Biological Defenses Research Articles

Good Health and Well- being in the Different Current Treatment Strategies for Coronavirus Disease 2019 (COVID-19): A mini Review

People of all ages must lead healthy lives and advance wellbeing in order for sustainable development to occur. The global economy is being weakened by COVID-19, which is also disrupting the lives of billions of people worldwide. By the end of 2019, the novel coronavirus that causes severe acute respiratory syndrome (SARS-CoV2) abruptly began to spread, giving rise to the term coronavirus disease 2019 (COVID19). There is currently no proven treatment for COVID-19. Finding efficient therapies is urgently needed to care for patients and control the spread of SARS-CoV2 among humans. The treatment medicines that may be employed to fight the SARS-CoV2 infection were emphasized for the current review. Numerous medications have been repurposed for COVID19 therapy since the disease's emergence. Regarding the treatment of COVID-19, existing medications such as chloroquine (CQ), Along with chloroquine, We also investigated monoclonal antibodies, restorative plasma, Chinese herbal treatment, and natural compounds, including remdesivir, hydroxychloroquine (HCQ), and nucleoside analogues. Although initial clinical trials demonstrated that CQ/HCQ had antiviral activities, further investigations revealed significant debate over its suitability for treating COVID-19. Preventing the virus from interacting with human cell receptors for angiotensin converting enzyme 2 is one of these medicinal medicines' biological defenses against SARS-CoV2. Many of studies about the role of nanomaterials in treating Covid-19, based on their unique physical, chemical and biological properties, which depend on shape and size, as the use of nanomaterials is considered a promising future to eliminate viruses, including Covid-19.

Biological Defenses and Regulation of Epithelial Tumor Development by the Gastric Gland Mucus-type Glycan

Biological Defenses and Regulation of Epithelial Tumor Development by the Gastric Gland Mucus-type Glycan

Modeling of Laboratory Animals Exposure Conditions behind Local Concrete Shielding Bombarded by 650-MeV Protons

Purpose: To estimate the radiation fields formed after the passage of high-energy protons through the concrete protection for subsequent radiobiological experiments on animals on this model.
 Material and methods: The results of the calculation of the secondary characteristics of a field of mixed radiation behind the local concrete with thickness 20, 40, and 80 cm, bombarded by a proton beam of 650 MeV at the JINR Phasotron and experimental estimation of the values of the absorbed dose phantoms of mice irradiated for protection during radiobiological experiments. 
 The calculation was performed by the Monte Carlo method according to the MCNPX program for secondary protons, neutrons, π-mesons, and gamma rays. To verify the adequacy of calculations was performed the comparison of calculated and measured in the experiment spatial distribution of activation threshold detectors for aluminum protection, as well as a comparison of the calculated values of absorbed dose for radiation protection with the results of absorbed dose measurements with a diamond detector.
 Results: The calculations made it possible to obtain the characteristics of the fields of mixed secondary radiation behind local concrete shields of different thickness irradiated with protons with an energy of 650 MeV and to estimate the values of absorbed doses in the irradiation sites of mice in the radiobiological experiment. The reliability of the calculations was confirmed by experimental verification of the activation of aluminum threshold detectors behind a 20 cm thick protection, as well as direct measurements using a diamond detector. 
 Conclusion: The calculated assessment of radiation fields formed after protons pass through the concrete protection and its comparison with the results of radiation dose measurements for the subsequent radiobiological experiment on animals on this model in the interests of designing protective structures on the Moon and other space bodies, as well as biological defenses on charged-particles accelerators.

A New Exposure Metric for the Cumulative Effect of Short-term Peaks of Exposure to Traffic-related Ultrafine Particles

Introduction Traffic-related ultrafine particles (UFPs) can cause adverse health outcomes through inflammatory reactions. Current epidemiology studies focus on either short-term health outcomes associated with UFP levels averaged over days or weeks, or long-term outcomes associated with a long-term (annual or longer) average exposure to UFP. We hypothesize that frequent and repeated exposure to short-term UFP peaks that last for just one or a few hours could overwhelm human’s biological defenses, which may result in long-term health effects. We propose a new exposure metric for measuring the cumulative effect of the peaks. Method Our study uses data collected by the Community Assessment of Freeway Exposure and Health (CAFEH) project, which recruited 704 participants from six “near-highway” or “urban background” neighborhoods in the Greater Boston Area between 2009 and 2012. The CAFEH project developed land use regression models to estimate hourly averages of ambient UFP level throughout the study areas, and applied time-activity adjustment to calculate the adjusted hourly estimate. Our alternative metric is the cumulative peak exposure, determined by the intensity (the 99th percentile of an individual’s adjusted hourly UFP estimates) and the frequency (the number of hours with the UFP level higher than the 99th percentile of all adjusted hourly UFP estimates of all participants) of UFP peaks. Results The cumulative peak exposure does not always correlate well with the annual average, especially in certain near-highway neighborhoods. (Pearson’s R between the intensity of UFP peaks and the annual average of hourly UFP estimates ranges from 0.33 to 0.98.) Thus, it appears that there is still sufficient variation within the residents’ UFP peak exposure after holding their annual average constant, which suggests they are distinct measurements. Conclusion Measuring the cumulative effect of peak exposures may provide a new exposure assessment metric that could be tested for association with long-term health outcomes.

Reproductive Toxicity of T Cells in Early Life: Abnormal Immune Development and Postnatal Diseases.

Immunity is a balanced status with adequate biological defenses to recognize and fight "non-self", as well as adequate tolerance to recognize "self". To maintain this immune homeostasis, a well-organized T cell immune network is required, which in part depends on the well-controlled development of alternative effector T cells, with different cytokine repertoires. Recent researches have pointed that developing fetal T cells network is a remarkably sensitive toxicological target for adverse factors in early life. Epidemiological and experimental studies showed an inseparable relationship between T cell developmental toxicity and immune diseases in adults. Considering that the inflammatory and immune disorders have become a growing health problem worldwide, increasing attention is now being paid to the T cell developmental toxicity. We propose that adverse factors may have programming effects on the crucial functions of immune system during early life which is critical for fetal T cell development and the establishment of the distinct T cell repertoires balance. The permanently disturbed intrathymic or peripheral T cell development may in turn lead to the immune disorders in later life. In this manuscript, we reviewed how adverse factors affected T cell development in early-life with the consequence of the immune dysfunction and immune diseases, and further elucidate the mechanisms. These mechanisms will be helpful in prevention and treatment of the increased prevalence of immune diseases by interfering those pathways.

Biological Defenses against Ultra-Violet, Visible Light, and Near-Infrared Exposure

Objective: Humans are increasingly exposed to artificial light and electromagnetic wave radiation, in addition to solar radiation. Many studies have shown the biological effects of ultra-violet and near-infrared exposure, but few have extensively investigated the innate biological defenses within human tissues against visible light and near-infrared exposure. Herein, we investigated spectral properties of endogenous human biological defenses against ultra-violet to near-infrared. Methods: A double-beam spectrophotometer (190 - 2700 nm) was used to measure the transmission spectra of a saline solution used to imitate perspiration, and oil to imitate sebum, as well as human skin, blood, adipose tissue, and muscle. Results: Saline (thickness, 0.5 mm) blocked 27.5% - 98.6% of ultra-violet, 13.2% - 34.3% of visible light, and 10.7% - 99.8% of near-infrared. Oil (thickness, 0.5 mm) blocked 50.5% - 100% of ultra-violet, 28.7% - 54.8% of visible light, and 19.0% - 98.3% of near-infrared. Blood thicknesses of 0.05 and 0.5 mm blocked over 97.8%, 100% of ultra-violet, over 94.6%, 99.7% of visible light, and over 75.8%, 99.4% of near-infrared, respectively. Skin thicknesses of 0.25 and 0.5 mm blocked over 99.4%, 100% of ultra-violet and over 94.3%, 99.7% of visible light, and over 74.7%, 93.5% of near-infrared, respectively. Adipose tissue thickness of 0.25 and0.5 mm blocked over 98.3%, 100% of ultra-violet, over 94.7%, 99.7% of visible light, and over 88.1%, 98.6% of near-infrared, respectively. Muscle thickness of 0.25 and0.5 mm blocked over 95.4%, 99.8% of ultra-violet, over 93.1%, 99.5% of visible light, and over 86.9%, 98.3% of near-infrared, respectively. Conclusions: Humans possess endogenous biological protection against ultra-violet, visible light and near-infrared exposure on multiple levels, including through perspiration, sebum, blood, skin, adipose tissue, and muscle. Since solar and artificial radiation affects human tissues, biological defenses made of biological materials may be induced to protect subcutaneous tissues against these wavelengths.

Oxidative damage and the pathogenesis of menopause related disturbances and diseases.

The postmenopausal phase of life is frequently associated in women with subjective symptoms (e.g. vasomotor) and real diseases (atherosclerosis with coronary ischemia, osteoporosis, Alzheimer-type neurodegeneration, urogenital dystrophy), which together determine the post-menopausal syndrome. Observations that oxidative damage by reactive oxygen/nitrogen species in experimental models can contribute to the pathogenesis of these disturbances stimulated research on the relationships between menopause, its endocrine deficiency, oxidative balance and the "wellness" in postmenopausal life. The connection among these events is probably due to the loss of protective actions exerted by estrogens during the fertile life. Most recent studies have revealed that estrogens exert an antioxidant action not by direct chemical neutralization of reactants as it was expected until recently but by modulating the expression of antioxidant enzymes that control levels of biological reducing agents. Also nutritional antioxidants apparently act by a similar mechanism. From this perspective it is conceivable that a cumulative control of body oxidant challenges and biological defenses could help in monitoring between "normal" and "pathological" menopause. However, as clinical studies failed to confirm this scenario in vivo, we have decided to review the existing literature to understand the causes of this discrepancy and whether this was due to methodologic reasons or to real failure of the basic hypothesis.

A mitochondrial superoxide theory for oxidative stress diseases and aging.

Fridovich identified CuZnSOD in 1969 and manganese superoxide dismutase (MnSOD) in 1973, and proposed ”the Superoxide Theory,” which postulates that superoxide (O2•−) is the origin of most reactive oxygen species (ROS) and that it undergoes a chain reaction in a cell, playing a central role in the ROS producing system. Increased oxidative stress on an organism causes damage to cells, the smallest constituent unit of an organism, which can lead to the onset of a variety of chronic diseases, such as Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis and other neurological diseases caused by abnormalities in biological defenses or increased intracellular reactive oxygen levels. Oxidative stress also plays a role in aging. Antioxidant systems, including non-enzyme low-molecular-weight antioxidants (such as, vitamins A, C and E, polyphenols, glutathione, and coenzyme Q10) and antioxidant enzymes, fight against oxidants in cells. Superoxide is considered to be a major factor in oxidant toxicity, and mitochondrial MnSOD enzymes constitute an essential defense against superoxide. Mitochondria are the major source of superoxide. The reaction of superoxide generated from mitochondria with nitric oxide is faster than SOD catalyzed reaction, and produces peroxynitrite. Thus, based on research conducted after Fridovich’s seminal studies, we now propose a modified superoxide theory; i.e., superoxide is the origin of reactive oxygen and nitrogen species (RONS) and, as such, causes various redox related diseases and aging.

Nanotechnology for Chemical and Biological Defense - By Margaret E. Kosal

Nanotechnology for Chemical and Biological Defense - By Margaret E. Kosal

Xenohormesis: Sensing the Chemical Cues of Other Species

Many plant molecules interact with and modulate key regulators of mammalian physiology in ways that are beneficial to health, but why? We propose that heterotrophs (animals and fungi) are able to sense chemical cues synthesized by plants and other autotrophs in response to stress. These cues provide advance warning about deteriorating environmental conditions, allowing the heterotrophs to prepare for adversity while conditions are still favorable.

Theoretical and Experimental Approaches to Address Possible Thresholds of Response in Carcinogenicity

The determination and utilization of the actual low dose-response relationship for chemical carcinogens has long interested toxicologists, experimental pathologists, modelers and risk assessors. To date, no unequivocal examples of carcinogenic thresholds in humans are known. However, at least 5 examples of thresholds of preneoplastic foci or tumors have been observed in animals. The two largest dose-response studies utilized 20,880 mice (2-acetylaminofluorene) and 7,200 rainbow trout fry (aflatoxins). In both of these studies linear relationships were observed for DNA adducts and for liver tumors. A threshold relationship was observed for 2-acetylaminofluorene induced mouse urinary bladder cancer. Other comprehensive dose-response studies have examined the chemicals 2-amino-3,8-dimethylimidazo[4,5-f]-quinoxaline, 2-amino-1-methyl-6-phenolimidazo[4,5-b]pyridine and diethylnitrosamine. Taken collectively, the DNA adduct data for these 6 well studied chemicals are fairly linear. The foci and tumor data show either supralinear, linear or threshold curves, making it difficult to generalize. All the 6 studied chemicals cause multiple biological effects including genotoxicity, cytotoxicity and cell proliferation in complex dose and time dependent patterns that are not fully understood. We do know that there are multiple possible biological defenses (at least 7 pharmacokinetic and 7 pharmacodynamic) against the development of cancer. Currently, we have limited scientific and regulatory understanding of chemicals that act simultaneously or sequentially via both linear and nonlinear carcinogenic pathways (genotoxic and nongenotoxic). If an 100% experimental approach is used to elucidate the dose-response of chemicals of dual carcinogenic dose-response properties (linear and non linear), this would require studying 2 or more such chemicals in a large scale coordinated fashion employing at least 1,000 animals, 5 different treatment groups, 7 different study parameters and 8 different scientific disciplines.

Physiologically Based Modeling of Nonsteady State Dermal Absorption of Halogenated Methanes from an Aqueous Solution

Dermal absorption of organic chemicals from aqueous solutions are a concern in both the workplace and the home. Organic chemicals are generally not very soluble in water and the exposure may never reach steady state because the concentration of chemical decreases during the exposure.In vivoanimal studies which mimic human exposures, but are carefully controlled, are one way to measure absorption. Whole animal studies are superior to excised skin measurements, because the physiological responses including blood flow, metabolism, and biological defenses are present. In this study, we develop a physiologically based model for nonsteady state exposures to organic chemicals in aqueous solutions. A key feature of this model is a compartment which describes loss of chemical in the exposure solution due to absorption into the skin. We exposed rats to a range of aqueous concentrations of dibromomethane (2.4 to 9.4 mg/ml) and bromochloromethane (3.6 to 12.8 mg/ml) and measured blood concentrations during 24-hr exposures. The blood concentrations peaked at about 1–2 hr and diminished to nearly nothing at 24 hr. Physiologically based models were used to estimate permeability coefficients for each of the exposures, although none of the exposures reached steady state due to the decreasing concentration of chemical on the surface of the skin. A constant permeability coefficient adequately described the blood concentrations during the prolonged exposure. Physiologically based models can be used to estimate permeability coefficients when the concentration of chemical on the skin is not constant. These permeability parameters can subsequently be used for assessing the risks in human exposure situations.

Toxicity of Heavy Metals and Biological Defense: Principles and Applications in Bioinorganic Chemistry-VII

Discussion of the adverse/toxic effects of metallic elements, particularly the heavy metals (Cd, Pb, Hg), and biological defenses against these species.

Early childhood, the critical stage in human interactions with disease and culture

This paper examines the continuous interactions between evolving Homo sapiens and the multiple health-related factors that significantly have shaped the course of human evolution. Early childhood, particularly the precarious post-weaning stage, is seen to be the most critical period determining survival in disease confrontations. Selection for the fundamental biological defenses predated human emergence; however, human cultures add a significant dimension to disease patterns. Specific configurations of disease are intimately related to human economies, social structure and political interactions as well as macro- and micro-environmental factors.

Nonmilitary Defense: Chemical and Biological Defenses in Perspective

This publication of the American Chemical Society directs attention to the problems of defense against chemical and biological warfare (CW-BW). The book is a compilation of an important portion of our civil defense programs and, as suggested early in the text, it portrays a defensive rather than offensive philosophy. It is a concrete demonstration of assuming responsibility to our families, our neighbors, and ourselves. Less apathy and more public support for sound civil defense programs should fulfill our moral responsibilities better than withdrawal in horror. An eminent American physician who had just spent a full day being briefed on the nature of CW-BW remarked, "Now that I've seen the potentialities of this type of warfare, I am no longer afraid of atomic warfare." This is an oversimplification, but it points up the fact that in this type of warfare a new concept is involved. An enemy may be able to

Defense Against CW and BW

Summary of several papers given at the Symposium on Chemical and Biological Defenses in Perspective of the American Chemical Society, in Cleveland, Ohio, April 8, 1960.

The BW Threat

Below is a summary of a paper given by Dr. LeRoy D. Fothergill, at the Symposium on Chemical and Biological Defenses in Perspective of the American Chemical Society, in Cleveland, Ohio, April 8, 1960. Dr. Fothergill has been associated with the army biological warfare laboratory, Fort Detrick, Frederick, Maryland.