#Adenosine deaminase

[jcrmhscasereports]

Diagnostic value of pleural Fluid Adenosine deaminase in patients with Pleural Tuberculosis by Sina Parsay M.D in Journal of Clinical Case Reports Medical Images and Health Sciences  

ABSTRACT

Background and Objectives: Extra-pulmonary tuberculosis occurs in about 10-20% of patients with tuberculosis. It most commonly manifests as tuberculous lymphadenitis or pleural effusion. Pleural fluid Adenosine deaminase (ADA) activity considered as a useful biomarker for detecting pleural tuberculosis. The purpose of this study was to evaluate the diagnostic accuracy of pleural fluid adenosine deaminase level in patients with pleural tuberculosis.

Methods: In this study, 113 patients with exudative pleural effusion with unknown underlying diagnosis, were enrolled. Physical examination, chest CT, ADA level of pleural fluid, direct thoracoscopic examination, and biopsy of pleura were obtained for all individuals. ADA level and thoracoscipoc appearance of the lesions was then compaierd among the patients with regard to the pleural biopsy report as the diagnostic goldstandard.

Results: The diagnosis of tuberculous pleurisy was established in 40 individuals based on the pathology reports. The mean ADA level of the TB and the non-TB group was 39.90±22.93 IU/L and 30.74±38.27 IU/L, respectively (P-value=0.167). Sensitivity, specificity, positive predictive value, and negative predictive value of ADA test were 35%, 86.30%, 58.33%, and 70.79%, respectively.

Conclusion: Based insuffiecient sensitivity and specificity of ADA, in patients with unexplained exudative pleural effusion especially in those with a high suspicion of tuberculous pleurisy, despite the low level of ADA, direct thoracoscopic pleural evaluation with obtaining multiple biopsies of pleura is highly recommended.

Keyword: Pleural Effusion, Thoracoscopy, Tuberculosis, Diagnostic Accuracy, Extra-pulmonary tuberculosis, Adenosine deaminase

INTRODUCTION

Tuberculosis is a chronic bacterial infection caused by Mycobacterium tuberculosis. It remains a disease with a high rate of mortality in the world especially in developing and low-income countries 1. Extrapulmonary tuberculosis occurs in about 10% -20% of patients and the most common forms of involvement are tuberculous Lymphadenitis and tuberculous pleural effusion 2.

Pleural tuberculosis (TB) which is the topic of this study, is characterized by symptoms such as chest pain, cough, and fever. Chest Radiography of these patients shows a small to moderate unilateral pleural effusion which is lymphocyte dominant in serologic evaluations. The condition also could be bilateral within the minority of cases 1, 3. The prevalence of tuberculosis among all patients with pleural effusion is between 4-22%, and pleura is involved in 3-23% of patients with tuberculosis 4, 5.

Different diagnostic methods have been used to diagnose pleural tuberculosis, including thoracentesis, measurement of serum and pleural fluid adenosine deaminase (ADA) level, pleural biopsy, and thoracoscopy assisted pleural examination and biopsy 3.

Measuring ADA activity in pleural fluid is an easy, inexpensive, fast, and useful way for diagnosing TB in endemic areas, such as South Africa, Asia, Brazil, Spain, and Eastern Europe 6-8. Based on literature a cut-off point of 40 U/L of ADA activity in a lymphocyte dominant pleural fluid is diagnostic for pleural TB. But the validity of the test is not generally accepted by consensus 9-11

With the advancement in endoscopic techniques and video equipment, thoracoscopy has been suggested as a diagnostic and therapeutic modality in patients with pleural tuberculosis, and become more popular among the physicians. Thoracoscopic findings of these patients include caseous necrosis, miliary nodules, exudative pleural effusion, and pleural adhesion or fibrotic septa 12-14.

Considering the important role of ADA in the diagnosis of pleural tuberculosis, evaluating the correlation between pleural ADA level and thoracoscopic findings of pleural tuberculosis seems necessary

15, 16.

This study aims to determine the correlation of the pleural fluid ADA activity and its diagnostic accuracy in histologically confirmed cases of pleural tuberculosis.

MATERIALS AND METHODS

In this cross-sectional study, 113 patients from those who referred to the cardiothoracic surgery department of Tabriz University of Medical Science with unexplained exudative pleural effusion were enrolled. The study population was measured by GPOWER software with a confidence interval of 95% and a test power of 80%. All patients had a pleural effusion with unknown etiology and candidated for thoracoscopy and biopsy. Patients were excluded from the study in case of transudative pleural effusion, post-traumatic effusion, known pulmonary disorders, history of pulmonary or pleural malignancies, and history of radiotherapy on the thoracic cavity.

All patients underwent thoracoscopic study with direct evaluation of the pleural cavity. Multiple pleural biopsies and pleural fluid specimen for ADA analysis were obtained. All tissue samples were evaluated by a certain pathologist and ADA was measured using ADA Reagent Kit in an acredited laboratory of the affiliated university. The ADA level of greater than or equal to 40 U/L considered as diagnostic for TB. According to the pathologic reports, patients were divided into two TB and non-TB groups. The demographic data, examination and thoracoscopic findings, as well as ADA levels were compared between two groups.

Data were collected and analyzed by IBM SPSS statistic for windows version 23.0. (IBM Corp., Armonk, N.Y., USA). Descriptive data were reported using mean, standard deviation, relative, and absolute frequencies. Chi2, paired sample t-test, independent t-test. and repeated measure ANOVA were used for analytical comparison of the variables between the groups as needed. The p-value of less than 0.05 was considered statistically significant. Sensitivity and specificity were calculated based on patient-level analysis of gathered data using confusion matrix and relying on pathologic results as the gold standard diagnostic test.

ETHICAL CONSIDERATION

The study was approved by the ethics committee of Tabriz University of Medical Science under the approval number of 5/d/8716-94/5-6/3. All diagnostic and therapeutic interventions were performed regarding the routine management of patients; no additional intervention or cost was imposed on participants in this study. Patients’ data were recorded as encoded variables without mentioning the name of any participant. None of the patients' personal information was included in this research.

Informed consent was obtained from each participant; nevertheless, patients were excluded from the study in cases they were reluctant to participate in the study.

RESULTS

Of the total 113 patients, 73 (58.4%) were male, and 40 (32.0%) were female, and 42 (33.6%) were smokers. The mean age of the patients was 49.77 ± 18.71 years.

The diagnosis of TB was confirmed in 40 patients according to the histopathologic reports. These patients were stratiffied as the case group (known as group A), and the other 73 with a diagnosis of nontuberculous pleural effusion were considered as the control group (known as group B).

As depicted in Table-1 dyspnea, cough, and pleuritic chest pain were the dominant symptoms of patients at the time of admission with a frequency of 66.37%, 48.67%, and 40.7% respectively. The frequency of fever and weight loss were30.97%, and 28.31%, respectively among the patients. Table-1 also demonstrates demographic data of individuals separately for each study groups.

Regarding the thoracoscopic examination, pleural effusion, pleural adhesion band, miliary nodules, and caseous necrosis were found in 100%, 67.5%, 70%, and 60%, of the group A respectively (Table-2). Among the control group (group B), pleural effusions, thickening of pleura and miliary nodules were the dominant manifestations with a frequency of 100%, 46.57%, and 30.13% respectively (Table-2). The underlying cause of pleural effusion among the patients in control group was: metastasis (23.28%), mesothelioma (5.47%), inflammation (32.87%), fibrosis (36.98%), and fungal infection (1. 36%) as depicted in Table-2.

The mean ADA level was 39.90 ± 22.13 IU/L in group A and 30.74 ± 38.27 IU/L within group B individuals which did not differ statistically significantly between the two study groups (p=0.167).

As delineated in Table-3, 35% of patients in group A has ADA level of greater than 40 (as a diagnostic cut-off for TB) compared to 13.7% in group B (p>0.05). Bar chart for these amounts is also illustrated in figure-1. Sensitivity, specificity, positive predictive value, and negative predictive value of ADA test were measured 35%, 86.30%, 58.33%, and 70.79% respectively (Table-4). Figure-2 demonstrates the ROC curve of ADA test measures.

Figure 1: Chest X-ray reveals pulmonary edema after ICU admission

Figure 1: Chest X-ray reveals pulmonary edema after ICU admission

Figure 1: Chest X-ray reveals pulmonary edema after ICU admission

After 24h of fully controlled mechanical ventilation and 6800ml of diuresis the sedation medication was terminated and the patient extubated uneventfully. No further ventilation support or vasoactive medication was required. The patient recovered in the matter of 72 hours and was discharged from the hospital on the day 7 with a mild arterial hypertension, that was treated by Hydrochlorthiazide 25mg a day.

After 24h of fully controlled mechanical ventilation and 6800ml of diuresis the sedation medication was terminated and the patient extubated uneventfully. No further ventilation support or vasoactive medication was required. The patient recovered in the matter of 72 hours and was discharged from the hospital on the day 7 with a mild arterial hypertension, that was treated by Hydrochlorthiazide 25mg a day.

DISCUSSION

In this study, 113 patients (73 males and 40 females) with unexplained pleural effusion were evaluated for probable pleural tuberculosis by using thoracoscopic examination and biopsy. Meanwhile, the ADA level was measured for all individuals regardless of pathologic findings. The diagnosis of pleural TB established only in 40 individuals according to the histopathologic reports. The ADA level among these tuberculous pleurisy patients was 39.90 ± 22.13 IU/L compared to a level of 30.74 ± 38.27 IU/L in nontuberculous individuals, which was not statistically significant. Based on our results, the ADA test yield a sensitivity, specificity, positive predictive value, and negative predictive value of 35%, 86.30%, 58.33%, and 70.79% respectively.

In a study performed by Van et al., the causes of pleural effusion were evaluated among 95 patients in Netherland. According to their results, they have found tuberculous pleurisy just in five patients, among them the high ADA activity was only detected in four individuals. On the other hand, the underlying pathologies other than TB could raise the ADA activity based on their study. The authors conclude that the high ADA activity level in a country with low tuberculosis incidence is not accurate enough to establish the diagnosis of tuberculous pleurisy 17.

Tian et al. found a sensitivity and specificity of 84.4% and 91.8% for ADA in diagnosing tuberculous pleurisy by evaluating 190 patients with pleural effusion. The cause of pleural effusion was TB in 141 patients of their study population 18. The difference between the results of our study compared to the recently mentioned research is explainable by the high overall incidence of TB in the country in which Tian et al., performed their study.

Valdes et al., in their study, revealed that measuring pleural ADA level is a useful parameter for the diagnosis of tuberculous pleurisy by evaluating 405 patients with pleural effusion. All 91 cases of pleural TB in their study showed an ADA level of greater than 47 IU/L, compared to the elevation just in 5% of non-tuberculous patients 15.

Zemlin et al. demonstrated that measuring the ADA2 isoenzyme is more accurate, and it is superior to ADA in diagnosing tuberculous pleurisy by performing a study on 951 pleural fluid samples, including 387 patients with TB. They suggested that measuring ADA2 level is better to use as a routine test among patients with pleural effusion in endemic areas for TB 11.

Technically, the predictive value of an indicator such as ADA does not only depend on its sensitivity and specificity, but also the incidence of the disease in the study region is also effective 8, 9, 11, 16, 19, 20. The inconsistency between the results might have happened due to the variable prevalence of TB and different sample sizes in which the mentioned studies were performed.

The strength of this study was the use of pathlogical confirmation for the diagnosis of the underlying cause of the pleural effusion in the studied patients. The patients with the diagnosis other than pleural tuberculosis was also considered as a reliable corntol group for calculating the diagnostic accuracy of the applied method. Somehow, the shortness of the study sample size was a weakness of our study. Howere, it should be considered that the overall prevalence of the TB within the population in which the study takes place may alter the results of the study; then, it should also be considered as a limitation of the study.

By comparing our results with previous studies, it can be concluded that the sensitivity, specificity, and accuracy of this test are not suffiecient enough; so, ADA is not utterly useful in diagnosis of pleural TB. Therefore, in patients with pleural effusion with undetermined origin and in patients with a high level of suspicion of TB infection, despite the low ADA level, thoracoscopic evaluation of pleural cavity with obtaining multiple biopsies of pleura would be more appropriate.

Also, in cases with high ADA level and lack of proper response to TB treatments, for further investigation and rule out the other diagnosis, thoracoscopy and pleural biopsy could be beneficial.

However, further studies with larger sample size are suggested.

Acknowledgments: Not applicable

Source of Funding : None

For more information: https://jmedcasereportsimages.org/about-us/

For more submission : https://jmedcasereportsimages.org/

[brightlotusmoon]

"D-ribose supplements can offer health benefits for those with certain conditions like heart disease, fibromyalgia, or myoadenylate deaminase deficiency (MAD). More research is needed, but emerging studies look promising.

D-ribose is a critically important sugar molecule.

It’s part of your DNA — the genetic material that contains information for all the proteins produced in your body — and also makes up part of your cells’ primary energy source, adenosine triphosphate (ATP).

Though your body naturally produces ribose, some believe that D-ribose supplements can improve health or exercise performance."

_

Years and years ago, my mother suggested Ribose and I completely forgot. My tub of ribose power arrived today and I mixed it in my bedside water bottle.

D-Ribose powder is nifty. It's almost like MSM (methylsulfanomethane). It's odorless, colorless, tasteless, and dissolves fast in liquid.

...where was I? Right, Australia. Anyway, let's see what a daily 5 grams will do.

[science-sculpt]

Evolution of Gene Therapy: A Journey Through History

Gene therapy stands as one of the most promising frontiers in modern medicine, offering potential solutions to a myriad of genetic disorders and diseases. Its journey through history is both fascinating and complex, marked by remarkable breakthroughs, challenges, and ethical considerations.

The concept of manipulating genetic material to treat diseases dates back to the mid-20th century. In 1953, the discovery of the DNA double helix structure by Watson and Crick ignited the imagination of scientists worldwide, laying the foundation for genetic research. It wasn't until the 1970s that the term "gene therapy" emerged, coined by researchers Richard Mulligan and Theodore Friedmann. The 1980s marked the first foray of gene therapy into the clinical realm. The 1970s witnessed the first milestone in gene therapy with the successful introduction of foreign DNA into mammalian cells. This breakthrough, accomplished by Paul Berg in 1972, laid the groundwork for subsequent research endeavors. In 1980, Martin Cline performed the first gene therapy trial on a patient with beta-thalassemia, though ethical concerns arose due to the lack of proper patient consent and scientific rigor. Despite setbacks, the 1990s saw a surge of research, with gene therapy trials targeting various conditions like cystic fibrosis and severe combined immunodeficiency. However, tragic events, such as the tragic death of a young teenager in 1999, a young participant in a 1999 gene therapy trial, highlighted the need for stringent safety measures.

One of the landmark achievements in gene therapy occurred in 1990 when the first successful gene therapy trial took place. Researchers corrected a rare genetic disorder called Adenosine deaminase (ADA) deficiency in two young girls. This groundbreaking feat marked a crucial turning point, demonstrating the potential of gene therapy to treat genetic diseases.

Luxturna became the first gene therapy approved by the U.S. Food and Drug Administration (FDA) in 2017 for the treatment of an inherited retinal disease called Leber congenital amaurosis. This milestone underscored the therapeutic potential of gene therapy and paved the way for future advancements. The development of CRISPR-Cas9 revolutionized the field of gene editing, offering a versatile and precise tool for modifying DNA. This breakthrough has accelerated research in gene therapy and holds immense promise for the treatment of genetic diseases.

Gene therapy isn't a monolith; it dons various hats depending on the target and approach. Here are the major types:

Somatic vs. Germline: Somatic gene therapy: This targets non-reproductive (somatic) cells, impacting only the treated individual's lifespan and not passing changes onto offspring. This is the more prevalent and ethically accepted approach. Germline gene therapy: This modifies genes in reproductive cells, potentially impacting future generations. Ethical and safety concerns surround this approach, and it is not currently used in humans.

Ex Vivo vs. In Vivo: Ex Vivo gene therapy: Cells are extracted from the patient, modified in a laboratory, and then reintroduced. This allows for precise targeting but involves complex procedures. In Vivo gene therapy: The therapeutic gene is delivered directly to the target cells within the body. This offers minimally invasive approaches but poses challenges in targeting specific cells.

Gene Editing vs. Gene Replacement: Gene editing: Utilizes tools like CRISPR to modify existing genes, correcting mutations or fine-tuning their expression. This offers unparalleled precision but raises concerns about unintended consequences. Gene replacement: Introduces a functional copy of a missing or defective gene into the cells, restoring their normal function. This approach is well-established but may require permanent expression of the new gene.

The journey of gene therapy from its conceptual origins to clinical reality is a testament to human ingenuity and perseverance. With each passing year, advancements in technology and scientific understanding propel this field forward, offering hope to millions affected by genetic disorders. The evolution of gene therapy is a testament to human ingenuity and perseverance in the quest to conquer genetic diseases. From humble beginnings to cutting-edge innovations, the journey of gene therapy has been marked by triumphs and challenges alike. As researchers continue to unravel the complexities of the genome and refine therapeutic approaches, the future of gene therapy shines brighter than ever, holding the promise of transformative treatments and cures for diseases once deemed incurable.

[moleculardepot]

Human Adenosine deaminase

Human Adenosine deaminase Catalog number: B2018654 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 1 mL Molecular Weight or Concentration: N/A Supplied as: Solution Applications: a molecular tool for various biochemical applications Storage: -20°C Keywords: ADA1 Grade: Biotechnology grade. All products are highly pure. All solutions are made with Type I ultrapure water…

[twinkl22004]

“ADA Immune Deficiency”, Victor McKusick, “Mendelian Inheritance in Man”, 1966.

ABOVE is the twenty-four (24) hour day of  CHROMOSOMIC CLOCK and this time is twenty (#20).  Here I present: “ADA Immune Deficiency”, Victor McKusick, Mendelian Inheritance in Man’, 1966. INTRODUCTION. The ADA gene encodes adenosine deaminase (EC# 3.5.4.4), an enzyme that catalyzes the irreversible deamination of adenosine and deoxyadenosine in the purine catabolic pathway. T cell-negative…

[biopharmaceuticalindustry]

Global Regulatory Landscape for Cell and Gene Therapies

Traversing the dynamic gene therapy regulatory landscape

Navigating the complex and dynamic gene therapy regulatory landscape has been a persistent challenge for developers and manufacturers. Ensuring these life-changing therapies successfully pass critical regulatory milestones on the journey to market requires gene therapy producers and their partners to demonstrate both flexibility and agility.

With gene therapy being a fast-paced yet relatively new therapeutic area, regulatory bodies have struggled to keep up with continuous technological advancements and our expanding knowledge of genetics, virology and molecular biology. With no blueprint to follow, a practical approach has been necessary to ensure regulations and guidance can safeguard the quality, efficacy and safety of new therapies entering the market.

In this article, Kai Lipinski, Ph.D., Chief Scientific Officer; Xiaojun Liu, Director of AAV Process Development; and Jing Zhu, VP of Nucleic Acid & Virus Technology at ReciBioPharm, explore the current gene therapy regulatory landscape and provide their expert insights into the tactics developers and manufacturers must employ to overcome regulatory challenges.

The evolution of gene therapies

For many years, researchers and developers have striven to realize the potential of therapeutics that introduce specific cells or genetic material to patients for disease treatment and prevention. Owing to breakthroughs and advancements in technology and genetic engineering in the last two decades, we are now at the dawn of a new cell and gene therapy (CGT) era.

There are currently 15 approved gene therapies and 12 cell-based immunotherapy products. Although the gene therapy space has come a long way since the first approved therapy in 1990, which utilized a retroviral vector to deliver functional adenosine deaminase genes, most gene therapies approved today still harness the delivery capabilities of viral vectors.

Read more: https://www.pharmafocusamerica.com/strategy/global-regulatory-landscape?divya

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[sisil-slot]

Rakyat yang sangat suka untuk menampilkan kasino online back online tahu cukup efektif bahwa banyak menarik dan hebat adalah slot rekreasi . pada dasarnya bergantung pada keberuntungan Anda bahwa berapa secara signifikan Anda bisa mendapatkan sorting olahraga dan jika Anda memukul jackpot dan Anda menerima maka itu sama seperti Anda telah mengubah gaya hidup dengan keberuntungan Anda . Adenosine deaminase berbeda cara menikmati slot seperti yang Anda dapat terlibat dalam one-armed bandit seperti Anda dapat terlibat dalam mereka dengan hanya menuju ke kasino di mana beraneka ragam jenis slot perangkat ditempatkan atau Anda dapat terlibat bahkan di entanglement hanya dengan duduk di rumah Anda . disarankan untuk pemula bahwa mereka mulai Dari di web slot dan beberapa time slot gulungan . Untuk bermain melalui beberapa Sisil4d gulungan benar-benar mudah dan itu bukan subjek untuk besar uang . Jika Anda langsung ingin melakukan one-armed bandit lie maka peluang Dari Persian kalah pertandingan menjadi lebih jadi sungguh lebih besar untuk mulai Dari tiga slot gulungan . Anda dapat sangat mudah menyadari kebijakan rekreasi ini dan bahkan prinsip sangat lurus maju. Berbeda tema untuk slot on-line dan 3 slot gulungan Ada berbeda tema diberikan di slot di net dan tiga slot gulungan seperti Dari binatang hutan hingga Amerind Amerika dan Dari Persian 7 lautan hingga buah-buahan . Itu benar-benar bergantung pada pilihan dan keingintahuan Anda yang jenis Dari tema yang ingin Anda pilih . Segera setelah ini Anda dapat stat boast . Jika Anda berpartisipasi dalam slot on internet maka Anda tidak harus menjadi cemas tentang contoh Dari permainan dan time slot yang Akan Anda dapatkan Dari Persian sejak itu sebenarnya terkait dengan slot individu yang Anda temukan di kasino yang berbasis tergantung . Pada slot on the web , kasino menggunakan sort curriculum perangkat lunak yang menghasilkan angka secara acak.

[rnomics]

Adenosine deaminases that act on #RNA, then and now. [Perspective]

In this article I recount my memories of key experiments that led to my entry into the RNA editing/modification field. I highlight initial observations made by the pioneers in the ADAR field, and how they fit into our current understanding of this family of enzymes. I discuss early mysteries that have now been solved, as well as those that still linger. Finally, I discuss important, outstanding questions and acknowledge my hope for the future of the RNA editing/modification field. http://rnajournal.cshlp.org/cgi/content/short/rna.079990.124v1?rss=1&utm_source=dlvr.it&utm_medium=tumblr

[tumimmtxpapers]

High-throughput virtual screening to identify potential small molecule inhibitors of the Zα domain of the adenosine deaminases acting on RNA 1(ADAR1)

Changes in RNA editing are closely associated with diseases such as cancer, viral infections, and autoimmune disorders. Adenosine deaminase (ADAR1), which acts on RNA 1, plays a key role in adenosine to inosine editing and is a potential therapeutic target for these various diseases. The p150 subtype of ADAR1 is the only one that contains a Zα domain that binds to both Z-DNA and Z-RNA.The Zα domain modulates immune responses and may be suitable targets for antiviral therapy and cancer... http://dlvr.it/T0G4sH

[astuteanalyticablog]

Gene Therapy: A Revolutionary Strategy to Genetic Disorder Treatment

Gene therapy is currently an important subject in the biotech sector, with numerous medicines under research and various recent approvals. However, the way has not always been easy. It has been one of the biggest achievements of the twenty-first century. Genetic disorders were formerly thought to be incurable, engraved in stone within the genomes of individuals unfortunate enough to be born with them in genetic life. In this blog, let’s explore gene therapy.

A growing number of firms are entering the market. US FDA expects to receive more than 200 new applications for cell and gene therapy each year, with 10-20 therapies approved each year. Thus, this factor is anticipated to boost market growth. In addition, according to a research report by Astute Analytica, the Global Gene Therapy Market is likely to increase at a compound annual growth rate (CAGR) of 24% over the forecast period from 2023 to 2030.

Historical Overview of Gene Therapy:

In 1972, US scientists Richard Roblin and Theodore Friedmann released a study in Science titled ‘Gene therapy for human genetic disease?’ in which they discussed the enormous potential of inserting DNA sequences into patients’ cells for treating people with genetic illnesses. They did, however, urge caution in the technology’s growth, pointing out numerous important barriers to scientific knowledge that needed to be overcome.

Following 18 years of more research, the first gene therapy experiment began in 1990. A four-year-old girl called Ashanthi DeSilva had a 12-day treatment for severe combined immunodeficiency, a rare genetic illness. DeSilva lacked a critical enzyme known as adenosine deaminase (ADA), which damaged her immune system and put her at risk of developing a potentially fatal infection.

Gene Therapy Products:

Gene therapy products are being researched for the treatment of diseases such as cancer, hereditary diseases, and viral infections.

Wide range of gene therapy products, such as:

Viral vectors:

Viruses can naturally deliver genetic material into cells, and several gene therapy products are developed from viruses. Once viruses have been changed so that they no longer have the ability to cause infectious disease, they can be employed as vectors (vehicles) to deliver therapeutic genes into human cells.

Human gene editing technological advances:

Gene editing aims to either disrupt dangerous genes or fix mutated genes.

Bacterial vectors:

Bacteria can be created to avoid producing infectious illnesses and then utilized as vectors (vehicles) to deliver therapeutic genes into human cells.

Products generated from patients for cellular gene therapy: Cells are extracted from the patient, physically changed (sometimes with the help of a viral vector), and back to the patient.

Plasmid DNA:

Therapeutic genes can be delivered into human cells via circular DNA molecules that have been genetically modified.

The Current Situation Of Gene Therapy

Several gene therapies have been approved by regulatory organizations such as the FDA for the treatment of several ailments such as uncommon diseases, certain types of cancer, genetic disorders, and inherited eye diseases. However, numerous problems remain in the research and administration of gene therapies, such as safety concerns, ethical concerns, and the high price of treatment.

Source: A Revolutionary Strategy to Genetic Disorder Treatment

[moleculardepot]

Human Recombinant DPP-4/CD26 Extracellular Domain

Human Recombinant DPP-4/CD26 Extracellular Domain Catalog number: B2016986 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 25 µg Molecular Weight or Concentration: 112 kDa Supplied as: Powder Applications: a molecular tool for various biochemical applications Storage: -80°C Keywords: ADABP ADCP2 Adenosine Deaminase Complexing Protein 2, Dipeptidyl Peptidase 4, DPP-IV, T-cell…

[cytoart1]

CAR T-cell therapy is a promising new approach to cancer treatment. It involves genetically modifying a patient's T-cells to recognize and attack cancer cells. CAR T ADA, or adenosine deaminase, is an enzyme that can improve the effectiveness of CAR T-cell therapy.

[juniperpublishersoceanography]

Prospect of Marine Bioactive Peptides as DPP4 Inhibitor

Authored by:  Md Morshedul Alam

Abstract

Dipeptidy peptidase 4 (DPP4) is an enzyme that plays important role in metabolism and due to its exacerbating role in glucose metabolism, it is essential to inhibit its function to ameliorate Type 2 Diabetes Mellitus (T2DM). Vildagliptin, sitagliptin and some other drugs are being used worldwide. As a new source, marine derived bioactive peptide having DPP4 inhibitory effect would have a promising role to control its regulatory effect on disease manifestation.

Keywords: DPP4 inhibition; Marine derived origin; Marine bioactive peptide

Abbreviations: DPP4: Dipeptidy Peptidase 4; T2DM: Type 2 Diabetes Mellitus; GIP: Glucose-Dependent Insulinotropic Polypeptide; GLP1: Glucagon-like Peptide-1; ROS: Reactive Oxygen Species, RAGE: Receptor for Advanced Glycation End Products; FDA: Food and Drug Administration; APCs: Antigen-Presenting Cells

    Introduction

Dipeptidyl peptidase 4 (DPP4)/CD26 is a serine exopeptidase enzyme that cleaves the N-terminal dipeptides with proline or alanine amino acids from the N-termini of polypeptides leading to regulate the activities of a number of peptide hormones and chemokines. It is known that DPP4 is responsible for the degradation of several incretins such as glucagon-like peptide-1 (GLP1), glucose-dependent insulinotropic polypeptide (GIP), thus regulating the blood glucose level by sensitizing insulin secretion [1]. Upon T cell stimulation, DPP4 expression is markedly up-regulated along with its increased release in soluble form in the blood, which also suggests DPP4 as a T cell co-stimulatory molecule that exerts its effect through binding to adenosine deaminase and interacting with T cell receptor complex. Bunch of studies suggests that DPP4 is a novel adipokine, which is correlated with the amount of adipose tissue inflammation, and insulin resistance as well. Several reports suggest that DPP4 is also released in soluble form exerts lots of cellular effects such as stimulation of reactive oxygen species (ROS), induction of inflammation in smooth muscle cells. Generally, soluble DPP4 interacts to cell surface receptor(s) and executes numerous effects such as activation of T cells, induction of smooth muscle cells inflammation, stimulation of insulin resistance in various tissues, augmentation of CD86 in antigen-presenting cells (APCs), enhancement of smooth muscle cell proliferation, stimulation of reactive oxygen species (ROS) generation and induction of receptor for advanced glycation end products (RAGE) gene expression, and so on [2].

To manage the excessive adverse effects of DPP4 at the cellular level, scientists are suggesting some pharmacological intervention as a drug and in this case vildagliptin, sitagliptin, approved by the Food and Drug Administration (FDA), are most widely used. Beside these two drugs, saxagliptin and alongliptin are also being suggested [3]. Most of the cases these drugs are approved to be used in a combinatorial therapy like in combination with metformin, sulphonylureas, thiazolidinediones etc. As an alternative source of DPP4 inhibitor, marine derived sources would have a great potential in therapy [4] and more specifically marine derived bioactive peptides production would be one of the areas of utmost interest in DPP4 inhibitor activity. It is known that ficin digested gliadins-derived peptides possess strong dipeptidyl peptidase 4 inhibitory activity as well as antihypertensive and antioxidant activities. As a functional food or dietary supplement, marine peptides derived from seaweeds, sponges, fish-skin, fish-bones, fish-scales, mollusks, crustaceans and marine byproducts including substandard muscles, viscera and trimmings would have a great potential targeting DPP4 inhibition. It is known that Gly-Pro-Ala peptide works as a DPP4 inhibitor, which has a great relevance as a natural source for Type II diabetes mellitus (T2DM) management in both in vitro and in vivo through incretin effect. In one study using RubisCO of Halophila stipulacea, a sea grass, lots of bioactive peptides were found by using chymotripsine digestion, which showed strong DPP4 inhibitory activities such as GL, PL, GF, KY, RL, TY, VF. In the same species, trypsine digestion gives DPP4 inhibitory activity with the bioactive peptide sequence of DF. Proteinase K digestion also gives DPP4 inhibitory function with TP, SP, KP, EP, QP, AY, EY, GV, HI, QV, RI, TP and so on. In line with these, pancreatic elastase digestion provides several important bioactive peptide sequences having DPP4 inhibitory role such as RA, PL, WT, ET, KG, KT, NV, RG, and so on [5]. Thus, marine source as a bioactive peptide would have huge potential.

The recent age, blue economy emerged a lot of potential and various countries are now focusing on exploring the marine resources in their coastal region. Various pharmaceutical companies are also searching for new sources of secondary metabolites and as a DPP4 inhibitory agent, bioactive peptide from marine origin would open a new window to explore this field.

To Know More About Oceanography & Fisheries Open Access Journal Please click on: https://juniperpublishers.com/ofoaj/index.php

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