephrine sensitivity in DDMS-treated arteries of HS-fed rats. HS diet increased vascular 20-HETE production and CYP4A protein levels by ∼24% and ∼31%, respectively, although these differences were not significant. Conclusions:  These findings

support the hypothesis that the 20-HETE/CYP4A system modulates vessel responses to norepinephrine and vascular relaxation to reduced PO2 in mesenteric resistance arteries R428 of SS rats fed HS diet. “
“Cells require energy to carry out their functions and they typically use oxidative phosphorylation to generate the needed ATP. Thus, cells have a continuous need for oxygen, which they receive by diffusion from the blood through the interstitial fluid. The circulatory system pumps oxygen-rich blood through a network of increasingly minute vessels,

the microcirculation. The structure of the microcirculation is such that all cells have at least one nearby capillary for diffusive exchange of oxygen and red blood cells release the oxygen bound to hemoglobin as they traverse capillaries. This review focuses first on the historical development of techniques to measure oxygen at various sites in the microcirculation, including the blood, interstitium, and cells. Next, approaches are described as to how these techniques have been employed Selleckchem Rapamycin to make discoveries about different

aspects of oxygen transport. Finally, ways in which oxygen might participate in the regulation of blood flow toward matching oxygen Myosin supply to oxygen demand is discussed. Overall, the transport of oxygen to the cells of the body is one of the most critical functions of the cardiovascular system and it is in the microcirculation where the final local determinants of oxygen supply, oxygen demand, and their regulation are decided. “
“Please cite this paper as: Quinn, Hamilton, McCann, Agnew, Millar, Lockhart, Harbinson and McVeigh (2011). Ocular Blood Flow Analysis Detects Microvascular Abnormalities in Impaired Glucose Tolerance. Microcirculation 18(7), 532–540. Objective:  Waveform analysis has been used to assess vascular resistance and predict cardiovascular events. We aimed to identify microvascular abnormalities in patients with IGT using ocular waveform analysis. The effects of pioglitazone were also assessed. Methods:  Forty patients with IGT and 24 controls were studied. Doppler velocity recordings were obtained from the central retinal, ophthalmic, and common carotid arteries, and sampled at 200 Hz. A discrete wavelet-based analysis method was employed to quantify waveforms. The RI was also determined.

Urinary incontinence status was ascertained using the selleck compound library International Consultation on Incontinence Questionnaire-Short Form. Results: Among the 683 eligible male participants, 49 men (7.2%) experienced urine leakage for the past 2.6 years (standard deviation [SD] 1.9). Their prevalence of alcohol drinking (beer, sake, shochu, wine, whisky) was lower than others without the condition, even though the daily mean ethanol intakes were similar between the two groups, 31.8 g (SD 45.4) and 31.3 g (SD 41.9), respectively. Relative to non-drinkers, the adjusted odds of urinary incontinence were 0.43 (95% CI 0.19 to 0.96) for low ethanol intake, and up to 32 g per day and 0.53 (95% CI 0.22 to 1.28) for drinking, at most, one can

(350 mL) of beer daily. However, higher levels of alcohol consumption had no significant benefit in reducing the incontinence risk. Conclusion: The findings suggested an inverse association between urinary incontinence and low alcohol consumption particularly beer in middle-aged and older Japanese

men. “
“Most men with lower urinary tract symptoms have both storage and voiding symptoms. Overactive bladder symptoms occur in 50–75% of men with benign prostatic obstruction. Alpha-blockers are usually the first option in medical therapy. Even though voiding symptoms are alleviated by the use of medicines or transurethral resection of the prostate, storage symptoms continue in 30–65% of patients. Combination therapy with an alpha1-receptor antagonist and an anticholinergic agent Protease Inhibitor Library clinical trial in benign prostatic hyperplasia patients with overactive bladder symptoms significantly alleviates symptoms and improves quality of life. In clinical practice, the efficacy and safety of anticholinergic combination therapy may not be comparable with well-controlled studies. Overactive bladder symptoms usually require long-term treatment, and benign prostatic hyperplasia

tends to progress with time. When male LUTS patients are treated with anticholinergic combination therapy, there are still some concerns about the development of acute urinary retention, voiding difficulty, and other anticholinergic side-effects. If the drug is prescribed in a relatively low dosage, however, this approach could be appealing regarding adverse effects. There is a Amisulpride relatively small number of clinical reports about low-dose combination therapy, which is in its early stages. Promising results are being reported, though the level of evidence is low. We await the final results. Lower urinary tract symptoms (LUTS) are found commonly in elderly men, and benign prostatic obstruction (BPO) is a common cause of LUTS.1 The prevalence of overactive bladder (OAB) increases with age, and it is similar to the natural history related to benign prostatic hyperplasia (BPH).2 Most men with LUTS have both storage and voiding symptoms, which suggests that BPO and detrusor overactivity (DO) may coexist. OAB occurs in 50–75% of men with BPO.

This is an important strategy of pathogens to cross various barriers. Serine protease plasmin degrades many blood plasma proteins, mostly

fibrin clots. In serum, free plasmin is quickly inactivated by α1-antiplasmin and α2-antiplasmin (Mayer, 1990); however, cell surface-associated plasmin cannot be regulated by the serum inhibitor and degrades high–molecular weight glycoproteins such as fibronectin, laminin, and collagen IV which are essential for proper BBB function Fig. 3. Most of the bacterial plasminogen receptors CP-673451 ic50 are extracellular metabolic enzymes (Pancholi et al., 2003), which fall into two major categories: (1) filamentous protein structures that are morphologically similar to fibrin–fimbriae proteins and (2) nonfilamentous surface proteins, usually abundant proteins, with enzymatic activity and multiple-binding properties (Mayer, 1990). The nonfilamentous plasminogen receptors Dinaciclib have relatively low affinity for plasminogen, which recognizes the lysine-binding

sites of a receptor molecule (Lahteenmaki et al., 1995). Fimbriae and flagella form a major group of plasminogen receptors in Gram-negative bacteria, whereas surface-bound enzyme molecules and M protein-related structures possess affinity to plasminogen in Gram-positive bacteria (Lahteenmaki et al., 2001). For the first time, binding of human plasmin to bacteria was reported for Streptococcus Group A. Over the next years, exploitation of host’s plasmin and plasminogen for proteolysis

of ECM, mediated by their surface proteins, was showed in many other bacteria like Staphylococcus aureus, N. meningitidis, Neisseria gonorrhoeae, Yersinia pestis, B. burgdorferi, and Cronobacter sakazakii. Binding of plasminogen to receptors of B. burgdorferi, Borrelia hermsii, M. tuberculosis, and Streptococcus Group A takes place via lysine residues (Coleman et al., 1995). ErpP, ErpA, and ErpC proteins are the major plasminogen-binding proteins of B. burgdorferi (Brissette et al., 2009). It has been shown that plasminogen bound to the surface of B. burgdorferi can be activated and turn into plasmin by urokinase-type plasminogen activator (Hu et al., 1995). Similarly, outer membrane protease (Cpa) of C. sakazakii causes uncontrolled plasmin activity Miconazole by converting plasminogen to plasmin and inactivating the α2-antiplasmin (Franco et al., 2011). GlnA1, one of the few plasminogen receptors of M. tuberculosis, binds host’s fibronectin to degrade ECM (Xolalpa et al., 2007), while C. albicans binds both plasminogen and plasmin. Binding of Candida enolase to plasmin is also lysine-dependent and can be inhibited with arginine, aspartate, and glutamate (Jong et al., 2003). Direct binding of plasmin and plasminogen in Streptococcus group A is mediated by three receptors: 1) plasminogen-binding group A streptococcal M-like protein, 2) α-enolase, and 3) glyceraldehyde-3-phosphate dehydrogenase (Lahteenmaki et al.

The authors further investigated the mechanism responsible for the different bacterial loads in double check details Casp1−/− Casp11−/−, Casp11−/− and Casp1−/− mice by analyzing neutrophils and macrophages, both of which regulate IL-1β processing by the NLRP3/ASC/caspase-1 axis [22] and are important for defense against Salmonella. Total neutrophil counts were significantly reduced in all three mutants compared with wild-type, but no difference was found between the three genotypes. Notably, the proportion of neutrophils carrying Salmonella (Salmo+) was much higher in double Casp1−/− Casp11−/− tissues compared with tissues from the

two single Casp1−/− and Casp11−/− mice. Moreover, the percentage of Salmo+ neutrophils inversely correlated with the percentage of Salmo+ macrophages. These observations, together with MG-132 cost the fact that caspase-1 and caspase-11 regulate macrophage death, led the authors to propose the following mechanism: in the absence of both caspase-1 and caspase-11, lysis of macrophages is delayed, allowing more bacteria to be retained intracellularly. Consequently, neutrophils could not then uptake and eliminate Salmonella, which could expand

extracellularly. When caspase-11 is present in the absence of caspase-1, bacterial release from macrophages undergoing pyroptosis is accelerated, causing a higher bacterial burden. The increased susceptibility observed in Casp1−/− Casp11Tg mice depends on pyroptosis induced by caspase-11

and not on IL-1β and IL-18 release, since the same number of bacteria was recovered from Il1r1−/− or Il1b−/− Il18−/− mice compared with Casp1−/− Casp11−/− mice. Although preliminary, these studies indicate that caspase-11 is an important component of the inflammatory response that, depending on the physiological circumstances, can control or exacerbate bacterial burden. Further studies undoubtedly will shed more light on the pathogenic or protective mechanisms driven by caspase-11 underlying host–pathogen interaction. The discovery of caspase-11 represents an important new achievement in the advancement of our understanding of the control of cytokine release and pyroptotic cell death regulated by inflammasomes. Caspase-11 activation is regulated via the TLR4/IFN pathway in response to Gram-negative bacteria. Moreover, by contributing to phagosome–lysosome fusion and pyroptosis Interleukin-2 receptor caspase-11 also plays an important role in host defense against cytosolic bacteria. Despite these important advances, our knowledge of the mechanisms underlying caspase-11-mediated processes is limited and several important questions remain to be addressed. The signal(s) that activate caspase-11 remain to be identified. Indeed, LPS alone, without the whole Gram-negative bacterium, induces procaspase-11 expression, as well as production of cytokine precursors and NLRP3 priming, but not caspase-11 activation, IL-1β/IL-18/IL-1α release or pyroptosis.

044 (−.034 for the original stimuli) for /buk/ and .023 (.034 for the original stimuli) for /puk/. Importantly, the variance in both was much lower in the present experiment (/buk/: SDoriginal = .0046, SDmodified = .0023; /puk/: SDoriginal = .026, SDmodified = .0026). Thus, by both relative measures, the variance in the information

available for voicing was minimized dramatically. Given the relatively slight contribution of this cue to perception in adults, it is clear that we have significantly reduced (if not altogether eliminated) variation in contrastive information in Experiment 3. A final concern was that the coda (/uk/) portion of the two words was not physically identical between /buk/ and /puk/ tokens within a speaker, as it was in Experiments 1 and 2. Coda information could have provided an additional source of constrastive information about voicing. It seems unlikely that such information would be sufficient to distinguish the Doxorubicin research buy words for two reasons: first, if coda information was necessary to distinguish the word-initial voicing, prior experiments using natural recordings that preserved coda information (Pater, Stager, & Werker, 2004; Rost & McMurray, 2009) would have provided sufficient information selleckchem for categorization in this task. Second, the effect of voicing on the vowel is small: most of the established cues to word-initial

voicing are found at the release or the aspiration/voicing juncture (Allen & Miller, 1999). Nonetheless, if there was information correlated with voicing, then variability in these cues could have helped the infants. Experiments 1 and 2 rule out contrastive variability alone (particularly as the contrastive cues varied there were much more robust cues to voicing than anything in the coda), but it is possible that these cues, combined with the noncontrastive variability we manipulated, were driving Thalidomide the effect. To

determine if the coda portions of the words contained any information that could contribute to a voicing decision, we measured a number of cues to voicing: the length of the syllable (measured from the release to the onset of closure), the pitch (F0), and the first and second formant frequencies. Measurements of F0, F1, and F2 were conducted twice, once during the first pitch pulse after the onset of voicing and once at the midpoint of the vowel (see Table 1). All of the measurements showed substantial variability. For example, at voicing onset, F0 had an SD of 84 Hz for /buk/ at onset and 97 Hz for /puk/. Similarly, F2 varied by well over 150 Hz at both points. This is perhaps to be expected given the variability in speakers (especially the variability in gender) and register across the Experiment 3 stimulus set and it validates our assumption that these stimuli had substantial variation. However, none of these measures showed significant differences as a function of the word.

Exosomes released from cancers contain oncoproteins and miRNAs which may promote cancer progression. A novel technology which consists of immobilized affinity agents in the outer-capillary space of hollow-fibre plasma separator cartridges that integrate into standard dialysis

machines has been selleck products devised. This technology is currently being evaluated for its efficacy for capturing exosomes secreted by cancer cell lines and present in biological fluids from cancer patients[106] and could potentially be applied to other situations such as atherosclerosis in which circulating microvesicles might have pathogenic roles. While there is an increasing appreciation of the existence and potential functions of exosomes and other vesicles, some very fundamental questions remain. Are there distinct cell-specific types or families of exosomes with well-defined sizes, cargos and differing functions? How is exosomal cargo modified? What are the physiological and pathological stimuli to their production, release and uptake? What are their physiological signalling roles in the circulation and urine? What receptors or other mechanisms define their target cells? What is the effect of renal Birinapant clinical trial function and disease

on the levels and nature of circulating and urinary exosomes? Addressing these questions should provide new insights in the intercellular communication mechanism and enable a more sophisticated translation of the use of exosomes as novel biomarkers and therapeutic intervention strategies. “
“Aim:  Haemodiafiltration (HDF) is the most efficient blood purification method and can remove a wide spectrum of solutes of different molecular weights (MW). The purpose of this study was to investigate whether the removed amounts of solutes, especially the larger molecules, could be

increased by changing the HDF filtration Bay 11-7085 procedure. Methods:  A new first-half intensive HDF treatment (F-HDF) was designed, whereby convective clearance is intensively forced during the first half of a HDF session. We compared the removed amounts of solutes in the same group of nine patients treated by F-HDF, constant rate-replacing HDF (C-HDF) and a high-flux haemodialysis (HD). Results:  F-HDF can remove significantly larger amounts of α1-microglobulin (MG), molecular weight (MW) 33 000, compared with HD and C-HDF (30.1 ± 15.1 vs 12.4 ± 0.3, 15.0 ± 3.1 mg, P < 0.01). Regarding the removal amounts and clear space of β2MG, MW 11 800, there were no significant differences between the three treatment modalities. Regarding amounts of creatinine, urea nitrogen and phosphorus, there were no significant differences between the three treatment modalities.

Although the treatment for leishmaniasis was introduced in the early 20th century, parenteral administration of pentavalent antimony compounds (meglumine antimoniate and

sodium stibogluconate) remains the first-choice treatment for all forms of leishmaniasis [7]. In the case of antimonial resistance, the second-choice treatment includes amphotericin B (deoxycholate or liposomal formulation) [7]. However, each of these therapies has important limitations, such as long-term selleck parenteral administration, toxic side effects, high cost in endemic countries and an increase in number of resistance cases [8]. A major breakthrough in chemotherapy of VL was the discovery of miltefosine, an analogue of phosphatidylcholine initially developed as an anticancer agent [9]. It is not recommended during pregnancy as teratogenicity has been observed in one species during preclinical development. Moreover,

its cost is another limiting factor [10]. Till date, no ideal drugs are available that fulfil the major requirements for efficient antileishmanial therapy, including high efficacy, low toxicity, easy administration, low costs and avoiding occurrence of drug-resistant parasites [11]. Cisplatin (cis-diamminedichloroplatinum II; CDDP) is a platinum-based anticancerous drug, which mediates its action by forming cross-link of DNA ultimately triggering apoptosis, or programmed cell death [12], and is also known to enhance the cytotoxic immunity [13]. An in vivo antileishmanial study with cisplatin at low dose also resulted in decreased parasite burden, increased Cobimetinib delayed-type hypersensitivity (DTH) response, initial transient and reversible increase in various liver and kidney function tests [14]. It is well known that nephrotoxicity is a dose-limiting factor of cisplatin, so later on, Sharma et al. [15] investigated the protective efficacy of high dose of cisplatin in combination with antioxidants (Silibinin, vitamin C and

vitamin E) which effectively reversed the toxic side effects caused by the drug. So an auxiliary therapeutic measure that might enhance the efficacy of these antileishmanials or reduce the resulting toxicity would be valuable. Immunochemotherapy Tau-protein kinase has been used with various combinations of drugs and vaccines mostly in case of cutaneous leishmaniasis. Some of them are sodium stibogluconate with poly ICLC (Polyinosinic-po lycytidilic acid) plus arginine [16], antimony with interferon–gamma [17], N-methyl meglumine antimoniate with recombinant Leish-110f plus MPL-SE vaccine [18], killed Leishmania promastigotes with antimonials [19] and alum precipitated autoclaved Leishmania promastigote (ALUM/ALM) plus BCG with sodium stibogluconate [20]. Chemotherapy of leishmaniasis is often compromised due to suppression of immune function during the course of infection.

Clearly, several approaches may be taken to enhance DC tolerogenecity. We previously Selleckchem Torin 1 demonstrated that genetic modification of immature DCs

with inhibitory cytokines such as IL-10, TGF-β or soluble TNF receptor could inhibit pathogenesis of autoimmune diseases or prolong allograft survival 14–16. In addition, exosomes derived from IL-10-treated or IL-4 gene-modified DCs could also suppress inflammation and attenuate progression of autoimmune diseases 17, 18. In spite of the existing findings, new approaches to enhance DC tolerogenecity or utilizing new subsets of tolerogenic/suppressive/regulatory DCs for the control of inflammation and autoimmune diseases with increased efficacy and identifying the underlying mechanisms remains a hot topic in immunology. Ligation of Fc receptors for IgG (FcγRs) by immune complexes Neratinib supplier (IC) may trigger two opposing signals, activating or inhibitory, depending on the FcγR subtypes 19. Three FcγR subtypes are currently known: FcγRI, FcγRIIa and FcγRIII that trigger cell activation by the presence

of an immunoreceptor tyrosine-based activation motif in their cytoplasmic fragments 19, and FcγRIIb that deliveries inhibitory signal through its intracellular domain containing an immunoreceptor tyrosine-based inhibition motif 20. Accumulating evidences have shown that inhibitory FcγRIIb is important for the maintenance of peripheral tolerance, Lumacaftor ic50 and FcγRIIb deficiency is associated with the pathogenesis of experimental autoimmune models and of systemic lupus erythematosus (SLE) 21, 22. SLE is characterized by high levels of autoantibodies in circulation. Tissue deposition of IC plays a major role in the pathogenesis of inflammatory injuries in SLE. Therefore, enhancement

of FcγRIIb expression and function may be useful to the prevention and treatment of inflammatory autoimmune diseases such as SLE. Disorders of DC subsets and functions are associated with the pathogenesis of SLE. High level of type I IFN from overactivated plasmocytoid DCs (pDCs) are also involved in the pathogenesis of SLE 23. SLE patients have significantly decreased expression of BDCA2, a negative regulator of TLR9-dependent activation and, accordingly, have markedly elevated IFN-α levels 24. Furthermore, the decrease in myeloid DCs with a tolerizing phenotype was reported in SLE patients 25. Given these lines of evidence, it is plausible that intervention of DC function may be another approach for the treatment of SLE.

Then, the cells were pelleted down by centrifugation at 300 g. The supernatants

were collected and stored at −80°C for the measurement of IFN-γ by enzyme-linked immunosorbent assay (ELISA) kits (BD Biosciences), according to the manufacturer’s protocol. All data are represented as the mean ± standard deviation (s.d.). Univariate and multivariate linear regression was Protein Tyrosine Kinase inhibitor applied to calculate the correlation coefficient and significance among different parameters using STATA software (StataCorp, College Station, TX, USA). Statistical significance was assessed by Mann–Whitney U-test and a P-value less than 0·05 was considered statistically significant. The demographic and clinical data of the AS patients were recorded and are summarized in Table 1. The expression profile of 270 miRNAs in T cells from five AS patients and five healthy controls is shown in Fig. 1a. Each scatter-spot represents the average of normalized miRNA levels of T cells from five AS patients and normal controls. We noted that the expression of eight microRNAs, including miR-150, miR-16, miR-342-5p, miR-221, Ensartinib mouse let-7i, miR-99b, let-7b and miR-513-5p, were significantly higher and five microRNAs including miR-218, miR-409-3p, miR-30e, miR-199a-5p and miR-215 were significantly lower in AS T cells than in normal

T cells (fold change >4·5 and P < 0·05; Fig. 1b). Then, we chose only the five most differentially expressed miRNAs (defined as fold change >6 and P < 0·05), including miR-150, miR-16, miR-342-5p, miR-221 and let-7i for further validation. In the second step, T cells from another 22 AS patients and 18 healthy controls were compared. We confirmed that the expression levels of miR-16, miR-221 and let-7i (fold change: 2·34, 2·38 and 3·17, Fludarabine respectively; all the P values < 0·05) were significantly higher in AS T cells than in normal T cells (Fig. 1c). We then intended to correlate

different clinical parameters with the expression levels of miR-16, miR-221 and let-7i in AS T cells by univariate and multivariate linear regression analysis. We found that the expression of miR-221 (P = 0·022) and let-7i (P = 0·031) were associated positively with BASRI of lumber spine. The expression of miR-16 (P = 0·086) was associated positively with BASRI of lumbar spine (Fig. 2). After adjusting for age and gender, the expression of miR-221 (fold change = 1·58, P = 0·033) and let-7i (fold change = 1·75, P = 0·029), but not miR-16 (fold change = 1·67, P = 0·059), were still correlated positively with BASRI of lumbar spine, which reflects inflammatory activity in the lumbar spine (Table 2). However, expression of miR-16, miR-221 and let-7i did not correlate with serum C-reactive protein levels or sacroiliitis by radiography in AS patients (Table 2). Several studies have demonstrated that miR-16, miR-221 and let-7i regulate the protein expression of Bcl-2, c-kit and TLR-4, respectively [29-31].