**Acknowledgements**

the ones of commercial terahertz detectors at room temperature like Golay cells, pyroelectric detectors, and Schottky diodes [47]. However, the Si/SiGe MODFET presents the advantage of

**Figure 10.** Responsivity (a) and NEP (b) measured under excitation of 0.15 (blue dots) and 0.3 THz (red squares) of the

**Hz) RV (V/W) NEP (nW/√**

**\_\_\_ Hz)**

To test the ability of the strained-Si MODFETs as detectors in THz imaging, a single transistor (D1) was used as the sensor in the terahertz imaging system shown in **Figure 3**. **Figure 11** shows the visible image of a standard copper RT/duroid® laminate where the logo of the Nanotechnology Group at Salamanca University has been etched (a) and its terahertz image at 0.3 THz (b) when it was wrapped around with a paper. THz radiation passes through in the regions were the metal layer was etched off and it is reflected in the regions covered with copper. A pixel-by-pixel image was taken using D1 as the detector; the gate of the transistor

**Figure 11.** Visible (a) and 0.3 THz (b) images obtained at room temperature using the strained-Si MODFET with a shorter

working at higher modulation frequencies as compared to other detectors.

**0.15 THz 0.3 THz**

Device 1 68.6 0.08 46.4 0.12 Device 2 74.5 0.06 36.2 0.13 Device 3 41.1 0.12 33.3 0.14

**\_\_\_**

**RV (V/W) NEP (nW/√**

**Table 2.** Calculated NEPs and RV for the different devices under studio.

strained-Si MODFET with 100-nm gate length.

66 Design, Simulation and Construction of Field Effect Transistors

gate as sensor.

We would like to acknowledge Thomas Hackbarth (Daimler AG) who fabricated the strained-Si MODFETs used in this work. Our work was financially supported by the Spanish Ministry of Economy and Commerce and FEDER (ERDF: European Regional Development Fund) under the Research Grant #TEC2015-65477-R and FEDER/Junta de Castilla y León Research Grant #SA045U16. Both Research Grants #TEC2015-65477-R and Salamanca University partly support Open Source publications. Y. M. Meziani acknowledges the financial support from RIEC nation-wide Collaborative Reseach Project, Sendai, Japan.


**5. Assessment of intracranial hypertension and hydrocephalus syndrome**

#### **5.1 CSF infusion test or infusion-load test (ILT)**

ILT with the calculation of resorption resistance of the CSF was one of the fundamental methods in choosing of surgical treatment of patients with hydrocephalus [9].

#### **Figure 3.**

*A—Bolus INT circuit with recorded parameters: Po—initial liquor pressure; Pp—maximum pressure after bolus injection. Pt—liquor pressure after bolus injection after 1 minute in the relaxation phase; ΔV—volume of injected fluid. B is the type of pulse wave of ICP with a compensated state of intracranial compliance. P1—Systolic peak, P2—Vascular peak, P3—Diastolic peak. C—pathological Lundberg waves of type B caused by an increase in ICP without depletion of intracranial compliance. D—pathological Lundberg waves of type A caused by increased ICP with depletion of intracranial compliance.*

During ILT, the bolus infusion technique of A. Marmarou is used. To do this, a ventricular catheter is inserted into the cavity of the lateral ventricle. The distal part of the ventricular catheter is connected to the ILT system. Within 2 minutes the background intracranial pressure, background spectral components of wave oscillations are recorded. Next, a saline solution is injected with a bolus volume of 2 ml at a rate of 1 ml/sec with an interval between boluses of 1 min [4, 10, 15, 17] (**Figure 3**, **A**).

From the ratio of the injected volume, the magnitude of the maximum increase in pressure and pressure after 1 minute during the relaxation period, according to A. Marmarou's formula, both the production rate (A) and the resorption resistance index (R) (a value proportional to the inverse value of its absorption) are calculated using an infusion-liquor test, which is based on excretion and administering a certain volume of CSF by boluses or once and measurement of the time during which the cerebrospinal pressure is restored as a result of CSF production or suction [15, 25].

The calculation is carried out according to the formulas:

1.CSF production rate (A) (Eqs. (3) and (4)):

$$\frac{\Delta V\_1 \cdot \lg\left(\frac{P\_1}{P\_m}\right)}{t\_1 \cdot \lg\left(\frac{P\_0}{P\_m}\right)}\tag{3}$$

2.CSF resorption resistance (R) (Eq. (4)):

*CSF Bypass Surgery in Children with Hydrocephalus: Modern Possibilities, Prospects… DOI: http://dx.doi.org/10.5772/intechopen.110871*

$$
\Delta V\_2 \cdot \lg \left[ \frac{P\_2 \cdot \left( P\_p - P\_0 \right)}{P\_p \cdot \left( P\_2 - P\_0 \right)} \right] \tag{4}
$$

The evaluation of ILT results consists in the determination of intracranial pressure, fluctuations of CSF (amplitude-frequency changes), as well as registration of resorption resistance of CSF, followed by obtaining one of the variants of pressure-volume curves (P/V): normotensive, hypertensive, and atrophic [15].

#### **5.2 Monitoring biomechanical properties of CSS in case of ICH**

Currently, discrete values of intracranial pressure are of low practical importance, since they do not display indicators of intracranial compliance (ICC). To assess the severity of the pathological process in patients with increased ICP of various etiologies, including hydrocephalus and congenital malformations of the skull bones, an assessment of the pulse curve recorded when measuring ICP is used. These changes are typical of ICC changes of any etiology and characterize the amplitude of pulse oscillations, the morphology of pulse curve peaks, and the formation of plateau waves with a significant decrease in compliance. The classical view of the pulse curve is shown in **Figure 3**, **B**.

One cardiac cycle forms three peaks due to the increase in intracranial volume in the systole and its decrease in the diastole.

Accordingly, the P1 (systolic) peak turns out the most pronounced one on the normal ICP curve. Immediately upon reaching the pulse wave of the microcirculatory bed of the brain, a P2 peak should appear as the reaction of the arterial bed muscular layer to compensate systolic pressure and normalize the curve, and reduce the amplitude of pulse oscillations. At the moment of diastole, a dicrotic P3 peak is formed, which characterizes a decrease in intracranial blood volume and relaxation of the vascular bed. The morphology of the pulse curve depends on the initial state of the ICC and the volume of increase in the intracranial contents, which manifests clearly and underlies the infusion-load testing.

Formulas were used for discrete assessment of biomechanical properties and liquor circulation [15]:

$$PVI\_d = \frac{dV\_b}{\lg\frac{\left(meanICP\_p\right)}{\left(meanICP\_o\right)}}\tag{5}$$

where PVId is the discrete value of the PVI index; meapISRo is the average liquor pressure before bolus administration; mean ICPp is the average liquor pressure after bolus administration; dVb is injected (with a plus sign)/output volume (with a minus sign) of the bolus, ml.

$$C\_d = \frac{0,4343 \cdot PVI\_d}{memICP\_o} \tag{6}$$

where *Cd* is a discrete assessment of craniospinal compliance.

$$I\_d = \frac{PVI\_d \lg\left[\frac{\left(memICP\_p\right)}{\left(memICP\_t\right)}\right]}{dT} \tag{7}$$

where Id is a discrete estimate of the rate of resorption/production of CSF; dT is the time interval in minutes from the moment of bolus injection/withdrawal to the current meanICPt average pressure.

$$R\_d = \frac{dT \cdot meanICP\_o}{PVI\_d \lg\left[\frac{meanICP\_t\left(meanICP\_p - meanICP\_o\right)}{(meanICP\_t - meanICP\_o)meanICP\_p}\right]}\tag{8}$$

where Rd. is a discrete estimate of the resorption resistance of the CSF.

In addition to changes in the pulse curve, the classic signs of an increase in ICP and a decrease in ICC are the appearance of pathological plateau waves (Lundbergwaves) on the ICP monitoring chart. There are three types of waves—A, B, C—while only type B and C waves are indicative of this or that change in compliance. Type C waves are associated with respiratory and cardiac cycles, manifested by an increase in ICP of a small amplitude. Their duration does not exceed the specified cycles. Type B waves are manifested by an increase in ICP to 30–50 mmHg and a duration of 1–5 minutes (**Figure 3**, **C**). Most often, the appearance of these waves is considered to provoke ICC without its obvious depletion. The appearance of type A waves—prolonged, up to 40 minutes, persistent increases in ICP up to 50 mmHg and above—is associated with the depletion of ICC (**Figure 3**, **D**).

The universality of these parameters resulting from compliance changes of any etiology seems to be significant. The identification of the ICP increase plateau is a significant diagnostic criterion for "latent" ICH, which is most often encountered in the long course of the pathological process. HCG in hydrocephalus can serve as an example of such condition, developing in patients with congenital malformations of the skull bones, or in patients with subcompensated forms of hydrocephalus in the neonatal period, when classical clinical signs of ICH are extremely rare.

#### **5.3 Imaging methods, indices of the ventricular system of the brain**

Modern imaging methods make it possible to identify hydrocephalus, establish the cause of the development of this process, conduct dynamic observation, and evaluate the effectiveness of the performed liquor bypass surgery. Currently, magnetic spiral computed tomography (MSCT) is considered to be the optimal method of radiation diagnosis of hydrocephalus, the use of which allows you to quickly measure the size and count the indices of the ventricular system of the brain, which is especially important in childhood when planning surgical treatment [26, 27].

*CSF Bypass Surgery in Children with Hydrocephalus: Modern Possibilities, Prospects… DOI: http://dx.doi.org/10.5772/intechopen.110871*

When interpreting the conducted radiation examination, the symmetry, degree of expansion, configuration, and contours of the ventricular system are taken into account.

**The index of the anterior horns of the lateral ventricles** is calculated in relation to the maximum distance between the most distant external parts of the anterior horns and the maximum bitemporal diameter of the skull multiplied by 100. Normally, the value of this index ranges from 25.4 (under the age of 5 years) to 29.4–31.0 (aged 71 to 80 years) (**Figure 4**, **A**).

**The index of the central sections of the lateral ventricles** is calculated with respect to the smallest distance between their outer walls in the recess area and the maximum bitemporal diameter of the skull on the same slice multiplied by 100. Normally, the value of this index ranges from 18.2 to 26.0 (**Figure 4**, **B**).

**The index of the III ventricle** is estimated in relation to its maximum width in the posterior third at the level of the pineal gland to the largest transverse diameter of the skull on the same section, multiplied by 100. Normally, the value of this index increases with age, reaching 3.0 at the age of 5 years and 4.8—from 71 to 80 years (**Figure 4**, **C**).

**The index of the IV ventricle** is calculated in relation to its largest width to the maximum internal diameter of the posterior fossa of the skull on the same slice. Normal indicators of this index are 11.9–14.0 (**Figure 4**, **D**).

Intraventricular hypertension is characterized by the appearance of periventricular edema, there are four stages of these changes:

Stage 1—blurring of the contours of the upper-outer corners of the anterior horns or a clearly limited border of reduced density of the same localization;

#### **Figure 4.**

*MSCT of the brain. Measurement for calculating the index of the anterior horns of the lateral ventricles (A), measurements for calculating the index of the central divisions of the lateral ventricles (B). Measurement for calculating the index of the III ventricle (C), measurements for calculating the index of the IV ventricle (D).*

Stage 2—reduction of density in the anterior and posterior horns;

Stage 3—edema along the perimeter of the lateral ventricles;

Stage 4—scalloped contours of the lateral ventricles and thinning of the brain substance.

Conducting magnetic resonance imaging (MRI) or MSCT with ventriculometry, in combination with a CSF examination, allows to timely diagnose hydrocephalus, to determine the severity and evaluate the results of the treatment.


*2.1. Chronic Inflammation Disease and Cancer*

Chronic inflammation is recognized as a leading promoting factor of diseases including carcinogenesis [24], which continues to be the leading cause of mortality and disability around the world [25–28]. Tumour-promoting inflammation is recognised as an enabling hallmark of cancer [29]. Cancer and inflammation are linked by intrinsic and extrinsic pathways. Intrinsically, oncogenes regulate the inflammatory microenvironment, whereas extrinsically, the inflammatory microenvironment promotes the growth and spread of cancer [30]. Various cell types involved in chronic inflammation can be found in tumours, both in the surrounding stroma and within the tumour itself. Neoplasms, including some of epithelial origin, contain a significant inflammatory cell component [31]. Multiple studies on human clinical samples have revealed that inflammation influences epithelial cell turnover [32,33]. Significantly, human susceptibility to breast, liver, large bowel, bladder, prostate, gastric mucosa, ovary and skin carcinoma is increased when proliferation occurs in the context of chronic inflammation [32–37].

Chronic inflammation is linked to approximately 25% of all human cancers and increases cancer risk [38] by stimulating angiogenesis and cell proliferation, inducing gene mutations and/or inhibiting apoptosis [38]. Chronic inflammation can develop from acute inflammation if the irritant persists, although in most cases the response is chronic from the start. Chronic inflammation is characterized by the infiltration of injured tissue by mononuclear cells such as macrophages, lymphocytes and plasma cells, as well as tissue destruction and attempts at repair [31]. *Helicobacter pylori* infections in gastric cancer, human papillomavirus infections in cervical cancer, hepatitis B or C infections in hepatocellular carcinoma and inflammatory bowel disease in colorectal cancer (CRC) are common causes of chronic inflammation associated with cancer development [39,40]. Inflammation also causes epigenetic changes that are linked to cancer development.

Natural PAs from diverse food and medicinal plants and their derivatives exert multiple bioactivities, including anti-inflammatory properties [41]. PAs can impact inflammation through known and unknown pathways. Evidence supports that PA compounds improve human health by stimulating anti-cancer and anti-inflammatory mechanisms [3]. These PAs contain triple bonds that functionality convert them into highly alkylating compounds that are reactive to proteins and other biomolecules. This unique molecular structure might be the key to understanding the beneficial effects of PAs such as their anti-inflammatory and cytoprotective function [41]. Recent research has suggested that the anti-cancer role of certain foods might be attributed to their anti-inflammatory function. Root vegetables, and particularly carrots, are promising natural sources in this respect thanks to their rich content of PAs [3,41–43]. The anti-inflammatory properties of purple carrots have been suggested to be due to the high levels of anthocyanin pigments [44]; however, another study showed that PAs, not anthocyanins, are responsible for the anti-inflammatory bioactivity of purple carrots [45]. In vitro and in vivo studies have demonstrated that the health-benefitting effects of carrots and other root vegetables might be attributed to PAs, such as FaOH and FaDOH [46]. Other dietary compounds, including several different phytochemicals, have been examined in the context of cancer chemoprevention; however, until now the measured effects [47–50] have been quite small and inconsistent compared with those found for PAs.

#### *2.2. Inhibition of Nuclear Factor Kappa B (NF-κB) Pathways*

NF-κB is a transcription factor that regulates the expression of many genes involved in the regulation of inflammation and autoimmune diseases [51,52]. Moreover, NF-κB plays a significant role in inflammation-induced cancers, as NF-κB is one of the major inflammatory pathways that are triggered by, for example, infections causing chronic inflammation [39,40,53]. Cellular immunity, inflammation and stress are all regulated by NF-κB signalling, as are cell differentiation, proliferation and apoptosis (Figure 2) [54,55]. Both solid and hematologic malignancies frequently modify the NF-κB pathway in ways that promote tumour cell proliferation and survival [56–58].

NF-κB, a key factor in the inflammatory process, provides a mechanistic link between inflammation and cancer, and the components of this pathway are targets for chemoprevention, particularly in CRC [59]. There are two major signalling pathways for NF-κB activation, namely the canonical and the non-canonical NF-κB signalling pathways. The canonical pathway activates NF-κB1 p50, RELA and c-REL, which are also called canonical NF-κB family members. The non-canonical NF-κB pathway, on the other hand, selectively activates p100-sequestered NF-κB members, mostly NF-κB2 p52 and RELB, which are also called non-canonical NF-κB family members [60]. LPS and proinflammatory cytokines, among other pathogenic substances, activate NF-κB through degrading inhibitors of κB (IκBs) [61] to release the common subunit P65 (RELA). In order to trigger the transcription of these genes, activated NF-κB travels into the nucleus and attaches to its associated DNA motifs. When activated, the NF-κB p65 subunit binds to the promoter regions of genes involved in inflammation, leading to the production of *IL-6*, *IL-1β* and *TNF-α* [62].

**Figure 2.** NF-κB target genes implicated in the onset and progression of inflammation. NF-κB is a transcription factor that is inducible. After activation, it can regulate inflammation by activating the transcription of several genes. NF-κB regulates cell proliferation, apoptosis and differentiation in addition to promoting the production of pro-inflammatory cytokines and chemokines. Endoplasmic reticulum (ER) stress results in an inflammatory unfolded protein response (UPR). Stress on the ER induces apoptosis by activating inflammation. This can be accomplished by stimulating IKK complex (element of the NF-κB) or (X-box binding protein 1) XBP1 and (protein kinase R-like ER kinase) PERK through a mediator. These trigger the release of pro-inflammatory molecules, hence accelerating cell death.

Carrot PAs, particularly FaOH and FaDOH, were studied for their anti-inflammatory properties [3,63], in part by inhibiting the transcription factor NF-κB [64]; however, their exact mechanism of action is still unknown. Mice fed a diet containing FaOH were less likely to develop severe inflammation after being exposed to LPS [5]. FaOH from *Saposhnikovia divaricata (S. divaricata)* significantly reduced the levels of LPS-induced *TNF-α* and *IL-6* in cultured BV-2 microglia cells and murine serum [61]. FaOH and FaDOH purified from carrots were demonstrated for their preventative effects on colorectal precancerous lesions in azoxymethane (AOM)-induced rats. Biopsies of neoplastic tissue were analysed for gene expression, and the results showed that FaOH and FaDOH inhibited NF-κB and the downstream inflammatory markers *TNF-α, IL-6 and COX-2* [46]. FaOH from Radix Saposhnikoviae (dried roots of *S. divaricata*, Apiaceae) inhibited LPS-induced NF-κB p65 activation and IκB-α phosphorylation in BV-2 microglia cells [61]. Treatment using FaOH from the roots of *Heracleum moellendorffii* (*H. moellendorffii*) inhibited LPS-induced NF-κB signalling activation by inhibiting IκB-α degradation and nuclear accumulation of p65 [65] in RAW264.7 cells. In addition, FaDOH reduced the level of LPS/IFNγ-induced NF-κB, IKK-α and IKK-β activation in rat primary astrocytes [64].

Prostaglandin (PG) synthesis is a hallmark of inflammation. Two enzymes, cyclooxygenase (COX) 1 and 2, catalyse the first step of PG synthesis, but *COX-2* is the major one that responds to inflammatory signals to produce PG at inflammatory sites [66]. However, *COX-2* can be suppressed by inhibiting the NF-κB translocation pathway (Figure 2) [67]. *COX-2* expressions in healthy tissues are low, but they can quickly increase in response to growth factors, cytokines and signals promoting tumour invasion, metastasis, aberrant proliferation and angiogenesis [68].  Mechanistically, *COX-2* promotes carcinogenesis through the creation of prostaglandins (PGs), which suppress apoptosis and stimulate the development of blood vessels in tumour tissue, which helps in sustaining tumour cell

viability and growth [39,75], suggesting that anti-inflammatory drugs targeting *COX-2* might be beneficial in the treatment of different types of cancer.

PAs modulate inflammation via suppressing *COX-2* expression, which depends on NF-κB activation by inflammation [76]. FaOH inhibited LPS-induced *COX-2* expression in RAW264.7 cells, thus blocking PGE2 overproduction [65]. FaOH isolated from American ginseng (*P. quinquefolius*) effectively reduced the severity of colitis in mice treated by dextran sulphate sodium (DSS) induced for a week before FaOH treatment. FaOH reduced the number of CD11b+ macrophages in the lamina propria and the inflammation hallmark protein *COX-2*. These data suggest that macrophages expressing *COX-2* might be an essential factor for colitis development. Interestingly, FaOH treatment prior to DSS did not prevent colitis or reduce colitis severity in mice [8]. Quiescent macrophages in the lamina propria in a healthy mouse might offer protection against colitis induction, as depleting macrophages prior to induction of colitis may exacerbate DSS-induced colitis [77]. However, when colitis develops, there is an increase in the number of activated macrophages that secrete pro-inflammatory cytokines to boost the inflammatory response, thus exacerbating colitis. At this stage, an overactive macrophage response to enteric microbiota greatly contributes to the pathogenesis of colitis [78]. Treatment with FaOH to target macrophages was shown to be highly effective in suppressing colitis at this stage, highlighting the utility of FaOH in the treatment of a hyper-inflammatory disease (Figure 3) [79]. In an azoxymethane (AOM)-induced rat colorectal cancer model, FaOH and FaDOH downregulated *COX-2* in precancerous lesions of CRC [46] and also reduced the number of malignant tumour foci.

**Figure 3.** Schematic representation of the possible mechanism of immunoregulation activity of poly-acetylenes (PAs) in macrophages. (Interferon-γ) IFN-γ activates macrophage cells to M1, and PAs downregulate NF-κB activities in M1 macrophages by inhibiting *iNOS, COX-1* and *COX-2*. PAs suppress the inflammatory response by inhibiting cytokines (*IL-16, IL-1β* and *TNF-α*) and upregulating Nrf2 pathway (*HO-1* and *NQO1*) in macrophages. PAs structure modified from Mplanine (2022) https://www.wikiwand.com/en/Falcarinol#Media/File:Falcarinol\_3D\_BS.png (accessed on 1 January 2023).

#### *2.3. Oxidative Stress*

2.3.1. Inhibition of Nitric Oxide Synthase (NOS) and Pro-Inflammatory Cytokine Pathways

Nitric oxide (NO) is essential in a number of physiological functions, such as host defence, where it prevents the spread of disease-causing microbes within cells by stifling their reproduction [80]. The upregulation of NO expression in response to cytokines or pathogen-derived chemicals is a crucial part of the host's defence against different types of intracellular pathogens. Different cell types produce the enzyme NOS, which catalyses the synthesis of NO, at high levels in a number of different tumour types [81]. Inflammation induces a specific form of NOS, i.e., the inducible isoform of nitric oxide

synthase (iNOS), via activating *iNOS* gene transcription (Figure 2) [82]. iNOS is involved in complex immunomodulatory and antitumor mechanisms, which have a role in eliminating bacteria, viruses and parasites [83].

A considerable number of studies have been published on the role of PAs in *iNOS* expression in inflammation. Studies have demonstrated that FaOH extracted from *P. quinquefolius* inhibited *iNOS* expression in ANA-1 mΦ macrophage cells that were polarized to M1 [8] and LPS-induced iNOS expression in macrophages [84,85], leading to colitis suppression [8]. Moreover, FaDOH was tested on rat primary astrocytes for its impact on LPS/IFN-γ-induced *iNOS* expression. FaDOH blocked 80% of LPS/IFN-γ-induced *iNOS* by reducing *iNOS* protein and mRNA in a dose-dependent manner. FaDOH was shown to suppress *iNOS* expression, and it inhibited *IKK, JAK, NF-κB* and *Stat1* (Figures 2 and 3) [64].

Another study showed a dose-dependent reduction in nitric oxide production in macrophage cells, where treatment with an extract of purple carrots containing PAs significantly reduced iNOS activity and *iNOS* expression in macrophage cells [45]. PAs reduced nitric oxide production in macrophage cells without cytotoxicity [45]. In vivo, purple carrots also inhibited inflammation in colitic mice and reduced colonic mRNA expression of *iNOS* [44]. FaOH from *H. moellendorffii* roots inhibits the LPS-induced overexpression of *iNOS* in RAW264.7 cells [65]. FaOH and other PAs from *P. quinquefolius* such as panaxydiol have a suppressive effect on *iNOS* expression in macrophages treated with LPS [85].


*7.2.5 Lipidic substitutes eyedrops*

Is used when a lipid deficiency is detectected, (Rosacea), meibomian gland disfunction. They are developed to enhance the lipidic layer of the tear-film, by different substances. Comercial eyedrops available are Systaine Balance and Optive Advance (no commercial interest) [48].


**Preface to Transitioning to Zero Hunger**

#### **Delwendé Innocent Kiba**

#### **1. Introduction**

Food insecurity is a worldwide concern. Today, the quest for a world where everyone has access to sufficient, safe, and nutritious food has never been so crucial. In 2021, around 2.3 billion people were food-insecure, seriously affecting around 11.7% of the world's population (FAO et al. 2022). Food insecurity has been exacerbated by the social and health crises the world has been experiencing since 2019. The COVID-19 crisis and the Russia–Ukraine conflict have fundamentally affected food supply both for agricultural products and for the inputs used to produce them. These crises have disrupted supply chains, limited access to markets, and increased the vulnerability of marginalized populations (Ben Hassen and El Bilali 2022).

Experts agree that food security can only be achieved through inclusive, resilient, and sustainable agrifood systems (FAO 2023). Agrifood systems go beyond simple access to food and encompass the entire food chain, including the production, processing, distribution, and consumption of agricultural and food products (Neik et al. 2023). Agrifood systems are weakened by climate change, the loss of biodiversity, and rising poverty. Although advancements in technology offer promising avenues to enhance food production while minimizing environmental impact (Foley et al. 2011), agrifood systems still generate significant hidden costs linked to environmental, social, and health problems, as stated in the 2023 report of the FAO.

Since the adoption of the SDGs in 2015, efforts and initiatives to promote sustainable agriculture, ensure food and nutrition security and eradicate hunger have been deployed around the world. Today, there are many signs that the "zero hunger" objective set out in the Sustainable Development Goals (SDGs) will not be achieved. The FAO estimates that nearly 670 million people will still be suffering from hunger in 2030. This was made clear at the UN Summit on Food Systems in 2021, where several nations made a firm commitment to implement policies aimed at transforming agrifood systems.

This book analyzes the factors behind hunger and the sustainability of food production, and highlights approaches aimed at a transition to zero hunger.

Chapter 2 deals exhaustively with the links between SDG 2 and the other SDGs, in particular the global resolution of problems such as poverty, health,

education, and climate change, while Chapter 3 highlights the essential role of social capital in combating the structural factors of hunger and provides a critical analysis of agroecology. The analyses of agroecology and conventional food production are expanded in Chapter 4. Chapters 5 and 6 deal with the resilience and productivity of production systems and their sustainability, with a particular focus on agroforestry and agrobiodiversity. Chapters 7 and 8 deal with case studies of yam farming in West Africa and coconut-based livestock farming in Sri Lanka, respectively, as contributions to achieving food security and improving people's incomes. Finally, in Chapter 9, approaches aimed at limiting food waste are presented as solutions for achieving the "Zero Hunger" objective while contributing to environmental sustainability.

#### **2. Highlights**

#### *2.1. Pathways to Zero Hunger*

SDG 2 aims to eradicate hunger and ensure food and nutritional security by 2030. Achieving this goal necessarily involves a phase of promoting sustainable food production. This transition phase towards zero hunger requires tackling various issues relating to the production, distribution, access, and use of foodstuffs. The transition to zero hunger will undoubtedly require coordinated efforts at the national, regional, and international level, with complex and multi-faceted challenges to reconcile increased agricultural productivity with environmental protection and global social and economic objectives (Okello et al. 2021). To this must be added efforts to guarantee physical and economic access to sufficient, healthy, and nutritious food, considering individual food preferences. Today, more than ever, it is necessary to integrate nutrition into food production, as malnutrition is recognized as a global phenomenon affecting both underdeveloped and developed countries (Beyerlee and Fanzo 2019). It is important to consider indigenous food systems, particularly the development of traditional crops that are often best adapted to their biophysical, socio-economic, and cultural contexts, but which have unfortunately been neglected until now (FAO 2022). In addition, the production of healthy, balanced, and sufficient food requires access to innovations and technologies such as precision agriculture, digital technologies, biotechnologies, and innovative solutions for the storage and transport of foodstuffs. Access to innovations does not guarantee their adoption by stakeholders. The adoption of innovations requires a good connection between research and development through a transdisciplinary approach that enables them to be co-created and correspond to the real needs of stakeholders. (Kiba et al. 2020; Jacobi et al. 2022). Participatory and adaptive solutions that consider

local institutional capacities, the diversification of agroecosystems and ecological management, and the quality of local diets should therefore be favored (Blesh et al. 2019). Sustainable land management is essential if the world is to achieve food security. Soil, an essential support for agricultural production, is being degraded at an exponential rate, although the extent and impact of this degradation cannot be accurately assessed. It should be possible to develop a global approach to disentangle the natural and anthropogenic causes of soil degradation, based on ecological approaches to production and remote sensing (Bindraban et al. 2012).

None of the approaches toward zero hunger are possible without eradicating poverty (SDG 1) and inequality (SDG 10) and improving the livelihood of people (SDG 3). Finally, policy and governance around trade, land tenure, soil health, and regulations that affect food production and distribution are necessary, as are good partnerships between governments, non-governmental organizations, businesses, and the research community to share the necessary knowledge and resources.

#### *2.2. Case Studies*

In Chapter 2, Lile et al. explore the complex relationship between SDG 2 and the other SDGs to identify direct and indirect links. They show that SDG 2 does not stand alone but is instead closely linked to all the other SDGs. To achieve zero hunger, the authors stress the urgent need to find answers to the issues of poverty, health, education, inequality, and climate change in a comprehensive manner. They point out that given the interconnections between the different SDGs, zero hunger cannot be achieved through isolated efforts, but rather through a synergy of actions between government agencies, international organizations, civil society, private companies, and other stakeholders, each naturally playing its role according to its area of expertise. The authors suggest that policies and programs to tackle the root causes of hunger should be formulated transparently and integrated into national development programs that can be regularly monitored and evaluated.

In Chapter 3, Gian L. Nicolay examines the essential role of social capital in combating the structural factors contributing to hunger. The author analyzes the drivers of hunger, including poverty, wars, pandemics, climate change, gender, age, race, societal divisions, and capitalism. He shows that social capital is a key parameter for predicting and solving the problem of hunger. These include extension systems, agencies that link farmers to markets and external agencies, innovation platforms, farmer field schools, cooperatives, and business groups. According to the author, these social organizations enable sustainable intensification to succeed as an important element of the food system in low-income countries and improve

economic performance. The author also makes a critical analysis of agroecology, comparing it with industrial agriculture, and proposes a morphological analysis and solutions for a sustainable food production.

In Chapter 4, Epule and Chehbouni discuss the implications of agroecology and conventional agriculture for food security in Africa. They highlight the fact that the continent faces the daunting challenges of climate change and variability and examine the contributions, benefits, and challenges associated with agroecology and conventional agriculture. The authors stress the need to promote agroecology so that it achieves the same yields as conventional agriculture. However, they recognize the difficulty of getting out of the agroecology/conventional agriculture dilemma, given the involvement of several factors in the African context. Looking ahead, the authors suggest innovations to make conventional agriculture cleaner and more sustainable, the multiplication of pilot studies on agroecology, and a political approach that is both bottom-up and top-down to guarantee the success of the various initiatives.

The study by Dissanayaka et al. (Chapter 5) presents agroforestry—combining trees, crops, and animals—as an important multi-purpose approach for the productivity and resilience of production systems. They highlight different agroforestry practices and the potential benefits in terms of land use, food production, biodiversity conservation, and adaptation to climate change. Factors such as site selection and planning, component selection, planting, system management and harvesting, and the use of products are presented as key elements in the implementation of agroforestry, although these elements may vary according to the context and objectives. Finally, the authors discuss the limitations of agroforestry systems and suggest ways of improving them.

Achieving food and nutritional security requires crop diversification, as demonstrated by the authors Weerasekara and Plooger from Sri Lanka (Chapter 6). In this chapter, the importance of agrobiodiversity and the need to diversify global food production are discussed, as are the risks of losing this agrobiodiversity. The authors recommend the use of local traditional food plants to achieve food and nutritional security. The study identified 85 species of food plants of great importance. Traditional food preparation and preservation methods are presented and discussed. From the authors' analysis, it emerges that traditional local crops are less costly and more environmentally friendly sources of food, since they are well adapted to unfavorable climatic and edaphic conditions and have good resistance to pests and diseases.

In Chapter 7, Aighewi et al. show the potential of a traditional crop such as yam for achieving food security and improving household incomes in West Africa. They also outline the challenges faced by yam farmers, including poor seed quality. The authors present an initiative to improve yam production by setting up formal quality seed production systems as part of the project 'Yam Improvement for Income and Food Security in West Africa (YIIFSWA)'. This initiative has led to the production of certified yam seed and the development of yam seed markets. Virus detection tools and technologies for eliminating infected sources, as well as high-ratio propagation technologies, are presented as a strategy for improving yam seed quality and productivity, thereby contributing to food security and reducing household poverty.

In Chapter 8, Nuwarapaksha et al. show the importance of integrating coconut cultivation and livestock production in the Sri Lankan context as an innovative and sustainable approach offering mutual benefits, including increased productivity, improved soil health, and reduced dependence on mineral fertilizers. The authors argue that although this system provides livelihoods for farmers while conserving natural resources, further research is needed to identify the most appropriate animal and plant species.

Achieving zero hunger requires good management to minimize food waste. Chapter 9 by Balan et al. looks at limiting food loss and waste, a pervasive problem that persists despite global efforts. The authors map food losses around the world. They highlight the importance of reducing food loss and waste in the context of SDG 2 and propose key measures to mitigate these challenges at all stages of the food chain, including production, storage, processing, distribution, retail and food services, and household losses. Furthermore, the authors believe that it is essential to identify and assess the factors contributing to food waste to effectively tackle the problem. This chapter provides useful guidelines for authorities, businesses, organizations, and consumers to help them adopt sustainable practices and promote effective food management.

#### **3. Conclusions**

The transition to zero hunger calls for innovation throughout the chain of the agrifood system. This book has examined the links between SDG 2 and the other SDGs, as well as the role of social capital, agroecology, agroforestry, crop diversification, innovative farming systems, and reducing food losses as essential elements in achieving food and nutrition security. The book provides analyses and solutions from a variety of authors that can be used by policy makers, researchers, and practitioners engaged in the global effort to combat food and nutrition insecurity. The

discussions highlight the need for holistic and collaborative approaches to address the complex web of challenges associated with achieving SDG 2 and related goals.

**Funding:** This research received no external funding.

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

#### **References**

© 2023 by the author. 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 (http://creativecommons.org/licenses/by/4.0/).


**5. Results obtained**

### **5.1. 1D simulations**

### *5.1.1. Compression loads response*

Responses from the evidence to compressive loads can be seen in Figure 7. Figure 7a shows the negative shift of the solid component that increases its value negatively with increasing loading time. The time initially is zero (0) for t = 0.67s and reaching figures of -15x10-4mmN-1s-1 at the time of maximum loading, t = 45s for x = 0.3. As the liquid flows, the behavior is similar to a linear elastic behavior, because the only component that supports the load is solid.

Figure 7b shows the decrease in pressure due to the fluid outlet presented by the compression of the tissue. For an initial time t = 0.67s the pressure exerted on the fluid in the tissue is 2 MPa, but as the permanence of the compressive, the pressure decreases and takes values close to 0 MPa, thereby external pressure is balanced, also zero.

**Figure 7.** Response of tissue to compression forces. a. Displacement of solid matrix. b. Changes in the fluid pressure in the tissue in presence of the displacement of the same.

### *5.1.2. Tensil loads response*

208 Injury and Skeletal Biomechanics

*4.3.2. Boundary conditions*

*4.3.3. Loading conditions*

frequency equivalent to 0.1 Hz

*5.1.1. Compression loads response*

**5. Results obtained**

**5.1. 1D simulations**

Simulation was performed so as not to allow displacement at the bottom. Load was applied on the upper edge, allowing the fluid outlet only at the bottom of the tissue fragment, as shown in Figure 6a. For 2D, a condition of tissue confinement was simulated, as shown the Figure 6b, so as to present only flow at the bottom. The burden was placed at the top and lateral and bottom movement were restricted, similar conditions to those reported in several experimental studies, including that of Ateshian et al, 1997; Frijns, 2000 and Wu et al, 1999.

Calculations to simulate the applied load were performed from the data for the AC reported by Wu et al. For the 1D simulations, a load was applied of -2.033 N/m in compression, 2.033 N/m in tension and cyclic loading with frequency equal to 0.1 Hz. In 2D simulations a load was applied on the upper face of cartilage fragment corresponding to the value -4.0397e-6 N/m in compression, 4.0397e-6 N/m in tension. For cyclic loading, it was applied at a

Responses from the evidence to compressive loads can be seen in Figure 7. Figure 7a shows the negative shift of the solid component that increases its value negatively with increasing loading time. The time initially is zero (0) for t = 0.67s and reaching figures of -15x10-4mmN-1s-1 at the time of maximum loading, t = 45s for x = 0.3. As the liquid flows, the behavior is similar

Figure 7b shows the decrease in pressure due to the fluid outlet presented by the compression of the tissue. For an initial time t = 0.67s the pressure exerted on the fluid in the tissue is 2 MPa, but as the permanence of the compressive, the pressure decreases and takes

to a linear elastic behavior, because the only component that supports the load is solid.

values close to 0 MPa, thereby external pressure is balanced, also zero.

**Figure 6.** AC scheme for the confinement conditions in (a) 1D and (b) 2D.

Figure 8 summarizes the results obtained for tensile strength. Figure 8a shows the positive displacement of the solid component in response to tensile load imposed on tissue. The figure shows how the displacements are positive in presence of tension maintained over time. From an initial value of 0 mmN-1s-1 at t = 0.67s, displacement increases up to a maximum of 16x10-4 mmN-1s-1 at a maximum load time t = 45s.

**Figure 8.** Response of tissue to tensile forces. a. Displacement of solid component tissue upward. b. Change in the fluid pressure generated by the redistribution of fluid in the tissue.

Figure 8b shows the increase of fluid pressure generated by the entry thereof into the tissue due to the pressure difference between the internal and external environment (fluid suction). This pressure difference is caused by displacement of the solid component in the positive direction in response to imposed tensile load. It is shown that this progression of the increase of pressure manifests over time, creating a redistribution of the fluid in the tissue.

### 210 Injury and Skeletal Biomechanics

### *5.1.3. Oscillating loads response*

Responses obtained in the simulation of oscillating charges can be seen in Figure 9. Figure 9a shows the alternating displacement presented at each oscillation.

Mechanical Behavior of Articular Cartilage 211

**5.2. 2D simulations**

*5.2.1. Compression loads response*

Figure 10a corresponds to the displacement of the solid in the *y* axis for each time instant. The displacements are small in the first moments of the load and it can be seen that as the load increases, the time of displacement increases toward more negative values, demonstrating a greater deformation of the solid phase of the tissue. These displacements are produced by the fluid outlet in response to the maintained compression load and it is observed that the greatest displacement occurs in the upper layers of the tissue responsible for receiving the load

**Figure 10.** 2D - Response to compressive load. a. *y* displacements during 45 seconds. b. Behavior of the

Figure 10b shows the behavior of the fluid pressure at each instant of time. It is observed that the pressure decreases rapidly in all tissue layers reaching values close to 0 MPa in a very short time. This variation of fluid pressure corresponds to the decrease of the same in function of the load exerted over the time and poro-elastic tissue behavior which allows the

Results obtained from the tensile simulation are shown in Figure 11. Figure 11a shows the displacement of the solid in the *y* axis for different time instants. There are major shifts in the early stages of loading (t = 0.67s) and displacement decreases with increasing load time. It is further noted that with a sustained tensile load at a given time, the greater displacement or elongation occurs in the upper layers of the tissue where the stress is felt in the first instant, which is why the transfer of deformation is smaller at a greater depth of tissue. In this case the fluid pressures tend to increase because the tissue seeks to balance the inside and the outside

fluid pressure *p* due to its outflow in presence of the load.

fluid outlet.

*5.2.2. Tensil loads response*

directly, while the displacement transference is less at a greater tissue depth.

**Figure 9.** Response to cyclic load. a. Alternate displacement of the solid component. b. Changes in the fluid pressure in oscillate form. c. Delay between the solid deformation and fluid pressure variation.

Initially the movements of the solid are small, close to 0 mmN-1s-1 for t = 0.67s. However, they increase over time reaching a value of 6x10-4 mmN-1s-1 or -6x10-4mmN -1s-1, at t = 45s, according to the tissue load, tension or compression respectively. Figure 9b shows the development of the process of oscillation in the fluid pressures in response to movement that the solid matrix undergoes upon perceiving the cyclic loading. Initially the pressure lowers and then makes an adjustment that increases, being in inverse phase with the evolution of the deformation of the solid phase of the tissue. I.e., once the solid is deformed in the positive direction, the pressure changes, becoming more negative and vice versa.

The obvious alternating deformation processes of the solid in the face of the application of cyclic loads shows that the displacements are caused by the loads exerted on the tissue and the mobilization of fluid from or into the interior as applied tension or compressive loads respectively. These loads, in turn, generate alternation with respect to each instant of time between the variation of the pressure pattern and the variation of the displacement pattern. However, this action is not in complete phase with displacement. One can appreciate the presence and delay of alternating processes described above, because the equation that represents the displacements is elliptical and corresponds to a displacement equation in space while the equation that represents the pressure corresponds to a parabolic equation and represents a much slower diffusion process than the process of displacement (See Fig. 9c).

### **5.2. 2D simulations**

210 Injury and Skeletal Biomechanics

9c).

*5.1.3. Oscillating loads response*

Responses obtained in the simulation of oscillating charges can be seen in Figure 9. Figure

**Figure 9.** Response to cyclic load. a. Alternate displacement of the solid component. b. Changes in the fluid pressure in oscillate form. c. Delay between the solid deformation and fluid pressure variation.

Initially the movements of the solid are small, close to 0 mmN-1s-1 for t = 0.67s. However, they increase over time reaching a value of 6x10-4 mmN-1s-1 or -6x10-4mmN -1s-1, at t = 45s, according to the tissue load, tension or compression respectively. Figure 9b shows the development of the process of oscillation in the fluid pressures in response to movement that the solid matrix undergoes upon perceiving the cyclic loading. Initially the pressure lowers and then makes an adjustment that increases, being in inverse phase with the evolution of the deformation of the solid phase of the tissue. I.e., once the solid is deformed in the positive direction, the pressure changes, becoming more negative and vice versa.

The obvious alternating deformation processes of the solid in the face of the application of cyclic loads shows that the displacements are caused by the loads exerted on the tissue and the mobilization of fluid from or into the interior as applied tension or compressive loads respectively. These loads, in turn, generate alternation with respect to each instant of time between the variation of the pressure pattern and the variation of the displacement pattern. However, this action is not in complete phase with displacement. One can appreciate the presence and delay of alternating processes described above, because the equation that represents the displacements is elliptical and corresponds to a displacement equation in space while the equation that represents the pressure corresponds to a parabolic equation and represents a much slower diffusion process than the process of displacement (See Fig.

9a shows the alternating displacement presented at each oscillation.

### *5.2.1. Compression loads response*

Figure 10a corresponds to the displacement of the solid in the *y* axis for each time instant. The displacements are small in the first moments of the load and it can be seen that as the load increases, the time of displacement increases toward more negative values, demonstrating a greater deformation of the solid phase of the tissue. These displacements are produced by the fluid outlet in response to the maintained compression load and it is observed that the greatest displacement occurs in the upper layers of the tissue responsible for receiving the load directly, while the displacement transference is less at a greater tissue depth.

**Figure 10.** 2D - Response to compressive load. a. *y* displacements during 45 seconds. b. Behavior of the fluid pressure *p* due to its outflow in presence of the load.

Figure 10b shows the behavior of the fluid pressure at each instant of time. It is observed that the pressure decreases rapidly in all tissue layers reaching values close to 0 MPa in a very short time. This variation of fluid pressure corresponds to the decrease of the same in function of the load exerted over the time and poro-elastic tissue behavior which allows the fluid outlet.

### *5.2.2. Tensil loads response*

Results obtained from the tensile simulation are shown in Figure 11. Figure 11a shows the displacement of the solid in the *y* axis for different time instants. There are major shifts in the early stages of loading (t = 0.67s) and displacement decreases with increasing load time. It is further noted that with a sustained tensile load at a given time, the greater displacement or elongation occurs in the upper layers of the tissue where the stress is felt in the first instant, which is why the transfer of deformation is smaller at a greater depth of tissue. In this case the fluid pressures tend to increase because the tissue seeks to balance the inside and the outside environment. Then displacement occurs in response to stress and produces a reorganization of the fluid within the tissue, interfering with the variation in the pressure thereof.

Mechanical Behavior of Articular Cartilage 213

response to the compression of the tissue. This is due to the rapidity with which compressive and tensile loads are alternated, loads which prevent the behavior of cartilage during the cyclic loading from exhibiting the behavior that corresponds exclusively to the

**Figure 12.** 2D - Response to oscillate load. a. *y* displacements. b. Oscillation of the pressure *p* within the

There are several theories explaining the behavior of AC in the presence of load conditions, summarized in computational models that include the swelling process and the properties of the anisotropic structure of collagen. The most frequently used tests to determine the mechanical qualities of the AC are the confined compression, the unconfined compression, the indentation and the swelling tests (Wilson, et al., 2005), carried out using numerical

For purposes of meeting the stated objectives, we simulated a condition of confinement of the tissue that allows the flow at the bottom to restrict lateral and bottom movement. Conditions were similar to those reported in practical experiments as the papers presented by Ateshian et al., 1997; Frijns, 2000 and Wu et al., 1999; among others. The data obtained from the simulations confirm the theory of biphasic articular cartilage, first proposed by Mow et al., 1980; and supported by several authors as Haider et al., 2006; Wilson et al., 2005, Haider & Guilak , 2007; Meng et al., 2002; Wu et al., 1997, Terada et al., 1998, Donzelli et al.,

Results allow us to conclude that articular cartilage exhibits a displacement response of the solid component (matrix) and a variation in the pressure of fluid component due to the exit or entrance thereof, with decreases in pressure in response to compressive loads and increases at the same tensile loads. The displacement is caused by outflow of fluid in response to the maintained compressive load. However it is important to note that once the tissue reaches its maximum displacement, it behaves as a solid rather than as a poro-elastic material. From this point the fluid can't flow out of the tissue because the pressure is

case of tension or compression.

tissue according to the load.

**6. Final discussion**

approximation tools.

1999 and Donzelli & Spilker, 1998; among others.

balanced with the external fluid begins to bear part of the load.

**Figure 11.** 2D-tensile load response. a. *y* displacements. b. . Behavior of the fluid pressure *p* due to its inflow in presence of the load.

Figure 11b shows the behavior of the fluid pressure *p* for different time instants. It is observed that the fluid pressure is increased by small amounts in response to sustained tensile load. This action is due to the compensation of the tissue in response to deformation in elongation by the solid phase of the tissue that requires a redistribution of fluid into the tissue. However, it is evident that at the end of the tensile load time (approximately at t = 27s), the tissue can't undergo greater deformation in elongation and hence the fluid pressure also tends to stabilize at the inside thereof, causing a steady pressure maintained close to zero which balances with the external pressure.

### *5.2.3. Oscillating loads response*

Figure 12a corresponds to the displacement of the solid in the *y* axis at different time instants. It is noted that the displacements or deformations occur alternately; at the times 1, 3 and 5 (t = 0.67s, t = 27s = 6.57s respectively) the displacements are made positive, behavior similar to that observed during exposure to stress loads. Conversely, at the times 2, 4 and 6 (t = 3.37s, t = 16.5 s and t = 45s respectively) the displacements are negative, consistent with the behavior exhibited by the matrix to compressive loads.

Figure 12b shows the behavior of the fluid pressure *p*. Similar to what happened with the deformations of the solid phase, the pressure oscillation in response to cyclic loading imposed on the tissue is evident. Note that at times 1, 3 and 5 (t = 0.67s, t = 6.57syt = 27s respectively) the pressure tends to decrease due to the redistribution of fluid in response to perceived stress loads. Because the loads are not maintained, the tissue can't compensate with fluid inlet from the outside which is why the pressure is not increased. Thus, at times 2, 4 and 6 (t = 3.37s, t = 16.5 s and t = 45s respectively), the pressure tends to increase in response to the compression of the tissue. This is due to the rapidity with which compressive and tensile loads are alternated, loads which prevent the behavior of cartilage during the cyclic loading from exhibiting the behavior that corresponds exclusively to the case of tension or compression.

**Figure 12.** 2D - Response to oscillate load. a. *y* displacements. b. Oscillation of the pressure *p* within the tissue according to the load.


*3.2. Classifier*

The classifier has the ability to learn the concept during the training phase, mine the situations and assign the context label during the recognition phase in real time. The extracted feature vectors (i.e., Section 3.1.2) are provided to the classifier for the classification. In the first stage, accelerometer data are classified into "active" or "still". In the second stage, audio data are classified by the classifier. In the audio data classifier, we take into consideration only two contexts, while the rest of the contexts are recognized as "sedentary-unknown context". The following sections explain the training and testing of the classifier.


**6. Conjugation of NDDS with transdermal route**

Transdermal drug delivery systems (TDDS) are topically administered medications in the form of patches, which can deliver certain medication to systemic circulation in a more convenient and effective way than is possible with conventional dosage form. The potential of skin as a path of drug administration has been amply demonstrated by the acceptability of marketed therapeutic systems [32]. Administration of systemic drugs using a transdermal patch represents a noninvasive route, with improved patient compliance. This route of administration prevents passage through the gastrointestinal tract and maintains constant plasma levels for prolonged periods of time [33]. A transdermal patch is a medicated adhesive patch placed on the skin to deliver a time-released dose of medication through the skin for treating topical or systemic illness. Since early 1990, this dosage form of transdermal therapeutic system has been available in the pharmaceutical market. Such a system offers a variety of significant clinical benefits over others, such as tablet and injection [32, 33]. Transdermal route is a potential mode of delivery of lipophilic drugs in the systemic circulation. Some factors are responsible for transdermal drug delivery such as area of application, amount applied, release kinetics and prolongation of application time [34].

**135**

*Drug Delivery through Targeted Approach with Special References to Phytosomes*

**7. Feasibility of phytosome as novel vehicle for transdermal drug**

Lipophilic drugs could be easily transfused by transdemal route which enhance the bioavalibility of phytoconstitutent. Drug would be delivered into systemic circulation by transdermal route transdermal route. Drug has to pass three different skin layers before reaching to systemic circulation. The outermost layer, *Stratum corneum* provides hindrances to such type of drugs delivery due to its lipophilicity. The Phytosomal form of phytoconstituents can pass this barrier easily and helps to deliver the phytoconstituents in systemic circulation. The research studies from two decades show the phytosome technology has enough potency to be used as novel carrier of Phytoconstituents. Phytosomal carrier has enough potency to be used transdermally for increasing bioavailability of

Ever since the advent of human civilization, man is dependent on nature to fulfill all his need. Traditional system of healing human aliment was also derived from natural resources. In an era of development, devised various means of treatment primarily based on synthetic chemicals and popularly known as allopathic system of treatment. The inherent side effects of this system led to the shift in focus from contemporary to either conventional system of medication or to evolve the Novel drug delivery system. Novel drug delivery vehicles that can be used for the poorly soluble, pH sensitive and less potent drug to make them safe and target oriented. These novel drug delivery vehicles can also be utilized to deliver herbal formulations to its targeted site with lesser side effect. This phenomenon can be further augmented by conjugation of transdermal drug delivery system with novel drug delivery vehicle containing nanobiomedicine as herbal constituents. Phytosomes have shown the potential to be good carrier of herbal constituents for novel drug delivery systems. The combination of Transdermal route and Phytosomal drug delivery opens up an arena for better treatment for the patient suffering from skin diseases, Burn, allergies and bone

Authors want to acknowledge the Department of Pharmaceutical Sciences, Kumaun University campus bhimtal, for providing support for library and litera-

*DOI: http://dx.doi.org/10.5772/intechopen.86644*

**delivery**

Phytoconstituents [34, 35].

**8. Conclusion**

fracture.

ture search.

**Acknowledgements**

**Conflict of interest**

There is no conflict of interest.


**4. Summary**

The presence of foreign body inside the spinal canal was not shown to be associated with increased risk of infection, regardless of the previous path of the bullet, prior to its final location in the spinal canal [92, 93]. Thus, we do not consider bullet removal as an indication for

is shown outside of the patient's spine; (e) C1 ring following osteosynthesis.

80 Essentials of Spinal Cord Injury Medicine

**Figure 2.** A 30-year-old patient, who sustained a low-velocity gunshot wound. He had a few entry wounds in his head and neck. He was conscious, alert, and hemodynamically stable with normal neurological status. The following images describe the evolution of events. (a) Plain radiograph showing the patient's skull with a bullet located at the center; (b) axial CT scan showing the broken arc of C1 with the bullet located next to the dens; (c) trans-oral approach to C1 vertebra with the bullet at the base of the surgical dissection. The smiley gives the orientation of the patient's face; (d) the bullet

> This chapter is an overview of two relatively rare-penetrating spinal cord injuries, their epidemiology, mechanism of injury, initial evaluation, and emergency primary and late definitive treatment. We also reviewed the complication and prognosis of each injury.

**References**

1916

[1] Conran J. Characteristics and outcomes of gunshot-acquired spinal cord injury in South

Penetrating Spinal Cord Injury

83

http://dx.doi.org/10.5772/intechopen.76857

[2] McCaughey EJ, Purcell M, Barnett SC, Allan DB. Spinal cord injury caused by Stab Wounds: Incidence, natural history, and relevance for future research. Journal of Neurotrauma. 2016 Aug 1;**33**(15):1416-1421. DOI: 10.1089/neu.2015.4375. Epub 2016 Mar 18

[3] Sidhu GS et al. Civilian gunshot injuries of the spinal cord: A systematic review of the current literature. Clinical Orthopaedics and Related Research. 2013;**471**(12):3945-3955 [4] Wilkins RH. Neurosurgical Classics. 2nd ed. Park Ridge, Illinois: American Association

[5] Arthur John Brock (translator). Introduction. Galen. On the Natural Faculties. Edinburgh.

[6] Lipschitz R, Block J. Stab wounds of the spinal cord. Lancet. 1962 Jul 28;**2**(7248):169-172 [7] Peacock WJ, Shrosbree RD, Key AG. A review of 450 stab wounds of the spinal cord.

[8] Velmahos GC, Degiannis E, Hart K, Souter I, Saadia R. Changing profiles in spinal cord injuries and risk factors influencing recovery after penetrating injuries. The Journal of

[10] Farmer JC, Vaccaro AR, Balderston RA, Albert TJ, Cotler J. The changing nature of admissions to a spinal cord injury center: Violence on the rise. Journal of Spinal Disorders.

[11] Miyamoto S, Ide T, Takemura N. Risks and causes of cervical cord and medulla oblongata injuries due to acupuncture. World Neurosurgery. 2010 Jun;**73**(6):735-741

[12] Enicker B, Gonya S, Hardcastle TC. Spinal stab injury with retained knife blades: 51 consecutive patients managed at a regional referral unit. Injury. 2015 Sep;**46**(9):1726-1733.

[13] De Régloix SB, Baumont L, Daniel Y, Maurin O, Crambert A, Pons Y. Comparison of penetrating neck injury management in combat versus civilian trauma: A review of 55

[14] Sakar M, Dogrul R, Niftaliyev S, Bayri Y, Dagcınar A. Direct withdrawal of a knife lodged in the thoracic spinal canal in a patient with normal neurologic examination: Is it

[15] Johnson S, Jones M, Zumsteg J. Brown-Séquard syndrome without vascular injury associated with Horner's syndrome after a stab injury to the neck. The Journal of Spinal Cord

[9] Holtz A, Levi R. Spinal Cord Injury. New York: Oxford University Press; 2010

of Neurological Surgeons. 1992. ISBN: 978-1-879284-09-8. LCCN:<PHONE_NUMBER>

Africa. South African Medical Journal. 2017;**107**(6):518-522

South African Medical Journal. 1977;**51**:961-964

cases. Military Medicine. 2016 Aug;**181**(8):935-940

safe? Spinal Cord Series and Cases. 2016 Jul 7;**2**:1-3

Trauma. 1995;**38**:334-337

1998;**11**:400-403

DOI: 10.1016/j.injury

Medicine; 2016;**39**(1):111-114

**Table 1.** Summarized table comparing evaluation, treatment, and complications between NMPSCI and MPSCI.

In order to emphasize the differences between these entities, we present a summarized table that compares between them (**Table 1**).


*2.3. Variables*

Demographic variables collected included student's gender, race and ethnicity, maternal education, language spoken at home, living situation, living arrangement due to finances, and grade level (details of these questions are located in Appendix A Table A1). We selected HYS questions regarding adolescent risk and protective factors and risk-taking behaviors by cross-referencing Jessor's Domains of Adolescent Risk Behavior and the 2014 HYS Questionnaire Form B/B Enhanced [13]. Categorization of chosen questions reflected the HYS framework for risk and protective factors and risk-taking behaviors [8]. HYS questions were reviewed for validity and reliability by experts in public health, injury prevention, and school health prior to inclusion in the administered survey [8]. The behaviors and factors chosen include unintentional injury behaviors (e.g., life jacket wear, exposure to swimming lessons), protective factors (e.g., eating dinner with family, having supportive adults), and risk-taking behaviors and risk factors (e.g., texting while driving, alcohol use, involvement in physical fighting) (Appendix A Table A1). These factors were not specifically related to water behavioral factors, but general lifestyle factors.

 (Appendix A Table A1). These questions were developed by drowning prevention experts at Seattle Children's Hospital, Washington State Department of Health and Public Health Seattle and King County and reviewed and approved by Washington State Department of Health prior to their inclusion in the HYS. Life jacket wear (Q7) was added to the HYS starting in 2002, and both swimming questions (Q5 and Q6) were added in 2014.

For this study, we used responses to the question about comfort in water (Q6) as a validated indicator of swim ability [5]. Taking formal swimming lessons and wearing life jackets are both validated drowning prevention indicators [9,10].


**Acknowledgements**

The authors would like to acknowledge the significant contributions of Professor Patrick Crookes who was an academic member of the Project Team. Also the contributions of Mr Ravi Daga and the IGNOU team including: Professor Marmar Mukopadhyay, Professor Madhu Parhar and Ms. G. Mythili. Additionally the academics and senior higher education leaders from Australian and New Zealand institutions who provided feedback on the framework, which helped shape it. Finally the University of Wollongong for the provision of two funding grants that was critical in the development of the Framework.