*2.1. Materials*

Human serum albumin (HSA), methylglyoxal (MG), nitro blue tetrazolium (NBT), 2,4-Dinitrophenylhydrazine (DNPH), caffeic acid, p-coumaric acid and porcine pancreatic α-amylase were purchased from Sigma-Aldrich, Milwaukee, WI, USA. All other chemicals, unless stated otherwise, were high grade and purchased from local vendors. All the blanks were run replicating the same conditions and acted as a control. All the buffers were filtered before use.


*3.1. Data Information*

Datasets 1 and 2 are derived from the online communication system (OCS) of ABC Software Co. and uses data accumulated over a 12-week period. Datasets 1 and 2 show that the cumulative number of failures at *t* = 1, 2, ··· , 12 is 14, 17, ··· , 81, and 11, 17, ··· , 81, respectively [14]. Dataset 3 is the test data of a medical record system consisting of 188 software titles and data for one of three releases. It shows that the cumulative number of failures is 90, 107, ··· , 204 for *t* = 1, 2, ··· , 17, respectively [36]. Table 2 shows the accumulated failure data for datasets 1, 2, and 3. We compare the fit between the software reliability models with two failure datasets obtained from OCS and one dataset from Lee et al. [29], which showed good performance as the dependent models (DPF).


5. Conclusion

4. Future of photocatalytic H2 evolution

sunlight (Eq. 13):

Water Chemistry

photostability.

dioxide [108].

doped SrTiO3 [5].

190

The literature examples of photocatalytic water splitting activities show improvements in visible light utilization, charge separation, and prevention of back-oxidation reactions via fine tuning of photocatalyst materials that

enabled more efficient water splitting systems. The efficiency of these systems working under sunlight is better defined with solar-to-hydrogen energy conversion efficiency (STH), i.e., hydrogen production rate times the Gibbs free energy for generating 1 mole of H2 divided by the power of incident

> STH ¼ ð Þ mmol H2=s ∗ 237 ∗ 103 J=mol P mW cm2

The estimated STH required for the particulate photocatalytic systems to be economically compatible with current H2 production technologies is 10% [104]. However, the highest STH values obtained with current developed photocatalysts are in the order of 1–2% (1.8% at 400–475 nm using Rh/Cr2O3-loaded GaN:Mg/ InGaN:Mg photocatalyst [69] and 2% at 420 nm using CDots-C3N4 [70]). The STH conversion efficiency depends both on the catalytic activity and the extent of the utilization of sunlight that depends on the bandgap of the semiconductor. With current photocatalysts having absorption edges around 500 nm, even 100% apparent quantum yields would not guarantee 10% STH values [106]. For a photocatalyst to show 10% STH values, it should have absorption edges at least at 600 nm with apparent quantum yields around 60%. Under the light of these calculations, it can be said that the present photocatalysts having adsorption edge values around 450 nm and quantum yields around 10% are far from being utilized in commercial systems. In order to achieve targeted STH values, the photocatalysts with lower bandgap energies such as (oxy)nitrides and (oxy)sulfides should be improved for H2 evolution activities while ensuring their thermal stability and

Large-scale photocatalytic water splitting reactors are implemented with current low STH values as of 2015. The first example of large-scale photocatalytic water splitting utilized Pt-loaded C3N4 photocatalyst with sacrificial electron donor triethanolamine in a flat-panel-type photocatalytic reactor system in 2015 [107]. The solar-to-hydrogen conversion efficiency is reported to be 0.12%, for which the photocatalytic activity is monitored for 30 days. In such systems, where a sacrificial reagent such as triethanolamine or methanol is irreversibly oxidized at a more negative potential than water (thermodynamically more favorable) at the oxidation centers, the photo-generated charges can be more efficiently separated,

thus increasing H2 evolution rates. However, in those systems, hydrogen production is not solely due to the water splitting; as the carbon- and hydrogencontaining "sacrificial agents" are being oxidized at the oxidation centers, they produce hydrogen as well as aldehydes, carboxylic acid, and carbon

Another large-scale photoreactor is reported by Domen et al., who used Aldoped and RhCrOx-loaded SrTiO3 photocatalyst sheets in their 1 � 1 m water splitting panel [45]. The achieved STH value under simulated sunlight is 0.6% at 331 K and limited to a maximum value of 1.4% due to the large bandgap energy of the photocatalyst (3.2 eV). Improved STH values (reaching 1.1%) are shown to be possible on a two-step excitation system in 2016 using photocatalyst sheets having smaller bandgap energy values such as Mo-doped BiVO4 (2.4 eV) and La- and Rh-

∗ A cm2 ð Þ � 100 (13)

The developments in the photocatalytic water splitting reactions are explained here with the emphasis on the one-step photocatalysis systems. The early photocatalyst improvements with bandgap engineering, co-catalyst usage, and size reductions are shown to contribute to the increased visible light-driven H2 evolution activity values. The main drawbacks in the present systems are discussed to be the charge recombination, back-oxidation reactions of the products into water, and mass transfer limitations especially in the three-phase systems. Using defect-free small crystals of photocatalysts and making use of phase junctions or metal cocatalysts are suggested to decrease charge recombination rates. Back-oxidation of H2 into water or oxygen reduction reaction to water is expected in many noble metal-containing particulate photocatalyst systems. The prevention of these unwanted secondary reactions is shown to be possible to some extent by modification of the noble metal surfaces. Some examples of these modifications are anion coating, partial adsorption of a poison, or nanolayer coating of the co-catalyst or the whole photocatalyst. Selective permeation property of the nanolayer coatings such as Cr2O3 is reported to suppress the back-oxidation rates, resulting in enhanced H2 and O2 evolution rates. Possible mass transfer limitations, limiting the observed rates in three-phase systems, are predicted especially in the liquid–gas interfaces. The literature examples attracted attention for the liquid–gas interfaces in suspended systems and internal mass transfer limitations for the immobilized photocatalyst systems. It is concluded that, in addition to the required developments in activities with suppression of charge recombination, back-oxidation, and mass transfer limitations, future of the photocatalytic systems would necessitate active and stable photocatalysts with narrower bandgap energies (to be activated at >600 nm) for achieving targeted 10% solar-to-hydrogen energy conversion efficiency value.


Genetics and Periodontal Disease: An Explicit Insight

*Santo Grace Umesh, Lakshmi Ramachandran, Janani Karthikeyan and Anitha Mani*

#### **Abstract**

A branch of Biology which deals with the science of hereditary influences on living organisms is termed as Genetics. There has been a broad study related to hereditary influence on human tissue linking to health and disease conditions. A vital role is played by genetics in the proper functioning, adaptive repair, regeneration and remodelling of hard and soft tissue. A major segment of genes are related to periodontal disease. Periodontal disease, being multifactorial in origin is directly or indirectly known to be caused by genetic factors also. A study on human and animals validates the concept that genetics could have influenced periodontal disorders and also plays a key role in the predisposition and progressiveness of the condition. The role played by genetics to damage the inflammatory and immune response system of the host tissues during periodontal conditions has been proved and this section will give a clear insight on the influence of genetics in this condition.

**Keywords:** Genetics, Periodontal disease, Hereditary influence, Polymorphism, Syndromes, Genetic study design

#### **1. Introduction**

A distinct approach is required for periodontal pathologies that produces lesions within the tooth- supporting tissues, once associated with risk factors which are complementary to systemic diseases [1]. Bacterial plaque is the prime aetiology of periodontal diseases, accelerating tissue damage. However, the role of plaque is debated when the vulnerability to periodontal diseases persist despite regular conditions. According to the majority of researchers' perspective, periodontal disease cannot occur in the absence of plaque and tartar, and also suggests that a systematic predisposition merely progresses the tissue destruction caused by microbial flora. On the other hand, few authors claim that there is no concrete evidence establishing cause-effect relationship between the nonspecific bacterial plaque and severity of tooth supporting tissue injury [2].

The host immune response system, the integrity of the tissues, humoral and cellular immunity, and certain endocrine and nutritional factors are the major factors for the development and progression of periodontal disease. Multitude of other factors are also related to periodontal diseases including age, intraoral sites that are more prone to infection and specific microbial agents such as Captosinofaga, Actinomyces naeslundi and Actinobacillus actinomycetemcomitans [2]. Apart from the host immune response system, these factors also add on to the vulnerability to periodontal disease, presenting simple to complex signs. Furthermore, the presence of associated metabolic disorders would also lead to periodontal damage [2].

Genetic elements play a vital role in influencing the inflammatory and immune response of the periodontal disease. Due to the key role played by the immune system in the pathophysiology of the disease, research is directed to identify the genetic mutation or polymorphism related to the various aspect of immunity. The result of these genetic variations might be minor or unimportant or very important and severe based on its effect and infectivity [3]. Genetic diseases are broadly classified into two entities: Simple Mendelian Disorders and Complex Genetics Disorders. Simple Mendelian Disorders are otherwise known as monogenic or single-gene disorders since they are caused by alterations of a single gene, acquired through autosomal recessive or dominant type of inheritance. Several monogenic gene disorders with biochemical defects present with severe periodontitis as one of their clinical manifestations. In these conditions, genetic alteration occurs at a single locus, producing the clinical phenotype which is responsible to cause the disease. Such a genetic alteration, that is associated with a disease phenotype in all families and there is no alternative mechanism to overcome the impact of the genetic defect, is termed as mutation [4].

Complex genetic diseases prevail in more than 1% of the population and are known to be more dominant than Simple Mendelian disorders. Being affected by environmental and lifestyle factors, complex genetic diseases occur as a result of genetic variations at multiple areas of the genes. Alterations in multiple genes, with each contributing a little to these complex genetic diseases, are called polymorphisms. Specific allele occurring in at least 1% of the population is known as genetic polymorphism. Single base mutation that replaces one nucleotide for another is said to be the simplest type of polymorphism and is termed as a single nucleotide polymorphism (SNP). Restriction fragment length polymorphism (RFLP) and simple tandem repeats (STRs), comprising of nucleotide or allele repetition are other types of polymorphism [5]. These genetic polymorphisms are not directly associated with the disease as in monogenetic disorders, however, specific alleles are found with greater incidence in the affected individuals than healthy individuals. The results prove to be true only when two different genetic variations coexist. Complex periodontal disorders are chronic, slowly progressive and are mostly of mild phenotype [5].

Variations in numerous genes encoding different proteins result in a genetic predisposition to a clinical phenotype. Environment and lifestyle play a significant role in impacting the development of complex diseases. Host response influenced by the genetic makeup is responsible for the progression of periodontal disease. Genetic defects or alterations can raise the incidence of periodontal disease. If the physiological process elicited by the gene is related to the occurrence and severity of disease, that specific gene is considered as a contributory element in periodontal disease [6]. Literature evidence reports that the genetic variants play a major role in the aetiology of syndromic and non-syndromic periodontitis.

#### **1.1 Terminologies**

#### *1.1.1 Allele*

One of two or more alternate forms of a gene or marker at a particular locus on a chromosome. (A glossary of relevant genetic terms –Dialogues in clinical neuroscience) [7].