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Causes and Effects of Unhealthy Blood in the Human Body

Explain the causes and effects of unhealthy blood in the human body
The blood is composed by red cells (erythrocytes), white cells (leucocytes) and platelets (thrombocytes), suspended in a pale yellow fluid as known as plasma (Titmuss, 1970 and Pallister and Watson, 2011). In the initial of the 20th century, Karl Landsteiner, a scientist in Vienna, “took red cells suspensions and serum from six men in his laboratory (including himself); by mixing them in different combinations and noting the agglutination patterns, he first described the A, B and 0 blood groups” (Iles and Docherty, 2012 and Daniels and Bromilow, 2014). Because of that, Landsteiner received the Nobel Prize in 1930. According to Ilyas, Akram and Nawaz (2014), in the moment, researchers present approximately 20 different blood groups and 400 antigens have been discovered. But the most respectful among them is ABO blood group antigens discovered by Karl Landsteiner. “Blood group systems are all related to groups of proteins that have specific psychological function” (Pallister and Watson, 2011). This specific function happened because the molecule cannot be an antigen if it is not recognised by an antibody (Daniels and Bromilow, 2014). Antibodies are formed by a blood protein in result of and counteracting a specific antigen (OMDT2). For instance, ABO antibodies are basically IgM (Knight, 2013). Our body need all this working together in harmony. If some of their components are abnormal, can be dangerous for our body health. The causes of unhealthy blood come over from genetic or environment and can develop diseases as anaemia and in cardiovascular system.
First of all, one important cause of unhealthy blood can drop by genetic influential. All genes coded by proteins actually implicates varies DNA elements affecting transcription and expression (Dodge and Rutter, 2011). A massive among of genes are pleiotropic which means that have numerous effects. For example, the effects of ApoE4 gene in connection with Alzheimer’s disease can come over by an ageing, but also cholesterol metabolism. The biological pathways are always affected by genes which are significant for multiple variations. “Genetic effects are crucially dependent on gene expression (which is subject to environmental influences, chance variation and background genetic effects)” (Dodge and Rutter, 2011). This means that if researchers only look at the DNA, they cannot make conclusions. However, it is an extremely important part to make it.
Second prominent cause of unhealthy blood can come over by the environment. A great quantity of cases shows that the environment causes disease (Ahmed et al., 2006). However, many researchers alleged that environmental causes are erroneous because they fail to consider a lot of variability. “Nongenetic effects may involve developmental (perturbations brought about through stochastic effects) rather than specific environmental hazards” (Ahmed et al, 2006). Although, they probably miss the fact that environmental characteristics consist of urban aspects like neighbourhood safety, healthy food availability and social capital (Berke et al., 2007; Clarke et al, 2008). In addition, researchers suggested that environment is not always gruesome. They said that the environment can bring a positively influence in health too (Berke et al., 2007).
However, environment can, at least in some cases, triumph over biology. Sometimes, without a specific environment the disease cannot manifest. Dodge and Rutter (2011) affirmed that there are three important reasons for supposing that genetics x environment can be both relatively similar and fully influential. This three mainly reasons was: “genetically influenced differential response to the environment constitutes the mechanism thought to give rise to evolutionary change” (for instance, the evolution in pathogenic organism of resistance to antibiotics), “ to suppose that there is no genetics x environment would see to require the assumption and certainly one that is highly implausible” and “a wide range of human and animal naturalistic and experimental studies have shown huge heterogeneity in response to all manner of environmental features, both physical and psychosocial” (Dodge and Rutter, 2011). However, both genetic and environment can influence, together, the health of blood.
The consequence of an unhealthy blood can be Anaemia. “Anaemia is functionally defined as an insufficient red cell mass to adequately deliver sufficient oxygen to peripheral tissues to meet physiological needs” (Pallister and Watson, 2011). It can be classified according to mean cell volume and divided into microcytic anaemia (small cells – low cell volume), normocytic anaemia (cells of normal size – normal cell volume) and macrocytic anaemia (large cells – high cell volume) (Iles and Docherty, 2012; Bain et al., 2012; Ahmed et al, 2006). Microcytic anaemia is caused by iron deficiency. While the body’s iron stores are depleted, normal haemoglobin levels are controlled. When this happen, haemoglobin levels start to fall and then it can be said that the anaemia is present. Hereditary haemochromatosis is a defective iron absorption which is a hereditary. This can be inherited and it is an autosomal recessive disorder (Iles and Docherty, 2012). In addition, normocytic anaemia is caused by acute haemorrhage, chronic diseases and bone marrow infiltration. The treatment of the cause is always the best solution. And the macrocytic anaemia can be subcategorized into megaloblastic (deficient in vitamin B12 and in folate) and nonmegaloblastic (normal in pregnancy) (Iles and Docherty, 2012; Murphy and Pamphilon, 2009). Anaemia is a symptom. Further evidence of this is that anaemia is the most common symptoms of leukaemia (Bain et al., 2012).
Another effect of unhealthy blood in the human body is related with the cardiovascular system. It is necessary a fluid component called blood to this system works correctly. When the blood is unhealthy, it can come over in a cardiovascular disease which is a collective term, used to define a lot of component illnesses (Foster, 1992; Iles and Docherty, 2012). It is basically a heart disease of the heart or blood-supply vessels (Foster, 1992; Wintour and Owens, 2006). “Chest pain may occur when the heart muscle, the myocardium, is deprived of oxygen and nutrients due to diseased coronary arteries in angina, myocardial infarction, or a lack of blood reaching the coronary arteries in heart valve disease” (Iles and Docherty, 2012). It is well known that the leading factor in cardiovascular disease is hypertension (Society of Actuaries, 1959 and Li, 2009). Any irregularity in blood can affect this entire system. According to Iles and Docherty (2012) and Foster (1992), irregularities in blood pressure (hypertension) are typically in whole world, but normally do not show symptoms. For best acknowledgment, diseases in heart are subdivided into two groups, congenital (hereditary) and acquired after birth (environmental) (Foster, 1992; Wintour and Owens, 2006). Heart defects in child can be genetic, or may be caused by viral infections (Brown, 1979). However, some individuals have a tendency to increase the production of one or more distinct types of cholesterol (Foster, 1992). Thus, cardiovascular disease is also a reflection of unhealthy blood in the human body.
In conclusion, genetic and environment can together influence some disease in blood. Foster (1992) affirmed that health is not only function of medical care, but also lifestyle, environment and biology. He also concluded that “since major changes in the gene pool are unlikely in the foreseeable future, large scale improvements to health seem most likely to result from alterations to either, or both, individual personal behaviour and to the environment” (Foster, 1992). As a result of that, some individuals are more genetic predisposed for some disease in blood. Thus, it is important to know about your probability genetic disease but also about in which environment are you in.
Ahmed, N., Dawson, M., Smith, C.

Detection of Fungal Infections in Plants

Histopathological Technique for Detection of Fungal Infections in Plants
Vijai Kumar Gupta and Brejesh Kumar Pandey
Microscopic examination of the interaction between pathogenic fungi and their host plants has been instrumental in deciphering the biology of this relationship and can serve as a useful diagnostic tool. In this chapter, we describe the technique of fixing fungal infections of plant samplings for histopathological experiments. Toludine blue O’ staining methods coupled with stereoscopic microscopy are used to scan the infection structures of the fungus Fusarium spp. and host response in Psidium guajava L. root tissues.
Key Words: fungal infections, histopathological experiments, microscopy, staining techniques, Toluidine blue O’, Fusarium spp., Psidium guajava L.
INTRODUCTION The ability to observe the growth of fungal structures in host tissues under the microscope is an important tool in the study of plant pathogenesis. Over the years many staining techniques that highlight fungal structures in plant tissues have been reported. In particular, technologies such as stereoscopic microscopy have enhanced our ability to visualize hyphae in plant tissue. [1-4]
The use of certain staining techniques can facilitate considerably microscopic observations and experimental research on plant pathology by allowing plant and fungal tissues to be differentiated. More specifically, staining can aid examination of fungal colonization and infection processes, such as differentiating hyphae in life cycles that involve a transition from a biotrophic to a necrotrophic phase. Staining of specific tissues also can simplify identification of fungal inoculum or hyphal presence in asymptomatic plant tissue. The effectiveness of a particular staining technique can vary greatly depending on the particular fungus and plant species. Toluidine blue O’ has been used to stain and identify callose deposition produced by host plants in response to intracellular infection of plant cells by fungi in some plant-fungus interactions.[5] Toluidine blue O’ staining techniques was applied to examine the infection structures of the fungus Fusarium in root tissues wilt infected guava plants. The usefulness of this staining method was based on the visual contrast between host plant tissue and fungal hyphae provided by polychromatic dye and resolution, and the relative ease of preparation and use. [6] This study describes an improved method for fixation of sampling of fungal infected plant parts, and staining and observation of fungal infections in plant tissue for histopathological visualization.
MATERIALS Sterilized water
0.1% HgCl2
Glass slides
Whatman filter paper no. 41
Glacial acetic acid
Paraffin wax
Toluidine blue O’
Microprocessor based automatic tissue processor (Electra, YSl 104, Yorko )
Microtome (MICROM – HM 350)
Stereoscopic microscope (Leica – LEITZ – DM RBE)
The methods presented in the following sections describe general procedures for fixation, staining, and microscopy of fungal infections of plant samplings. Modifications that may be needed to fix the sampling properly from different types and sources of material are also described.
Killing and Fixation
Roots samples were collected from wilt-affected and healthy plants. Root pieces 2 to 4 cm long were cut and surface sterilized using 0.1% HgCl2, washed two to three times in sterilized water, and the excess water absorbed on Whatman filter paper 41. Then samples were kept in formaldehyde: acetic acid: alcohol (5 ml: 5 ml: 90 ml) for a minimum of 48 hours (see Note 1).
The samples were processed with the alcohol:xylene series (as per the flow chart depicted in Figure 13.1) using an automatic tissue processor (Yorko) (see Note 2).
Infiltration and Embedding
The samples were embedded in melted paraffin wax (54-56° C) for at least 4 to 8 hours in order to completely replace the xylene with paraffin wax in a square-shaped block (see Note 3).
Section (10 [mu]m thick) cutting was done using a microtome. Blocks were prepared in paraffin wax and thin sections 10 [mu]m thick were cut with the help of a microtome (MICROM – HM 350S). At least 20 slides were prepared for each sample (see Note 4).
Staining and Mounting
The sections were stained in 0.1% aqueous toluidine blue O’ and were mounted in DPX after bringing them to xylene through the alcohol:xylene series. The detailed procedure is given in the flow diagram depicted in Figure 13.2 (see Note 5).
Microscopy and Imaging
Samples were mounted in 50% (v⁄v) DPX mount and viewed under a stereoscopic microscope (Leica – LEITZ DM RBE) using a Hoya CM500S filter (IR cut-off 650 nm). Images were captured using a CCD camera with a Bayer Array RGB filter for brilliant pictures (Interline transfer frame readout CCD – ICX252AQ) and Leica DFC Twain and Leica Image Manager analysis software (soft microscopy with imaging control software system).
NOTES The FAA solution is prepared based on the type of material, that is, soft tissue, moderate tissue, or hard tissue (use 25% ethanol for very delicate material, 50% for normal use, and 70% ethanol for very tough material).The samples were left in the FAA solution at least 48 hours or until they were processed further. This depends on the hardness of the tissue.
This process removes the water from the plant tissues and facilitates sectioning.
Infiltration and embedding of the material was done in paraffin wax to remove the xylene from the tissues. The blocks of wax were prepared in L molds in which the material was embedded.
Sectioning of the material was done with the automatic microtome (MICROM – HM 350 S).
Sections were stained in 0.1% aqueous Toluidine blue O’ and were mounted in DPX after bringing them to xylene through the alcohol:xylene series as described by Jensen. [7] The samples were examined for anatomical details as per the technique described by Pandey. [3]
The authors are very grateful to Director, CISH; Head, Department of Crop-Protection, Central Institute of Subtropical Horticulture (CISH), Lucknow, and Prof. Shakti Baijal, Dean, FASC, MITS University, Rajasthan for providing the necessary research grants.
Johansen DA. Plant microtechnique. NewYork; McGraw-Hill; 1940.
Meyberg M. Selective staining of fungal hyphae in parasitic and symbiotic plant-fungus associations. Histochemistry. 1988;88: 197–9.
Pandey BK. Studies of chickpea blight caused by Ascophyta rafiei (Pass) Labr. with special reference to survival in crop debris [PhD thesis]. Pantnagar, UP, India: Department of Plant Pathology. G. B. Pant University of Agriculture