6
Results and Discussion
The UVGI from sunlight can be trapped by using the outer glazing wall surface of
a building or house considering the photon energy emission on the glazing wall
surface area [15, 16, 6]. The glazing wall surface area has the ability to have
consistent solar irradiance emission, and UVGI generation from sunlight has got a
unique dynamic mode of solar energy penetration into the outer glazing wall
surface. Simply, the UVGI is being trapped by the glazing wall surface from the
electromagnetic radiation (EM) of the light spectrum in relation to short-wavelength
photon-induced solar energy penetration on the glazing wall surface. Thus, this EM
radiation is being determined by the wavelength of UVGI sinusoidal monochromatic waves, which in turn is being classified by the EM spectrum of the photon
particles by using PHOTO-ELECTRO-METER.
Subsequently, the EM waveform is being determined using the spectral analysis
of photonic frequency considering its energy content which is the spectral density
of the solar energy. Thus, the random electromagnetic radiation of UVGI is being
determined by the wideband forms of solar radiation from the unique sinusoidal
wave field of the photon energy.
The EM field of the solar energy thus suggests that once the outer glazing wall
surface emits light between 254 and 280 nm it allows to add a mass-term sunlight
energy transformed into UVGI naturally. Since UVGI has the extraordinary ability to destroy the DNA and/or RNA of the fatal pathogens in seconds regardless
of the pathogens’ frequent changing mechanism of mutants and pathways, the
UVGI light wavelength implantation suggests that EM field has been paved for
the solar irradiance to penetrate uniformly into the pathogen bodies. Since DNA
and/or RNA of the pathogens is composed of double- or single-strand bonds consisting of chemically coded nucleotide adenine (A), thymine (T), guanine (G),
and cytosine (C) which are very sensitive to UBGI, UVGI light penetration into
their bodies directly interferes these bonds between the nucleotides in the DNA
and/or RNA and completely damages their cyclobutane pyrimidine dimers (CPD)
and 6–4 pyrimidine pyrimidone photoproducts (6–4PPs), and its Dewar isomers
[5, 9]. Simply it can be explained that once UVGI penetrates into the pathogen
bodies, it forms the CPDs which are the two adjacent pyrimidine bases (thymine—TT or cytosine—CC) and it becomes covalently linked to produce a cyclic
ring structure and thus 6–4PPs result from a single covalent bond formed between
the 5′ end of C6 and 3′ end of C4 of adjacent pyrimidines [17, 18]. This leads to
the formation of an unstable oxetane or azetidine intermediate end base of the
thymine or cytosine dimers. Consequently, spontaneous rearrangement of these
intermediate ends gave rise to 6–4PP and eventually the pyrimidine dimers
caused a kink into the DNA strands, halting transcription and protein synthesis
(Fig. 1.2). The 6–4 pyrimidine pyrimidone adducted isomerization and caused
severe damage to cellular function (Fig. 1.2). Subsequently, UVGI radiation does
additional function to cause damage to the DNA and/or RNA via absorption of
photon energy by cellular chromophores to enforce to generate the reactive
1 Design a Better World
Results and Discussion
The UVGI from sunlight can be trapped by using the outer glazing wall surface of
a building or house considering the photon energy emission on the glazing wall
surface area [15, 16, 6]. The glazing wall surface area has the ability to have
consistent solar irradiance emission, and UVGI generation from sunlight has got a
unique dynamic mode of solar energy penetration into the outer glazing wall
surface. Simply, the UVGI is being trapped by the glazing wall surface from the
electromagnetic radiation (EM) of the light spectrum in relation to short-wavelength
photon-induced solar energy penetration on the glazing wall surface. Thus, this EM
radiation is being determined by the wavelength of UVGI sinusoidal monochromatic waves, which in turn is being classified by the EM spectrum of the photon
particles by using PHOTO-ELECTRO-METER.
Subsequently, the EM waveform is being determined using the spectral analysis
of photonic frequency considering its energy content which is the spectral density
of the solar energy. Thus, the random electromagnetic radiation of UVGI is being
determined by the wideband forms of solar radiation from the unique sinusoidal
wave field of the photon energy.
The EM field of the solar energy thus suggests that once the outer glazing wall
surface emits light between 254 and 280 nm it allows to add a mass-term sunlight
energy transformed into UVGI naturally. Since UVGI has the extraordinary ability to destroy the DNA and/or RNA of the fatal pathogens in seconds regardless
of the pathogens’ frequent changing mechanism of mutants and pathways, the
UVGI light wavelength implantation suggests that EM field has been paved for
the solar irradiance to penetrate uniformly into the pathogen bodies. Since DNA
and/or RNA of the pathogens is composed of double- or single-strand bonds consisting of chemically coded nucleotide adenine (A), thymine (T), guanine (G),
and cytosine (C) which are very sensitive to UBGI, UVGI light penetration into
their bodies directly interferes these bonds between the nucleotides in the DNA
and/or RNA and completely damages their cyclobutane pyrimidine dimers (CPD)
and 6–4 pyrimidine pyrimidone photoproducts (6–4PPs), and its Dewar isomers
[5, 9]. Simply it can be explained that once UVGI penetrates into the pathogen
bodies, it forms the CPDs which are the two adjacent pyrimidine bases (thymine—TT or cytosine—CC) and it becomes covalently linked to produce a cyclic
ring structure and thus 6–4PPs result from a single covalent bond formed between
the 5′ end of C6 and 3′ end of C4 of adjacent pyrimidines [17, 18]. This leads to
the formation of an unstable oxetane or azetidine intermediate end base of the
thymine or cytosine dimers. Consequently, spontaneous rearrangement of these
intermediate ends gave rise to 6–4PP and eventually the pyrimidine dimers
caused a kink into the DNA strands, halting transcription and protein synthesis
(Fig. 1.2). The 6–4 pyrimidine pyrimidone adducted isomerization and caused
severe damage to cellular function (Fig. 1.2). Subsequently, UVGI radiation does
additional function to cause damage to the DNA and/or RNA via absorption of
photon energy by cellular chromophores to enforce to generate the reactive
1 Design a Better World