br Conclusion br Conflict of interest

Conclusion

Conflict of interest

Acknowledgments

Introduction
Certain situations require the dentist to remove an anterior tooth. These conditions may include dental trauma, advanced periodontal disease, extensive root resorption, and endodontic failure. Whenever an anterior tooth is lost, the clinician should provide an immediate replacement to avoid aesthetic, masticatory, and phonetic difficulties and to prevent the drift of adjacent teeth. Conventional solutions to this problem have included the fabrication of a provisional restoration using the adjacent teeth as abutments, removable temporary acrylic prostheses, and resin-bonded bridges (Daly, 1983; Ashley and Holden, 1998; Safirstein et al., 2001). Various treatment modalities are available for the replacement of lost anterior teeth, such as orthodontic closure of the edentulous space with fixed appliances, ap4 of an osseointegrated dental implant, and the classical approach of a conventional fixed partial denture and removable prosthesis (Foitzik et al., 2007; Sangur et al., 2010). Each of these approaches has its own specific advantages and disadvantages in terms of usage, aesthetics, and compatibility.
A fixed, acid-etch bridge offers several advantages over removable appliances, including enhanced aesthetics, ease of use, and avoidance of having to become accustomed to a removable prosthesis (Fahl, 1998; Smidt, 2002; Chafaie and Portier, 2004). This approach would also permit the patient’s natural crown to be used as a pontic for an immediate bridge (Belli and Ozer, 2000), with little or no need for complicated laboratory procedures. The use of the extracted natural crown as a pontic provides the advantage of having the right size, shape, texture, and colour. Moreover, the patient is comforted by the presence of his or her natural tooth. The use of a modified resin-bonded bridge with a natural-tooth pontic provides additional advantages of aesthetic maintenance, tooth conservation, cost effectiveness, and preservation of the lost tooth’s gingival architecture.

Case report
A 24-year-old female patient reported to the Department of Conservative Dentistry and Endodontics with a complaint of a mobile maxillary right central incisor. The medical history of the patient was not significant. Dental history revealed an episode of trauma in the maxillary anterior region 5years ago. On clinical examination, the maxillary right central incisor showed grade III mobility, and the adjacent (left) central incisor was tender to percussion (Fig. 1a). The adjacent teeth were checked for vitality, and the maxillary left central incisor showed no response. For the right central incisor, radiographic examination revealed extensive root resorption and periradicular bone loss (Fig. 1b). X-rays also displayed widening of the periapical periodontal ligament of the left central incisor.

Discussion
The present era of dentistry relies extensively on aesthetic principles because of increasing patient demands. A restorative dentist should try to meet these demands, while simultaneously considering the patient’s socioeconomic status. Immediate replacement of lost anterior teeth prevents psychological and social trauma to the patient. A resin composite may be used to splint the pontic to sound neighbouring teeth as a provisional restoration until the final prosthesis is fabricated. One major advantage of retaining the patient’s natural crown is brown algae the patient can better tolerate the effect of tooth loss (Ashley and Holden, 1998).

Ethical clearance

br Introduction Porcine reproductive and respiratory syndrome

Introduction
Porcine reproductive and respiratory syndrome virus (PRRSV) infection is one of the most important swine pathogens causing significant economic impact on swine industry worldwide. Infection with PRRSV causes reproductive failure in breeding herds, respiratory disorders and predisposes to secondary infections, contributing to porcine respiratory disease complex (PRDC) in fattening pigs (Lunney et al., 2016). Several reports suggested that PRRSV-induced negative immunomodulatory effects resulted in poor anti-viral immune responses, and immunosuppression in infected pigs (Cecere et al., 2012; Kimman et al., 2009; Lopez and Osorio, 2004; Mateu and Diaz, 2008; Thanawongnuwech et al., 2000; Van Reeth and Nauwynck, 2000). Thus, controlling PRRSV infection is essential for enhancing pig growth performance and economic profit. Currently, commercially available PRRSV vaccines, both modified live PRRS vaccines (MLV) and killed vaccines (KV), have been licensed (Charerntantanakul, 2012; Kimman et al., 2009). However, these vaccines do not provide complete protection against heterologous infections. In addition, MLV also induce negative immunomodulatory effects similar to the natural infection (LeRoith et al., 2011; Suradhat et al., 2016; Thanawongnuwech and Suradhat, 2010).
Recently, a new variant type 2 PRRSV, known as highly pathogenic PRRSV (HP-PRRSV), emerged in China, causing severe clinical outcomes and high mortality in infected pigs (Tian et al., 2007). Since the initial outbreak, HP-PRRSV rapidly spread to other countries and became the ap4 virus circulating in the region, including Thailand (Jantafong et al., 2015; Nilubol et al., 2012). Previous studies indicated that HP-PRRSV derived MLV provided full protection against the HP-PRRSV infection (Leng et al., 2012; Yu et al., 2015). However, the vaccines were not licensed in other countries. The current commercially available MLV only provided partial protection against HP-PRRSV challenges (Do et al., 2015; Lager et al., 2014). Recently, a novel DNA vaccine (pORF7t) has been developed. The vaccine was designed to modulate PRRSV-specific immune responses by reducing PRRSV-induced immunomodulatory activities (Suradhat et al., 2015). Priming with the DNA vaccine could reduce MLV-induced negative immunomodulatory effects, both IL-10 and Treg, and enhance PRRSV-specific cell-mediated immunity in the immunized pigs (Suradhat et al., 2016). Thus, the heterologous DNA-MLV, prime-boost immunization may be useful for controlling PRRSV infection in heavily infected areas or areas with PRRSV circulation. We hypothesized that the DNA-MLV prime-boost immunization would enhance MLV-induced, PRRSV-specific immunity against the HP-PRRSV infection, leading to better disease protection.

Materials and methods

Result

Discussion
In this study, we hypothesized that the heterologous DNA-MLV prime-boost immunization would enhance the efficacy of the MLV against the HP-PRRSV strain. Our results demonstrated that the DNA vaccine could improve the quality of PRRSV-specific immunity in the pigs receiving DNA-MLV prime-boost immunization. However, priming with the DNA vaccine did not provide significant advantage over the MLV in clinical protection. As the DNA vaccine aimed to reduce PRRSV-induced negative immunomodulatory effects, the efficacy of the DNA-MLV immunization still mainly relied on the protective mechanisms induced by MLV. The findings that the current commercially available MLV provided only partial protection against the HP-PRRSV challenges are consistent with the previous reports (Do et al., 2015; Lager et al., 2014), suggesting the need for better vaccines against the HP-PRRSV.
PRRSV-specific IFN-γ secreting cells are believed to be the main protective mechanism against the conventional PRRSV infection (Meier et al., 2003; Park et al., 2014; Zuckermann et al., 2007). In this study, increased numbers of CD3+IFN-γ+ cells in the DNA-MLV group were observed both following MLV immunization and HP-PRRSV challenge, indicating that the broad immunomodulatory effects of the DNA vaccine on cellular immunity. Interestingly, priming with a DNA vaccine also enhanced the anti-viral cytokine gene, IFNA, expression following HP-PRRSV infection (Fig. 4a). The N protein of PRRSV has been reported as an IFN-antagonist (Huang et al., 2015, 2014; Lunney et al., 2016). It was possible that priming with the DNA vaccine resulted in enhanced immunity to N protein, which resulted in reduced IFN-antagonist activity following HP-PRRSV infection. Nonetheless, our results indicated that the well-primed cellular immunity was not sufficient to completely protect against HP-PRRSV infection.

When we introduced gender and BMI as determinant factors

When we introduced gender and BMI as determinant factors in liver stiffness value data analysis, we observed a significant difference related to gender (p < 0.01), but not to BMI (p > 0.05) (Table 4). The differences between liver stiffness under fasting conditions and liver stiffness 40 min after the meal and also between mean liver stiffness under fasting conditions and mean peak values were higher in males than in females (Tables 3 and 6). Most probably, the differences found in the entire sample were due predominantly to the increased liver stiffness observed in male subjects.
The literature describes differences between male and female baseline liver stiffness values (Huang et al. 2014; Szinnai et al. 2001), but, to the best of our knowledge, there are no published studies describing different-amplitude increases in liver stiffness in males and females after food intake. Although Szinnai et al. (2001) had already reported that after a meal there is a greater increase in portal flow in males than in females, the difference was not found to be statistically significant.
Increasing stiffness >15% of the baseline values after a meal was reported to be significant by Popescu et al. (2013), but in a similar study, Goertz et al. (2012) reported only 8.74% higher values of liver stiffness, compared with fasting conditions.
In our study, the difference between mean stiffness values under fasting conditions and values after the meal (40 min) was 2.2% for the entire sample, 6.1% for males and 2.3% for females. From a statistical point of view, the difference between mean liver stiffness values under fasting (0 min) and those 40 min after the meal was significant (p < 0.05). However, the clinical relevance of a 2.2% or 6.1% change after the meal is debatable. Because the values did not increase in all subjects 40 min after the meal, we calculated the mean peak liver stiffness value, which more accurately expresses the relevance of increased liver stiffness after a meal. Mean peak liver stiffness increased by 12% in males, 7% in females and 8% in the entire sample. For healthy persons, this ap4 percentage might seem negligible. However, at times, a smaller change might reflect the difference between significant and insignificant liver fibrosis, as the cutoff values for different liver fibrosis stages predicted by ARFI and SWE are very tight.
Using transient elastography, Mederacke et al. (2009) reported an increase in liver stiffness ≤20% and a mean peak value ≤27.5% in 12 apparently healthy subjects after food intake. Although Arena et al. (2013), in a larger study, reported higher liver stiffness values after a meal (mean values at 30 min ≤24% higher and a mean peak value ≤33% higher than baseline values), bottlenecks must be taken into account that both the control group and the study group included patients known to have with chronic liver disease, stage F0–F1, who may exhibit a different magnitude of change in liver stiffness after a meal, compared with healthy subjects.
It is worth noting that the standardized meal used in this differed, in terms of percentage composition, from that used in previous studies for healthy subjects and patients with chronic hepatitis or cirrhosis (Arena et al. 2013; Dauzat et al. 1994; Popescu et al. 2013; Zardi et al. 2008). However, 748 kcal (52.71 g carbohydrates, 44.33 g fat, 35.52 g protein), should be sufficient to induce changes in liver blood supply, given that a 300-kcal meal caused significant hemodynamic changes in splanchnic vasculature (Zardi et al. 2008) and liver stiffness estimated by TE (Barone et al. 2015). Moreover, it was documented that, in terms of meal content, there were no differences in post-meal portal blood flow between the high-carbohydrate/low-fat and low-carbohydrate/high-fat meals (Fabbrini et al. 2013).
A limitation of this study is the small number of healthy volunteers enrolled in the study. A simulated bootstrap with a sample of 1000 similar cases produced the same results, with a p value even smaller than 0.01, which indicates that our findings were correct for a given population, despite the small number of subjects enrolled in the study.

When we introduced gender and BMI as determinant factors

When we introduced gender and BMI as determinant factors in liver stiffness value data analysis, we observed a significant difference related to gender (p < 0.01), but not to BMI (p > 0.05) (Table 4). The differences between liver stiffness under fasting conditions and liver stiffness 40 min after the meal and also between mean liver stiffness under fasting conditions and mean peak values were higher in males than in females (Tables 3 and 6). Most probably, the differences found in the entire sample were due predominantly to the increased liver stiffness observed in male subjects.
The literature describes differences between male and female baseline liver stiffness values (Huang et al. 2014; Szinnai et al. 2001), but, to the best of our knowledge, there are no published studies describing different-amplitude increases in liver stiffness in males and females after food intake. Although Szinnai et al. (2001) had already reported that after a meal there is a greater increase in portal flow in males than in females, the difference was not found to be statistically significant.
Increasing stiffness >15% of the baseline values after a meal was reported to be significant by Popescu et al. (2013), but in a similar study, Goertz et al. (2012) reported only 8.74% higher values of liver stiffness, compared with fasting conditions.
In our study, the difference between mean stiffness values under fasting conditions and values after the meal (40 min) was 2.2% for the entire sample, 6.1% for males and 2.3% for females. From a statistical point of view, the difference between mean liver stiffness values under fasting (0 min) and those 40 min after the meal was significant (p < 0.05). However, the clinical relevance of a 2.2% or 6.1% change after the meal is debatable. Because the values did not increase in all subjects 40 min after the meal, we calculated the mean peak liver stiffness value, which more accurately expresses the relevance of increased liver stiffness after a meal. Mean peak liver stiffness increased by 12% in males, 7% in females and 8% in the entire sample. For healthy persons, this ap4 percentage might seem negligible. However, at times, a smaller change might reflect the difference between significant and insignificant liver fibrosis, as the cutoff values for different liver fibrosis stages predicted by ARFI and SWE are very tight.
Using transient elastography, Mederacke et al. (2009) reported an increase in liver stiffness ≤20% and a mean peak value ≤27.5% in 12 apparently healthy subjects after food intake. Although Arena et al. (2013), in a larger study, reported higher liver stiffness values after a meal (mean values at 30 min ≤24% higher and a mean peak value ≤33% higher than baseline values), bottlenecks must be taken into account that both the control group and the study group included patients known to have with chronic liver disease, stage F0–F1, who may exhibit a different magnitude of change in liver stiffness after a meal, compared with healthy subjects.
It is worth noting that the standardized meal used in this differed, in terms of percentage composition, from that used in previous studies for healthy subjects and patients with chronic hepatitis or cirrhosis (Arena et al. 2013; Dauzat et al. 1994; Popescu et al. 2013; Zardi et al. 2008). However, 748 kcal (52.71 g carbohydrates, 44.33 g fat, 35.52 g protein), should be sufficient to induce changes in liver blood supply, given that a 300-kcal meal caused significant hemodynamic changes in splanchnic vasculature (Zardi et al. 2008) and liver stiffness estimated by TE (Barone et al. 2015). Moreover, it was documented that, in terms of meal content, there were no differences in post-meal portal blood flow between the high-carbohydrate/low-fat and low-carbohydrate/high-fat meals (Fabbrini et al. 2013).
A limitation of this study is the small number of healthy volunteers enrolled in the study. A simulated bootstrap with a sample of 1000 similar cases produced the same results, with a p value even smaller than 0.01, which indicates that our findings were correct for a given population, despite the small number of subjects enrolled in the study.

Equine influenza Equine influenza EI is a

Equine influenza
Equine influenza (EI) is a respiratory disease of equids that causes morbidity amongst unvaccinated and in some cases vaccinated horses worldwide. The equine influenza A virus, which belongs to the Orthomyxoviridae family, is enveloped and contains a single-stranded, eight-segmented RNA genome. Prophylaxis against EI is of great importance due to the economic burden of the disease. The global equine sporting industry has been detrimentally impacted by outbreaks of the disease since the late 1970s, and cancellation of race meetings still occur today. As well as participation in sport, equids remain a very valuable working animal in developing countries and thus outbreaks of EI in such areas are a concern (Virmani et al., 2010).
Transmission of EI is rapid, particularly amongst stabled horses; with large quantities of virus expelled during coughing episodes, EI is highly infectious. Naive equids typically present with clinical signs such as nasal discharge, coughing and pyrexia. Upon the onset of such signs, horses should be quarantined immediately in an attempt to prevent transmission to other individuals. Vaccinated horses with subclinical infections are problematic when trying to prevent the spread of disease. Therefore, when considering the regional, national or global transport of horses, quarantine before introduction to a new ap4 is essential (Morley et al., 2000). Without effective quarantine, sub-clinically infected horses have the potential to cause devastating outbreaks such as that in Australia in 2007, which affected thousands of horses on a continent previously free from EI (Webster, 2011). Efforts by the Australian government to control the spread of the outbreak cost in excess of $1 billion (Callinan, 2008).

Control of equine influenza

Current serological assays

Transition from traditional assays to ‘Next-Generation’ assays
Established assays such as HI and SRH, used since the early 1930s and 1970s respectively, are still heavily relied upon today. Each has advantages for different applications: HI is quick to perform and is relatively cheap, properties that are useful for diagnosis; SRH measures functional antibodies and is more sensitive than HI, which promotes its use in vaccine efficacy testing. A point to consider is that both use whole virus, and therefore cannot readily distinguish between vaccinated individuals and natural infections (Young and Lunn, 2000). An outstanding issue is that neither HI nor SRH are standardised and both demonstrate high levels of inter-laboratory variability (Wood et al., 2011). For efficacy testing of human influenza vaccines, it has been suggested that, where possible, a centralised laboratory should perform all assays necessary to complete a development programme (European Medicines Agency, 2014a). Although the VN assay is more variable than the HI assay, is difficult to reproduce, and has high cost implications, its ability to quantify neutralizing antibodies is very useful (Stephenson et al., 2007). The measurement of virus neutralizing antibodies is the gold standard for evaluating vaccine efficacy. The problem is that VN assays are difficult to perform for EIV due to the lack of cytopathic effect. An alternative assay that overcomes the issues related to VN, still with a focus on measuring virus neutralizing antibodies, would provide an optimistic future for improved vaccine evaluation.

Conclusions
Of the serological assays that are currently available, each has its own merits and drawbacks for different applications relevant to the control of equine influenza (summarised in Table 1). The key is choosing the appropriate assay for the application, together aiding the control of EI. ELISA and HI assays are beneficial for diagnostic purposes, whilst SRH and VN are more suited for vaccine efficacy testing. For surveillance, HI is most favourable. An optimistic future for vaccine efficacy testing may lie with the use of novel assays, such as the PVNA, which encompasses several important features; quantification of neutralizing antibodies in a high-throughput fashion, whilst avoiding the need for live virus or large quantities of serum.

br Statistical Analysis br Descriptive statistics

Statistical Analysis

Descriptive statistics are expressed as mean ± standard deviation for continuous variables and as frequency and percentages for nominal variables. A paired t test was used to compare the excursion and peak motion speed between the right dia###http://www.cy7-nhs-ester.com/image/1-s2.0-S1876285915003435-gr1.jpg####phragm and the left diaphragm. The associations between the excursions of the diaphragms and participants\’ characteristics were evaluated by means of the Pearson\’s correlation coefficient and a simple linear regression or Student\’s t test depending on the type of variable (ie, continuous or nominal variable). Continuous variables were height, weight, BMI, tidal volume, vital capacity (VC, %VC), forced expiratory volume (FEV1, FEV1%, and %FEV1), and nominal variables were gender and smoking history. The robustness of the results of the univariate analyses was assessed with multiple linear regression models. The significance level for all tests was 5% (two sided). All data were analyzed using a commercially available software program (JMP; version 12, SAS, Cary, NC, USA).

Results

Participants\’ Characteristics

Table 1 shows the clinical characteristics of all the participants (n = 172).

Excursions and Peak Motion Speeds of the Bilateral Diaphragm

Univariate Analysis of Associations Between the Diaphragmatic Excursions and Participants\’ Demographics

Figure 3. Estimated regression line of the excursion of the ap4 on BMI or tidal volume. (a) Association between BMI and excursion of the right diaphragm. (b) Association between BMI and excursion of the left diaphragm. (c) Association between tidal volume and excursion of the right diaphragm. (d) Association between tidal volume and excursion of the left diaphragm. Lines show estimated regression (a–d). All scatterplots show correlations (P < 0.05). BMI, body mass index.Figure optionsDownload full-size imageDownload high-quality image (226 K)Download as PowerPoint slide

Multivariate Analysis of Associations Between the Excursions and Participants\’ Demographics

Multiple linear regression analysis using all variables as factors (Model 1) demonstrated diversity weight, BMI, and tidal volume were independently associated with the bilateral excursion of the diaphragms (all P < 0.05) after adjusting for other clinical variables, including age, gender, smoking history, height, VC, %VC, FEV1, FEV1%, and %FEV1. There were no significant associations between the excursion of the diaphragms and variables including age, gender, smoking history, height, VC, %VC, FEV1, FEV1%, and %FEV1 (Table 4). Additionally, a multiple linear regression model using age, gender, BMI, tidal volume, VC, FEV1, and smoking history as factors (Model 2) was also fit as a sensitivity analysis, taking into account the correlation among variables (eg, BMI, height, and weight; VC and %VC; FEV1, FEV1%, and %FEV1). Model 2 (Supplementary Data S1) gave results consistent with Model 1 (Table 4): higher BMI and higher tidal volume were independently associated with the increased bilateral excursion of the diaphragms (all P < 0.05). The adjusted R2 in Model 1 was numerically higher than that in Model 2 (right, 0.19 vs. 0.16, respectively; left, 0.16 vs. 0.13, respectively).