*2.2. Method*

The collected data included both a time-series dimension and a cross-sectional dimension, and were thereby transformed into panel-data form. Each firm is observed repeatedly in the vertical dimension with a length of (the number of individuals), I × (the number of periods), T, and the dependent and independent variables K are presented in the horizontal dimension. The overall size of the matrix equals I × T × K observations.

What is typical to panel data and distinguishes them from simple time-series regression is the presence of unobserved heterogeneity that is due to the cross-sectional dimension. Unobserved heterogeneity is the time persistent differences between the individual studied units also called "individual effects" that cannot be estimated with the simple pooled (OLS) regression [38]. When heterogeneity is present in the data, which is typically the case, a model able to take it into account should be used. For this reason, fixed effects and random effects -models that can handle longitudinal and heterogeneous data are used in this research. The fixed effects (FE) or "within"-estimator used has the following form:

$$\mathcal{Y}\_{it} = \beta\_0 + \sum\_{k=1}^{K} \beta\_k \times \mathcal{X}\_{it}^k + e\_{it} + a\_i \tag{4}$$

The within-estimator models the time-invariant heterogeneity in the unknown parameter *ai* . The data are transformed by time demeaning all the variables, a.k.a. subtracting the variables' individual means over time from all the variables. The result is a formulation in terms of deviations from the individual means. The *ai* term, as well as the constant *β*0 (see, Equation (4)) that is simply the individual mean, and all the time-invariant independent variables cancel out in this calculation. This eliminates the problem of individual effects, hence it is said to be "fixed" [38].

The coefficients of the FE model can be interpreted as the effect that the unit of change from the individual mean of the respective independent variable has on the same individual's dependent variable from its mean. The main downside of the FE estimators is that one cannot include time-invariant independent variables since they would be canceled out in the model estimation. This simplifies the estimation process but fails to account for the time-invariant variables although they could potentially be significant in determining the values of the dependent variable. To deal with the possible handicaps of the FE in the context of the studied data, a random-effects (RE) model is also applied.

In the random-effects model (RE), the individual differences are allowed and the variation between the individuals is assumed to be random and uncorrelated with the independent variables. The random individual effects are modeled as the error term *ui* . The RE-effects model used is defined as follows:

$$Y\_{it} = \beta\_0 + \sum\_{k=1}^{K} \beta\_k \times X\_{it}^k + e\_{it} + u\_i \tag{5}$$

In Equation (5), the intercept corresponds to the mean of the unobserved heterogeneity and the error term *ui* is the random time-invariant heterogeneity specific to the individual unit. In the random-effects model, the generalized least squares (GLS) estimator is used. The data are "quasi time-demeaned", which means that a part of the within-individual variation is taken out. For a more comprehensive introduction to the Random Effects model, see [39].

The application of fixed-effects and random-effects models was considered to be sufficient for the purposes of this research in terms of the reliability of the results. We point out that the use of more advanced methods, such as the generalized method of moments (GMM), which control for the violations of the random-effects model and the possible endogeneity problems in the data may reveal deeper and better results from the same data. The use of more advanced methods is left as a topic for future research.


**Author details**

Madhavi Latha Routhu1 \* and Gudikandula Krishna2

1 Department of Radiology, MGM Hospital, Warangal, Telangana, India

2 Viral Research and Diagnostic Laboratory, Kakatiya Medical College, Warangal, Telangana, India

\*Address all correspondence to<EMAIL_ADDRESS>
© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


**2. Molecular diagnosis in hematological malignancies**

Hematological malignancies are heterogeneous in both clinical and biological aspects. The association of genomic profile changes associated with hematological malignancies is complex and variable including translocations, karyotypic improvements, transformations and adjustments of post-translational alteration and some genetic changes are needed, to induce the onset of disease. This proof in relationship with the development of molecular techniques has prompted an alteration of the current authoritative opinion concentrating on a solitary quality or single pathway analysis [4].

The advancement in molecular biology techniques has not just permitted the individualized molecular diagnosis of hematological malignancies but have also prompted the disclosure of genetic or targeted therapeutic schemes with cytotoxic, anti-metabolic or immunomodulatory properties [4].

Utilizing karyotype analysis and the new technique of polymerase chain reaction (PCR), chromosomal microarrays (CMA), fluorescence in situ hybridization (FISH) and new generation sequencing technique (NGS), it is conceivable to configuration better hazard stratification classes and decide if there is complete remission or presence of minimal residual disease (MRD).

New molecular and cytogenetic methods have been connected to determination of diagnosis and treatment. As to, the reasonableness of those strategies expands the precision and the speed of results while screening can be even more successfully performed. In regard to treatments, immunomodulatory and target therapies assurance better outcomes with less hematological side effects.

The molecular basis of hematological malignancies has developed aberrant genes expression and/or pathological expression of natural genes [5]. Also other new somatic mutations detected by Next Generation Sequencing NGS have prompted the revelation of already unknown molecular and pathological genes as well as diagnostic and therapeutic value [6].

Genetic changes plays a vital role to diagnose and classify the stage of disease and determine the prognosis of diseases and choice of treatment in most hematological malignancies [7–9]. Molecular diagnostic technology in patients with HMs is useful for diagnosis and prognosis and selecting the proper treatment, and to monitor the degree of response to new therapies [5, 8].

The majority of leukemia, specifically predictable by gene expression profiles [9]. Vulnerability tests are being developed through the explicit treatment of targeted therapies such as imatinib in acute lymphoblastic leukemia BCR-ABL positive (ALL) and farnesyltransferase inhibitors in acute myeloblastic leukemia (AML) [10].

Myelodysplastic syndrome (MDS) and acute leukemia (AML and ALL) are intensely influenced by epigenetics [11]. Targeted epigenetic therapies may be particularly attractive as long-term treatment in post remission period, if they could target certain subclones once standard chemotherapy has produced targeted cytoreduction to induce remission of acute leukemia [12]. Personalized targeted therapy have just upset treatment results in some HMs, especially, chronic myeloid leukemia (CML), non-Hodgkin's lymphoma (NHL), multiple myeloma (MM) and acute promyelocytic leukemia (APL) [12, 13].

### **3. Detection of molecular markers in hematologic malignancies**

**The molecular markers and genetic studies in hematologic malignancies include**: (1) **AML**: FLT3-ITD, CEBPA, RUNX1, NPM1, PML-RARA, *ASXL1*, IDH1, IDH2, DNMT3A, TET2 and BCR-ABL1; (2) **ALL**: IKFZ1, CDKN2A/B, BCR-ABL1, BCR-ABL1-like, NOTCH1, ETV6, and RUNX1; (3) **chronic myeloproliferative** (CMPNs): CAL-R, MPL, JAK2, SRSF2, SETBP1, *TP53*, CSF3R and ASXL1; (4) **CML**: BCR-ABL1; (5) **MDS**: RUNX1, *JAK2*, EZH2, SF3B1, IDH1/2, *N-RAS*, TP53, TET2, *KIT*, SRSF2, and ASXL1; (6) **CLL**: ATM, TP53, BIRC3, del11q, SF3B1 and NOTCH1 mut; (7) **Hodgkin's lymphoma (HL):** BCL6, SOC1, JUNB, MAP3K14, STAT6, MDM2, JAK2, XPO1, NFKBIE, GNA13, MAFB,IKBA, TNFIP3, BCL3, NFKBIA, PD-L1, PD-L2, and REL6; (8) **B-cell lymphomas**: MYC/BCL2, MYC/BCL2/BLC6, SOX11, CCND1/2, *CCND3* and *TCF3*; (9) **T-cell lymphomas**: TP63, IRF4, DUSP22 and ALK; (10) **Hairy cell leukemia (HCL)**: BRAFV600E, *IGHV4-34*, *MAP2K1*; and (11) **MM**: KRAS, CCND1, CCND2, CCND3, TP53, DI53, NRAS, MAF, FAM46C and BRAF [5, 10, 14–17].

#### **4. Personalized target therapy: Monoclonal antibodies**

In the late 1970s, the technology development of monoclonal antibody (MoAb) was possible to produce antibodies targeting specific antigens to the surface of cancer cells. The antibodies target an antigen present at high concentrations on cancer cells

**3**

*Introductory Chapter: Advances in Hematologic Malignancies*

and missing or present at low fixations on typical cells. The MoAbs, is given as monotherapy or target therapy with chemotherapy, have excellent outcome in different types of neoplasm's with improve quality of life and survival rate and time. An assortment of components has been proposed that would allow monoclonal antibodies to kill cancer cells, including apoptosis, inhibition of cell growth, cellular cytotoxicity. The development of molecular and genetic technology play important role in the modernization and modification of the (2016 WHO Edition) for classification of tumors of hematopoietic and lymphoid tissues, is being published by World Health Organization, the aims to provide these data with essential clinical characteristics, morphology and immunophenotyping relevant to targeted and novel therapies

The targeted and novel therapies currently used in the treatment of hematological malignancies are: (1) Acute myeloblastic leukemia subtypes: lintuzumab, midostaurin, gemtuzumab, ulocuplumab, sorafinib, navitoclax, panobinostat, vorinostat, Dr383-IL3 and lestaurtinib; (2) acute myeloblastic leukemia (promyelocytic type): all trans-retinoic acid gemtuzumab ozogamicin and arsenic trioxide; (3) acute lymphoblastic leukemia: tyrosine kinase inhibitors, rituximab, inotuzumab ozogamicin, nelarabine, blinatumomab, and CAR T-cells; (4) myelodysplastic syndrome: azacitidine, decitabine, and lenalidomide; (5) chronic myeloid leukemia: imatinib, nilotinib, dasatinib and ponatinib; (6) chronic myeloproliferative neoplasms: ruxolitinib; (7) chronic lymphatic leukemia (CLL): rituximab, idelalisib, ibrutinib, venetoclax obinutuzumab, and duvelisib; (8) HL: brentuximabvedotin, nivolumab, rituximab and everolimus; (9) B-cell lymphomas: tositumomab, rituximab, ibritumomab tiuxetan and CAR T-cells; (10) T-cell lymphomas: romidepsin, alemtuzumab, epratuzumab, denileukin and nelarabine; (11) hairy cell leukemia: vemurafenib; and (12) multiple myeloma: bortezomib, carfilzomib, lenalidomide,

pomalidomide, daratumumab milatuzumab, and ixazomib [17–26].

therapies have proven to be a great success.

**5.1 Enasidenib for** *IDH***-mutated AML**

**5. Examples of advance treatment in AML**

**5.2 Gemtuzumab ozogamicin for CD33+ AML**

The targeted treatments are directed to the cancer cell and do not harm or affect the healthy cell, which is of course a breakthrough in the treatment of hematological malignancies, but is still in the process of research despite the success of the experiments, which have been conducted and targeted therapies exist for many types of cancers, including: Chronic leukemia and lymphoma is used in making there are opportunities for no need for bone marrow transplantation, and targeted

Mutations in isocitrate dehydrogenase (IDH) occur in 20% of AML cases and are also found in gliomas and cholangiocarcinomas. Enasidenib was approved in August 2017 by FDA for treatment acute myeloblastic leukemia patients (AML) refractory or relapsed to chemotherapy with presence of IDH2 mutation. IDH2 mutations are relatively common in hematological malignancies, which occur in ~12% of AML patients [27]. The follow up of patients for a period of 6.6 months, 23% of patients experienced a complete remission [28]. The dose of enasidenib is

Gemtuzumab ozogamicin (Mylotarg) is an antibody-drug conjugate to treat patients who are more than 60 years old in first relapse AML with CD33+ and not candidates for chemotherapy and also for pediatric patients, more than 2 years old

100 mg once daily and continuously was chosen for the extension stage.

*DOI: http://dx.doi.org/10.5772/intechopen.88777*

against incurable diseases [18].

*Introductory Chapter: Advances in Hematologic Malignancies DOI: http://dx.doi.org/10.5772/intechopen.88777*

*Advances in Hematologic Malignancies*

ence of minimal residual disease (MRD).

well as diagnostic and therapeutic value [6].

acute promyelocytic leukemia (APL) [12, 13].

ance better outcomes with less hematological side effects.

monitor the degree of response to new therapies [5, 8].

and new generation sequencing technique (NGS), it is conceivable to configuration better hazard stratification classes and decide if there is complete remission or pres-

The molecular basis of hematological malignancies has developed aberrant genes expression and/or pathological expression of natural genes [5]. Also other new somatic mutations detected by Next Generation Sequencing NGS have prompted the revelation of already unknown molecular and pathological genes as

Genetic changes plays a vital role to diagnose and classify the stage of disease and determine the prognosis of diseases and choice of treatment in most hematological malignancies [7–9]. Molecular diagnostic technology in patients with HMs is useful for diagnosis and prognosis and selecting the proper treatment, and to

The majority of leukemia, specifically predictable by gene expression profiles [9]. Vulnerability tests are being developed through the explicit treatment of targeted therapies such as imatinib in acute lymphoblastic leukemia BCR-ABL positive (ALL) and farnesyltransferase inhibitors in acute myeloblastic leukemia (AML) [10]. Myelodysplastic syndrome (MDS) and acute leukemia (AML and ALL) are intensely influenced by epigenetics [11]. Targeted epigenetic therapies may be particularly attractive as long-term treatment in post remission period, if they could target certain subclones once standard chemotherapy has produced targeted cytoreduction to induce remission of acute leukemia [12]. Personalized targeted therapy have just upset treatment results in some HMs, especially, chronic myeloid leukemia (CML), non-Hodgkin's lymphoma (NHL), multiple myeloma (MM) and

**3. Detection of molecular markers in hematologic malignancies**

**4. Personalized target therapy: Monoclonal antibodies**

**The molecular markers and genetic studies in hematologic malignancies include**: (1) **AML**: FLT3-ITD, CEBPA, RUNX1, NPM1, PML-RARA, *ASXL1*, IDH1, IDH2, DNMT3A, TET2 and BCR-ABL1; (2) **ALL**: IKFZ1, CDKN2A/B, BCR-ABL1, BCR-ABL1-like, NOTCH1, ETV6, and RUNX1; (3) **chronic myeloproliferative** (CMPNs): CAL-R, MPL, JAK2, SRSF2, SETBP1, *TP53*, CSF3R and ASXL1; (4) **CML**: BCR-ABL1; (5) **MDS**: RUNX1, *JAK2*, EZH2, SF3B1, IDH1/2, *N-RAS*, TP53, TET2, *KIT*, SRSF2, and ASXL1; (6) **CLL**: ATM, TP53, BIRC3, del11q, SF3B1 and NOTCH1 mut; (7) **Hodgkin's lymphoma (HL):** BCL6, SOC1, JUNB, MAP3K14, STAT6, MDM2, JAK2, XPO1, NFKBIE, GNA13, MAFB,IKBA, TNFIP3, BCL3, NFKBIA, PD-L1, PD-L2, and REL6; (8) **B-cell lymphomas**: MYC/BCL2, MYC/BCL2/BLC6, SOX11, CCND1/2, *CCND3* and *TCF3*; (9) **T-cell lymphomas**: TP63, IRF4, DUSP22 and ALK; (10) **Hairy cell leukemia (HCL)**: BRAFV600E, *IGHV4-34*, *MAP2K1*; and (11) **MM**: KRAS, CCND1, CCND2, CCND3, TP53, DI53, NRAS, MAF, FAM46C and BRAF [5, 10, 14–17].

In the late 1970s, the technology development of monoclonal antibody (MoAb) was possible to produce antibodies targeting specific antigens to the surface of cancer cells. The antibodies target an antigen present at high concentrations on cancer cells

New molecular and cytogenetic methods have been connected to determination of diagnosis and treatment. As to, the reasonableness of those strategies expands the precision and the speed of results while screening can be even more successfully performed. In regard to treatments, immunomodulatory and target therapies assur-

**2**

and missing or present at low fixations on typical cells. The MoAbs, is given as monotherapy or target therapy with chemotherapy, have excellent outcome in different types of neoplasm's with improve quality of life and survival rate and time. An assortment of components has been proposed that would allow monoclonal antibodies to kill cancer cells, including apoptosis, inhibition of cell growth, cellular cytotoxicity.

The development of molecular and genetic technology play important role in the modernization and modification of the (2016 WHO Edition) for classification of tumors of hematopoietic and lymphoid tissues, is being published by World Health Organization, the aims to provide these data with essential clinical characteristics, morphology and immunophenotyping relevant to targeted and novel therapies against incurable diseases [18].

The targeted and novel therapies currently used in the treatment of hematological malignancies are: (1) Acute myeloblastic leukemia subtypes: lintuzumab, midostaurin, gemtuzumab, ulocuplumab, sorafinib, navitoclax, panobinostat, vorinostat, Dr383-IL3 and lestaurtinib; (2) acute myeloblastic leukemia (promyelocytic type): all trans-retinoic acid gemtuzumab ozogamicin and arsenic trioxide; (3) acute lymphoblastic leukemia: tyrosine kinase inhibitors, rituximab, inotuzumab ozogamicin, nelarabine, blinatumomab, and CAR T-cells; (4) myelodysplastic syndrome: azacitidine, decitabine, and lenalidomide; (5) chronic myeloid leukemia: imatinib, nilotinib, dasatinib and ponatinib; (6) chronic myeloproliferative neoplasms: ruxolitinib; (7) chronic lymphatic leukemia (CLL): rituximab, idelalisib, ibrutinib, venetoclax obinutuzumab, and duvelisib; (8) HL: brentuximabvedotin, nivolumab, rituximab and everolimus; (9) B-cell lymphomas: tositumomab, rituximab, ibritumomab tiuxetan and CAR T-cells; (10) T-cell lymphomas: romidepsin, alemtuzumab, epratuzumab, denileukin and nelarabine; (11) hairy cell leukemia: vemurafenib; and (12) multiple myeloma: bortezomib, carfilzomib, lenalidomide, pomalidomide, daratumumab milatuzumab, and ixazomib [17–26].

The targeted treatments are directed to the cancer cell and do not harm or affect the healthy cell, which is of course a breakthrough in the treatment of hematological malignancies, but is still in the process of research despite the success of the experiments, which have been conducted and targeted therapies exist for many types of cancers, including: Chronic leukemia and lymphoma is used in making there are opportunities for no need for bone marrow transplantation, and targeted therapies have proven to be a great success.

### **5. Examples of advance treatment in AML**

#### **5.1 Enasidenib for** *IDH***-mutated AML**

Mutations in isocitrate dehydrogenase (IDH) occur in 20% of AML cases and are also found in gliomas and cholangiocarcinomas. Enasidenib was approved in August 2017 by FDA for treatment acute myeloblastic leukemia patients (AML) refractory or relapsed to chemotherapy with presence of IDH2 mutation. IDH2 mutations are relatively common in hematological malignancies, which occur in ~12% of AML patients [27]. The follow up of patients for a period of 6.6 months, 23% of patients experienced a complete remission [28]. The dose of enasidenib is 100 mg once daily and continuously was chosen for the extension stage.

#### **5.2 Gemtuzumab ozogamicin for CD33+ AML**

Gemtuzumab ozogamicin (Mylotarg) is an antibody-drug conjugate to treat patients who are more than 60 years old in first relapse AML with CD33+ and not candidates for chemotherapy and also for pediatric patients, more than 2 years old with relapsed or refractory CD33+ AML. Subsequent studies with positive findings resulted in the resurrection of gemtuzumab ozogamicin and its approval in 2017.


*Review* **E**ff**ect of LDHs and Other Clays on Polymer Composite in Adsorptive Removal of Contaminants: A Review**

**Maleshoane Mohapi 1, Jeremia Shale Sefadi 2,\*, Mokgaotsa Jonas Mochane 1,\*, Sifiso Innocent Magagula 1 and Kgomotso Lebelo 1**

Received: 15 August 2020; Accepted: 15 October 2020; Published: 22 October 2020

**Abstract:** Recently, the development of a unique class of layered silicate nanomaterials has attracted considerable interest for treatment of wastewater. Clean water is an essential commodity for healthier life, agriculture and a safe environment at large. Layered double hydroxides (LDHs) and other clay hybrids are emerging as potential nanostructured adsorbents for water purification. These LDH hybrids are referred to as hydrotalcite-based materials or anionic clays and promising multifunctional two-dimensional (2D) nanomaterials. They are used in many applications including photocatalysis, energy storage, nanocomposites, adsorption, diffusion and water purification. The adsorption and diffusion capacities of various toxic contaminants heavy metal ions and dyes on different unmodified and modified LDH-samples are discussed comparatively with other types of nanoclays acting as adsorbents. This review focuses on the preparation methods, comparison of adsorption and diffusion capacities of LDH-hybrids and other nanoclay materials for the treatment of various contaminants such as heavy metal ions and dyes.

**Keywords:** layered double hydroxides (LDHs); other nanoclays; organically modified LDH; water purification; adsorption; adsorption interaction; diffusion


**5. Conclusions**

This research does not respond to the modern challenges with a "yes" or "no", in the juridical logic of *h. alal¯* or *h. aram¯* , permissible or forbidden. Instead, it fits into a different kind of reasoning: the human conscience makes decisions in difficult and complex situations after long deliberation. The text nourishes the ethical conscience but does not replace it. The believing conscience starts from the text to listen to history and respond to the needs of the time. The hermeneutics of the text is not separate from the interpretation of the signs of the times. Islamic nonviolence theology is a reading oriented towards the higher finalities of the Qur" an. It touches the heart of religious reform, which can only be interreligious and ¯ interdisciplinary.

Inclusive and universal peace, the project of radical nonviolence, is found in many religions as a messianic dream, postponed until the end of history and then to Paradise. It is often seen as a meta-historical and eschatological hope. Today, the prevailing opinion is the theory of a just or defensive war, which many religions consider a challenge to be overcome. We sometimes also see a regression back to a preventive and offensive warfare theory. The theory of permanent warfare is not yet dead, and it is found in the form of great or lesser powers that do not even recognize the minimum moral conditions of war. The debate is still open, but the awareness of nonviolence as a fundamental solution to the tragedies of conflict, killings and displacements has begun to crystallize and present itself as an alternative and a new horizon. Can humanity overcome war and violence in the same way as it has overcome slavery? We need to redefine religion and engage in radical reform or a nonviolent spiritual revolution in order to concretize this hope. At the same time, we need to rethink modernity and the economic and political systems that produce violence. Violence and nonviolence today are questions of life and death concerning the survival of humanity and the planet. This urgency forces us to face our historical and collective responsibility: it is not a dream but a roadmap that we should construct together since there are no separate destinies or ways to salvation.

**Funding:** This research was funded by the Fondazione per le Scienze Religiose (FSCIRE), 90137 Palermo, Italy.

**Conflicts of Interest:** The author declares no conflict of interest.


Light-Emitting Diodes - New Perspectives

*Edited by Chandra Shakher Pathak and Uday Dadwal*

Published in London, United Kingdom

Light-Emitting Diodes - New Perspectives http://dx.doi.org/10.5772/intechopen.100741 Edited by Chandra Shakher Pathak and Uday Dadwal

#### Contributors

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4.3.1. Al

Al poisons the effect of grain refinement with Zr, which is the main reason for which Mg-Al alloy cannot be grain-refined using Zr. Tamura et al. [72] found that even the trace addition of 0.015% Zr could severely coarsen the grain size of high-purity Mg-9Al alloy; Kabirian et al. [64] found that the dendrites of AZ91 alloy were greatly coarsened by the addition of 0.2~1.0% Zr; Balasubramani et al. [65] found the grain size of Mg-1Zr was sharply coarsened from 114 ± 38 μm to 1550 ± 38 μm with the addition of 0.2% Al (Figure 10). Two reasons have been proposed. One is that Zr poisons the surface of the native Al-carbide nuclei (such as Al4C3 [73]) that are originally present in high-purity Mg-9Al alloy. Another is that the consumption of solute Al by Zr (or solute Zr by Al) reduces the extent of the CS effect. The Al-Zr compounds were identified to be Al2Zr [64], Al3Zr2 [64] or Al3Zr [65]. Despite the negative effect on grain refinement, Al-Zr compounds can increase the thermal stabilities of grain during heat treatment, refine grains during hot deformation [74], and increase creep resistance [75].

**Figure 10.** SEM BSE images showing: (**A**) blocky Zr particles and fine Zr particles in Mg-1Zr alloy; (**B**) faceted Zr*x*Al*y* particles in Mg-1Zr-Al-Be alloy; (**C**) Zr clusters surrounded by fine precipitates of Zr*x*Al*y* particles in Mg-1Zr-Al-Be alloy, EDS testing point 1 is rich in Al and Zr, whereas point 2 is rich in Zr. The samples were cut from the bottom of an ingot to observe the clusters [65]. Reprinted with permission from ref. [65]. Copyright 2004 Elsevier.

## 4.3.2. Fe

Fe is one of the most common impurities in Mg alloys, and may result from the raw materials, fluxes, crucible, and stirring tools used. Fe is detrimental to the effect of grain refinement with Zr. This can be understood from two perspectives.

On the one hand, Fe can react with Zr in the Mg melt, forming the compound Fe2Zr, as verified by Cao et al. [66]. As a result, the Zr content is rapidly consumed, and the grain refinement effect is remarkably reduced. This effect has also been observed during the remelting process of pre-alloyed or commercial ingots of Zr-bearing Mg alloys when using an Fe crucible. An obvious loss of dissolved Zr takes place due to the diffusion of Fe through the Mg melt, finally leading to the addition of extra Zr in order to achieve the required level of grain refinement [76].

On the other hand, trace Fe and Si impurities on tiny Zr particles may alter the surface chemistry of the Zr particles, upsetting the coherent match between the Zr and Mg lattices, as reported Davis et al. [77]. Therefore, the nucleating potency of the Zr particles is decreased, reducing the grain refinement effect.

On the basis of these analyses, it can be seen that when an Fe crucible and Fe stirring paddle are used during melting of Mg alloys, a protective coating (e.g., BN coating [66]) should be pre-coated to inhibit the dissolution of Fe into the Mg melt. However, it has been reported that, by taking advantage of the effective removal of Fe by Zr, high-purity Mg alloys containing less than 1 ppm Fe can be produced [78].