Evaluation of Profile Errors in Drug Infusion by Anesthesiologists: An Overview

Introduction

Patient safety can be defined as the reduction and mitigation of unsafe acts within the health care system, as well as the use of practices aiming at achieving good results for the patient [1]. The culture of patient safety has been progressively becoming a subject of general interest in health [2]. This is not only focused on harmless health care but also on its timely, effective and equitable performance, based on the best scientific information and the full and individual needs of both the patient and the patient. of their family [3]. The national system for reporting adverse events, or potential risk situations, is already known but almost not practiced by health professionals. This system is composed by records and analyzes of the problem origin in the occurrence of patient damage. The aim of these communications is avoid preventable failures, to disseminate this information and introduce changes in the system or practices, in order to prevent the same mistakes from recurring in the future.

The understanding the concept of patient safety is important for problem evaluation and to detect the various factors involved. Studies on diseases caused by health care have been published for some years and the good practices and error decreases resulting from a health care that are crucial to guarantee patient safety in care settings [4]. The goal of these approaches is that the increased and more effective records and analyses of such situations could lead to a reduced occurrence of errors or failures. It has been suggested that the large number of errors observed in medical practice is precisely the absence of mechanisms that diminish its occurrence, or that intercept the error before the patient arrives [5], since it starts from the mistaken assumption that a health professional does not make mistakes and, therefore, no mechanisms of prevention and correction are created. In this way, some related events were defined above.

Adverse Reaction

The adverse drug reaction is defined by the World Health Organization (WHO) as any unintentional and unintended harmful event occurring during the use of a medicinal product used at usual therapeutic doses for treatment, prophylaxis or diagnosis.

Adverse Events

The adverse event is defined as the occurrence, in humans, of any undesirable effect resulting from the use of products under sanitary surveillance. This has to be reported to the responsible sectors of health institutions and / or regulatory agencies. Promoting the adoption of preventive measures ensures greater patient care. (Resolution-DRC No 23 from Apr. 4th, 2012). The adverse drug event involves different situations, including adverse drug reaction and therapeutic ineffectiveness [6]. According to TOMÁS and GIMENA [7], the incidence of adverse events in emergency services is estimated between 1.6 and 14%, considering different studies and methodologies adopted. In Brazil, a study with patients admitted to hospitals in Rio de Janeiro observed 5.6% of adverse drug events [8]. Another study carried out in the country, in the Center-West region, revealed a frequency of 8% of adverse drug events in hospitalized patients [9] and the adverse events to severe drugs are the most reported because they cause harm to patients [10]. Thus, the importance of monitoring and reporting of adverse events is evidenced, justifying the accomplishment of this communication.

Medication Error

Medication error, according to the National Coordinating Council for Medication Error Reporting and Prevention is any avoidable event that causes or induces the inappropriate use of a medication, being the medication in the control of the health professional, patient or consumer [11,12]. Researchers who studied the subject in Brazilian public hospitals, have identified problems in the administration of 30% of cases4, in the present communication, it was observed that the use of drug in the treatment of disease is not a problem. National Agency of Sanitary Surveillance [13] states that medication error is any avoidable event that, in fact or potentially, may lead to inappropriate use of medication. The error can be related to professional practice, products used in the area of health, procedures, communication problems, including prescription, labels, packaging, names, preparation, dispensing, distribution, administration, education, monitoring and use of medicines. It is important for institutions to encourage notification and for professionals included in the practice to have awareness of their importance beyond their knowledge. The lack of notification of the error related to medication is a worldwide problem, because even today there is a punitive culture, compromising the veracity of the data [14].

Causes of Medication Errors

The commitment with medicine is from different health professionals, such as doctor, by prescription; pharmacist, for the release and distribution; and the nursing team, by management and supervision. It is crucial to each step of the medication process, however, in the preparation stage, the error must be distinguished, since it is the stage that precedes administration to the patient [15]. Non-existent knowledge and inexperience were also identified as relevant factors for the occurrence of errors [3]. Yamamoto [14] also reported that the higher incidence of errors with medication was associated with the incorrect rate of drug infusion. It was then realized that this type of error is linked to the infusion pump programming and its malfunction due to the handling, proving that the training of the professionals is of paramount importance. Most of the errors observed in medical practice were noted by the absence of mechanisms that diminish their occurrence, or that intercept the error before reaching the final consumer - the patient. According to Carvalho et al. [15] are environmental, psychological and physiological factors combined that provide the error in the practice of medicine. The figure below presents the main factors that interfere in the occurrence of errors (Figure 1).

Figure 1: De Andrade et al. [13].

ANVISA Legislation

According to the National Agency for Sanitary Surveillance (ANVISA) Medicines Labeling Regulation16, parenteral solutions, families of similar medicines should be of the same label color, this color being pre-established in a specific annex. It is, however, clear that medications with different potencies and similar names, such as Ephedrine and Epinephrine (Figure 2), may be confounding factors. It can still be mentioned the fact that there is nothing on the form of ampoules, but drugs of quite different potencies, but from the same family have the same color of the label and the same ampoule format, these factors being confusing, especially in situations of urgency (Figure 3).

Figure 2: De Andrade et al. [13].

Figure 3: De Andrade et al. [13].

Conducting the Medication Error

Describing failings and explaining their cause and reason for that, in health area or elsewhere, is not only to talk about people-related issues, but also analyze and detect the external circumstances and environmental factors that provide this human error [12]. Among the activities with the purpose of promoting scientific knowledge, it is worth mentioning continuing education, an approach that allows the development and improvement of health professionals and ensures the quality of customer service [16,17].

To aim these procedures ANVISA, also recommends a medication error prevention program based on the following topics:

a) Promotion of search and identification of human and institutional errors.

b) Promoting the prevention of accidents in health care.

c) Encouraging the incorporation of new knowledge on the origin of medication and patient safety.

d) Raising awareness and creating communication to improve patient safety.

e) Development of information, collaborative and educational approaches that promote patient safety.

Many studies present continuing education as a way to minimize avoidable medical failures. From these findings, it becomes important to evaluate and study possible medical errors that can cause damage to the patient´s health.

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Does Blood Group Influence on Tomato Likeliness?

Introduction

Blood Group System

The term blood group system is clarified as system in human species where cell surface antigens are managed at a single locus or by two or more very meticulously linked homologues genes. Karl revealed that blood chunking was an immunologic process which eventuate when the beneficiary of blood adulteration has antibodies in paradox of the contributor blood cells. He was bestowed noble premium in Phytology in 1930. The alteration in human gore (blood) are due to the existence of or nonappearance of undeniable protein fragments termed antigens and antibodies. The determinant are situated on the exterior of the RBCs and the antiserums (antibodies) are in the blood claret. There are supplementary than 20 genetically resolute blood group systems identified currently. The ABO and Rhesus (Rh) methodology are the utmost significant ones castoff (used) for lifeblood transfusions. ABO blood collections are furthermost vital in auspicious of safe lifeblood transfusion. The blood set A has antigen A on RBCs.

While blood set B has antigen B and antibody A. AB has A and B antigen and Not any antibody. O has nope antigen but Anti-A and Anti-B [1]. Rh antigens are transmembrane proteins with circlets manifested at the outward of red blood compartments. They are baptized (named) for the rhesus monkey. RBCs that are Rh positive prompt the antigen nominated D. Rh system gets more intricated because here the antigen is Rh antigen [2]. Actually different people have different blood groups. So, We had collected different information about this correlation from different people. According to our research, most of the students had B+ and o+ blood groups. Then, according to our research, We had collected the information about their correlation with Tomato. So, B+ and O+ people like more tomatoes. While others like A- and AB- had very less likeness towards tomatoes. Purpose of the recent study was to match blood grouping with Tomato likeliness.

Materials and Methods

Blood Grouping

First of all, We introduced our self to the person whom blood I was going to draw. Then, We washed and sanitized our hands. After this, We selected the appropriate needle depend on the patient’s age and physical characteristics. We asked him to sit in a chair and made sure that his arm is not bent at thee elbow. Asked him to made a fist and then traced his veins with my index finger. Disinfected the area that We planned to puncture with an alcohol wipe. Then, We interleaved the spike into the vein and permitted the tube to fill. Finally, We detached the needle and blood was collected.

Project Designing

The main goal of my project was to correlate blood group with tomato likeliness. For this estimate, I collected information from different people about their blood groups and their likeliness towards tomato. They gave different point of views about their tomato likeliness and unlikeness. In this way, I completely designed my project. The overall of 170 subjects. The subjects were scholars of Bahauddin Zakariya University Multan, Pakistan.

Statistical Analysis

Statistical analysis were achieved by using MS Excel.

Results

Does blood group influence on tomato likeliness is given in Table 1.

Table 1: Does blood group influence on tomato likeliness.

Discussion

Questionnaire constructed studies have given an essential advancement in recent researches. Alma Lee, Health consultant at pH Labs had worked on the relationship between blood group and tomato lovers. Tomatoes are good for every blood group. The NIH reported that epidemiological studied had associated tomato consumption with a decreased risk of prostate cancer. Tomatoes are truncated in calories, yet occupied with nutrition, said Heather Mangieri. Tomatoes are higher in fiber and a virtuous cause of vitamin A, C, B2…folate and chromium.

Conclusion

It was concluded from the current study that B+ and O+ people like more tomatoes. While others have very little likeliness towards tomatoes. B+ were 25.8% and O+ were 21.1%.

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Contemplate of Nail Fungus Infection Among Different Scholars of University

Introduction

Nail Fungus

Fungoid nail contamination is an ordinary disorder that commences as white or yellow speckle underneath the spike of our fingernail or toenail. It provoke nail to blemish, congeal, and smash at the extremity. If our illness is not trifling and upsetting us, we may not require therapy [1]. But if it is aching, then self-aid steps and treatment may benefit. We may have nail contagion if our nails are condensed, white or yellow-brown streak, fragile, flakey, inaccurate in form, sniffing somewhat obscene. This contagion is typically instigated by numerous fungoid organisms or fungi. The most common source is a sort of fungus communal in grown person. Toe nail taint can begin from sportsperson’s foot and it can extend from one to another nail. Being adult, lessen blood movement, perspiring severely, rambling unadorned foot, having nail grievance, diabetes etc., these aspects can upsurge our danger of emerging nail fungus [2]. A critical situation of nail infection can be throbbing and may create everlasting injury to our nails. And it may conduct other somber infections. So, there are some anticipations alike rinse hands and feet frequently, snip nails, attire perspiration-gripping socks, remove old shoes, hand over nail paint (Table 1). The basic motive of this work was to assess the knowledge about nail fungus infection. So, we had collected different information about this infectious disease from different people in university [3]. Then according to our research, some were aware of this disease, some were suffering from this infection, even there were some who were not aware of this disease [4] (Table 2).

Table 1: Feedback to estimate acknowledgement about analysis of Nail Fungus.

Table 2: Feedback to estimate opinions about familiarity of Nail fungus.

Materials and Methods

Feedback to estimate awareness about Nail fungus Infection

Nail Fungus Yes No

a) Nail Fungus Infection is a Metabolic disease

b) Nail Fungus Infection is a Genetic disease

c) Nail Fungus Infection is a Fungal disease

d) Nail Fungus Infection is a Viral disease

e) Nail Fungus Infection is a Bacterial disease

Ever experienced from Nail fungus Yes No

a. Ever you suffered from nail fungus

b. Ever your family member suffered

c. Ever your relative experienced from this infection

d. Ever your neighbor agonized from this infection

e. Ever any of your friend experienced

Nail fungus Infection Is usually mediated by Yes No

a) Infection is transmitted by Contacts or Blood transfusion

b) From parents to progeny

Nail fungus infection may be medicated by Yes No

a. Medication

b. Treated by Surgery

c. There is no need of cure

Conclusion

It was concluded from that project, most of the people were not aware of this infectious disease (Table 3). While there were some, who were suffering from this nail fungus infection [5]. So, many diverse methods to resolving the problem of nail dispersion have been struggled recently. There were numerous factors that may subsidize to the high rate of fungal nail infection reappearance [6- 8]. It was proved that it is fungal disease. It is most common in aged people (Table 4). 45% of the students said that it is transmitted by contacts or blood transfusion. 83% of the scholars said that it is medicated by medicines and 39% said it is treated by medicines. As for as knowledge is concerned, it is detected that female were more aware of nail fungus than male [9,10].

Table 3: Feedback to estimate interpretations about spread of Nail Fungus.

Table 4: Feedback to evaluate views about aspiration for Nail fungus infection.

Discussion

Questionnaire studies have given a significant improvement in current researches. Endeavor Clinical Tribunals and Dr. Richard had worked on the contemplate of nail fungus infection among different people. They led a study to determine the protection and efficiency of a contemporary solution for the treatment of Nail fungus. A contemplate (survey) of nail fungus infection and awareness among different people had been done by Jeetun Omar, Dr. Rajesh.

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Does Pulse Rate Influence Tomato Likeliness?

Introduction

In medical science, a pulse signifies the tangible arterial inspection of the heartbeat by proficient finger-extremity. The beat could be palpated in any location that permits an artery to be squeezed nearby the exterior of the body. Pulse is equal to calculating the heart frequency. The heart rate can also be estimated by hearing to the heart beat by percussion and calculating it for a minute. The heart rate may be larger or smaller than the pulse rate relay on physiological requirement. The pulse rate can be accustomed to verifying in general heart health and strength level. A fragile pulse shows fine pulse force. It may be because of little cardiac productivity. A standard heart speed for adults ranges from 60 to 100 beats for each minute. There are diverse factors that can manipulate heart rate, such as age, being a smoker one, strength and action levels, temperature of air, feelings, size of the body, medications. Usually a lesser heart rate in relax position implies more well-organized heart function and improved cardiovascular strength.

Eating some foods or drinking some type of beverages, could cause your heartbeat to increase above your regular resting heart rate. Every individual has dissimilar blood group. So, for this project, we had assembled various data about the association of tomato likeliness with blood group and pulse rate from diverse people. According to our study work, different scholars have dissimilar blood groups and different pulse rates. Then we gathered the data about their link with tomato. So, individual having blood group B positive and O positive were most attracted to tomatoes. While other people of different blood groups had very little likeliness to tomatoes. We also concluded that pulse rate is not affected by eating tomatoes. The main goal of this recent research was to corelate regular pulse rate with tomato likeliness.

Materials and Methods

An overall of 220 subjects participated in this project. The subjects were scholars of Bahauddin Zakariya University Multan, Pakistan. Then, we recorded the pulse rate of diverse scholars. Mainly ECG sensors are used, that determine the electrical action of heart over a period. It is detected by electrode attached to the exterior of skin and recorded by a machine outside to body. The common way of checking pulse is to place two fingers between the bones or within the patient’s wrist. Then, push it softly next to the pulse and then note any irregularity in force and beat or regularity. In this way, we measured pulse rate of different students.

This project was designed to correlate pulse rate with tomato likeliness.

Statistical Analysis

Statistical analysis was achieved by applying the M state software. t-Test was used to evaluate the result. P < 0.05 was regarded as a most significant value.

Result

Table 1 From this project, we concluded that pulse rate has no influence on person’s life. For instance, we perceive that pulse rate affected when we saw lizard and if we had temperature or our health is distressed then pulse rate would be exaggerated. About 202 students took part in this investigation and we observe different people had diverse pulse rates. Most of the people who said ‘Yes’ is 155.04 with STDEVA 884.25. While other people who said ‘No’ is 78.60 with STDEVA 16.02. And T-test gave value of 0. 329.So, from this analysis it is observed that result is non-significant because value of P is greater than 0.05.

Table 1: Relationship of normal pulse rate with tomato likeliness is given in the below table.

Conclusion

We concluded from this survey that person or individual having high pulse rate had no effect on tomato likeliness, while one with low pulse rate had effect on tomato likeliness.

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Garlic Polyphenols: A Diet Based Therapy

Garlic Polyphenols: A Diet Based Therapy

Introduction

Garlic (Allium sativum L.) belongs to the family Alliaceae and has been derived from the Celtic word ‘all’ meaning pungent and nature’s boon to mankind. More than 5000 years, garlic has been used as curative and food based bioactive agent for physiological disorders. Garlic plant is mentioned in the Ancient Israel (The Talmud), Egypt (Codex Ebers), Bible and India (Vedas and Purans, Charak Sanghita). Chinese people believe that consumption of garlic as diet based therapy is most effective against human metabolic syndromes such as aging, oxidative stress, cancer, wound healing, diabetes, heart diseases and obesity [1]. Hippocrates observed that garlic was inhibited the cancer cells lines and also prevented from the intestinal and extra-intestinal diseases. Prophet Hazrat Mohammad (PBUH) recommended it for treating scorpion stings and cured health’s related disorders. In Historia Naturalis by Pliny, it was more effective against dog & snake bites as well as gastro-intestinal disorders. Allicin is sulfur containing compound formed through the action of alliinase enzyme on alliin and show the anti-platelet and hypolipidemic activity on human health. There are multiple evidences which confirm the uses of garlic as nature tonic to cure diarrhea in ancient times. In Nigeria, it is used to treat diarrhea, abdominal discomfort, respiratory tract, and otitis media infections.

In Europe, India and Pakistan, consumption of garlic was found to cure asthma, hay fever, and common colds, respectively [2,3]. Garlic is a promising source of bioactive compounds such as allicin, disulfides, alliin, allyl sulfides, cycloalliin, ajoene, allyl disulfides, methionine, cysteine, cystine, diallyl sulfides, glutathione, pseudoscordinine, dimethyl sulfides, sulfones, allyl trisulfides, thiosulfates, scordinine, methyl sulfides, tetra thiol, trisulfides cysteine, and sulfoxides [4]. It is prominent source of calcium, phosphorous, iron, nicotinic acid, thiamine, riboflavin, and vitamin C, respectively. Garlic comprises of citral, linalool, geraniol, α-phellandrene, valeraldehyde, and propionic aldehyde components [5]. They play a significant role against cancer, cataract, cardiovascular disease (CVD), hypercholesterolemia, obesity and hypertension. Maceration of garlic produces oil that good source of 3-vinyl-[4H]-1,2-dithiin, 2-vinyl-[4H]-1,3-dithiin, ajoene and allyl sulfides, whilst steam distillation of garlic oil (SDGO) gives diallyltrisulfide and diallyl disulfide [6] (Tables 1 & 2).

Table 1: Nutritional profile of raw garlic/100g.

Table 2: Health perspectives of garlic.

Antioxidant Potential of Garlic

Nencini et al. [7] determined the antioxidant potential of 15% hydroethanolic extracts of aged diverse parts (bulblets, bulbs, flowers, leaves, and flower bulblets) of Allium subhirsutum L, Allium roseum L. Allium neapolitanum for 20 months. The aged garlic leaves extracts show the higher antioxidant potential followed by flowers and bulbs, whilst bulblets and flower bulblets exhibit no antioxidant potential. Nencini et al. [8] also determined the effect of garlic (bulbs or leaves, 250mg/kg) daily for 5 days in liver of ethanol induced male albino rats. They determined that garlic enhances the GSH and lowers the MDA levels, GR, CAT and SOD activities in liver injury through ethanol. Park et al. [9] evaluated the antioxidant potential garlic extracts through providing different diverse processing conditions. Aged-garlic extract (AGE) yields total phenolic contents (562.6 ± 1.92 mg/100 g GAE) as compared to heated garlic extract (HGE) or raw garlic extract (RGE). In H2O2 induced DNA damage of rats, the ED50 (19.3μg/mL) and inhibition activity (70.8%) of aged garlic extract were reported, whereas ED50 value (38.6μg/mL) of raw garlic extract for 4-hydroxynonenal induced DNA damage followed by aged garlic extract>heated garlic extract was observed. Raw and aged garlic comprises of high quantity of phenolic contents and exhibit high anti-genotoxic activity. They showed chemopreventive role against deleterious effects of H2O2 against DNA and 4-hydroxy-2,3-trans-nonenal (HNE) [9].

Health Perspectives

Anticancer Role: Garlic and garlic oil have been found to provide significant protection against N-nitrosodiethylamine-induced hepatocarcinogenesis. Garlic contains fat and water soluble sulfur compounds that exhibits the anti-cancer mechanisms through the ameliorating oxidative stress, improving immune function, and inhibiting metabolic carcinogenic activation [10]. A group of peers, Choi and Park [11] determined that garlic oil has anticancer role by inducing apoptosis, inhibiting differentiation & tumor angiogenesis and reversing multidrug resistance. Garlic is a potential phytochemical candidate against colon cancer cells, glioblastoma cells and hepato carcinoma cells. It induces apoptosis mechanism in different cancer cells. Allicin, which is the most abundant component in garlic, could induce autophagic cell death in Hep G2 cells [12]. Garlic consists of diallyl disulfide (DADS), diallyl sulfide (DAS), and diallyltrisulfide (DATS) which protect from the carcinogenesis. The supplementation of garlic triggers the production of ROS in glioblastoma cells and induces apoptosis through regulating phosphorylation of p38 MAPK and redox-sensitive JNK1 pathway.

JNK (c-Jun N-terminal kinases) is a potent inhibitor and dominantly lower the cell death by enhancing intracellular free [Ca (2+)], activating caspase-4, calreticulin, calpain, caspase-3 and caspase-9, mitochondrial release of cytochrome c and Smac into the cytosol, down-regulating Bcl-2, and overexpression of Bax [13]. Garlic dietary phytochemicals inhibit, delay or reverse skin carcinogenesis due to presence of organosulfur compounds i.e. ajoene, allicin, S-llyl cysteine (SAC) and allyl sulfides. The oral administration of garlic prevents the mice from chemical carcinogen induced skin papillomagenesis [14]. It up-regulates the carcinogenesis progression and down-regulates the lipid peroxides, as well as also modulates PI3K/Akt signaling pathways and the p53 in the skin papilloma cells [15]. Similarly, in another study conducted by Cherng et al. [16], they investigated that supplementation of DAS significantly decreased the expression of apoptotic sunburn cells, proliferative cell nuclear antigen (PCNA), UVB-induced thymine dimer-positive cells, and terminal deoxynucleotidyl transferasemediated dUTP nick end labeling whilst enhanced the p21/Cip1- positive cell population and p53 in the epidermis. Moreover, suppression of COX-2, prostaglandin E2 (PGE2), NF-κB, and NO level were reported after DAS administration, respectively [16].

There are different methods like digital rectal examination (DRE) and prostate specific antigen (PSA) use in blood sera and enhance the prostate cancer diagnosis among male population at early stages [17]. The use of androgen drugs suppresses the hormone stimulation of the prostate; on the other side, show deleterious effects on body [18]. Garlic bioactive components inhibit the proliferation of various cancer cells through the histone deacetylase (HDAC) inhibitory activity, down-regulation of the Akt and up-regulation of apoptosis of prostate cancer cells [19,20]. The earlier findings of Kim et al. [10] reported that administration of garlic compounds prevented the in vitro and in vivo rats from the prostate cancer. These compounds induced repression of the androgen receptor (AR), apoptosis, and cell cycle arrest in prostate cancer cells. Besides this, they also enhanced the histone acetylation and apoptosis in prostate cancer cells of mice [21, 22]. The administration of S-allylcysteine at the rate of 1-100 mmol/L in A2780 cells in concentration- and time-dependent fashions momentously suppressed the proliferation of cells. It also induced apoptosis, accompanying by lowering the expression of pro-caspase-3, Parp-1, and Bcl-2, and enhancing active caspase-3 and Bax. Similarly, it also reduces the migration of A2780 cells, and significantly decreases the protein expression of Wnt5a, p-AKT and c-Jun [23].

Antidiabetic Role: Diabetes is a metabolic disorder and produces the abnormal levels of glucose in the bloodstream. It is growing emerging public health problem and estimated to be 333 million people by 2025. Herbal plants are being consumed as food by the patient as well as healthy person. Synthetic oral antihypoglycemic agents are more effective to lower the hyperglycaemia level but on other side, they produce the side effects [24]. Allicin is a bioactive component and prevent from the diabetes through lowering the blood glucose level. The oral administration of allicin enhances the free amino acid content and hepatic glycogen, lowers the triglyceride and glucose in serum sucrose-fed rabbits. Similarly, the administration of garlic extracts to streptozotocin-diabetic rats reduced the sugar level, inhibited superoxide formation and lipid per-oxidation. S-allyl cysteine inhibits the AGEs synthesis [25]. DATS, AM, and DAS show the hypoglycemic action that augmented the hepatic metabolism, and insulin release [26]. Allicin controls the blood glucose level in serum and alters the activities of liver hexokinase glucose-6-phosphatase and haemoglobin coenzyme-A reductase in rabbits. It significantly increases the free amino acids and liver glycogen that lower the liver serum proteins, triglycerides level (aorta and liver) and fasting blood sugar (FBS) as compared to high sucrose-fed diet rabbits [1].

The supplementation of diallylthiosulfinate and S-methyl cysteine sulfoxide (SMCS) to alloxan diabetic rats that activates 3-hydroxy- 3-methyl-glutaryl (HMG) Co-A reductase, hexokinase, glucose-6-phosphatase, and lecithin- cholesterol acyltransferase (LCAT) enzymes [27]. Padiya et al. [28] also determined the hypoglycaemic effect of garlic that enhanced the insulin sensitivity and lowered the body weight gain in fructose fed rats. The previous findings of Osman et al. [29], they reported that daily intraperitoneal administration of allicin at the rate of 8 mg/kg diabetic experimental volunteers for 30 days. It effectively reduced the antiislet cell antibodies ICA level through following mechanism (1) the lowered pan B cell marker (CD19), lowered pan T cell marker (CD90), decreased pan innate cells marker (CD11b), prevented from the damage of langerghans islet cell.The hypoglycaemic action of garlic polyphenols could possibly due to release of bound insulin and high pancreatic secretion of insulin from β-cells. These polyphenols lower the blood glucose level, TG, LDL, VLDL and enhance the HDL level in streptozotocin and alloxan-induced diabetes mellitus rats. S- allyl cysteine restores its function in streptozotocin-diabetic rats by preventing free radicals production through modulating the NADPH oxidase. DAT lowered the fasting blood glucose (FBG), LDL and increased the HDL level in diabetic patients for 12 weeks [30].

Antimicrobial Activity: Antimicrobial drugs have failed to provide response to micro-organisms due to their expensive prices, side effects and greater risk of death [31]. The garlic containing extracts show antimicrobial activity against different types of bacteria such as gram positive (A streptococcus, s. pneumonia group, s. aureus and bacillus anthrax) and gram negative (salmonella species, citrobacter enterobacter, kilabsella and E. coli) [32]. Hindi [33] reported that thiosulfinates in garlic are responsible for the antimicrobial activity in rats. Allicin also exhibits the antibacterial action against some fish pathogenic bacteria. The 10% v/v solution of allicin in dimethyl sulfoxide (DMSO) was also showed anti-bacterial activity against aeromonas veronii, aeromonassobria, aeromonascaviae, aeromonashydrophila and streptococcus iniae. The allicin (MICs; 125 µg/ ml) concentration for aeromonashydrophila and 250-500µg/ml for aeromonas veronii, aeromonas caviae and aeromonas sobria in dimethyl sulfoxide was found to be effective [34].

Cardiovascular Role: Allicin, DATS, DADS and AM polyphenols perform their antioxidant mechanism and prevent from cardiovascular disease by enhancing fibrinolytic antioxidant activity, inhibiting platelet aggregation, reducting serum lipids and blood pressure levels [35]. The previous findings of Thomson et al. [36] reported that single intravenous dose of garlic extract (10- 100mg/kg) dose-dependently suppressed the blood thromboxane B2 concentration in rats. Garlic also up-regulates the cellular glutathione levels in vascular endothelial cells and prevents endothelial dysfunction. The prophylactic supplementation of aged garlic extract prior to ischemia reperfusion suppresses the production of free radicals and prevent from the depletion of glutathione antioxidant enzyme. Similarly, they also suppress the fibrosis development in kidney and liver organs by inhibiting the neutrophil migration. Allicin and DATS suppress the angiotensin converting enzyme activity that lowered the blood pressure and cardio-protective effect in kidney and liver. The aged garlic extract (AGE) reduces the pulse pressure (PP) and improves the pliability of the artery. Additionally, they lower the deleterious effects that produce the papilloma in the forestomach, lower erythrocytes and enhance reticulocytes [37].

Blood Coagulation, Fibrinolysis and Circulatory Effects: In oxidized erythrocytes of rats, the supplementation of aged garlic extract has been found to enhance the blood circulation via preventing hemolysis and lipid peroxidation. Allicin, AM improve the erythrocytes fluidity, whereas unable to protect the erythrocytes from t-butyl hydroperoxide-induced hemolysis [38]. They also modulate the production and function of both constricting factors (endothelin-1) and endothelium-derived relaxing factor (NO) in pulmonary arteries of mice [39]. Garlic juice and g-glutamylcysteines have been proved to show the beneficial effects on heart rate and may lower the blood pressure through inhibiting angiotensin-converting enzyme in vitro [40].

Immunomodulatory Activity: Aged garlic extract, and their bioactive components exhibit the immunomodulatory properties due to presence of organosulfur compounds. The concentration of garlic extract is dominantly effective on IL-2 and INF-γ gene expression of stimulated lymphocytes. These compounds also reduce the macrophage infection through the induction of NO production in vitro [41]. Allicin prevents from the immunemediated liver damage of T cells of mice and as well as also inhibit the NF-kappa B activation. A group of researchers [42], they investigated that allicin supplementation prevented from the intestinal inflammation though inhibitory effect on peripheral blood, and intestinal epithelial cells [42].

Antiallergic Role: Allergic responses are the activation of FceRI receptor on the plasma membrane of mast and basophilic cells is known to liberate the b-hexosaminidase, histamine, cytokines, prostaglandins and leukotrienes allergic mediators. Likewise, arachidonic acid metabolites such as prostaglandins and leukotrienes cause acute and chronic allergic inflammatory reactions [43]. Supplementation of allicin and AM can inhibit the passive cutaneous anaphylaxis (PCA) and immunoglobulin E-mediated allergic response in RBL-2H3 cells. Similarly, ethyl acetate extract of garlic polyphenols inhibits the release of TNF-a and b-hexosaminidase. They suppress the cPLA2, Syk, COX- 2 and 5-LO factors in rats [44].

Conclusion

Garlic is mainly used as commodity worldwide for its health promoting perspectives in human such as prevention from cancer insurgence and diabetes, lowering the cardiovascular complications, allergy responses, and aging. Bioactive compounds from garlic exert anti-carcinogenic potential target multiple pathways, inclusive of the cell cycle, apoptotic cell death and angiogenic pathway. The active form of alliinase enzyme can be stabilized into biocompatible materials such as alginate beads and layered double hydroxides. This review encompasses the multiple health effects of garlic and its bio-active constituents with references to health perspectives.

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A Case of Huge Follicular Adenomatoid Odontogenic Tumor Treated by Fenestration and Delayed Enucleation

A Case of Huge Follicular Adenomatoid Odontogenic Tumor Treated by Fenestration and Delayed Enucleation

Introduction

Adenomatoid odontogenic tumor (AOT), first described by Stafne in 1948 [1], is a rare and benign epithelial tumor that most commonly occurs in the anterior maxillary region (especially in the canine region) of younger women [2]. There are three types of AOT: follicular, which has a central lesion associated with an impacted tooth; extrafollicular, which has no relation with an impacted tooth; and peripheral [3]. The follicular type is often associated with the crown and part of the root of an impacted tooth, typically affecting the maxillary canines but rarely affecting the permanent molars [4]. Radiographically, a cystic lesion containing teeth and a calcified body may be present, while histologically, the tumor cells appear as duct- or corolla-like structures with calcified material [5]. In this report, we describe a rare case of a huge follicular-type AOT that extended into the maxillary sinus of a young woman.

Case Report

A 26-year-old woman presented to our department with swelling of the left cheek for several months. There was no history of trauma, discharge, or any altered sensation. Intraorally, she complained of pain from the left upper central incisor to the left upper first premolar, and examination revealed that the buccal and palatal gingiva overlying this area was swollen. However, the swelling was non-tender to palpation and had a firm consistency. Also, the left upper canine was not present. Extra-orally, the swelling was diffuse and extended on the left cheek. Panoramic X-ray examination revealed a radiolucent area with an impacted left upper lateral incisor extending into the left maxillary sinus (Figure 1A). The roots of the left upper median incisor and canine were separate, but the roots of left upper premolars and first molar had been absorbed. Subsequent contrast-enhanced computed tomography (Figures 1B & 1C) revealed the presence of a lesion measuring 40 × 40 × 36 mm. Many radiopacities were found within the radiolucent lesion, including calcified material and impacted tooth. The lesion extended to the nasal cavity and maxillary sinus, the buccal cortical bone was thinning, and the palatine bone had been absorbed.

Figure 1: Panoramic X-ray and CT at first visit and 6 months after fenestration.

The size of lesion on Panoramic radiograph (A) and CT (B,C) at first visit was approximately 40×40×36 mm and Many radiopacities were found within the radiolucent lesion, including calcified material and impacted tooth. Changes in the lesion were monitored by follow-up CT(D,E), and a reduction in the tumor size with accompanying bone renewal were confirmed about 6 months after the fenestration procedure.

Biopsy was performed under local anesthesia in an outpatient clinic. Serous liquid, calcified material, and a thick fibrous capsule were encountered after perforating the labial cortical plate, and a jelly-like specimen was collected that had a cystic appearance. At this time, we therefore performed a fenestration to reduce the tumor size, stimulate bone renewal, and improve the chance of a favorable cosmetic outcome. A histologic diagnosis of folliculartype AOT was made from the biopsy sample. Changes in the lesion were monitored by follow-up CT, and a reduction in the tumor size with accompanying bone renewal were confirmed about 6 months after the fenestration procedure (Figures 1D & 1E). Therefore, we performed enucleation of the maxillary tumor and apicoectomy of the left upper canine under general anesthesia (Figure 2A). The tumor was approached intraorally via a reflected mucoperiosteal flap extending from the right upper lateral incisor to the left upper first molar. To remove bone from around the fenestration, the firm mass was separated from the adjoining bone along its margin and removed with the involved tooth (left upper lateral incisor).

Apicoectomy was also performed for the involved canine, but no other teeth were associated with the lesion. Hemostasis was achieved, and primary closure was completed with absorbable sutures. The total size of the enucleated tissue, including the impacted tooth, was about 35 mm and had a thick cyst-like coating (Figures 2A & 2B). As at biopsy, the contents of the enucleated tumor had a jelly-like consistency. The histopathological report of the enucleated lesion confirmed the diagnosis of follicular-type AOT. Ova-l and polygon-shaped cells were present with ductal and corolla-like structures (Figures 2C & 2D). A mass of calcifications was also present. At 1 year after the final surgery, the left cheek swelling, and the facial asymmetry had greatly improved (Figure 3). Bone renewal was also confirmed and the deformity of the bone of the front wall of the maxillary sinus and the alveolar bone of the buccal side had improved. Of note, there had been no surgical site infection or clinical recurrence.

Figure 2: Intraoperative views, enucleated tumor and histological image.

We performed enucleation of the maxillary tumor and apicoectomy of the left upper canine under general anesthesia (A). The total size of the enucleated tissue, including the impacted tooth, was about 35 mm and had a thick cyst-like coating (B). The histopathological report of the enucleated lesion confirmed the diagnosis of follicular-type AOT. Ova-l and polygon-shaped cells were present with ductal and corolla-like structures (C,D).

Figure 3: CT findings at 1 years after surgery.

At 1 year after the final surgery, the left cheek swelling, and the facial asymmetry had greatly improved. Bone renewal was also confirmed and the deformity of the bone of the front wall of the maxillary sinus and the alveolar bone of the buccal side had improved.

Discussion

AOT was first described in 1905 by Steensland. In 1907, Dreibladt called this lesion a pseudo-adenoameloblastoma, while in 1915, Harbitz proposed the term adamantoma; however, it was not until 1948 that Stafne [1] considered the lesion to be a distinct entity. Although it has since been thought of as a subtype of ameloblastoma, in 1969 Philipsen et al. coined the term “adenomatoid odontogenic tumor” that was adopted by the World Health Organization (WHO) classification for odontogenic tumors in 1971 [6]. It has been reported that AOTs account for 2%–7% of all odontogenic tumors [4-8]. They are more common in the maxilla than in the mandible (a ratio of 2:1), and they also occur more frequently in females (64%–65%) and between the ages of 10 and 29 years (74%–81%) compared with other groups [7,8]. Philipsen [2,4] also reported that the male to female ratio was 6:5, nearly all cases occurred during the second decade of life (age 8 to 39 years), and most cases occurred in patients of Asian origin.

The typical presentation is with a maxillary swelling that can be either painless or painful. AOT is a slow-growing benign tumor that is not prone to recurrence. It has intraosseous and peripheral forms, with the former being differentiated into follicular and extrafollicular types based on radiographic findings [9]. Philipsen reported that the follicular, extrafollicular, and peripheral types occurred in 70.9%, 26.7%, and 2.3% of cases, respectively [2,4]. AOTs usually measure 10–30 mm, but they may grow to as large as 70 mm [10]. Horino [9] reported that the average size was 27.6 mm, but that the average of those that developed into the maxillary sinus was only 41.6 mm. Our maxillary case was consistent with this average. As mentioned, AOTs are usually solid, but may occasionally be cystic; indeed, only 11 cases have been described that arise in association with a dentigerous cyst [4]. That said, AOT has previously been described as an adenomatoid odontogenic cyst based on its form and histology [2]. Our case is therefore consistent with these alternative reports.

AOT often occurs in anterior areas, and about 70% of all cases are associated with an impacted tooth. The maxillary canines account for 41.7% of these cases, with all four canines involved in 60.1% of cases [4-10]. Therefore, it is perhaps unsurprising that 77% of follicular-type AOTs are initially diagnosed as dentigerous cysts [7]. Although the first premolar, third molar, second molar, and lateral incisor have been reported to be involved, the maxillary canine is the most often involved tooth. Interestingly, Philipsen reported that only one casehad a well-defined radiopaque mass, finding that all other lesions appeared as circumscribed unilocular radiolucent lesions around an unerupted tooth. Our patient was a young Asian woman with an AOT associated with an unerupted maxillary lateral incisor that was displacing the maxillary canine. Philipsen et al. [2] postulated that follicular-type AOT develops from cell nests within the dental lamina that surround the tooth. Furthermore, they suggest that the extrafollicular variants form from the epithelial nests situated at the borders of the conduit of tooth eruption. Consequently, the tooth would not be embedded by the developing AOT during eruption. As noted in the macroscopic observations, the tumor in the current case had a tissue tag that was attached to the epithelial lining in the bony depression.

Microscopic examination revealed that the tissue tag belonged to the epithelial lining of the dentigerous cyst. This raised three possibilities. First, the dentigerous cyst with the unerupted lateral incisor may have developed initially, and through a stimulus that is yet to be determined, the AOT arose from the epithelial nests in the dental lamina within the odontogenic cystic lining. Second, the findings reflect two different pathologies that were occurring concurrently in the lesion. Third, this may have been an entirely new variant. However, AOT has been reported to derive from a calcifying epithelial odontogenic cyst [2]. AOT is usually encapsulated and has few recurrences, allowing definitive treatment by surgical enucleation and curettage at presentation. However, our case was relatively large, and the maxillary deformity was a concern for the enucleation surgery. At biopsy, the tumor had a cyst-like structure with liquid or jelly-like material, so we initially performed fenestration to reduce the tumor size and improve the facial deformity. As a result, we could perform the enucleation with minimal surgical invasion, and satisfactory clinical results could be obtained without leaving unsatisfactory facial deformity. In cases such as ours, where the AOT has a cystic component and the patient has facial deformity, we advocate performing enucleation surgery after reducing the tumor size by fenestration surgery.

Preventive Medicine

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Promoting an All-Inclusive Epidemiological Studies of Parkinson Disease (PD) in Ethnic Minorities of African Descent

Promoting an All-Inclusive Epidemiological Studies of Parkinson Disease (PD) in Ethnic Minorities of African Descent

Introduction

Parkinson Disease (PD) is a neurodegenerative disease characterized by the loss of the Substantia Nigra (SN) accommodating dopaminergic neurons responsible for the production of dopamine (DA), an excitatory neurotransmitter, in the mid brain [1,2]. Because DA is involved in the relay of messages to the part of the brain that controls movement and coordination (Motor Cortex) via the Basal Ganglia and the Thalamus, its loss results in the complete or partial loss of movement [3]. PD symptoms can be categorized into four groups based on the individual and severity. These include tremor of the hands, arms, legs, jaw and face; bradykinesia or slowness of movement; rigidity or stiffness of the limbs and trunk; and postural instability or impaired balance and coordination [4]. It is termed a progressive neurological disorder because it worsens with time [4]. The cause of PD is not fully understood. So far, no cure has been found for PD, but certain treatments are recommended for patients based on the severity of the symptoms. Because PD’s pathology is linked to loss of dopaminergic neurons that produces DA, most drugs are designed and produced as synthetic or semisynthetic DA to replenish insufficient endogenous DA in order to reverse the symptoms. The most prominent drug in this category is the levodopa, a semi-synthetic form of DA [5]. The final conversion of levodopa to DA is facilitated in the brain [6]. Although this drug and other variants have been shown to mitigate the symptoms of PD, they have not been able to reverse them completely. Apart from medications, surgical therapy, lifestyle modifications, physical therapy and change of diets are other alternative therapies that may be recommended on an individual basis [4].

Etiology and Pathophysiology

Most PD development can be traced to the loss of the SN in the mid brain (National Parkinson Foundation). The brain SN accommodates dopaminergic neurons that produce DA, an excitatory neurotransmitter that plays a critical role in movement and coordination [1,2]. Thus, the decreased production of DA results in movement disorder, characterized by tremors in people with PD [4]. Apart from the damaged or loss of SN, genetic mutations of some certain genes have been implicated in PD development. Some of these genes include PARK2 (parkin), PARK7, PINK1 (PARK6), LRRK2 (PARK8) and SNCA (PARK1), PARK 7(DJ-1) and PARK2 (ATP13A2) [7]. In most cases, mutations of these genes have been linked to the impairment of the SN [8], although the mechanisms are yet to be clearly defined in many cases. It is also possible that PD may be caused by mutations in some other genes that are yet to be discovered. Scientists and researchers have also discovered a correlation between PD and protein aggregates of alpha-synuclein, the major component of Lewy bodies, and a signature and marker for dementia and other neurodegenerative, neurological and cardiovascular diseases [9,10]. Drugs that can dissolve this protein aggregates have been developed and in preclinical testing stages [11]. While the pathology and pathophysiology of most PD development can be accounted for, about 15% are idiopathic [12].

Prevalence of PD in the United States

Because of the lack of adequate statistics, especially in the sub-Sahara (SS), it is very difficult to state categorically how many people are living with this disease worldwide. However, according to the Parkinson’s Disease Foundation, about one million people are living with this disease in the United States (US). Also, about sixty thousand new cases are detected each year minus those that go undetected. Studies have also shown that PD is about one and a half time as common in men as in women and people with a family history are 10% more likely to have it than people with no family history [4,13]. Although the basis for the prevalence of PD in men compared to women has not been fully understood, studies have shown that it may not be unconnected with exposure of men to toxic chemicals or head injuries, both of which have been characterized as possible PD risk factors [13]. It is also believed that estrogen may provide additional protection for females’ nervous system [13]. The elucidation of the underlying mechanism of the gender-based discrimination against PD development will definitely shed more light on the pathophysiology of PD. Apart from gender, other factors that may influence PD prevalence include age, genetics, social life and family history.

Prevalence of PD in Ethnic Minorities in the United States

Most data available on the prevalence and incidence of PD are based on studies done in the US, Europe and some parts of Asia. Data are lacking on the prevalence and incidence of this disease in the Sub-Saharan (SS). Although available data of studies done in the US, with the second largest population of black people after Nigeria and Brazil, showed that black people may have a low incidence of PD compared to Caucasians [14], this does not necessarily translate to the overall low prevalence of PD among black people. Many of these studies are really vulnerable to statistical biases and their outcomes have been termed unacceptable. It is necessary and important to conduct more comprehensives studies to really ascertain the prevalence of PD in minorities, especially of African descent. In Africa, the historical ancestral homeland of black minorities in the US, reliable and substantial data are lacking on the prevalence and incidence of PD. Except for South Africa, Nigeria, Ghana and Zambia, research studies both at the molecular and epidemiological levels on PD are essentially nonexistent. The unreliable epidemiological data on PD in American minorities of African descent and the lack of substantial data in Africa makes it difficult to make any substantial conclusion on the prevalence and incidence of PD between Caucasian and Blacks vis-à-vis sex, age, demography etc.

Why Epidemiological Studies of PD of Minorities is Essential

The importance of a comprehensive report on the incidence and prevalence of PD in African American, and Black people in general, cannot be overemphasized. It will definitely provide a platform to organize a comprehensive treatment scheme to manage the disease among this ethnic minority. Also, reliable epidemiological data on this disease on blacks could reveal new novel information about the genetic and environmental basis of the development and evolution of this disease. This is predicated on the fact that epidemiological studies of some diseases have revealed novel pattern of inheritance and polymorphisms, providing more information on genetic variations and diversities. Africa has been termed a dark continent when it comes to the knowledge of most neurological diseases, including PD [15]. It is generally believed PD prevalence and incidence in black people are actually more than reported in few countries where they are reported. Many factors are responsible for this development. Firstly, there is a paucity of qualified trained staff and personnel that can diagnose PD. It is projected that there will be a significant shortage of neurologists that can manage PD in the US by 2025 if the present rate of turnover is not increased [16]. Secondly, the reluctance of people to participate in clinical trials and epidemiological studies. Cultural beliefs, religious sentiments and prejudice, especially in Africa, may also discourage people with PD from coming out to declare their status.

Correcting PD Management Disparities in African Americans

Comprehensive Epidemiological Studies

The first step in correcting the disparities of the management of PD in African American minorities is to conduct comprehensive epidemiological studies on this group of people. While comprehensive epidemiological studies of this disease are also recommended in the sub-Saharan to provide a comprehensive conclusion on the prevalence and incidence of this disease in black people as a whole, the financial and demographic burdens may be quite challenging. Therefore, for a start, the studies can be limited to Africans in the United States and the research extended to the subSaharan in the future. The epidemiological studies must emphasize the frequencies and pattern of PD distribution. The frequencies studies must emphasize the prevalence and incidence with respect to time, space, age, gender and social status.

Clinical and Genetic studies (Genome Wide Association Studies)

African Americans should be encouraged to participate in large scale screenings to identify potential gene mutations which could results in PD development. These genes include PARK2 (parkin), PARK7, PINK1 (PARK6), LRRK2 (PARK8) and SNCA (PARK1), PARK 7(DJ-1) and PARK2 (ATP13A2). More genetic studies are recommended for African Americans in order to identify novel genes mutations that can also cause PD. Genetics studies is a powerful tool that can reveal a lot of information about the vulnerability and susceptibility to a disease vis-à-vis sex, age, race and demography. For instance, genetic studies have shown that female ethnic minorities of African descent are vulnerable to having and dying from certain types of breast cancer compared to their Caucasian counterpart [17]. In addition, novel race-specific polymorphisms, including single nuclear polymorphisms and copy number polymorphisms can be identified and patients can be advised in advance of their chances of having PD.

Periodic Screening

Periodic screenings should be encouraged among minorities to access and examine their health conditions and their propensity to having PD. This screening may reveal past family histories of PD. People with family histories of PD have about ten chances of having PD compared to people with no family histories.

Affordable Health Care Provision

Although the government is doing a lot to make health care affordable to patients, there is still need for improvement especially with regard to minorities. This is predicated on the facts that most minorities, the majority of whom live below the middle class, cannot afford the minimum health insurance plans. Also, as PD requires a medical specialist attention, copayment should be waived by the Insurance companies. Many patients may be forced to hide their family histories of PD to avoid being classified as preexisting by the insurance companies since most preexisting classified patients are rejected by insurance companies or in the worst scenario case accepted with a high premium insurance rate which may be unaffordable to the patients. The implications of hiding a family history of a disease, including PD, is that it prevents early intervention measures. This should not only be discouraged but should be discontinued.

Individual Focused Interventions

There is a general misconception that health care disparities among ethnic groups can be eradicated by simply improving the quality of health care of the general population. Past studies have shown that this may not be true after all. A 15-year progress analysis of carried out to investigate black-white health disparities in the United States vis-à-vis improved general quality of health in Chicago area from 1990 to 2005 showed that rather than closing the health disparities gap, it was further widened, although the qualities of health care for the two groups were significantly improved [18]. A recent study showed that individual-focused interventions may be very effective in managing chronic diseases. This is based on the premise that it provides a combination of prevention interventions that consider individual lifestyle, genetics and environment rather than general characteristics [19]. Individually focused intervention should also be employed in the management of PD.

Sensitization of Local Communities

Also, efforts should be directed at increasing the number of health care providers, especially medical specialists in areas that are densely populated by minorities. Studies have shown that minorities with terminal diseases, including PD, are less likely to be accepted by specialists due to prejudice about their ability to pay. To prevent this situation, government and private agencies should encouraged private care providers to assist and educate minorities, especially those with low income on the need to enroll in the Medicare program of the government. They should be made to understand that been healthy at all time is a personal responsibility and no effort should be spared in getting access to adequate treatment, even when the patients cannot afford it.

Clinical Trials

Minorities should be encouraged to participate in clinical trials of potential new drugs for PD treatment. Because PD affects a relatively small number of people, pre-clinical trials to identify new drugs for its treatment has proven relatively difficult. Although studies have shown that a lot of minorities are skeptical about clinical studies and their outcomes, these sentiments and prejudice can be eradicated through proper education and sensitization about the importance of clinical trials in the management of diseases, including PD [20]. The idea of monetary compensation to encourage participation should also be encouraged.

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