Figure 1. Recent developments in diagnostic tools and bioanalytical methods for analysis of snake venom.

According to statistics from the World Health Organization, disability and death from venomous snake bites are still common phenomena in developing countries. Before the use of antivenom, there is still a general lack of feasible experimental methods for snake venom detection. At present, the clinical identification of snake bites mainly relies on the patient’s description of the snake’s morphology, the manifestations of the bite site and systemic symptoms, and simple tests such as coagulation, blood routine, and urine routine. However, the appearance of some non-venomous snakes is similar to that of venomous snakes. Clinically, it is also encountered that venomous snakes “dry bite” without detoxifying without poisoning. In addition, the limitations of these diagnostic methods include errors in patient description, or the time it takes for symptoms to appear after a venomous snake bite, and the lack of specificity in blood biochemistry and urine tests. Snake venom is a highly complex mixture. There are still certain differences in the composition and toxicological effects of snake venom between snakes of the same family, the same genus, or even different families and genera, or a certain snake species in different regions. Therefore, identification of the species of the injuring snake is crucial to the effectiveness of early use of monovalent antivenom in the treatment of venomous snake bites. For a long time, researchers have been committed to developing a stable, reliable, fast, simple, and specific snake venom identification method. Currently, there are radioimmunoassay, agglutination assay, enzyme-linked immunosorbent assay (ELISA), fluorescent immunoassay, and proteomics techniques have been used to detect various snake venoms and toxins.

Radioimmunoassay (RIA)

RIA uses radioactive isotopes (such as 3H, 125I, 131I, etc.) to label antigens or labeled antibodies to determine the corresponding antigen, and uses special instruments to monitor the metabolism of the labeled antigen or labeled antigen-antibody complex and calculate the number of antigens to be tested. Compared with double-antibody sandwich ELISA, this method has simpler operation steps and requires less body fluid. However, this method uses radioactive materials and is expensive. In addition to problems related to the short half-life of 125I, it also requires specialized and sophisticated reading equipment to measure isotope levels. It has proven impractical and not very operable in clinical patients. Compared with double-antibody sandwich ELISA, this method has simpler operation steps and requires less body fluid. However, this method uses radioactive materials and is expensive. In addition to problems related to the short half-life of 125I, it also requires specialized and sophisticated reading equipment to measure isotope levels. It has proven impractical and not very operable in clinical patients.

Enzyme-linked Immunosorbent Assay

ELISA is an immunological diagnostic technology that uses enzyme-labeled antigens or antibodies to bind to the corresponding antibodies or antigens in the sample to be tested. The basic principle is to physically adsorb the antigen or antibody to the surface of a certain solid phase carrier while maintaining immune activity, and the protease and the corresponding antibody or antigen are coupled to form an enzyme-labeled antibody or antigen, and the enzyme-labeled antibody or antigen is simultaneously It has immunological activity and enzymatic activity. After combining with the antigen or antibody on the surface of the solid-phase carrier, the enzyme is used as the detection signal. After the enzyme reaction substrate is added, it is catalyzed by the enzyme to produce a colored product. The amount of the product is equal to the amount of the antigen or antibody to be tested. Proportional, according to the color depth, it can be qualitative or a special microplate reader can be used to detect the adsorption signal for quantitative analysis. Use biotin or avidin to amplify the signal to further increase the sensitivity of the experiment. Due to its advantages of sensitivity, specificity and rapidity, ELISA is suitable for testing large quantities of samples and is an internationally recognized standardized diagnostic method.

Liquid Chromatography-Mass Spectrometry (LC-MS)

LC-MS can effectively separate and analyze complex organic mixtures. Liquid chromatography has strong separation capabilities and can effectively separate thermally unstable and high-boiling compounds in mixed organic matter. Combined with the powerful component identification capabilities of mass spectrometers, Analyze the isolated organic compounds one by one to identify the molecular weight, structure and concentration of the organic compounds. Due to the powerful electrospray ionization technology of LC-MS, its mass spectrum is simple and intuitive, and subsequent data processing is simple. Therefore, LC-MS is an essential tool for analyzing organic compounds. Snake venom is a mixture of proteins, enzymes, small amounts of metal ions, carbohydrates and amines with different molecular weights. Its composition is complex and has a variety of biological activities and pharmacological effects. Proteomics technology can be used to study the evolution of venom proteins in different snake genera or the same snake genus in different regions, the relationship between protein structure and function, and the classification status of venomous snakes. With the maturity of the development of proteomics technology, snake venom proteomics has been deeply studied, revealing the components of different snake venom proteins.

Polymerase Chain Reaction (PCR)

PCR is a molecular biology technology used to amplify and amplify target DNA or RNA fragments. The target DNA or RNA is replicated in vitro. The biggest feature of PCR is that it can greatly increase trace amounts of gene fragments.

Fluorescent Immunoassay (FIA)

FIA is a non-radioactive labeling immunoassay technology based on enzyme-labeled immunoreactants and highly active enzyme-catalyzed substrate color or luminescence methods to achieve the purpose of quantitative analysis. Fluorescence methods were introduced into immunological analysis to improve the sensitivity of immunoassays. 4-Methylumbelliferyl phosphate is widely used as a fluorescent substrate in combination with alkaline phosphates.

Immunosensor

Immune sensors are biosensors, also known as optical immune sensors. Their key information converters use photosensitive elements and work using optical principles. Biorecognition molecules (protein antigens, etc.) are solidified on the sensor and interact with light in the optical element, causing the optical signal to change. The immune response is detected by detecting the optical signal caused by the physical change in the thickness of the molecular film on the optical silicon chip. Therefore, the test object can be analyzed and measured.

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Figure 1. Schematic overview of invasive biomarkers.

Pathological Mechanism of AD

The pathological mechanism of AD is currently unclear, and is currently summarized as neurodegenerative changes and inflammatory response. Neurodegenerative changes involve neuronal degeneration, nerve cell apoptosis, and the generation of new neurons. Inflammatory response refers to the inflammatory response in the brain of AD patients, including the release of activated cytokines and inflammatory cytokines. In addition, many studies have shown that the pathological mechanism of AD is also affected by protein oxidative stress. Oxidative stress refers to the production of free radicals and the increase in reactive oxygen species under conditions of intracellular hypoxia or anoxia, leading to the destruction of cell structure and function. Studies have found that oxidative stress can affect the apoptosis and degeneration of nerve cells in the brains of AD patients, thus increasing the severity of the disease. There are reports that AD is also affected by neurotransmitters. The level of neurotransmitters in the brains of AD patients is lower than that of normal people. This may be one of the reasons for the cognitive impairment of AD patients. In addition, AD patients have obvious amyloidosis in their brains. Amyloidosis refers to a variety of pathological changes that occur in the brains of AD patients, including amyloid crystals, neuronal degeneration, and nerve cell apoptosis. Such lesions may be a key cause of AD and serve as diagnostic markers for AD.

AD Diagnostic Markers

Apolipoprotein Eε4

Apolipoprotein Eε4 (APOEε4) is a very clear risk gene for late-onset AD, which may advance the age of onset and accelerate the development of cognitive decline. It has been recognized as a genetic marker of AD. ApoE is a key component of plasma lipoproteins, which can produce β-amyloid peptide and maintain neurological function.

β⁃amyloid

Under the action of hydrolyzing amyloid precursor protein (APP), β⁃ and γ⁃secretase can produce β⁃amyloid protein (Aβ). Such polypeptides are distributed in many cells and can also be found in blood, cerebrospinal fluid (CSF) and brain interstitial fluid. The most widespread subtypes of Aβ are Aβ40 and 42. The latter are neurotoxic and are related to the formation of AD. Most of them are generated from microglia and astrocytes, have hydrophobic characteristics, and play a major role in plaque formation. Aβ42 in CSF is generally considered to be a biomarker of AD and is helpful in diagnosing preclinical AD. Lower levels of Aβ42 in the cerebrospinal fluid are associated with higher Aβ plaques in the brain, and the concentration levels of Aβ42 in the cerebrospinal fluid of AD patients are significantly reduced compared with normal controls. Currently, the detection of Aβ42 in cerebrospinal fluid can be carried out using immunological technology or mass spectrometry. However, the specificity of Aβ42 in detecting AD needs to be improved. Some studies have shown that the ratio of Aβ42/Aβ40 can be used to judge amyloid deposition in the brain in the early stages of the disease. The specificity of this method is significantly better than that of measuring Aβ42 alone. However, the detection of cerebrospinal fluid is invasive and is not conducive to early screening. Currently, more and more scholars are beginning to explore blood biomarkers. Aβ protein can be measured in plasma, but the Aβ concentration in plasma will be affected by factors such as platelets, and its correlation with AD is not as good as the Aβ concentration in cerebrospinal fluid. However, gratifyingly, studies have shown that using mass spectrometry to detect plasma Aβ concentration can show a significant correlation with cerebral amyloidosis. Therefore, exploring more effective measurement technologies is the core of breakthroughs in blood screening.

Tau

The microtubule system is a component of the neuronal cytoskeleton, and its composition contains tubulin and microtubule-related proteins, with the latter having a higher content of Tau protein. The main function of Tau protein is to bind tubulin and promote the production of microtubules. If Tau is over-phosphorylated, it can accumulate in cells, damage the function of microtubules, and damage the cytoskeleton or axonal transport of nerve cells, thus triggering neurodegeneration. It is generally believed that total⁃t tau (T⁃t tau) and phosphorylated⁃Tau (P⁃tau) concentrations are related to AD. The increase in T-tau reflects the degree of degeneration and damage of neurons and axons. High levels of P-tau suggest the formation of neurofibrillary tangles. CSF P-tau is regarded as the most specific marker of AD, and the concentration of CSF P-tau in AD patients will be significantly increased. Studies have shown that P-tau protein can be used to judge the conversion of MCI to AD, and therefore can be used as a key marker for early clinical diagnosis. Nowadays, P-tau levels in CSF can be measured through immunological methods such as ELISA.

Neurofilament lightweight peptide (NFL)

NFL is a peptide encoded by the NEFL gene. It is an intrinsic cytoskeletal protein that can be used as a biomarker of axonal injury and can be obtained in both cerebrospinal fluid and plasma. Neurons in the brain interstitium and cerebrospinal fluid release NFL after death, and then enter the blood. The serum or plasma level of NFL is closely related to CSF ​​NFL, and is increased in both familial and sporadic AD. In familial AD, patients show increased concentrations of NFL 10 years before the onset of significant clinical symptoms. . Therefore, plasma or serum NFL may be a reliable blood biomarker for neurodegenerative diseases in AD and other neurodegenerative diseases.

Plasma glial fibrillary acidic protein (GFAP)

GFAP is a key indicator used to monitor astrocyte viability. Previous studies have shown that GFAP is significantly increased in the brain and CSF of AD patients, suggesting that GFAP may become a potential biomarker of AD. Studies have shown that serum GFAP levels in AD patients are significantly higher than those in normal controls. In addition, reports also suggest that the plasma concentration of early-onset AD patients is significantly higher than that of normal controls. While the increase in GFAP concentration in the plasma of late-onset AD patients is not as significant as that of early-onset AD, it is also significantly higher than that of normal controls group. Therefore, GFAP is expected to become a member of the blood AD markers and provide new clues for the clinical diagnosis of AD.

Neurogranin (Ng)

Ng is also a potential biomarker for early diagnosis of AD and is usually expressed in granular structures in pyramidal cells in the hippocampus and cortex. Ng has been shown to be related to synaptic plasticity, synaptic regeneration and other functions mediated by the calcium/calmodulin signaling pathway. Some scholars have compared the levels of neurogranin in the cerebrospinal fluid of patients with AD, frontotemporal dementia, Lewy body dementia, Parkinson’s disease, etc. The results show that the concentration of neurogranin in the cerebrospinal fluid of AD patients is significantly higher than that of other diseases, further illustrating that Higher Ng protein concentration in cerebrospinal fluid has a specific screening effect on AD.

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Figure 1. Feline herpesvirus.

FHV-1 Genome Structure and Encoded Glycoproteins
FHV-1 is a double-stranded DNA virus with an envelope. The full genome sequence is 126-134 kbp, and the GC content in the base is about 50%. Its genome consists of a long unique region (UL) of 99 kbp and a short unique region (US) of 27 kbp. Its short fragment consists of inverted repeats (IRs) of 7.0-8.5 kbp long and 8-9 kbp segmented short unique sequences. US region contains genes such as gG, gD, gI, and gE, and the UL region contains gC, gH, and gB genes. The FHV-1 genome encodes a variety of proteins, 17 virus-specific proteins and 3 immunogenic glycoproteins have been reported. So far, seven glycoproteins, gB, gC, gD, gE, gG, gH and glI, have been identified, and they play an important role in virus recognition, invasion, causing infection, cell-to-cell dissemination and infection release. The four glycoproteins gC, gE, gI, and gG were not required when the virus was cultured, suggesting that these proteins are not essential for FHV-1 replication. Among them, gB is the main immunogenic protein, which is expressed in mammalian cells, causing cell fusion and polykaryon formation, and is necessary for virus replication; gD plays a major role in the firm adsorption of viruses and cells.

Structural Features of gB and gD Proteins

The gB glycoproteins are 108, 70, 64 and 58 kDa in size under denaturing conditions. Among these proteins, the 108 kDa glycoprotein FHV-1 gB has a structure similar to a heterodimer. Amino acid sequence analysis shows that it has two intracellular protease cleavage sites (RTRR/S and RSRR/S), one or two of these sites can be cleaved, and this enzymatic cleavage affects the spread of the virus between cells. The gB protein is encoded by 948 amino acids, contains 10 glycosylation sites at the nitrogen end, and contains 10 highly conserved cysteine residues in the sequence. Purified gB can induce high titers of virus neutralizing antibodies in mice, and gB-expressing vaccinia virus can also stimulate fairly high titers of virus neutralizing antibodies in rabbits. Therefore, gB can be used as a very important research object in a subunit vaccine against FHV-1 infection. The gD protein is the main component of the viral envelope. It exists on the infected cell membrane and is highly conserved and antigenic. It can specifically bind to molecules on the cell surface and induce cellular and humoral immunity in the body. It plays an important role in virus penetration into cells and is one of the main target cells of host cell immunity and humoral immune response. Nucleic acid sequence analysis showed that the FHV-1 virus genome is 1 125 bp long, encoded by 374 amino acids, and has a molecular weight of 43.2 kDa. Comparing the gD of FHV-1 with the gD gene products of other herpesviruses, it was found that the six cysteine skeletons that make up its disulfide bond are highly conserved. Anti-gD monoclonal antibodies have complement-independent virus-neutralizing properties. In other kinds of herpesviruses, although the biological functions of the gD genes are different, they are all non-essential genes for virus infection in vivo and replication in vitro.

Biological Functions of gB and gD proteins

The gB protein is a very conserved protein in the herpesviridae family and has high homology among the constituent proteins of all herpesviruses. In the herpesviridae, the gB genes of different viruses can substitute for each other, indicating that the gB genes of different herpesviruses are functionally very similar. Studies have shown that HSV-1 gB is an essential gene for virus adsorption, penetration and cell-to-cell spread, but the function of gB gene in FHV-1 replication is not very clear.
gD has hemagglutination properties and can produce hemagglutination and hemagglutination inhibition reactions. Heparin was unable to inhibit its haemagglutination properties on feline erythrocytes, suggesting that gD is insensitive to heparin. Studies have found that insect cells expressing FHV-1 gD protein can adsorb cat cell lines, but not bovine, porcine and dog cells, and this adsorption can be inhibited by the corresponding monoclonal antibody, which indicates that gD protein plays an important role in the selection of host cell . In addition, the FHV-1g D gene and the canine herpes virus gD gene can only agglutinate red blood cells of their respective hosts. It is speculated that the differences in the biological functions of the gD gene may be the reason why each member of the herpesviridae has its own unique characteristics. The gD glycoprotein is considered to be the main molecule on the surface of virions and in virus-infected cells, and monoclonal antibodies against this glycoprotein neutralize the virus after virus adsorption and show high neutralization titers, suggesting that gD may be involved in virus entry cells, and is an essential gene for virus replication, and glycoprotein D is an extremely conserved immunogenic protein. Therefore, FHV-1 gD may be one of the candidate genes for a subunit vaccine against FHV-1 infection.

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Sleep itself is thought to be a conservative behavior from vertebrates to invertebrates, including flies and nematodes. From the study of existing, it is known that the noradrenergic in the central nervous system regulates sleep. Most receptor subtypes have been screened for validation by studying the network of norepinephrine-regulating neurons. Previous studies have found that βARs in the brain mediate norepinephrine (NE) affecting wakefulness and rapid eye movement (REM) sleep. Clinically, β receptor blockers are widely used and can cause difficulty in falling asleep and keeping sleep, possibly due to reduced production and release of melatonin. In order to find control genes at the molecular level, scientists have screened for potential genes regulating animal sleep homeostasis through large-scale mutagenesis in animal models.

The First Short Sleep Gene: The Discovery of DEC2
As early as 2009, Dr. Ying-Hui Fu, a professor of neuroscience at the University of California, San Francisco, and his team discovered a mutation called DEC2 from a pair of “short sleep” mothers and daughters. It is because of this mutation that they only sleeps for 6 hours a night without significant adverse effects. This is much less than the traditional 7-hour adult sleep time. Further studies have found that DEC2-encoded proteins can reduce the body’s alertness at night by binding and inhibiting MyoD1, a gene that can open orexin. Before dawn, DEC2 levels are lowered, causing MyoD1 to stimulate the production of orexin, which wakes you up and keeps the body alert during the day. Mutations in humans with reduced sleep time diminished the ability of DEC2 to control MyoD1, resulting in excessive orexin production, causing these people to wake up longer. The function of DEC2 may be to ensure that the orexin is expressed at the correct level at the right time every day. Therefore, it is a controller that ensures that the level of the orexin is consistent with the circadian clock.

New Short Sleep Gene: Adrb1 Gene
After further exploration, the researchers found in a family of three generations of genetically “natural short sleep” that no one carried the DEC2 mutation. So what other genes are affecting “natural short sleep”? The researchers used gene sequencing and genetic linkage analysis to determine the exact chromosomal location of the mutation associated with a particular trait to sort out the family’s genome. The study found that a gene mutation called ADRB1, like the DEC2 mutation, is closely related to natural short-term sleep. Since then, the second “natural short sleep gene” has been found! How does this new genetic mutation work for short sleep?

In a batch of genetically engineered mice containing the same ADRB1 mutation as humans, the researchers found that β1AR is expressed at high levels in the dorsal pons (DP). Neuronal activity measured by calcium imaging in this region demonstrates that ADRB1 and neurons in DP are active in wake and REM sleep. Manipulating the activity of these ADRB1 and neurons changes the sleep/wake pattern. Among them, the ADRB1 gene is responsible for encoding the adrenergic beta receptor. In mutational mouse, mutantion results in decreased receptor stability and functional effects. The human mutation was designed into mice, and the mice were reduced in sleep for 55 minutes and immediately awake after light stimulation.

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Definition of Biomarkers

A biomarker, or biological marker generally refers to a measurable indicator of some biological state or condition. It is a biological characteristic, which can be molecular, anatomic, physiologic, or biochemical. These characteristics can be measured and evaluated objectively.  They act as indicators of a normal or a pathogenic biological process. They allow assessing the pharmacological response to a therapeutic intervention. A biomarker shows a specific physical trait or a measurable biologically produced change in the body that is linked to a disease or a particular health condition.

Potential biomarkers including proteins and protein fragments, metabolites, carbohydrate biomarkers, genomic biomarkers (RNA and DNA), cellular biomarkers (captured as the cell pellet from body fluids), and imaging biomarkers. These types of biomarkers can also be referred to as in vitro biomarkers (derived from in vitro diagnostics) versus in vivo biomarkers respectively. A biomarker may be used to assess or detect a specific disease as early as possible, the risk of developing a disease, the evolution of a disease and it can be predictive too.

Biomarkers can take a wide variety of forms. For example, some biomarkers can be used to indicate the presence of certain organisms, including a history of their presence even if they no longer exist. A classic example of such a biomarker is an antibody, a substance developed by the body to help it fight disease. Biomarkers can also be used to differentiate cells; some cancer treatments, for example, are designed to target specific cells, using their biomarkers like a tag.

Functions of Biomarkers

Biomarkers assays are becoming increasingly important in clinical development. Biomarker assays are also useful for identifying intermediate endpoints of success to decrease follow-up time.  The use of a specific biomarker assay can provide early indication of drug efficacy.

Biomarkers depicting prodromal signs enable earlier diagnosis or allow for the outcome of interest to be determined at a more primitive stage of disease. Blood, urine, and cerebrospinal fluid provide the necessary biological information for the diagnosis. In these conditions, biomarkers are used as an indicator of a biological factor that represents either a subclinical manifestation, stage of the disorder, or a surrogate manifestation of the disease. Biomarkers used for screening or diagnosis also often represent surrogate manifestations of the disease.

Biomarkers and Diseases
Since at least the 1980s, the necessity of using biomarkers as surrogate outcomes in large trials of major diseases, such as cancer and heart disease, has been widely discussed. Factors such as increasing prevalence of cancer and heart desease, increased awareness and acceptance of diagnostic tests, Creative Diagnostics provides biomarkers related reagents.

Biomarkers play a critical role in improving the drug development process as well as in the larger biomedical research enterprise. Understanding the relationship between measurable biological processes and clinical outcomes is vital to expanding our arsenal of treatments for all diseases, and for deepening our understanding of normal, healthy physiology.

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OTA mainly damage kidneys and livers of animals. Kidneys are the first target organs and only taking vast Ochratoxin A leads to liver disease. Pigs and fowls are most sensitive to
Ochratoxin A. The acute toxic reactions are depression,digestive disorders , enteritis visible mucosal bleeding , or diarrhea. Pregnant dams even have abortion. What is the toxic reactions of kidneys. First,kidney become fat and pale; the surface is uneven and have small bubbles; renal necrosis happens and renal cortical cells induce gap. Second, proximal tubule function degenerates;renal tubular permeability deteriorates, ability to concentrate decrease. Third, Plasma total protein , albumin and globulin decrease. The chronic poisoning actions are poor bone integrity , intestine and kidney damage fragile.

If found poisoning of animals, the primary thing to do is stopping feeding them with toxic feeds and change into the feeds which is easy to digest and is rich in vitamins. Give thesymptomatic treatment to animals with serious condition to protect them from dehydration. Phenylalanine injection is effective to treat OTA acute poisoning.

How to prevent Ochratoxin A from animals? Prevention is more important than treatment. There are some tips on prevention and control of Ochratoxin A. Ochratoxin A act steadily to heat, so it is not ideal to remove toxicity through heating. According to the report, adds some cholestyramine into the feeds and irradiates it with γ-rays and ultraviolet, which can promote remove toxicity. In addition, OTA and OTB can hydrolyze to phenylalanine and OA with less toxicity under the catalysis of carboxypeptidase A and chymotrypsin. Hydrolysis rate of OTB is six to seven times that of OTA and rumen microbes have a strong reactivity. According to the experiment, adds Carboxypeptidase into fluids with OTA, after few days, the OTA decrease a lot. So It can be an effective way to remove OTA.

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Analysis: first, the establishment of RPR,TPPA,PCR and ELISA promote the establishment of syphilis ELISA for automatic detection, RPR syphilis detection method of manual testing, syphilis TPPA and fluorescent quantitative PCR. The four methods work well. Second, one hundred and fifty blood samples are tested positive from thirty thousand volunteers through ELISA and the positive rate is 5%. Ninety blood samples are tested positive in thirty thousand volunteers through PRP and the positive rate is 3%. Then use the TPPA to test the total blood samples which has been tested positive in ELISA and PRP.
The total samples of two former two methods are two hundred pieces. Eighteen blood samples are tested positive by both ELISA and PRP and eighteen samples are positive though the test of TPPA. However, the thirty samples which are positive through RPR and are tested negative in ELISA are all tested negative in TPPA. Sixty samples are tested positive in ninety samples which are negative in RPR and are tested positive in ELISA. Finally,use fluorescent quantitative PCR to test the samples which are positive both in ELISA and PRP and the two blood samples are all negative.

Conclusion:there are statistical differences on positive rate when the thirty blood samples are tested through syphilis PRP and syphilis ELISA. Compared with the results of TPPA, PRP have both false positivity and false negativity but the the samples of ELISA just have false positivity. In addition, detection capability of syphilis ELISA of is stronger than RPR syphilis and it also be more fitting to blood screening. So in comparison of methodology and practical operation, PCR, TPPA and RPR are not fit for the large-scale blood screening and syphilis ELISA is the one which can be applied to a large-scale blood screening.

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Colorectal Cancer is the tumor with high prevalence rate and the mortality ranks the second among Common Malignancies in recent years. The incidence of Colorectal Cancer have shown a obvious upward trends. So it is urgent to use FOB to diagnose it in early stage to reduce the mortality. Fecal Occult Blood Rapid Test is regarded as the world-recognized screening method to Colorectal Cancer. Because most pathological changes have the presence of bleeding, it can give a clear signal. However, a large number of people do not take this test seriously, which always causes the delay of treatment.

Generally, the main symptom of Colorectal Cancer is hematochezia and other symptoms are diabetes, stomach ache, weight loss and Anemia. What needs to be noticed is that some Colorectal Cancer in early stage shows no clear symptoms, so patients fail to recognize hematochezia by themselves. So it is necessary to do the regular stool test. It is late to do the test when they have stomach ache, diabetes or see blood in stool. In addition, the patients of Colorectal Cancer become younger. According to some medical papers, young people with Colorectal Cancer have bad changes and cancer cells spread in a quicker speed. Sometimes, people think having difficulty in defecation as constipation and they do not choose to have a test. Thus it will leads irreparable loss.

Therefore, it is significant to do Fecal Occult Blood Rapid Test（FOB）to save patients’ life. It is known that the test is regarded as an important screening index in diagnosing digestive tract cancer. The accuracy of the stool test is the important reason. About 20 percent of patients having diagnose digestive tract cancer in early stage is positive in the test and over 90 percent of patients with advanced cancer are positive in the test.

So, to get regular Fecal Occult Blood Rapid Test（FOB）in hospital having high-quality stool test kits to avoid irreparable loss.

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