**1. Introduction**

Metrology is the science of measurements. In our everyday life, we are constantly surrounded by measurements: from reading the time to weighing apples, we continuously measure something. However, measurements are also somehow embedded in objects, since, for example, the apple we buy has already been measured before its arrival at the greengrocer, in order to determine its calibre. In these measurements, uncertainty plays a very important rule. Metrologists know that no measurement makes sense without an associated uncertainty value. Without it, no decision can be taken; no comparisons can be made; no conformity can be assessed.

It is hence pivotal to know the meaning of measurement uncertainty, understand the contributions to measurement uncertainty, know how these contributions affect the final measurement uncertainty, have a mathematical tool to represent measurement uncertainty and propagate it through the measurement procedure, and consider measurement uncertainty in any application.

This Topical Collection "Measurement Uncertainty" started as a Special Issue, but many contributions have been submitted showing how metrology—and, in particular, measurement uncertainty—is an open, interesting, and important topic.

Therefore, with my great pleasure, the Special Issue has become a Topical Collection. I invite Colleagues working on this issue to continue submitting papers, so that the Collection can grow and become a good place for a fruitful discussion.


**Author details**

Hua Li\*, Zhenning Li, Kaiyu Liu, Mingshan Ren and Yunkai Deng Department of Space Microwave Remote Sensing System, Aerospace Information Research Institute, Chinese Academy of Sciences, Beijing, China

\*Address all correspondence to<EMAIL_ADDRESS>
© 2022 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.

*The Present Situation and Development for Spaceborne Synthetic Aperture Radar Antenna… DOI: http://dx.doi.org/10.5772/intechopen.106040*


**7. Role of cysteine-oxidized wild type SOD1 in sporadic ALS**

In sporadic ALS, there had been no direct evidence that SOD1 was involved in the pathogenesis of the disease, except that some mutations of *SOD1* gene expressed familial ALS in a low penetration rate with seemingly 'sporadic' cases. The link between SOD1 and sporadic ALS was first introduced by the detection of SOD1 specifically modifiable with a chemical compound commonly in familial and sporadic ALS, although the molecular basis for it has not been determined in detail (Gruzman et al., 2007). It indicates that a similar conformational change in mutant and wild type SOD1 can trigger the phenotype of familial and sporadic ALS in common. In *in vitro* study, wild type SOD1 acquires toxic properties of mutant SOD1 through oxidation by hydrogen peroxide (Ezzi et al., 2007), implying that cysteine-oxidized wild type SOD1 may be a contributor to motor neuronal death in sporadic ALS.

Recently, a conformation-specific antibody generated against misfolded mutant SOD1 has been shown to recognize wild type SOD1 only when the protein was sulfonylated (-SO3H) at Cys111, and the antibody immunostained motor neurons in the spinal cords of sporadic ALS patients, but not of SOD1-unrelated familial ALS patients or controls (Bosco et al., 2010). Chemically oxidized or purified wild type SOD1 from sporadic ALS spinal cords inhibited kinesin-based fast axonal transport as did mutant SOD1, supposing that Cys111 mediated conformational change or misfolding of SOD1 is a shared pathological denominator of familial and sporadic ALS. Interestingly, most of the sporadic ALS-derived toxic SOD1 was soluble and non-aggregated, meaning that misfolding or monomerization is sufficient for SOD1 to gain the toxic property such as oxidative insult we have shown in mutant and wild type SOD1 (Kishigami et al., 2010). Further studies *in vivo* will be required to clarify the detailed mechanism of SOD1 toxicity mediated by oxidation of cysteine residues including Cys111.


*2.1. Plant Material*

We analyzed 208 maize accessions obtained from international and national gene banks in Africa (Supplementary Table S1). The maize panel comprised 190 landraces representing gene pools from Burkina Faso (58), Ghana (43), and Togo (89) (Supplementary Figure S1). The landraces from Burkina Faso and Togo were sourced from the gene bank at the International Institute of Tropical Agriculture (IITA), Ibadan, Nigeria, whereas those from Ghana were provided by the Plant Genetics Resources Institute (PGRI) at Bunso, Ghana. The majority of these landraces were collected from farmers' fields in the 1970s and 1980s. However, the eco-geographical data of the collection sites of the landraces were not available. The study also included a diverse set (18) of drought- and heat-tolerant open pollinated populations (hereafter referred to as reference populations) developed by the Maize Improvement Program at IITA (MIP-IITA), Ibadan, Nigeria.


**3. TBI physiopathology and oxygen importance**

TBI presents two main classifications for intracranial lesions: focal or diffused [7–9]. Focal brain damage is the consequence of cortical lacerations, compression, or concussion forces, compromising blood supply and culminating in neuronal and glial necrosis. The structural injury is resulted from the brain collision to rigid structures, depressed skull fractures, vascular injuries or penetrating trauma [8–11].

Diffuse brain damage is caused by acceleration/deceleration forces, that shears and stretches brain tissue, causing functional disturbance, culminating in brain swelling or diffuse axonal injury [8–11]. The co-existence of both types of injuries are frequently present, as a result from the mechanical distortion of the head that leads to a combination of neural and vascular events [10–13].

Additionally, the TBI process can be breakdown in two successive, intertwined, pathophysiological moments, labeled as primary and secondary injury.

#### **3.1 Primary injury**

The primary injury arises from the mechanical damage occurring at the time of the impact, being exclusively responsive to preventive measures [8, 14]. On the macroscopic level, damage can be recognized by shearing of white-matter tracts, diffuse swelling, focal contusions, and intracerebral and extracerebral hematomas [15–17].

On the cellular level, mechanoporation of axolemma (caused by the traumatic axonal injury) results in sodium channelopaty [18] and unregulated influx of Ca2+, which initiates calpain activation and mitochondrial swelling [19–22]. Calpain activation and cytochrome *c* accumulation increases axonal injury, detachment and apoptosis [23]. This cascade of events occurs 24 to 72 hours after the trauma and is denominated as secondary axotomy [11]. Injured axons are also susceptible to demyelination [17].

The microvasculature suffers from injury changes, such as swelling of perivascular astrocytic end-feet, increased adherence of intravascular leukocyte, perivascular hemorrhage, transvascular erythrocytes diapedesis, and increased activity of endothelial microvacuolation and micropseudopodia [24, 25].

#### **3.2 Secondary injury**

The second injury emerges from a complex series of molecular and cellular interrelated events, resulted from the biochemical cascades triggered by the trauma [9, 11]. An essential goal in the critical care is to establish recognition and treatment for secondary injury, and prevent secondary insults, which worsen patient's outcomes [26, 27].

Post-traumatic edema likely occurs by the dysfunction of sodium-potassium pump, due to pH-induced conformational change or cellular energy failure, resulting in water and sodium accumulation within the cell [11, 25]. Other factors that contributes to intracranial edema are excitotoxicity (induces intracellular sodium accumulation) [28], and membrane disruption [29] and depolarization (induced by influx of chloride, due to sodium influx) [30].

**155**

**Figure 1.**

*TBI's sequence of events.*

*Benefits of Early Tracheostomy in TBI Patients DOI: http://dx.doi.org/10.5772/intechopen.93849*

rupted and the ICP raises exponentially [7, 16].

Excitotoxicity is the result of the excess of excitatory amino acids (EAA) that are released in the extracellular space, such as glutamate and aspartate, which raises intracellular sodium, calcium, chloride and water [10, 15]. This accumulation results in organelle and plasma membrane swelling [31], apoptosis, activation of destructive enzymes (such as calpain, nitric oxide synthase) [32], positive feedback

Besides other secondary brain injuries, such as calcium dysregulation (which leads to cytoskeletal degradation), patients experience superimposed secondary insults (with intracranial or systemic repercussions) [10, 14, 15, 27]. Systemic repercussions are hypotension, hypoxia, hyperthermia, and hypoxemia. **Figure 1** recapitulate TBI's

Intracranial insults include cerebral ischemia, elevated ICP (or intracranial hypertension), and cerebral fluid-mediated swelling. The Monro Kellie doctrine (**Figure 3**) demonstrates the constancy relationship in the sum of volumes of brain, intracranial blood and cerebrospinal fluid (CSF) [7, 36, 37]. Once the brain suffers from the intracranial insults and equal volumes of CSF and intracranial blood are compressed, ICP remains normal (compensated state). When the brain enters in a decompensate state (after exhaustion of compensate state), the balance is inter-

It is important to mention that secondary injury does not have the same meaning

as a secondary insult [11, 14]. Secondary insult occurs at the organ system level, being considered as a second hit event, exacerbating the damage from the primary

loop by voltage-gated calcium channels [33], and necrosis [34].

sequence of events. **Figure 2** recapitulate TBI's neurometabolic cascade.

*Benefits of Early Tracheostomy in TBI Patients DOI: http://dx.doi.org/10.5772/intechopen.93849*

*Advancement and New Understanding in Brain Injury*

**3. TBI physiopathology and oxygen importance**

leads to a combination of neural and vascular events [10–13].

endothelial microvacuolation and micropseudopodia [24, 25].

influx of chloride, due to sodium influx) [30].

pathophysiological moments, labeled as primary and secondary injury.

injuries.

**3.1 Primary injury**

demyelination [17].

**3.2 Secondary injury**

outcomes [26, 27].

TBI can be classified following its severity: Mild, Moderate and Severe [7]. This classification is based on the Glasgow Coma Scale (GCS), with Mild - GCS Score 13–15; Moderate - GCS Score 9–12; and Severe - GCS Score 8–3. Subsequent TBI management will rely on the first evaluation and the prevention of secondary

TBI presents two main classifications for intracranial lesions: focal or diffused [7–9]. Focal brain damage is the consequence of cortical lacerations, compression, or concussion forces, compromising blood supply and culminating in neuronal and glial necrosis. The structural injury is resulted from the brain collision to rigid structures, depressed skull fractures, vascular injuries or penetrating trauma [8–11]. Diffuse brain damage is caused by acceleration/deceleration forces, that shears and stretches brain tissue, causing functional disturbance, culminating in brain swelling or diffuse axonal injury [8–11]. The co-existence of both types of injuries are frequently present, as a result from the mechanical distortion of the head that

Additionally, the TBI process can be breakdown in two successive, intertwined,

The primary injury arises from the mechanical damage occurring at the time of the impact, being exclusively responsive to preventive measures [8, 14]. On the macroscopic level, damage can be recognized by shearing of white-matter tracts, diffuse swelling, focal contusions, and intracerebral and extracerebral hematomas [15–17]. On the cellular level, mechanoporation of axolemma (caused by the traumatic axonal injury) results in sodium channelopaty [18] and unregulated influx of Ca2+, which initiates calpain activation and mitochondrial swelling [19–22]. Calpain activation and cytochrome *c* accumulation increases axonal injury, detachment and apoptosis [23]. This cascade of events occurs 24 to 72 hours after the trauma and is denominated as secondary axotomy [11]. Injured axons are also susceptible to

The microvasculature suffers from injury changes, such as swelling of perivascular astrocytic end-feet, increased adherence of intravascular leukocyte, perivascular hemorrhage, transvascular erythrocytes diapedesis, and increased activity of

The second injury emerges from a complex series of molecular and cellular interrelated events, resulted from the biochemical cascades triggered by the trauma [9, 11]. An essential goal in the critical care is to establish recognition and treatment for secondary injury, and prevent secondary insults, which worsen patient's

Post-traumatic edema likely occurs by the dysfunction of sodium-potassium pump, due to pH-induced conformational change or cellular energy failure, resulting in water and sodium accumulation within the cell [11, 25]. Other factors that contributes to intracranial edema are excitotoxicity (induces intracellular sodium accumulation) [28], and membrane disruption [29] and depolarization (induced by

**154**

Excitotoxicity is the result of the excess of excitatory amino acids (EAA) that are released in the extracellular space, such as glutamate and aspartate, which raises intracellular sodium, calcium, chloride and water [10, 15]. This accumulation results in organelle and plasma membrane swelling [31], apoptosis, activation of destructive enzymes (such as calpain, nitric oxide synthase) [32], positive feedback loop by voltage-gated calcium channels [33], and necrosis [34].

Besides other secondary brain injuries, such as calcium dysregulation (which leads to cytoskeletal degradation), patients experience superimposed secondary insults (with intracranial or systemic repercussions) [10, 14, 15, 27]. Systemic repercussions are hypotension, hypoxia, hyperthermia, and hypoxemia. **Figure 1** recapitulate TBI's sequence of events. **Figure 2** recapitulate TBI's neurometabolic cascade.

Intracranial insults include cerebral ischemia, elevated ICP (or intracranial hypertension), and cerebral fluid-mediated swelling. The Monro Kellie doctrine (**Figure 3**) demonstrates the constancy relationship in the sum of volumes of brain, intracranial blood and cerebrospinal fluid (CSF) [7, 36, 37]. Once the brain suffers from the intracranial insults and equal volumes of CSF and intracranial blood are compressed, ICP remains normal (compensated state). When the brain enters in a decompensate state (after exhaustion of compensate state), the balance is interrupted and the ICP raises exponentially [7, 16].

It is important to mention that secondary injury does not have the same meaning as a secondary insult [11, 14]. Secondary insult occurs at the organ system level, being considered as a second hit event, exacerbating the damage from the primary

**Figure 1.** *TBI's sequence of events.*

#### **Figure 2.**

*[35] TBI's neurometabolic cascade. (1) nonspecific depolarization; (2) neurotransmitter release - excitatory neurotransmitters (EAAs); (3) increase potassium efflux; (4) increased membrane pumping to restore homeostasis; (5) Hyperglycolysis to increase adenosine triphosphate (ATP) availability; (6) lactate accumulation; (7) calcium sequestration and mitochondria dysfunction resulting in oxidative metabolism; (8) decreased ATP production; (9) Calpain activation and apoptosis initiation. A - Axolemma and calcium influx. B - Neurofilament compaction. C - microtubule disassembly. D - axonal swelling and secondary axotomy. K+ : potassium; Na+ : sodium; Glut: glutamate; Mg2+: magnesium; Ca2+: calcium; NMDA: N-methyl-D-aspartate; AMPA: d-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid.*

TBI. The same reasoning is applied to the primary insult, which alters the cerebral metabolism and blood flow, resulting in cellular dysfunction and predisposition to cognitive impairment, seizures, hypotension and hypoxia [8].

#### **3.3 Oxygen and TBI**

The brain requires an uninterrupted supply of glucose and oxygen to maintain cellular viability and metabolism, consuming up to 20% of individual's total oxygen, with an average of cerebral metabolic rate of oxygen (CMRO2) between 3 and 3.8 ml/100 g/min [38–41]. Brain metabolism represents the largest source of energy consumption in the human body, since neuronal activity is supported through the production of adenosine triphosphate (ATP), which consumes nearly 60% of oxygen [42, 43]. When cerebral oxygenation is maintained, minimization of secondary insult can be achieved [44].

Brain's energy consumption fluctuates following neuronal activity on localized regions, and in order to provide adequate energy supply, neurovascular and neurometabolic coupling mechanisms are involved [42]. However, within hypoxia or low oxygen conditions, prolyl hydroxylase domain-containing enzymes (PHDs) are

**157**

**Figure 3.**

*The Monro Kellie doctrine.*

*Benefits of Early Tracheostomy in TBI Patients DOI: http://dx.doi.org/10.5772/intechopen.93849*

inhibited, reducing inproline hydroxylation, and altering availability of hypoxiainducible factor-1α (HIF-1α), which assist the metabolism adaptation and function during hypoxic conditions [42, 45–47]. Then, nuclear accumulation of HIF-1α enhance transcriptional activity within HIF-β, promoting gene expression that contains a hypoxia response element (HRE) [42, 46, 48]. Remarkably, HIF-2α is also induced in hypoxic brain, being expressed in astrocytes and endothelial cells [49]. This dysfunction is associated with poor neurological outcomes [50].

In order to cope hypoxia stress, this adaptive response converts cellular metabolism to anaerobic metabolism and inducts erythropoiesis, glycolysis, angiogenesis (by vascular endothelial growth factor), among other events [46, 48, 51]. Nevertheless, anaerobic glycolysis is unable to apport sufficient energy to sustain brain demands, depleting ATP stores, which results in failure of ATP dependent membrane ionic pumps [52]. Likewise, under chronic hypoxic conditions, there is an increase in oxidative stress, cell death, inflammation and the interruption of cerebral blood flow (CBF), directly affecting brain structure and function, leading to neuronal damage and death [51, 53, 54]. A normal average of CBF in adults is 44–45 ml/100 g/min. However, the CBF threshold for irreversible tissue damage (in TBI) occurs with the decrease to 15 ml/100 g/min [27, 41, 55] and cellular function is disrupted under 10 ml/100 g/min [56]. Neurons in the hippocampus, striatum and cortical regions die

after 5, 10, and 15–20 min of ischemia [57, 58], respectively.

*Benefits of Early Tracheostomy in TBI Patients DOI: http://dx.doi.org/10.5772/intechopen.93849*

*Advancement and New Understanding in Brain Injury*

TBI. The same reasoning is applied to the primary insult, which alters the cerebral metabolism and blood flow, resulting in cellular dysfunction and predisposition to

*: sodium; Glut: glutamate; Mg2+: magnesium; Ca2+: calcium; NMDA: N-methyl-*

*[35] TBI's neurometabolic cascade. (1) nonspecific depolarization; (2) neurotransmitter release - excitatory neurotransmitters (EAAs); (3) increase potassium efflux; (4) increased membrane pumping to restore homeostasis; (5) Hyperglycolysis to increase adenosine triphosphate (ATP) availability; (6) lactate accumulation; (7) calcium sequestration and mitochondria dysfunction resulting in oxidative metabolism; (8) decreased ATP production; (9) Calpain activation and apoptosis initiation. A - Axolemma and calcium influx. B - Neurofilament compaction. C - microtubule disassembly. D - axonal swelling and secondary*

The brain requires an uninterrupted supply of glucose and oxygen to maintain cellular viability and metabolism, consuming up to 20% of individual's total oxygen, with an average of cerebral metabolic rate of oxygen (CMRO2) between 3 and 3.8 ml/100 g/min [38–41]. Brain metabolism represents the largest source of energy consumption in the human body, since neuronal activity is supported through the production of adenosine triphosphate (ATP), which consumes nearly 60% of oxygen [42, 43]. When cerebral oxygenation is maintained, minimization of secondary

Brain's energy consumption fluctuates following neuronal activity on localized regions, and in order to provide adequate energy supply, neurovascular and neurometabolic coupling mechanisms are involved [42]. However, within hypoxia or low oxygen conditions, prolyl hydroxylase domain-containing enzymes (PHDs) are

cognitive impairment, seizures, hypotension and hypoxia [8].

*D-aspartate; AMPA: d-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid.*

**156**

**3.3 Oxygen and TBI**

*: potassium; Na+*

**Figure 2.**

*axotomy. K+*

insult can be achieved [44].

*The Monro Kellie doctrine.*

inhibited, reducing inproline hydroxylation, and altering availability of hypoxiainducible factor-1α (HIF-1α), which assist the metabolism adaptation and function during hypoxic conditions [42, 45–47]. Then, nuclear accumulation of HIF-1α enhance transcriptional activity within HIF-β, promoting gene expression that contains a hypoxia response element (HRE) [42, 46, 48]. Remarkably, HIF-2α is also induced in hypoxic brain, being expressed in astrocytes and endothelial cells [49]. This dysfunction is associated with poor neurological outcomes [50].

In order to cope hypoxia stress, this adaptive response converts cellular metabolism to anaerobic metabolism and inducts erythropoiesis, glycolysis, angiogenesis (by vascular endothelial growth factor), among other events [46, 48, 51]. Nevertheless, anaerobic glycolysis is unable to apport sufficient energy to sustain brain demands, depleting ATP stores, which results in failure of ATP dependent membrane ionic pumps [52]. Likewise, under chronic hypoxic conditions, there is an increase in oxidative stress, cell death, inflammation and the interruption of cerebral blood flow (CBF), directly affecting brain structure and function, leading to neuronal damage and death [51, 53, 54]. A normal average of CBF in adults is 44–45 ml/100 g/min. However, the CBF threshold for irreversible tissue damage (in TBI) occurs with the decrease to 15 ml/100 g/min [27, 41, 55] and cellular function is disrupted under 10 ml/100 g/min [56]. Neurons in the hippocampus, striatum and cortical regions die after 5, 10, and 15–20 min of ischemia [57, 58], respectively.

Considering that the brain is susceptible to ischemic injury, cerebral perfusion and oxygenation are vital to be maintained. In TBI setting, cerebral ischemia occurs due to different mechanisms: damage to blood vessels, hypotension, mechanical compression, and reduced perfusion (impaired autoregulation, which leads to greater propensity to hypoperfusion) [16, 59]. Hypoxemia can represent a relative risk of mortality of 75%, when associated with hypotension [7].

According to the Brain Trauma Foundation [60], patients with severe TBI present pulmonary aspiration risks or compromised airway function, and initial treatment goals include early airway protection, adequate supplemental oxygen, and circulation support, ensuring that adequate oxygen and blood flow are delivered to the brain [61].


*5.3.4 Ataxia with vitamin E deficiency*

Ataxia with vitamin E deficiency (AVED) is caused by variants in the APTT gene, which encodes the synthesis of the alpha-tocopherol transfer protein, responsible for incorporating vitamin E into very low-density proteins in the liver, which will transport it to the brain. The first manifestations are observed between 4 and 18 years of age in individuals with or without a history of malabsorption disorders [66]. Subjects with AVED develop a neurological phenotype very similar to Friedreich's ataxia [67]. AVED is characterised by progressive ataxia, areflexia, head tremor, loss of proprioception and retinitis pigmentosa [68]. Supplementation improves symptoms and prevents the progression of the disease [68].

### *5.3.5 Autosomal-recessive spastic ataxia of Charlevoix: Saguenay*

Autosomal-recessive spastics ataxia of Charlevoix Saguenay (ARSACS) is caused by mutations in the SACS gene which is located on chromosome 13q12.12 [69]. SACS gene encodes sacsin, a protein that has chaperone activity and interacts with the proteasome, but is also involved in mitochondrial function and affects axonal and dendritic transport [70]. The mean age at onset is approximately 6 years (range: 0–40 years) [71]. ARSACS is clinically characterised by early-onset progressive cerebellar ataxia, spasticity and peripheral neuropathy. Oculomotor disturbances and dysarthria are also common manifestations. A characteristic finding is the presence of yellow streaks of hypermyelinated fibres radiating from the edges of the optic disc seen on ophthalmologic examination. In the optical coherence tomography study, an increase in the thickness of the retinal fibre layer can be observed [72]. MRI imaging shows atrophy of the cerebellar vermis, atrophy of the posterior part of the corpus callosum, and linear hypointensities in the pons on T2 and T2-FLAIR [73].


**3. The architecture of the BDI ecosystem**

*Data Integrity and Quality*

**62**

**Authors** Saggi et al

Kim et al

**Table 12.**

*Comparative Analysis of curated survey papers with specific parameters.*

2020

Survey sample data approach to handle big

Recognition of overlapping units and

correction of misclassification errors

data integration

2018

**Year**

**Study Objectives**

To bridge the gap by big data processing

and analytics

**Advantages** A comprehensive review of big

data projects in terms of analytics,

management, and machine learning

**Disadvantages**

It is required to carry

Y

Y

N

Y

N

Y

out empirical research

based on qualitative

and quantitative

methods

Statistical inference

Y

Y

N

Y

N

Y

variance estimation

with non-parametric

propensity score

tuning is not covered

**1**

**2**

**3**

**4**

**5**

**6**

The outline architecture of the BDI ecosystem is shown in **Figure 5**. This architecture has four major components. These components are Data Sources, Data Operations, Virtual Databases and Business Intelligence. This architecture also shows the operations performed by each of these components. The business Big data would be collected from various distributed sources in different formats and sizes in Data Sources component. The Data Operations component shows the different operations which are performed on this heterogeneous Big data.

The Big data gathered from various types of physically distributed databases are integrated to form a unified logical virtual database. Business intelligence information is extracted from this virtual data source by performing the operations stated in Business Intelligence Component. This intelligent information would be used for real-time intelligent business decision-making process across the organization.

**Figure 5.** *The architecture of the BDI ecosystem.*


**Acknowledgements**

The authors would like to express our gratitude to Dr. Olorunnisola Kola Saheed for his effort in taking time to read through the manuscript and providing his valuable technical inputs.


**Preface**

Buildings play an indispensable role in urban development. As typical structures of transportation buildings, bridges serve as crucial nodes in connecting different regions, promoting economic growth, and ensuring social security. However, with the extension of their service life, the performance of bridges will inevitably decline. Performance monitoring and evaluation are crucial during the life cycle of bridges. The accelerating convergence of civil engineering, materials science, and artificial intelligence has sparked the interest of researchers from different disciplines in the emerging field of bridge state perception.

This book covers topics on condition monitoring and assessment of bridges, featuring 13 papers. These studies provide some novel methods, models, and technological applications for bridge condition monitoring and assessment, which are of great significance for the design, construction, and assessment of bridges.

> **Jingzhou Xin, Yan Jiang, Bo Wu, and Simon X. Yang** *Editors*


*8.4. Smoking*

While it is well-established that smoking increases risk for poor fetal growth, its relation to preeclampsia is more controversial and not consistent with the placental origins hypothesis considering that a meta-analysis showed that smoking is inversely associated with the incidence of preeclampsia [85]. However, smoking is known to increase maternal carbon monoxide levels, which inhibit levels of sFlt-1 and increase those of PlGF—the opposite of what occurs in preeclampsia [86,87]. Furthermore, carbon monoxide also has a protracted hypotensive e ffect, which would decrease the diagnosis of high blood pressure and, as a consequence, paradoxically reduce the prevalence of preeclampsia whilst increasing the risk of poor fetal growth [88].


*Article* **Spectral-Spatial Interaction Network for Multispectral Image and Panchromatic Image Fusion**

**Zihao Nie 1, Lihui Chen 1, Seunggil Jeon 2 and Xiaomin Yang 1,\***

**\*** Correspondence<EMAIL_ADDRESS>
**Abstract:** Recently, with the rapid development of deep learning (DL), an increasing number of DL-based methods are applied in pansharpening. Benefiting from the powerful feature extraction capability of deep learning, DL-based methods have achieved state-of-the-art performance in pansharpening. However, most DL-based methods simply fuse multi-spectral (MS) images and panchromatic (PAN) images by concatenating, which can not make full use of the spectral information and spatial information of MS and PAN images, respectively. To address this issue, we propose a spectral-spatial interaction Network (SSIN) for pansharpening. Different from previous works, we extract the features of PAN and MS, respectively, and then interact them repetitively to incorporate spectral and spatial information progressively. In order to enhance the spectral-spatial information fusion, we further propose spectral-spatial attention (SSA) module to yield a more effective spatialspectral information transfer in the network. Extensive experiments on QuickBird, WorldView-4, and WorldView-2 images demonstrate that our SSIN significantly outperforms other methods in terms of both objective assessment and visual quality.

**Keywords:** deep learning; spectral-spatial interaction network; spectral-spatial attention; pansharpening