The Relationship of Blood Prolactin, Cortisol and Thyroid Hormones in Prematural Newborns with Respiratory Distress Syndrome_ Crimson Publishers

 The Relationship of Blood Prolactin, Cortisol and Thyroid Hormones in Prematural Newborns with Respiratory Distress Syndrome by Baris Yilmaz* in

Research in Pediatrics & Neonatology_ The Journal of Pediatrics

 

 

 

Abstract

RDS is one of the leading causes of morbidity and mortality in preterm infants. It is well known that the main reason for RDS development is the deficiency of pulmonary surfactant. Various endogenous hormones such as prolactin, cortisol, testosterone, estradiol, estrone, thyroxine, and triiodothyronine play a major role in fetal lung maturation. Neonates with low birth weights and low gestational age are reported to have a higher risk of developing RDS than average. Several studies which investigated the relationship between thyroid hormones and RDS had shown that infants with RDS have lower free T4 (fT4) and total (tT4) serum levels than infants without RDS although both groups had similar gestational ages and birth weights. Serum prolactin level of neonates increases proportionally with their gestational ages and their birth weights.

Numerous studies have been shown infants who have lower serum prolactin levels have an increased risk of developing RDS, therefore prolactin might be an important factor in fetal lung maturation. A rise cortisol concentration in cord blood is recorded before the rise in lecithin/sphingomyelin ratio (an indicator of surfactant maturation), an inverse relationship between the cortisol concentration and RDS occurrence is found, and cortisol administration before conception in risky pregnancies seemed to speed up surfactant maturation. These findings favor the cortisol as one of the key factors in fetal surfactant maturation, therefore, making the cortisol administration a vital aspect of RDS prevention. 56 neonates without RDS and 61 neonates with RDS, in total 117 neonates younger than 37 weeks of gestational age were examined (prospectively or retrospectively). Blood samples from each of them were taken in their first 24 hours of life and TSH, fT4, tT4, cortisol, and prolactin quantities were measured. Some statistical differences were found when they grouped according to their RDS development and birth weights.

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NSAIDs - Associated Damage to the Stomach Mucosa (Experimental Study)_ Crimson Publishers

 NSAIDs - Associated Damage to the Stomach Mucosa (Experimental Study) by Trubitsyna IE* in Gastroenterology Medicine & Research_ Gastroenterology Open Access Journals

 

Abstract
NSAIDs remain dangerous drugs due to the damaging effect on the mucous membrane of the stomach, intestines. Experimental studies were conducted to study the damaging effects of nimesulide and lornoxicam. It was found that these drugs damage the mucous membrane of the stomach. a non-selective drug has a slightly greater damaging effect. The damaging effect of these drugs enhances motor impairment, a decrease in pH, and an increase in secretion volume. NSAIDs often lead to the formation of acute ulcers of the gastrointestinal mucosa. The development of NSAID-associated ulcerative lesions is due to an imbalance between the factors of defense and aggression in Summary non-steroidal anti-inflammatory drugs Summary nonsteroidal anti-inflammatory drugs the mucous membrane of the gastrointestinal tract [1,2]. AIM of our research was to establish factors that contribute to the development of NSAID associated ulcerative lesions of the gastric mucosa.

Material and Methods
The experiments were carried out on white Wistar rats of both sexes, weighing 190-210g. Before the operation, food was taken away for 18 hours with free access to water [3]. Under ether anesthesia, a laparotomy was performed and the pylorus was ligated, the drug solution was administered through the probe - experimental groups: Nimesulide - experiment 1 (O1) and Lornoxicam - experiment 2 (O2), pH of the solutions of the injected drugs = 4.0 - 4.5, volume - 1 , 0ml, dose - 15mg/kg, the solution was shaken before administration. Control (С) - ligation of the pylorus and the introduction of 1.0ml of physiological saline. Autopsy after 2 hours, the animals were opened under ether anesthesia, and the abdominal cavity was examined. The pH and volume of the gastric contents were measured. Then using a magnifying glass examined the mucous membrane. Damage Index (ID), the total score of the identified lesions was calculated and divided by the number of animals. Points: edema=1; hyperemia=2; single hemorrhages=3; hemorrhages fused = 4; erosion = 5; ulcer = 6.

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The Evolution of Future Medicine - WE Medicine - To Meet Unmet Medical Needs_ Crimson Publishers

The Evolution of Future Medicine - WE Medicine - To Meet Unmet Medical Needs by Yung Chi Cheng* in Novel Approaches in Cancer Study_ Journal of Cancer Research

 

Abstract

The medicines needed today are not just for the treatment of disease, but for the treatment of the whole person across his or her lifetime - from disease prevention to disease progression, modulating the efficacy and safety of other medicines, and improving quality of life.

Currently many pharmaceutical and biotech companies are focusing primarily on the treatment versus the prevention of disease, with the exception of developing vaccines against infectious agents as preventative measurement. Developing small molecule medicines still largely applies a reductionist approach focused on a particular target and developing selective and potent chemicals aimed at it. The advancement of knowledge and modern technologies has facilitated the reductionist approach and led to the discovery of a few interesting target- oriented drugs with varying degrees of success, however this approach has not been satisfactory for the treatment of more complex, heterogeneous diseases which are often associated with the aging process [1]. It is recognized that the selected target in most cases is not only important for the pathogenesis of disease, but also plays an important role in the normal functions of the body. With highly potent chemicals used on long term basis, toxicity in normal tissues will often evolve. Furthermore, there is heterogeneity of the tissue target phenotype due to the degree of nutrients, including oxygen, and interaction among cells in the tissue [2]. Drugs could have a different impact on cells depending on its target phenotype or other cellular components. The response of targeted cells to drugs could `be different. This is clearly evident in cancer tissue.

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