Pros And Cons Of Human Diseases

Currently the only existing forms of smallpox are in two secure laboratories; the CDC facility in Atlanta and Russian State Research Centre for Virology and Biotechnology in Koltsovo. These samples were scheduled to be destroyed in 1993 but there was and still is much debate about what should happen to them.

With all living organisms, a process known as cell respiration is integral in order to provide the body with an essential form of energy, adenosine triphosphate (ATP). Oxygen, although an essential part of this process, can form reactants from colliding with electrons associated with carrier molecules. (pb101.rcsb.org, 2017). Hydrogen peroxide is an integral product of this reaction but is known to impose negative effects on the body if high levels are introduced. Explicitly, this reaction is caused “If oxygen runs into (one of these) carrier molecules, the electron may be accidentally transferred to it. This converts oxygen into dangerous compounds such as superoxide radicals and hydrogen peroxide, which can attack the delicate sulphur atoms and metal ions in proteins.” (pdbh101.rcb.org, 2017). Research has suggested that the hydrogen peroxide can be converted into hydroxyl radicals, known to mutate DNA, which can potentially cause bodily harm due to DNA’s role in the synthesis of proteins. These radicals can cause detrimental effects on the human body, and studies have suggested a link to ageing. Due to the harmful effects of these H2o2, it is important that the body finds a way to dispose of hydrogen peroxide before concentrations are too great.

Why are humans stuck how they are? Why do some have lethal flaws? Why do theses flaws exist? The correct answer is they don’t have to: Human genetic engineering can solve some of theses lethal issues now and can solve more in the future. It can help the next generation experience what everyone strives to achieve. Human genetic engineering research should continue because it can save people's lives, improve human’s lives and improve the lives of the next generation of children.

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

Smallpox is among the most feared diseases around the world; it is an infectious disease spread through transmission of the valiola vera virus. In its 12,000 years of recorded history, it has been responsible for more human deaths than any other disease and in the 20th century alone, an estimation of 300-500 million people died from the virus (Oddee, 2007). In the present day, there are no uncontained samples of smallpox, with the only two known remaining specimens of various strains held in high security laboratories in Russia and America (Williams, 2014). There is much debate whether or not the samples should be stored for future use, or whether it should be completely eradicated to minimize immediate risk. In this investigation, the ethical

As well as this, Nox2 affects the level of HIF-2a, which is responsible for anti-oxidative activity, and decreases it that lead to increased oxidative responses and neuronal

There are links between high serum urate, hyperuricemia, and many inflammatory diseases, yet the mechanism is obscure. For humans, purine and ATP are broken down to urate, which builds up in plasma because we lack the enzyme uricase to promote its excretion as allantoin. Urate may benefit our health by acting as an antioxidant that scavenges reactive oxygen species. Yet, hyperuricemia is associated with gout, metabolic syndrome and cardiovascular disease. These inflammatory diseases are characterized by inflammation and oxidative stress. During oxidative stress urate is oxidized to several reactive electrophiles including urate hydroperoxide. This novel oxidant could promote the pro-oxidant effects of urate.

Chapter 9 in Diseases and Human Evolution discusses tuberculosis in humans and cattle. The first thing that comes to mind when I think of tuberculosis is the visits to the veterinarian whenever we wanted to cross state lines with livestock from our farm. Though Arizona is considered a tuberculosis free state, New Mexico is not. Even though our livestock was coming out of a TB free state, we still were required to take our goats to the vet and have blood draws done. The chapter reminded me of the relevance of tuberculosis in society today, both in livestock and humans, and how it is still a disease we are struggling to control in some countries, even though it has been around for several thousand years.

Many animal studies have shown that lead is capable of causing oxidative stress in many organs (Patra et al., 2001). Toxicity of lead is mainly attributed to the induction of oxidative stress by disruption of the pro-oxidant/anti-oxidant balance, elevation of reactive oxygen and nitrogen species (ROS and RNS, respectively) such as superoxide radicals, hydrogen peroxide, hydroxyl radicals and lipid peroxides, and nitric oxide (Kumar and Reddy, 2012). Currently, N-acetyl-L-cysteine (NAC), derives from L-Cysteine and the precursor of glutathione (GSH), is a well-established cyto-protective drug against drugs induced hepatotoxicity and nephrotoxicity (Whyte et al., 2007; Akbulut et al., 2014), where it exerts antioxidant properties. L-Cysteine was utilized as a chelator of heavy metal to conserve against oxidative stress and inhibit damage to cells and tissues. L-cysteine, a sulfur-containing amino acid, is a nutritionally occurring non-essential amino

A recent study investigated the effect of H2S deficiency on endothelial NO synthase (eNOS) function, NO production, and ischemia / reperfusion injury by on CSE- knocked out mice and control [12]. Significant Lower H2S levels among CSE- knocked out mice was confirmed by gas chromatography. From oxidative stress perspective; their results revealed significant higher levels of malondialdehyde (indicator for lipid peroxidation) in heart muscle among CSE- knocked out mice compared to

Alzheimer’s disease (AD) is a debilitating illness of the nervous system, affecting millions of geriatric population worldwide. Numerous factors are involved in the disease etiology viz. tau phosphorylation, amyloid β protein (Aβ) accumulation, lipid dysregulation, oxidative stress and inflammation. Among all factors oxidative stress plays a central role in the pathogenesis of AD leading to neuronal dysfunction and cell death (1). Oxidative stress is caused due to the increased production of reactive oxygen species (ROS) which denatures biomolecules such as proteins, lipids and nucleic acids through pathological redox reactions(2). Increased oxidative stress also results in excessive lipid peroxidation, weakening the cell membranes, causing

The generation of reactive oxygen species (ROS) has long been recognized as an important contributor to cisplatin-induced hearing loss (10-14). Antioxidants have shown good promise initially for treating cisplatin-induced hearing loss. However, concerns have been raised that these agents could inhibit the anti-tumor action of cisplatin (15), reducing interest in developing anti-oxidants as otoprotectants. Recent studies have shown that cisplatin-induced ROS stimulate the activation of mitogen activated protein kinase (MAPK) pathway which in turn activates

The pro-oxidant effects of urate could be the link between hyperuricemia and inflammatory disease, yet the mechanism is poorly understood. In humans urate builds up in our serum from dietary purine. Urate is an antioxidant of reactive oxygen species, yet, high serum urate (hyperuricemia) is associated with gout, metabolic syndrome and cardiovascular disease. The link between hyperuricemia and inflammatory disease is oxidative stress. Urate acts as a pro-oxidant by generating reactive oxygen species and promoting the oxidation of LDL. Urate’s switch from antioxidant to pro-oxidant could be concentration dependent, ergo the ‘dose makes the poison’.

“He will soon learn to have a thick skin about what he has” - my senior dermatologist told as we walked out of the unit for children with congenital skin disorder, in which skin peels off even with slightest friction. I had gone into dermatology for its challenging complex diseases and hoping for a future with intellectual explorations. I was shocked to see the lack of structure to deal with the psychological aspects of patients. Often, I sat besides bewildered patients, listening to their stories of stigmatization and rejection in the community because of their appearance. I believed in adapting individual approaches to different personality types and cultural backgrounds. I was unwilling to accept everything at its face value but felt satisfied seeking for causes, asking questions, and above all analyzing the biological, psychological and social aspects of diseases. As I analyzed, I saw each disease being defined by the individual’s experience - her/his way of “being in the world”.

The involvement of oxidative stress in cancer development and promotion is considered by many cancer researchers. The cause of oxidative stress may be an overproduction of ROS or insufficient antioxidant capacity (29). Thus, in this study we determined the enzymatic activities of ARE and AChE along with MDA and TAC levels in the patients with breast cancer. In the current study, the erythrocytic AChE activity was significantly lower in MBT compared to the control group (P = 0.003) . There was no significant difference between the BBD and control groups, as well as, MBT and BBD groups. Some studies have presented the involvement of AChE in oxidative stress that supports our results . Molochkina et al . documented ROS mediated inhibition of