AFP, alpha-fetoprotein; ALB, albumin; BMP4, Bone morphogenetic protein 4; EGFP, enhanced green fluorescent protein; ES cells, embryonic stem cells; Fapb1, fatty acid binding protein 1; FGF2, fibroblast growth factor 2; Fox, Forkhead box; GATA4, GATA binding protein 4; hiPS, human induced pluripotent stem cells; HNF, hepatocyte nuclear factor; huES cells, human embryonic stem cells; iPS cells, induced pluripotent stem cells; mRNA, messenger RNA; Rbp4; retinol binding protein 4; Sox17, Sex determining region Y box 17. Selleck BMN 673 Human

H9 (WA09) ES cells and iPS cells were cultured using standard conditions5 that are described in supporting information online. In most cases, assays relied on well-established procedures, and details are provided as supplemental material online. Antibodies used are provided in Supporting Table S1. Each array analysis was performed on three samples that were generated through independent differentiation experiments. Specific experimental details are provided as supporting material online.

All original gene array files are available through the Gene Expression Omibus (GEO) database (http://www.ncbi.nlm.nih.gov/geo/) accession number GSE14897. We first determined whether iPS cells were competent to follow a hepatic developmental program that produced all liver cell lineages by examining embryos derived solely from mouse iPS cells by tetraploid complementation. Mouse iPS cells were generated from C57BL/6J-Tg(pPGKneobpA)3Ems/J fibroblasts as described in Supporting Fig. S1. Embryos were then XL184 order produced from these iPS cells by tetraploid complementation using transgenic mice (Tg[CAG-EGFP]B5Nagy/J) that ubiquitously express enhanced green fluorescent protein (EGFP)

Exoribonuclease as donors of tetraploid embryos. Fig. 1A shows that control CAG-EGFP embryos ubiquitously express EGFP, whereas EGFP was not detected in wild-type CD1 embryos. When embryos were generated from mouse iPS cells, from which EGFP is absent, all embryos (n = 5), including their livers (Fig. 1B), were devoid of EGFP expression except in extra embryonic tissues that were derived from the donor tetraploid embryos.11 Gross examination of E14.5 iPS cell–derived embryos and their livers (n = 3) revealed that they appeared to be identical to controls (Fig. 1C). We therefore determined whether these livers contained the expected repertoire of hepatic cells by identifying the expression of proteins that are characteristic of specific cell types. Fig. 1D shows that, like control CD1 fetal livers, iPS cell–derived livers contained hepatocytes (hepatocyte nuclear factor [HNF]4a positive), endothelial cells (GATA binding protein 4 [GATA4] positive), sinusoidal cells (lymphatic vessel endothelial hyaluronan receptor 1 positive), and Kupffer cells/macrophage (F4/80 positive).

27-29 The Epworth Sleepiness Scale (ESS)

is an 8-item measure of daytime sleepiness that quantifies the likelihood of dozing during various activities. Summed scores 10-15 are indicative of moderate sleepiness and 16-24 of severe sleepiness. The ESS is one of the most widely used paper-pencil measures of daytime sleepiness in adults,[9] has established reliability,[31] and has been validated against polysomnographic recordings.[30] The Selleck MK-1775 Sleep Hygiene Index (SHI) is a 13-item measure assessing how frequently the respondent engages in behaviors comprising the International Classification of Sleep Disorders-Revised criteria[33] for ISH. Higher scores are indicative of more frequent maladaptive sleep behaviors (ie, poorer sleep hygiene). Although relatively new, test-retest reliability and internal consistency of the SHI appear superior to those of previously published sleep hygiene instruments.[32, 34] The Patient Health Questionnaire-9 (PHQ-9) is a 9-item measure of depression commonly used in medical settings. Scores of 10 or higher are indicative of significant depressive symptomatology. Validity has been established by comparing

the PHQ-9 to self-report measures of general health and symptom-related disability,[36] as well as to structured interview diagnoses of major depression.[37] The Generalized Anxiety Disorder-7 (GAD-7) PD-1/PD-L1 inhibition is a commonly used self-report measure of GAD symptomatology. Scores of 10 or higher are indicative of significant anxiety symptomatology

and demonstrate good sensitivity (89%) and specificity (82%) for identifying GAD.[38] Most recently, the GAD-7 has also been shown to be effective at detecting other anxiety disorders such as panic disorder, social phobia, and post-traumatic stress disorder.[39] As such, the GAD-7 was used as a general measure of anxiety symptomatology. The institutional review board at the eltoprazine University of Mississippi approved this study. Participants were undergraduate students recruited using an online research program. They self-selected for participation, provided written informed consent, and completed the aforementioned measures in small groups in exchange for modest course credit. Those who screened positive for migraine on the ID Migraine screening measure were administered the SDIH-R in a face-to-face interview with trained graduate students to confirm headache diagnoses. Those who met ICHD-II diagnostic criteria for episodic migraine comprised the migraine group, and those screening negative for migraine comprised the control group. Individuals with CM were excluded. Statistical analyses were conducted using SPSS 20.0 (IBM, Armonk, NY, USA). Histograms, Q-Q plots, and descriptive statistics data (ie, skewness, kurtosis) were used to assess data analytic assumptions for the total scores of interest and found satisfactory.

2, 8, 9 Moreover, it remains unclear whether the degree of steatohepatitis Enzalutamide price depends more upon total adiposity per se (i.e., body mass index; BMI) or the severity of

adipose tissue dysfunction and resistance to insulin action (i.e., liver exposure to elevated plasma free fatty acids; FFA). Adipose tissue is important under normal living conditions, being the primary source of FFA (∼70%) for hepatic triglyceride (TG) synthesis.10 Excess release of FFA plays a key role in the development of hepatic “lipotoxicity” in NAFLD.7, 11-13 Failure of insulin to inhibit TG lipolysis in insulin-resistant states leads to the oversupply of FFA to the liver, excess hepatic TG synthesis, and intracellular accumulation of toxic lipid products that impair insulin signaling and activate inflammatory pathways (i.e., nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor/nuclear factor kappa light-chain enhancer of activated B cells and Jun N-terminal kinase pathways, Toll-like receptor 4, and others). Adaption to this metabolic stress involves hepatic IR, dyslipidemia and

steatohepatitis with mitochondrial dysfunction, endoplasmic reticulum stress, release of reactive oxygen species, and hepatocellular damage.14 Whether the degree of hepatic IR and steatohepatitis is proportional to the magnitude of adipose tissue IR has not been carefully examined. Only one study has reported that http://www.selleckchem.com/products/bmn-673.html the severity of adipose tissue IR is closely correlated with histological damage in patients with nonalcoholic steatohepatitis (NASH) as well as its improvement with a thiazolidinedione (TZD) to the reversal of dysfunctional fat.9 To better understand the relationship between the degree of adipose tissue IR, hepatic steatosis, and NASH, we studied in depth the metabolic and

histological profiles of patients with and without NAFLD. If liver disease mirrors adipose tissue dysfunction, future therapies aimed at dysregulated adipose tissue may hold particular promise in NAFLD. A1c, test for glycated hemoglobin; Adipo-IR, Endonuclease Adipo-IRi, adipose tissue insulin resistance index; ALT, alanine aminotransferase; ANOVA, analysis of variance; AST, aspartate aminotransferase; BMI, body mass index; DXA, dual-energy X-ray absorptiometry; EGP, endogenous glucose production; FFA, free fatty acids; FPI, free plasma insulin; HDL-C, high-density lipoprotein cholesterol; HIRi, hepatic insulin resistance index; HSCs, hepatic stellate cells; IR, insulin resistance; LDL-C, low-density lipoprotein cholesterol; MetS, metabolic syndrome; MHO, metabolically healthy obese; MRI, magnetic resonance imaging; MRS, magnetic resonance imaging and spectroscopy; NAFLD, nonalcoholic fatty liver disease; NAS, NAFLD activity score; NASH, nonalcoholic steatohepatitis; OGTT, oral glucose tolerance test; Rd, insulin-stimulated glucose disposal; T2DM, type 2 diabetes mellitus; TG, triglyceride; TZD, thiazolidinedione. We recruited a total of 229 subjects.

Conclusion: most patients with superior alimentary canal foreign bodes have a history of abnormal deglutition, several with extreme personality

amd it is difficult to detect foreign body in stomach because there are too much food. Usually doctors need to use X-ray to make a definite diagnosis. Electronic gastroscope has important implications for the diagnosis and treatment of superior alimentary canal foreign bodies. Key Word(s): 1. foreign bodies; 2. gastroscope; 3. diagnosis; 4. treatment; Presenting Author: BIANYING LIU Additional Authors: YUFENG LEI, XIAOHUI LI, XUGANG LI Corresponding Author: BIANYING LIU Affiliations: selleck screening library shanxi coal hospital; shanxi coal hospital; Shanxi coal center hospital Objective: Study the imaging features of the normal small intestine under the intestinal endo-luminal ultrasound and its application in diagnosing disease of small intestine. Methods: The existing endoscopic ultrasonography (EUS) cannot detect the small intestine directly for the limited length of its probe. But it can do this on the patients whose digestive tracts have

been shortened after operations on esophageal, stomach, duodenum, large intestine or laparotomy. Thus the patients should be screened. 50 patients were chosen out of the patients who stayed in Shanxi Coal Center Hospital Digestive Endoscopy Center, and who have been checked with capsule intestine, gastroscope, colonoscopy check details and double-balloon enteroscopy, as well as the patients who stayed in General Surgery and Digestive Surgery and who had intestinal checking during the operation. All the 50 patients have intestinal endo-luminal ultrasound, observe the imaging features of the normal small intestine and those with diseases, and take down the thickness of every small intestine wall layer and the characteristics. If any disease is found, Tolmetin the patient should have US and SCT, so as to decide the value of intestinal endo-luminal ultrasound in getting the imaging features of

the normal small intestine and its application in diagnosing disease of small intestine. Results: Of the 50 patients, 47 had ISUS, of whom 10 have diseases. The normal small intestine wall has six layers while the jejunum and ileal has totally different imaging features and their separate characteristics. The jejunum wall and ileal wall which have tapetum is high-level echo – high-level ech – low-level echo – high-level echo – low-level echo – high-level echo from inside to outside. Those without tapetum is high-level echo – low-level echo – high-level echo – low-level echo – high-level echo from inside to outside. The layer thickness of jejunum is measured to be about 1.5–2.0 mm, ileal 1.8–2.2 mm, tapetum in jejunum 0.4 mm, tapetum in ileal 0.2 mm.

MRSA colonization was defined by a positive MRSA culture without clinical signs or symptoms of infection. MRSA infection was defined

as isolation of MRSA C59 wnt from a normally sterile site with clinical signs or symptoms indicating infection. For both cases and controls, we extracted the following data: demographics (age, gender and race), medical comorbidities (diabetes, chronic obstructive pulmonary disease, liver disease, renal disease, malignancy, dermatological disorders and neuropathy), social history (past or present alcohol use, past or present tobacco use, past or present IDU, sexual orientation, and past or current incarceration or homelessness), and psychiatric history (depression, dementia and psychosis). For patients

H 89 supplier who were MRSA colonized or infected, we documented CD4 cell counts and HIV viral loads at the time of colonization or infection, as well as antiretroviral therapy (ART) exposure, antibiotic exposure, and hospitalizations up to 5 years prior to their colonization or infection. For MRSA-negative patients, we documented the following data within the previous 12 months, and within the previous 5 years from their most recent visit: ART exposure, antibiotic exposure, and hospitalizations, as well as the most recent CD4 cell count and viral load. Similarly, we conducted a second case–control study among HIV-infected patients with MRSA to identify risk factors for colonization or infection with the USA-300 CA-MRSA strain. We compared HIV-infected patients with USA-300 CA-MRSA colonization or infection with HIV-infected patients colonized or infected with non-USA-300 strains. Pulsed-field gel electrophoresis (PFGE) was performed on available MRSA isolates to identify USA-300 strains. The antibiotic

susceptibility pattern was recorded for each isolate from MRSA-infected patients to allow for comparison of susceptibilities Rebamipide between USA-300 strains and non-USA-300 strains. Proportions were compared using χ2 analysis. Logistic regression was used to identify variables associated with the outcome of interest (MRSA colonization or infection, or USA-300 CA-MRSA colonization or infection). Clinically relevant variables with significant associations from the univariate analysis were included in multivariate analysis to identify factors independently associated with the outcome of interest (EpiInfo v3.4.3, 2007; CDC, Atlanta, GA, USA). A P-value of <0.05 was considered statistically significant. Seventy-two (8%) of 900 HIV-infected patients were found to be colonized or infected with MRSA over the study period. Sixty-five MRSA infections occurred among 60 patients. Fifty-four MRSA SSTIs occurred: seven bacteraemias, two pneumonias, and two bone or joint infections. Twelve patients were MRSA-colonized but did not have MRSA infection, and 15 patients had MRSA colonization with subsequent MRSA infection.

01]. Finally, we observed that more hepatotoxic events occurred during the first year of NNRTI therapy compared with the entire period after 1 year (6.6 vs. 2.8 events, respectively, per 100 person-years of treatment; P = 0.04). Long-term NNRTI use was not associated with a higher risk of clinically significant liver toxicity in patients who had been treated with NNRTI for at least 3 years. Following the introduction of highly active antiretroviral therapy Small molecule library (HAART), the life expectancy of HIV-infected patients has increased dramatically. In view of the facts that

HAART is a life-long therapy and a successful regimen is intended to be used for many years, the long-term side effects of these antiretroviral drugs are receiving increasing attention. The nonnucleoside reverse transcriptase inhibitors (NNRTIs) efavirenz (EFV) and nevirapine (NVP) are frequently used as components of current antiretroviral regimens. However, NNRTIs are known for their potential to cause hepatotoxicity, which can lead to morbidity and therapy switches. Different studies have reported a cumulative

incidence of severe hepatotoxicity www.selleckchem.com/products/AT9283.html varying from 1.4 to 15.6% in patients treated with NVP [1-5] and from 1.1 to 10% in patients treated with EFV [1-4]. However, the follow-up time in these studies was relatively short, up to 3 years. Data focusing on hepatotoxicity in long-term NNRTI use are scarce [6]. The aim MTMR9 of this retrospective cohort analysis was to evaluate whether the incidence of hepatotoxicity increases with increasing duration of an NNRTI regimen. All HIV-infected patients under follow-up at our clinic until 1 November 2009, who had been receiving an NNRTI-containing HAART regimen for ≥ 3 years, were identified. Patients were included in the analysis if they had continuously used the same NNRTI for a minimum of three years and if at least one serum alanine transaminase (ALT) value per year was available throughout the treatment period. The control group consisted of patients who had exclusively received a protease inhibitor

(PI)-based regimen for at least 3 years and for whom ALT data were available. Demographic, pharmacological and laboratory data at the start of therapy were retrieved from the clinical database and patient records. Patients were considered to have a hepatitis B virus (HBV) infection when HBV DNA and/or the HBV surface antigen (HBsAg) was found at baseline. Hepatitis C virus (HCV) infection was defined as the detection of HCV RNA by polymerase chain reaction. Patients for whom baseline ALT was unknown and those with acute viral hepatitis during NNRTI treatment were excluded from the analysis. Hepatotoxicity was graded according to the modified toxicity scale of the AIDS Clinical Trials Group [1]. Serum ALT values were used rather than serum aspartate aminotransferase (AST) or cholestatic liver enzymes, as ALT is considered to be a more specific marker for liver damage [7].

The WHO guidelines also recommend that premature modification from first-line to second-line treatment should be avoided, with the assumption that the provision of second-line drugs is in the public sector and the availability is usually limited. This may mean that clinicians are not willing to modify the regimen immediately in the presence of treatment failure if virological failure cannot be confirmed. The higher rate of modification after virological failure in TAHOD

than after immunological and clinical failure lends support to this interpretation. However, there remain a large R428 proportion of patients (nearly 40%) who continue the same failing regimen 1 year after identification of virological failure, which

is probably a result of the limited treatment options available. We found that advanced disease stage (CDC category C), a lower CD4 cell count and a higher HIV viral load were associated with a higher rate of treatment modification after failure. This probably indicates that the clinicians in TAHOD clinics were prioritizing treatment options to those failed patients with more advanced immune deficiency as a result of limited resources. In a case note and questionnaire-based audit in the United Kingdom [14], after virological failure (defined as a viral load rebound from undetectable, not reaching an undetectable level, and/or an increase in viral load), change of therapy was found to occur in <4 months in 43% of patients, in 4–6 months in 20% of patients MK-1775 clinical trial and in >6 months in 34% of patients. Of the patients with virological failure who had their treatment modified, 48% switched to three or more new drugs, 32% to two new drugs and 20% to one new drug. In another study from the United Kingdom, Collaborative HIV Cohort (CHIC) [15], only one-third of patients remained on a failing regimen for more than 6 months after virological rebound of >400 copies/mL, Fenbendazole and the

proportions were 20% and 9% at 1 and 2 years after rebound, respectively. The rate of treatment modification after treatment failure in TAHOD patients is clearly slower than that seen in the United Kingdom, where routine HIV viral load tests and second-line treatment options are readily available. Treatment failure was only one of the reported reasons for modification of treatment after identification of failure. These clinical data provide an insight into clinical practice with regard to HIV treatment and care in the Asia and Pacific region. Adverse events were reported to be a major reason for treatment change after initiation, both in TAHOD [13,16] and in other cohorts [14]. This suggests that the TAHOD clinicians are aware of the adverse effects associated with cART and are ready to change treatment if toxicity is present.

, 2002), and the mechanism by which it does so is probably related to its dd-CPase activity (Nelson et al., 2002; Ghosh Ulixertinib molecular weight & Young, 2003; Ghosh et al., 2008). However, E. coli also expresses PBP 6, which exhibits dd-CPase activity and is the most closely related homologue of PBP 5 (Goffin & Ghuysen, 1998; Ghosh et al., 2008). However, despite these resemblances, PBP 6 cannot substitute for PBP 5 in maintaining or restoring normal cell shape to PBP mutants (Nelson & Young, 2001; Nelson et al., 2002; Ghosh & Young, 2003). At least some of the relevant differences in the in vivo functions of these

two PBPs lie in a short stretch of residues in and near the active site (Ghosh & Young, 2003), but it is not known how selleckchem these sequence differences affect the enzymatic activities of these enzymes. Here, we investigated the kinetic properties of PBPs 5 and 6 and two mosaic proteins and found that the enzymes differ

in their substrate preferences and in the rates at which they remove the terminal d-alanine from these substrates. The results suggest that these differences correlate with the in vivo phenotypes of shape maintenance. PBP 5 is clearly a better dd-CPase than PBP 6. For example, depending on the substrate, the dd-CPase activity of PBP 5 was previously shown to be three to five times greater than that of PBP 6 (Amanuma & Strominger, 1980). In our assays, the dd-CPase activity of sPBP 5 was five times greater than that of sPBP 6 when tested against the substrate AcLAA. An even greater difference was observed when the enzymes were tested against the peptidoglycan mimetic substrate AGLAA, on which PBP 5 was active, but to which PBP 6 may not bind covalently or else it may bind, but may not cleave.

The failure of PBP 6 to act on this latter substrate is consistent with the observations of van der Linden et al. (1992). However, no dd-CPase activity was reported on AcLAA and UDP-muramyl pentapeptide Cell Penetrating Peptide substrates for either the membrane-bound or the soluble form of PBP 6 (van der Linden et al., 1992). We speculate that sPBP 6 exhibited a low level of dd-CPase activity toward the artificial substrate, AcLAA, possibly because the active site cleft of sPBP 6 might accommodate smaller substrates such as penicillin and AcLAA while being unable to bind a bulkier substrate such as AGLAA. The phenomenon of complete inertness of sPBP 6 toward the pentapeptide substrate is interesting in that it simultaneously raises a doubt as to whether it functions as dd-CPase in vivo at all. Previously, we found that the differences between PBPs 5 and 6 in complementing shape defects in vivo could be narrowed down to a short stretch of 20 contiguous residues within the active site (the MMD), where the two PBPs differ from one another by only seven amino acids (Ghosh & Young, 2003). Shape complementation was associated with the MMD from PBP 5 and not with that from PBP 6 (Ghosh & Young, 2003).

This resulted in three pure isolates, two of which grew in TSA minimal medium supplemented with a vitamin solution and one that occurred at a low frequency (<5%) and that grew only in soy broth. The latter isolate had a slightly smaller colony phenotype, while the two TSA-degrading organisms appeared indistinguishable. LY294002 Analysis of the fatty acid composition of the two TSA-degrading organisms (Table 1) did not result in an identification. On hindsight, it became clear that E. adhaerens and Achromobacter xylosoxidans lacked reference entries in the corresponding MIDI database

(version 5.0). The sequence of the complete 16S-rRNA gene of the isolated TSA-degrading organisms shared 99.0% and 99.6% identity with those of the type strains of the betaproteobacterium A. xylosoxidans DSM 10346 (Y14908) and the alphaproteobacterium E. adhaerens LMG 9954 (AM181735), respectively. The 16S-rRNA of the third strain had a 99% sequence identity with the type strain of the gammaproteobacterium P. nitroreducens DSM 14339 (AM088474). This organism was found to accelerate the growth of E. adhaerens on TSA alone as well as in combination with A. xylosoxidans (Table 2). The three newly recognized organisms (based on their 16S-rRNA sequences) click here have been deposited with the German Culture

Collection (DSMZ, Braunschweig, Germany) as A. xylosoxidans TA12-A (DSM 22913) and E. adhaerens TA12-B (DSM 23677). The TSA nondegrader, P. nitroreducens TA12-C, was also deposited (DSM 23662). While ‘strain TA12’ utilized TSA relatively rapidly (growth rate μ=0.09 h−1) without any additives, the growth of the pure cultures of A. xylosoxidans TA12-A and E. adhaerens TA12-B was slower and required the addition of vitamins in order to grow (Table 3). Thymidylate synthase The addition of biotin was subsequently found to be sufficient to restore a slow growth (μ=0.01–0.015 h−1) of pure cultures

of A. xylosoxidans TA12-A and E. adhaerens TA12-B, hence identifying it to be the most essential vitamin. Defined mixed cultures of E. adhaerens TA12-B with A. xylosoxidans TA12-A and E. adhaerens TA12-B with P. nitroreducens TA12-C were able to grow on TSA without the addition of vitamins, but growth remained slow. This shows a partial vitamin auxotrophy of the two TSA degraders. Growth rates in the absence of vitamin supplement could be increased up to threefold (μ=0.033 h−1) by cultivating all three pure strains as a mixture (Table 2). The results show that A. xylosoxidans TA12-A and E. adhaerens TA12-B can complement each other with regard to auxotrophy for vitamins and identified biotin as the lacking essential vitamin. However, a notable increase in the growth rate requires the presence of all three strains, indicating that P. nitroreducens TA12-C complements a supply of limiting vitamins. The corresponding mixed cultures were started with equal amounts of all three strains. Doubling the amount of P. nitroreducens TA12-C at the time of inoculation resulted in a slightly reduced growth rate on TSA (0.

Child questionnaires assessed coping styles, social support, and quality of life outcomes. Parents were also asked to complete questionnaires,

which assessed previous stressors/strains AZD6738 in vivo on the family, social support, healthcare satisfaction, and family impacts. Data related to the child’s dental injury were collected from clinical notes. Structural equation modelling and regression analyses were employed to analyse data. One hundred and eight children and 113 parents participated at baseline. Children’s gender, coping style, social support, and family functioning significantly predicted children’s oral health-related quality of life. Parents’ satisfaction with their children’s dental care significantly predicted parental quality of life outcomes. Children’s close friend support and healthcare satisfaction remained significant predictors of positive outcomes at follow-up. The findings revealed important psychosocial factors that influence child and family adaptation to childhood dental trauma. “
“International Journal of Paediatric Dentistry 2011; 21: 103–111 Background.  Early childhood caries (ECC) is the presence of caries in primary teeth

in children 71 months of age or younger. Despite a decreasing prevalence of caries in China, ECC and related risk factors selleck products in China have not been well studied. Aims.  This study aimed to investigate the status of ECC in children living in Xiamen city in China and to analyse the associated social and behaviour determinants. Design.  A stratified random sample consisted of 1523 children with normal birth records. Clinical examination was performed to record caries at the surface level. Parents filled in questionnaires regarding eating habits, family status, childcare provider, and oral intervention. Results.  Prevalence of ECC in studied child population was 56.8–78.31%, with an increasing tendency with age. The following factors were

found to be significantly associated with ECC: age, candy, carbonated drink, bedtime eating, late start of brushing, low education of parents, private childcare, increased number of siblings, rural residence, and lack of oral health Tacrolimus (FK506) knowledge. Using a stepwise forward logistic regression analysis, a prediction model was established. Conclusion.  Early childhood caries in children living in Xiamen city was strongly associated with eating habits, family- and childcare-related factors and tooth-brushing. The ECC-high-risk group is children in rural private childcare facilities. “
“Recent systematic reviews on clinical trials comparing the efficacy of chlorhexidine and fluoride varnish found that the evidence was inconclusive and further well-conducted randomized controlled clinical trials were advocated. To compare the effect of fluoride varnish (F) and Chlorhexidine–thymol varnish (CHX/T) with intensive application regimen on mutans streptococci (MS) levels in human dental plaque.