**5. Antimicrobial Activity of AgNPs**

To evaluate the antibacterial activity of the AgNPs against gram-negative bacteria (*E. coli* ATCC 25922, *K. pneumoniae* ATCC 700603, *P. aeruginosa* ATCC 27853) and gram-positive ones (*S. aureus* ATCC 25923 and MRSA ATCC 43300), MIC and MBC values were obtained. Afterwards, we studied how the TS influenced the bacterial growth rate (at the initial moment and after 3 and 6 h of incubation).

For therapeutic consideration, only antimicrobial activity obtained below 1 mM concentration was considered. The MIC and MBC of nanoparticles against pathogenic bacterial strains are as mentioned in Table 2. Thus, it is found that almost all tested solutions exhibit inhibitory activity on the growth of tested bacteria (except TS1, where the MIC was determined only for MRSA, at the maximum analyzed concentration). It can be seen that AgNPs obtained at pH = 9 (TS2, TS4) favor the inhibitory activity for the tested bacterial strains. They have a lower MIC compared to those obtained at pH = 4 (TS1, TS3). TS2 (for *E. coli*, *K. pneumoniae*, and *P. aeruginosa*) and TS4 (for *S. aureus*, *E. coli*, *K. pneumoniae*, and *P. aeruginosa*) have lower MIC and MBC compared to those obtained for the control beech bark extract. For the most part, the MBC was registered for the TS where the MIC was determined, the results being presented in Table 2. The lowest MBC was recorded for TS4 (MRSA, *E. coli*, and *P. aeruginosa*) and for TS2 (*E. coli*).

As can be seen from Figure 7, TS4 had a bactericidal effect on *E. coli* and inhibited the growth of *S. aureus* and *P. aeruginosa* after 6 h of incubation.

**Figure 7.** Graphical and visual representation of the growth rate for *S. aureus* (**A**,**D**), *E. coli* (**B**,**E**), *P. aeruginosa* (**C**,**F**) in the presence of TS4 (beech extract + AgC2H3O2 pH = 9) and in the absence of TS4 (Control) at: initial time—H0, 3 h—H1, and 6 h—H2.

ATCC—American Type Culture Collection; MIC—minimal inhibitory concentration; MBC—minimum bactericidal concentration; MRSA—methicillin-resistant *S. aureus*, BBE—beech bark extract; AgNO3—silver nitrate; AgC2H3O2—silver acetate; TS1—beech bark extract, pH = 4, AgNO3; TS2—beech bark extract, pH = 9, AgNO3; TS3—beech bark extract, pH = 4, AgC2H3O2; TS4—beech bark extract, pH = 9, AgC2H3O2.

The antibacterial mechanism might beexplained by the interaction between silver nanoparticles and bacterial DNA. AgNPs can cause DNA damage, and ultimately bacterial cell death. This effect has been demonstrated on *S. aureus* and *E. coli* strains [32].

However, the antibacterial mechanism is different, depending on the type of bacteria to be inhibited. For example, silver nanoparticles have an inhibitory effect on *Helicobacter pylori*, stating two theories of action: small amounts of AgNPs enter the bacterium and inhibit the respiratory chain, while another theory considers that AgNPs inhibit urease from *H. pylori* [33]. Evidence of bacterial growth inhibition have also been demonstrated for strains of *S. aureus*, *Streptococcus pneumoniae*, *Proteus mirabilis*, and *E. coli* [34].


**1. Introduction**

92 Dyslipidemia - From Prevention to Treatment

Watala C, Boncer M, Golanski J, Koziolkiewcz W, Trojanowski Z, Walkowiak B: Platelet

*Eur J Haematol* Vol.61, No.5, (November 1998), pp. 319–326, ISSN 1600-0609 Winocour, P.D., Watala, C. & Kinlough-Rathbone, R.L. (1992). Reduced membrane fluidity

*Med* Vol.120, No.6, (December 1992), pp. 921-928, ISSN 1532-6543

membrane lipid fluidity and intraplatelet calcium mobilization in type 2 diabetes.

and increased glycation of membrane proteins of platelets from diabetic subjects are not associated with increased platelet adherence to glycated collagen. *J Lab Clin*

> Dyslipidemia is characterized by an aggregation of lipoprotein abnormalities including low high density lipoprotein cholesterol (HDL-C), high serum triglycerides (TG) and increased small low density lipoprotein cholesterol (LDL-C). Lipoproteins, which contain lipids and proteins (apolipoproteins, APO) are responsible, primarily, for transporting water insoluble lipids (cholesterol, TG) in plasma from the intestines and liver, where they are absorbed and synthesized, respectively, to peripheral tissues (muscle, adipose) for utilization, processing and/or storage (Kwan et al., 2007). There are several subtypes of lipoproteins with specific functions including, from smallest to largest: 1) chylomicrons, which transport dietary TG from the intestines to the peripheral tissue and liver; 2) very LDL (VLDL) particles, which transport TG from the liver to peripheral tissues; 3) intermediate density lipoproteins (IDL), which are produced from VLDL particle metabolism and may be taken up by the liver or further hydrolyzed to LDL; and, 4) HDL, which is key in 'reverse cholesterol transport' or shuttling cholesterol from peripheral cells to the liver (Kwan et al., 2007).

> The Metabolic Syndrome (MetSyn) is a clustering of traits including dyslipidemia as well as hypertension (raised systolic and/or diastolic blood pressure), dysglycemia (high fasting glucose) and obesity (high body mass index (BMI) and/or waist circumference). Dyslipidemia is formally defined within the context of MetSyn. Various diagnostic definitions have been proposed for MetSyn by several organizations including the World Health Organization (WHO) (Alberti and Zimmet, 1998), European Group Insulin Resistance (EGIR) (Balkau and Charles, 1999), National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III, (2001), International Diabetes Federation (IDF, (Alberti et al., 2005), American Heart Association/National Heart, Lung, and Blood Institute (AHA/NHLBI) (Grundy et al., 2006) and, with the most recent joint interim statement proposed by the AHA/NHLBI, IDF and other organizations (Alberti et al., 2009). Although the recommendations differ widely on the obesity component, the dyslipidemia component has been fairly consistently defined as having TG ≥ 150 mg/l, HDL-C <40 mg/dL (1.03 mmol/l, in males) or <50 mg/dL (1.29 mmol/l in females) or drug treatment for elevated TG or low HDL-C (NCEP ATP III: (2001), IDF: (Alberti et al., 2005), Joint Statement: (Alberti et al., 2009)). However, the WHO (Alberti and Zimmet, 1998) proposed slightly lower limits for HDL-C (male: < 0.9 mmol/l (35 mg/dl); female: < 1.0 mmol/l (39 mg/dl)) and the EGIR (Balkau and Charles, 1999) recommended dyslipidemia be defined by HDL-C < 1.0 mmol/l (39 mg/dl) or TG > 2.0 mmol/l (177 mg/dl). There is currently no recommended value for

Dyslipidemia: Genetics and Role in the Metabolic Syndrome 95

Heritability estimates suggest there is a strong genetic component to dyslipidemia and MetSyn. Heritability estimates for dyslipidemia range from 0.20 to 0.60 (Edwards et al., 1997; Goode et al., 2007; Herbeth et al., 2010; Kronenberg et al., 2002; Wang and Paigen,

Multiple genetic variants in the form of single nucleotide polymorphisms (SNPs) (i.e., single DNA base changes) have been associated with manifestation of dyslipidemia and MetSyn. In this chapter, we review and summarize associations between common SNPs (i.e., those with a minor allele frequency (MAF) ≥0.05) in the most biologically plausible candidate genes and HDL-C, LDL-C and TG levels as well as MetSyn as a single, unifying trait. Previous estimates suggest all common variants together explain less than 10 percent of HDL-C levels in the general population (Kronenberg et al., 2002); however, more elegant statistical modeling methods that combine SNPs in a more biologically meaningful way may be needed to better understand the collective role of genetic variants in manifestation of dyslipidemia, MetSyn and other complex metabolic traits. As a result, at the end of this chapter, we review studies that have undertaken more complex modeling strategies to understand the aggregate effects of SNPs in manifestation of dyslipidemia and MetSyn and

As mentioned above, HDL-C is important for "reverse cholesterol transport" or the shuttling of cholesterol from peripheral cells to the liver. Many of the genetic variants associated with HDL-C levels have been summarized nicely in a recent comprehensive review by Boes et al. (Boes et al., 2009). In Table 1, we include common SNPs tabulated in Boes et al. (2009) review of large studies (ethnic group sample sizes ≥500) as well as common

**Size**

(GP)

(GP) 735 (HBP)

(GP )

(GP)

(GP)

(GP)

**Results (Effect Size, p-value)**

+1.9/+2.7 mg/dl (1/2copies); p=0.03 +1.9 /+5.0 mg/dl (1/2 copies); p=0.03

+0.7/+1.9 mg/dl (1/2 copies); p<0.02

**Reference**

2004b)

(Shioji et al. 2004b)

(Hodoglugil et al. 2005)

(Porchay et al. 2006)

(Kathiresan et al. 2008)

2004b)

p=0.0455 (Shioji et al.

p=0.006 (Shioji et al.

2005) and from 0.24 to 0.63 for MetSyn (Lin et al., 2005; Sung et al., 2009).

provide our insights for future directions in this field.

**2. Genetic variants in lipid metabolism and HDL-C levels**

SNPs in large studies that have been identified since their review.

**Gene Polym. rs Number MAF Ethn. Sample**

ABCA1 C (-297)T rs2246298 0.25 (T) A 1625

ABCA1 G (-273)C rs1800976 0.40 (C) A 1626

ABCA1 G (-273)C rs1800976 0.38 (T) Tu 2332

ABCA1 G378C rs1800978 0.13 (C) W 5040

ABCA1 rs3890182 0.13 (A) W 5287

ABCA1 rs2275542 A <1880

LDL-C levels in the context of MetSyn yet LDL-C remains the primary target of therapy for the management of high blood cholesterol per the most recent guidelines from the NCEP ATPIII, which recommended drug therapy for LDL-C values ranging from ≥100 mg/dl to ≥190 mg/dl depending on the presence/absence of other coronary heart disease (CHD) risk factors (Grundy et al., 2004). When LDL becomes lipid depleted, small dense LDL (sdLDL) particles are formed, which have a lower affinity for the LDL receptor (LDLR), more susceptibility to oxidation and a higher affinity for macrophages; and, thus, sdLDL particles contribute to the atherosclerotic process (Austin et al., 1990; Littlewood and Bennett, 2003) and likely MetSyn (Kruit et al., 2010).

Dyslipidemia and MetSyn are common in developed nations and the prevalence of both are rising worldwide, which may be attributed, in part, to the rising rates of overweight and obesity (Alberti et al., 2009; Halpern et al., 2010). According to the National Health and Nutrition Examination Survey (NHANES) III (1988-1994) in the United States (U.S.), which used the NCEP ATP III criteria, the age-adjusted prevalence of dyslipidemia defined by high TG or low HDL-C, was approximately 30.0% and 37.1%, respectively; and, the prevalence of MetSyn was approximately 23.7% (Ford et al., 2002). The prevalence of dyslipidemia and MetSyn generally increase with increasing age (Ford et al., 2002). However, in a more recent study that used the Health Survey for England (HSE) (2003-2006) survey data and NHANES (1999-2006) data with exclusion of persons over 80 years old, the prevalence of low HDL-C (defined in both males and females as <40 mg/dL) was 10.0% in England and 19.2% in the U.S. (Martinson et al., 2010). Thus, the prevalence can vary markedly depending on how these traits are defined (Cook et al., 2008). Interestingly, trends in the U.S. and England indicate during the past two decades an increase in the proportion of individuals diagnosed with high cholesterol (≥240 mg/dL) but who achieved therapeutic control (Roth et al., 2010). For example, in the U.S. in 2006, 54.0% of men (95% CI: 47.6–60.4) and 49.7% of women (95% CI: 44.3–55.0) with high total serum cholesterol were on cholesterol-lowering medication, as opposed to 10.8% of men (95% CI: 8.0–13.6) and 8.6% (95% CI: 6.7–10.6) of women in 1993 (Roth et al., 2010). In England, in 2006, 35.5% of men (95% CI: 32.8–38.3) and 25.7% of women (95% CI: 23.4–28.1) were on cholesterol-lowering medication as opposed to 0.6% of men (95% CI: 0.3–1.3) and 0.4% of women (95% CI: 0.1–0.7%) in 1993 (Roth et al., 2010). Thus, prevalence rates will also vary by whether or not relevant drug treatments have been considered and, perhaps, the list of relevant drugs should include cholesterol lowering therapies (e.g., statins) as well as other drugs (e.g., tamoxifen, glucocorticoids) known to alter TG and cholesterol levels (Garg and Simha, 2007).

Both dyslipidemia and MetSyn increase the risk of Type II diabetes mellitus (T2DM) (Adiels et al., 2006; Kruit et al., 2010) and cardiovascular disease (CVD) morbidity (Alberti et al., 2009; Linsel-Nitschke and Tall, 2005) and CVD mortality (Lewington et al., 2007). Patients with MetSyn have a five-fold increase in the risk of developing T2DM and are at twice the risk of developing CVD over the next 5 to 10 years compared to individuals without the syndrome (Alberti et al., 2009). In the presence of both MetSyn and T2DM, the prevalence of CVD is markedly increased with an odds ratio (OR) of 3.04 [95% confidence interval (CI) of OR: 1.98-4.11] in comparison to those with none of these conditions (Athyros et al., 2004). The importance of MetSyn is exemplified by its ICD-9 code (277.7), which was initially established as a diagnosis of "Dysmetabolic Syndrome X" (Einhorn et al., 2003; Kahn et al., 2005). In summary, both dyslipidemia and MetSyn are substantial public health problems, which require a better understanding of their respective etiologies to develop more effective lifestyle and therapeutic interventions.

LDL-C levels in the context of MetSyn yet LDL-C remains the primary target of therapy for the management of high blood cholesterol per the most recent guidelines from the NCEP ATPIII, which recommended drug therapy for LDL-C values ranging from ≥100 mg/dl to ≥190 mg/dl depending on the presence/absence of other coronary heart disease (CHD) risk factors (Grundy et al., 2004). When LDL becomes lipid depleted, small dense LDL (sdLDL) particles are formed, which have a lower affinity for the LDL receptor (LDLR), more susceptibility to oxidation and a higher affinity for macrophages; and, thus, sdLDL particles contribute to the atherosclerotic process (Austin et al., 1990; Littlewood and Bennett, 2003)

Dyslipidemia and MetSyn are common in developed nations and the prevalence of both are rising worldwide, which may be attributed, in part, to the rising rates of overweight and obesity (Alberti et al., 2009; Halpern et al., 2010). According to the National Health and Nutrition Examination Survey (NHANES) III (1988-1994) in the United States (U.S.), which used the NCEP ATP III criteria, the age-adjusted prevalence of dyslipidemia defined by high TG or low HDL-C, was approximately 30.0% and 37.1%, respectively; and, the prevalence of MetSyn was approximately 23.7% (Ford et al., 2002). The prevalence of dyslipidemia and MetSyn generally increase with increasing age (Ford et al., 2002). However, in a more recent study that used the Health Survey for England (HSE) (2003-2006) survey data and NHANES (1999-2006) data with exclusion of persons over 80 years old, the prevalence of low HDL-C (defined in both males and females as <40 mg/dL) was 10.0% in England and 19.2% in the U.S. (Martinson et al., 2010). Thus, the prevalence can vary markedly depending on how these traits are defined (Cook et al., 2008). Interestingly, trends in the U.S. and England indicate during the past two decades an increase in the proportion of individuals diagnosed with high cholesterol (≥240 mg/dL) but who achieved therapeutic control (Roth et al., 2010). For example, in the U.S. in 2006, 54.0% of men (95% CI: 47.6–60.4) and 49.7% of women (95% CI: 44.3–55.0) with high total serum cholesterol were on cholesterol-lowering medication, as opposed to 10.8% of men (95% CI: 8.0–13.6) and 8.6% (95% CI: 6.7–10.6) of women in 1993 (Roth et al., 2010). In England, in 2006, 35.5% of men (95% CI: 32.8–38.3) and 25.7% of women (95% CI: 23.4–28.1) were on cholesterol-lowering medication as opposed to 0.6% of men (95% CI: 0.3–1.3) and 0.4% of women (95% CI: 0.1–0.7%) in 1993 (Roth et al., 2010). Thus, prevalence rates will also vary by whether or not relevant drug treatments have been considered and, perhaps, the list of relevant drugs should include cholesterol lowering therapies (e.g., statins) as well as other drugs (e.g., tamoxifen, glucocorticoids) known to alter

Both dyslipidemia and MetSyn increase the risk of Type II diabetes mellitus (T2DM) (Adiels et al., 2006; Kruit et al., 2010) and cardiovascular disease (CVD) morbidity (Alberti et al., 2009; Linsel-Nitschke and Tall, 2005) and CVD mortality (Lewington et al., 2007). Patients with MetSyn have a five-fold increase in the risk of developing T2DM and are at twice the risk of developing CVD over the next 5 to 10 years compared to individuals without the syndrome (Alberti et al., 2009). In the presence of both MetSyn and T2DM, the prevalence of CVD is markedly increased with an odds ratio (OR) of 3.04 [95% confidence interval (CI) of OR: 1.98-4.11] in comparison to those with none of these conditions (Athyros et al., 2004). The importance of MetSyn is exemplified by its ICD-9 code (277.7), which was initially established as a diagnosis of "Dysmetabolic Syndrome X" (Einhorn et al., 2003; Kahn et al., 2005). In summary, both dyslipidemia and MetSyn are substantial public health problems, which require a better understanding of their respective etiologies to develop more effective

and likely MetSyn (Kruit et al., 2010).

TG and cholesterol levels (Garg and Simha, 2007).

lifestyle and therapeutic interventions.

Heritability estimates suggest there is a strong genetic component to dyslipidemia and MetSyn. Heritability estimates for dyslipidemia range from 0.20 to 0.60 (Edwards et al., 1997; Goode et al., 2007; Herbeth et al., 2010; Kronenberg et al., 2002; Wang and Paigen, 2005) and from 0.24 to 0.63 for MetSyn (Lin et al., 2005; Sung et al., 2009).

Multiple genetic variants in the form of single nucleotide polymorphisms (SNPs) (i.e., single DNA base changes) have been associated with manifestation of dyslipidemia and MetSyn. In this chapter, we review and summarize associations between common SNPs (i.e., those with a minor allele frequency (MAF) ≥0.05) in the most biologically plausible candidate genes and HDL-C, LDL-C and TG levels as well as MetSyn as a single, unifying trait. Previous estimates suggest all common variants together explain less than 10 percent of HDL-C levels in the general population (Kronenberg et al., 2002); however, more elegant statistical modeling methods that combine SNPs in a more biologically meaningful way may be needed to better understand the collective role of genetic variants in manifestation of dyslipidemia, MetSyn and other complex metabolic traits. As a result, at the end of this chapter, we review studies that have undertaken more complex modeling strategies to understand the aggregate effects of SNPs in manifestation of dyslipidemia and MetSyn and provide our insights for future directions in this field.


*Statistical Analysis*

Patient characteristics were expressed as median (and Interquartile range, IQR) and percentage when appropriate. The normality of data distribution was assessed with the Shapiro–Wilk test. To compare the characteristics between groups (i.e., in hospital and out-of-hospital setting), we performed the Mann–Whitney U-test and the Chi-squared test (or Fisher Test when appropriate) for continuous and categorical variables, respectively. A *p*-value < 0.05 was considered statistically significant. To evaluate the variables associated with our primary outcome (i.e., retention in care) we performed logistic regression analysis, including in the multivariable model variables which presented a *p*-value ≤ 0.1 at univariate

analysis. All of the analyses were performed by using IBM SPSS Statistics for (Windows, Version 24.0, Armonk, NY, USA).


**Abstract**

Folate is a naturally occurring essential nutrient which is vital for DNA replication and a necessary substrate in various enzymatic reactions which are involved in synthesis of amino acids and vitamin metabolism. The synthetic and oxidized form of folate is folic acid, it is mainly incorporated into fortified foods and dietary supplements for preventive measures against folate deficiency. Folate deficiency has been linked with several abnormalities in both mother (anemia, peripheral neuropathy) and fetus (congenital abnormalities). Folic acid supplementation taken around the time of conception has been known to alleviate the risk of neural tube defects in the off springs. Optimal intake and absorption of folates is required for the maintenance of the human body's normal functioning and keeping the genomic integrity intact.

**Keywords:** folate, folic acid, neural tube defects, folate deficiency, congenital abnormalities


*Article* **Fracture Modelling of a Cracked Pressurized Cylindrical Structure by Using Extended Iso-Geometric Analysis (X-IGA)**

**Soufiane Montassir 1, Hassane Moustabchir 2, Ahmed Elkhalfi 1, Maria Luminita Scutaru 3,\* and Sorin Vlase 3,4**

**Abstract:** In this study, a NURBS basis function-based extended iso-geometric analysis (X-IGA) has been implemented to simulate a two-dimensional crack in a pipe under uniform pressure using MATLAB code. Heaviside jump and asymptotic crack-tip enrichment functions are used to model the crack's behaviour. The accuracy of this investigation was ensured with the stress intensity factors (SIFs) and the J-integral. The X-IGA—based SIFs of a 2-D pipe are compared using MATLAB code with the conventional finite element method available in ABAQUS FEA, and the extended finite element method is compared with a user-defined element. Therefore, the results demonstrate the possibility of using this technique as an alternative to other existing approaches to modeling cracked pipelines.

**Keywords:** extended iso-geometric analysis; extended finite element method; crack; pipeline; ABAQUS


**Biocompatibility and Biological Performance of the Improved Polyurethane Membranes for Medical Applications**

Maria Butnaru, Ovidiu Bredetean, Doina Macocinschi, Cristina Daniela Dimitriu, Laura Knieling and Valeria Harabagiu

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/34653


*<IP_ADDRESS> Device description*

The parts of AuraGain are as follows (**Figures 12** and **13**):

polyvinylchloride, it is more flexible and less traumatic. Its fixed, anatomically curved shape is elliptical in cross section and aids easier insertion. It has two separate drain channels. At the machine end, they begin as the male and female suction ports. The channels then enter a chamber behind the cuff bowl. At the patient end, the chamber ends at the tip of the cuff. The device is flexible and stays in place if the patient's head is mobilised. A built-in bite block reduces the potential for damage to, or obstruction of the airway tube in the event of biting. Additionally, the LMA-Protector™ is available with a pilot balloon or the integrated Cuff Pilot™. The Cuff Pilot™ enables constant visualisation of intracuff pressure inside the mask cuff that provides easier adjustment and is colour coded for infla-

It is commercially available in size 3, 4 and 5. The manufacturer recommends using a size 4 device for normal adults. After insertion, the device is fixed in place and inflated to the recommended pressure. There should be a minimum of a 1 cm gap between the fixation tab and the patient's upper lip. The cuff should be inflated with sufficient air to prevent a leak with positive pressure ventilation, but it must not exceed either a pressure of 60 cm H2O or the specific device cuff volume maxima. If no manometer is available, inflate with just enough air to achieve a seal sufficient to permit ventilation without leaks. It provides high first attempt and overall insertion success rate. It helps rapidly achieve effective ventilation with reliable airway seal. Additionally, it acts as a conduit for FOB guided intubation

tion pressure [74].

**Figure 11.**

*LMA protector cuff pilot.*

[75, 76].

**264**

*<IP_ADDRESS> Size selection, practical aspect, adjuncts*

*Special Considerations in Human Airway Management*

The mask is designed to conform to the contours of the hypopharynx with its lumen facing the laryngeal opening. When correctly inserted, the distal tip of the cuff rests against the upper oesophageal sphincter. It is anatomically shaped with an integrated bite block.


**1. Introduction**

NiTi alloy, with a nearly equal atomic ratio, has the most excellent performance, which is the most common application among many known shape memory alloys. It has many advantages, such as superelasticity, the shape memory effect, fatigue resistance, a low elastic modulus, and biocompatibility [1–4]. As we know, the most widely used commercial methods for producing NiTi alloy parts are vacuum arc melting and vacuum induction melting, followed by hot working or cold working. It is likely that casting would lead to segregation defects [5]. Meanwhile, vacuum induction melting has the drawback of crucible contamination [6].However, when NiTi components undergo cold working, they encounter springback and make the overall dimension difficult to be shaped, hindering the application of nickel-titanium alloys.Additive manufacturing (AM), which has emerged in the past decade, is a new technology that can realize the integrated molding of complex components, and a lot of research results have been obtained [7–10]. Among them, selective laser melting (SLM) technology [11–14] and laser-directed energy deposition (LDED) technology [15–17] are typical metal additive manufacturing technologies, which could achievethe rapid formation of metal parts.

In the recent years, laser additive manufacturing has become an ideal preparation method for complex NiTi alloy components, and related technologies have developed rapidly, especially SLM technology [18–21].Dadbakhsh et al. [22] showed that SLM parameters have a great influence on the phase transition temperature and mechanical response of dense porous NiTi alloys. Meier et al. [23] studied the effect of deposition orientation on the compressive properties of SLM Ti-rich Ni50.2Ti49.8 (at.%) and found that crystal orientation

**Citation:** Yang, X.; Wang, S.; Pan, H.; Zhang, C.; Chen, J.; Zhang, X.; Gao, L. Microstructure Transformation in Laser Additive Manufactured NiTi Alloy with Quasi-In-Situ Compression. *Micromachines* **2022**, *13*, 1642. https://doi.org/10.3390/ mi13101642

Academic Editors: Jie Yin, Yang Liu and Ping Zhao

Received: 18 August 2022 Accepted: 19 September 2022 Published: 30 September 2022

**Publisher's Note:** MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

**Copyright:** © 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

had no significant effect on the compressive properties of these samples. Yang et al. [24] investigated the additivemanufacturing process of gradient NiTi alloys and obtained the gradient martensite phase by adjusting the process parameters. Bormann et al. [25] focused on the microstructure and texture of NiTi alloys fabricated by SLM and considered the effects of different processing parameters and the scanning rate. Haberland et al. [26] researched the superelasticity and cyclic response of NiTi alloys fabricated by SLM. Lu et al. [27] learned the simultaneous improvement of mechanical properties and shape memory properties by proper precipitation of the Ti2Niphase and its mechanism of action. It can be found that a lot of research has been carried out on NiTi alloys with SLM technology, from process parameters and structure to properties.

Compared toSLM technology, LDED technology has lower cost, faster formation, and the ability to form large components and has received extensive attention and research in the industry. Bimber et al. [28] studied the spatial anisotropy of NiTi alloys prepared by LDED and explored the differences of microstructures with different deposition heights. Wan et al. [29] studied the phase transformationbehavior, microstructure evolution, and elastocaloric properties of NiTi alloys prepared by LDED. It is confirmed that NiTi alloys prepared by the LDED process haveexcellent properties and arenot inferior to as-cast NiTi alloys. Research on the compressive properties of NiTi alloys prepared by AM technology has also been reported recently, but the research results are relatively few. Marattukalam [30] prepared NiTi alloys by means of LDED technology; 8% strain was recovered under a pre-compression of 10%, and the recovery rate was further improved after heat treatment. Andani et al. [31] fabricated and designed NiTi shape memory alloys with porous forms by selective laser melting, which exhibited a good shape memory effect, with a recoverable strain of about 5% and functional stability after eight cycles of compression. In addition, the stiffness and residual plastic strain of porous NiTi alloys were found to depend highly on the pore shape and the level of porosity. Moghaddam et al. [32] fabricated Ni-rich NiTi components by using the additive manufacturing process with 250 W laser power, 1250 mm/s scanning speed, 80 µm hatch spacing and without any post-process heat treatments. The results showed superelasticity with 5.62% strain recovery and a 98% recovery ratio.Chen et al. [33] successfully fabricated uniform and graded gyroid cellular structures of NiTi alloys by laser powder bed fusion additive manufacturing. The results showed that all laser powder bed fusion NiTi structures exhibited similar nominal compressive elastic moduli (5–7 GPa) ashuman bones. The resultsof Zhang et al. [34] showed that the energy input balances against the energy output during cyclic loading of porous NiTi alloys after performing several compression cycles as 'training' and the porous NiTi alloys exhibit reliable linear superelasticity and a stable elastic modulus, with strain as high as 4%.

Most of the research on NiTi alloys with AM technology has mainly focused on their functional properties and process parameters. However, there is little systematic in-depth study on the microstructure transformation of the material after compression, especially the microstructure transformation and recovery ability after compression under the LDED process. In this paper, an in-situ compression test was carried out on LDED NiTi samples, and the microstructure transformation and recovery ability of shape memory alloyswere researched in detail.


**7. The control system structures**

In Fig. 12 and Fig. 14 the voltage and current multi-scalar control system structure is shown. These structures are based on four PI controllers and contain: the modulator, the speed observer and decouplings blocks .

**Figure 12.** The voltage multi-scalar control system structure

**Figure 13.** The voltage multi-scalar adaptive backstepping control system structure

456 Induction Motors – Modelling and Control

11 x

r\_K ˆ

from 0.1 to -0.1 p.u., the estimated rotor speed \_ ˆ

x12\*

x22\*

x22

r ˆ r ˆ

**Figure 12.** The voltage multi-scalar control system structure

**7. The control system structures**

observer and decouplings blocks .

x21\*

x11\*

x11

x21

**Multi-scalar variables**

x12

r id ˆ

**Figure 11.** The Speed observer test: the estimated rotor speed x11 in backstepping observer is changed

In Fig. 12 and Fig. 14 the voltage and current multi-scalar control system structure is shown. These structures are based on four PI controllers and contain: the modulator, the speed

m1

m2

**Speed observer backstepping**

*r K* by Krzeminski's speed observer [Krzeminski Z.,

i

**Current Source Inverter**

**~**

ed ud

id

v1

v2

Ld

ua ub ia

ib **IM**

xy abc

xy abc

us us

is is

1999] and the multi-scalar variable: x12, x21, x22 are shown . The load torque m0 is set to -0.1 p.u.

**Figure 14.** The current multi-scalar control system structure.

**Figure 16.** Motor start-up (chapter 4.1- 4.2)

**Figure 17.** Motor reverse (chapter 4.1- 4.2)

**Figure 18.** Motor start-up (chapter 5)

In Fig. 14 the ed\_ref value is determined in ed reference block. The ed reference block can be PI current controller or other controller.

In Fig. 13 the voltage multi-scalar adaptive backstepping control system structure is shown.

In Fig. 15 generalized multi-scalar control system structure is presented. This control structure is divided into two parts: the control system of IM fed by VSI and the control system of IM fed by CSI.