ahmed R. G. | Beni-Suef University (original) (raw)

Papers by ahmed R. G.

Springer, 2022

This study aimed to explore behavioral changes of embryonic and larval zebrafsh caused by pseudoe... more This study aimed to explore behavioral changes of embryonic and larval zebrafsh caused by pseudoephedrine hydrochloride (PSE) and its underlying mechanism. Zebrafsh embryos were exposed to 0.5 µM, 2 µM, and 8 µM PSE at 4 h postfertilization (4 hpf) or 22–23 hpf. Mortality, hatching rate, coiling frequency, heart rate, behavior changes, and related gene expression were observed at diferent developmental stages. PSE below 8 µM did not afect zebrafsh mortality, hatching rate, and heart rate compared with the control group. For embryos, PSE caused an increase at 16–32 hpf in zebrafsh coiling frequency which could be rescued by serotonin antagonist WAY100635. Similarly, PSE caused an increase in the swimming distance of zebrafsh larvae at 120 hpf. PSE also elevated the expression of serotonin (5-HT)-related genes 5-htr1ab and tph2 and dopamine-related gene dbh. Behavioral changes in zebrafsh embryos and larvae caused by PSE may be closely associated with increased expression of 5-HT and dopamine-related genes. This may be refected that the behavioral changes in zebrafsh are a possible PSE monitoring indicator.

Elsevier, 2022

Neural plasticity, remodeling neural network is associated with learning and memory. Neurons r... more Neural plasticity, remodeling neural network is associated with learning and memory.
Neurons reorganize the strength and efficacy of synaptic transmission.
Epigenetic reprogramming is an established mechanism of neural plasticity.
Epigenetic signature proteins are the hallmark of epigenetic remodeling.
Natural bioactive compounds potentially modulate the epigenetic mechanism

Int. J. Dev. Neurosci. , 2020

The aim of this work was to clarify whether maternal lithium chloride (LiCl) exposure disrupts th... more The aim of this work was to clarify whether maternal lithium chloride (LiCl) exposure disrupts the neonatal neuroendocrine-cytokine axis. Pregnant Wistar rats were orally administrated 50 mg LiCl/kg b.wt. from gestational day (GD) 1 to postpar-tum day 28. Maternal administration of LiCl induced a hypothyroid state in both dams and their neonates compared to the control dams and neonates at lactation days (LDs) 14, 21 and 28, where the levels of serum free triiodothyronine (FT3) and free thyroxin (FT4) were decreased and the level of serum thyrotropin (TSH) level was increased. A noticeable depression in maternal body weight gain, neonatal body weight and neonatal serum growth hormone (GH) was observed on all examined postnatal days (PNDs; 14, 21 and 28). A single abortion case was recorded at GD 17, and three dead neonates were noted at birth in the LiCl-treated group. Maternal administration of LiCl disturbed the levels of neonatal serum tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta (TGF-β), interleukin-1 beta (IL-1β), interferon-gamma (INF-γ), leptin, adiponectin and resistin at all tested PNDs compared to the control group. This administration produced a stimulatory action on the level of neonatal cerebral serotonin (5-HT) at PND 14 and on the level of neonatal cerebral norepinephrine (NE) at PNDs 21 and 28. However, this administration produced an inhibitory action on the level of neonatal cerebral dopamine (DA) at all examined PNDs and on the level of neonatal cerebral NE at PND 14 and the level of neonatal cerebral 5-HT at PNDs 21 and 28 compared to the corresponding control group. Thus, maternal LiCl exposure-induced hypothyroidism disrupts the neonatal neuroendocrine-cytokine system, which delay cerebral development. K E Y W O R D S cytokine, dams, lithium chloride, monoamine, pups, thyroid

Dose-Response: An International Journal, 1-12. , 2019

The goal of this investigation was to evaluate the effects of gestational administrations of arse... more The goal of this investigation was to evaluate the effects of gestational administrations of arsenic trioxide (ATO; As 2 O 3) on fetal neuroendocrine development (the thyroid-cerebrum axis). Pregnant Wistar rats were orally administered ATO (5 or 10 mg/kg) from gestation day (GD) 1 to 20. Both doses of ATO diminished free thyroxine and free triiodothyronine levels and augmented thyrotropin level in both dams and fetuses at GD 20. Also, the maternofetal hypothyroidism in both groups caused a dose-dependent reduction in the fetal serum growth hormone, insulin growth factor-I (IGF-I), and IGF-II levels at embryonic day (ED) 20. These disorders perturbed the maternofetal body weight, fetal brain weight, and survival of pregnant and their fetuses. In addition, destructive degeneration, vacuolation, hyperplasia, and edema were observed in the fetal thyroid and cerebrum of both ATO groups at ED 20. These disruptions appear to depend on intensification in the values of lipid per-oxidation, nitric oxide, and H 2 O 2 , suppression of messenger RNA (mRNA) expression of nuclear factor erythroid 2-related factor 2 and peroxisome proliferator-activated receptor gamma, and activation of mRNA expression of caspase-3, nuclear factor kappa-light-chain-enhancer of activated B cells, cyclooxygenase-2, Bcl-2-associated X protein, and inducible nitric oxide synthase in the fetal cerebrum. These data suggest that gestational ATO may disturb thyroid-cerebrum axis generating fetal neurodevelopmental toxicity.

Toxicol. Res., 8, 196–205. , 2019

The objective of this examination was to explore the impact of gestational caffeine (1,3,7-trimet... more The objective of this examination was to explore the impact of gestational caffeine (1,3,7-trimethyl-xanthine) exposure on the maternofetal thyroid axis and fetal thyroid-cytokine communications during gestation. Pregnant rats (Rattus norvegicus) were intraperitoneally administered caffeine (120 or 150 mg kg −1) from gestation day (GD) 1 to 20. Both doses of caffeine resulted in maternal hyperthyroid-ism, whereas the elevation in the concentration of serum free triiodothyronine (FT3) and free thyroxine (FT4) was related to a depletion in the level of TSH at GD 20. Maternal body weight gain and food consumption were markedly increased, while fetal body weight was significantly reduced. These alterations caused fetal hypothyroidism and several pathological lesions in the fetal thyroid gland including a vacuolar colloid, destructive degeneration, atrophy and hyperplasia at embryonic day (ED) 20. The abnormalities in the fetal thyroid gland seemed to depend on the activation of caspase-3, Bcl-2, BAX, Cox2, and NF-κB mRNA expression. Both maternal caffeine doses caused a marked attenuation in the values of fetal serum GH, IGF-II, VEGF, TGF-β, TNF-α, IL-1β, IL-6, leptin and MCP-1, and a noticeable elevation in the value of fetal serum adiponectin at ED 20. Thus, gestational caffeine exposure might disrupt the fetal thyroid-cytokine axis.

I am editor for a book entitled "Growth Hormone Deficiency" with InTech organization ISBN: 978-1-... more I am editor for a book entitled "Growth Hormone Deficiency" with InTech organization ISBN: 978-1-83880-584-5. The experts in these subjects are invited to contribute their findings in the form of chapter/s. The project link and the news about the upcoming Growth Hormone Deficiency book:
https://mts.intechopen.com/welcome/889cf2b5a21e42ccdf34e5861c1cc0a4/

Thyroid hormones (THs) play an essential role during the fetal and neonatal development (Gereben ... more Thyroid hormones (THs) play an essential role during the fetal and neonatal development (Gereben et al.,

The steady in the functions of gestational thyroid hormones (THs) displays major actions in the d... more The steady in the functions of gestational thyroid hormones (THs) displays major actions in the developing brain in particular the development and differentiation of neurons, oligodendrocytes, astrocytes and microglial cells(El-bakry et al.

Toxicol. Res., 2019, 8, 196–205. , 2019

The objective of this examination was to explore the impact of gestational caffeine (1,3,7-trimet... more The objective of this examination was to explore the impact of gestational caffeine (1,3,7-trimethylxanthine) exposure on the maternofetal thyroid axis and fetal thyroid–cytokine communications during
gestation. Pregnant rats (Rattus norvegicus) were intraperitoneally administered caffeine (120 or
150 mg kg−1) from gestation day (GD) 1 to 20. Both doses of caffeine resulted in maternal hyperthyroidism, whereas the elevation in the concentration of serum free triiodothyronine (FT3) and free thyroxine
(FT4) was related to a depletion in the level of TSH at GD 20. Maternal body weight gain and food consumption were markedly increased, while fetal body weight was significantly reduced. These alterations
caused fetal hypothyroidism and several pathological lesions in the fetal thyroid gland including a vacuolar
colloid, destructive degeneration, atrophy and hyperplasia at embryonic day (ED) 20. The abnormalities in
the fetal thyroid gland seemed to depend on the activation of caspase-3, Bcl-2, BAX, Cox2, and NF-κB
mRNA expression. Both maternal caffeine doses caused a marked attenuation in the values of fetal serum
GH, IGF-II, VEGF, TGF-β, TNF-α, IL-1β, IL-6, leptin and MCP-1, and a noticeable elevation in the value of
fetal serum adiponectin at ED 20. Thus, gestational caffeine exposure might disrupt the fetal thyroid–
cytokine axis.

THs and their receptors can regulate the development and functioning of the auditory system. In a... more THs and their receptors can regulate the development and functioning of the auditory system. In addition, any dysfunctions in the activities of THs during the development may cause hearing loss. These disorders may delay the developmental cognitive behaviors and neonatal responses, cause numerous lifelong consequences and severely impact quality-of-life. The prevention with early detection and treatment of hearing loss may be amenable. Yearly audiological evaluation to monitor hearing should be done. The results may be depending on the age of hearing examination, the methods of hearing assessment, and the genetic factors in different patient populations. Further studies are required to determine the exact prevalence of hearing impairment in children with permanent congenital hypothyroidism.

A normal transportation of thyroid hormones (THs) from pregnant women to their fetuses/neonates i... more A normal transportation of thyroid hormones (THs) from pregnant women to their fetuses/neonates is required for the normal development, particularly the energy homeostasis, appetite, basal metabolic rate (BMR) and metabolic mechanisms. In addition, mild maternal thyroid insufficiency (isolated hypothyroxinaemia; reduction in the level of free thyroxine (FT4) and an increase in the free triiodothyronine (FT3) to FT4 ratios) with poor obstetric outcomes during gestation can cause several adverse metabolic defects such as insulin resistance, glycaemia, obesity, and lipid profile disorders (hyper-lipidaemia). Also, the association between the maternal hypothyroxinaemia and obesity was observed in iodine-deficient pregnant women. It was supposed that obesity-induced the activities of peripheral deiodinases (Ds) increasing the energy expenditure, the conversion of FT4 to FT3 and eventually the FT3 to FT4 ratio. Thus, any disruption in the levels of THs during the gestation may cause obesity and suppress the neonatal development. Women have to avoid the hypothyroxinemia and any excess in the body weight gain. Maintaining normoglycaemia during pregnancy may play an important role in a healthy life for the newborns. However, additional studies are essential to replicate these observations and to explore the harmful effects of maternofetal thyroid dysfunction (hypothyroidism or isolated hypothyroxinaemia) and obesity (adverse metabolic parameters) on long-term growth and neonatal development. Furthermore, the connection between the molecular and epidemiological studies is required. This argument is still ambiguous because of the difficulties of the direct observation of thyroid dysfunction on obesity.

The activities of maternal thyroid hormones (THs) are important for the advancement of the prenat... more The activities of maternal thyroid hormones (THs) are important for the advancement of the prenatal and postnatal development. The homeostasis between the levels of THs and the placental development regulates the electrolytes equilibrium between dams and their fetuses/newborns. On the other hand, hyponatremia, electrolyte abnormality, can cause by the excess free H2O intake and the impairment in its excretion due to arginine vasopressin (AVP) excess. Another probable cause of hyponatremia is hypothyroidism/myxedema. More importantly, possible mechanisms of hyponatremia associated with hypothyroidism can be explained as the following: (1) increased the syndrome of inappropriate antidiuretic hormone secretion (SIADH; increase urine Na+); (2) decreased the cardiac outputs; (3) increased the level of antidiuretic hormone (ADH); (4) salt-losing nephropathy and hypovolemia; (5) decreased the glomerular filtration rate (GFR); (6) low-iodine and solute intake; (7) decreased the water delivery to the kidney diluting segment; (8) decreased the excretion of water content; and (9) water retention. In addition, any disruption in the activities of maternal antepartum THs (hypothyroidism) may disturb the electrolyte equilibrium between the dams and their fetuses/neonates. My hypothesis is the maternal antepartum dyselectrolytemia may intensify the risk of pre-delivery and may cause neonatal disorders. Though, the mechanism of maternofetal dyselectrolytemia or metabolic derangement remains indeterminate. Thus, I advise to treat the maternal electrolyte imbalance and thyroid functions before the gestation or correct the dyselectrolytemia and thyroid functions in the neonates after the labor. Moreover, a care postpartum for both dams and their newborns may be required to get a good outcome.

The normal balance in the levels of dietary omega-3-fatty acids (anti-inflammatory actions) and m... more The normal balance in the levels of dietary omega-3-fatty acids (anti-inflammatory actions) and maternal THs may be necessary for the normal brain development during the prenatal and postnatal periods. In addition, the deficiency in their levels during the gestation may increase the risk of teratogenic consequences and brain disorders (depression, psychotic symptoms, mental retardation, schizophrenia, Alzheimer, cognitive dysfunction, and mood disability) in fetuses, neonates, and childhood. These disturbances may increase the susceptibility of the CNS to the inflammatory-immune diseases, may decrease the neurite growth, and may inhibit the development generally. However, their developmental, molecular and biochemical mechanisms are unclear until now. The disruptions in the fetal and neonatal development may be depending on the time and severity of these deficiencies. Thus, this report can be recommended the following: (1) avoid the deficiency in levels of dietary omega-3-fatty acids and maternal THs; (2) Pregnant can keep the normal levels of dietary omega-3-fatty acids by eating the fatty fish such as salmon, tuna, and trout; (3) overconsumption of fishes should be avoided for the mercury toxicity; and (4) following the levels of maternal THs before or during pregnancy to decrease or avoid the previous disorders. Additional experiments are important to study the influence of the deficiency in levels of dietary omega-3-fatty acids and maternal THs at different stages of pregnancy (following pregnancy duration and birth dimensions) on the developing neuroendocrine system of both fetuses and neonates. The developmental, molecular, biochemical and immunological mechanisms should be examined. This could support development novel therapeutic approaches and enhance maternal and infant health consequences.

Thyroid hormones (THs) are crucial for the standard development and thermogenesis, particularly t... more Thyroid hormones (THs) are crucial for the standard development and thermogenesis, particularly the myogenesis, contractile function, bioenergetic metabolism, the activity of the Na+-K+-ATPase in skeletal myotubes, the sarcoplasmic reticulum Ca2+ -ATPase, the differentiation of muscle progenitor cell, and regeneration of the skeletal muscle. It is significant to notice that during the normal development of the skeletal muscle, the dynamic changes in the activities of THs can change the fiber type profile and the muscle propriety as well. In addition, the regular effect of hypothalamus–pituitary–thyroid axis (HPTA) on the homeostasis of the skeletal muscle depending on the thyroid receptors (TRs; α and β), thyroid transporters [monocarboxylate transporters (MCT8 and MCT10)] and thyroid metabolism enzymes (deiodinases; D2, D3). On the other hand, the disorders in thyroid function can cause the following: (1) reduce the metabolism and glucose level; (2) disrupt the activities of Ds (DIO2 activity and DIO3 mRNA); (3) diaphragm muscle dysfunction; (4) loss of muscle strength; (5) muscle fatigue; (6) diminish the mitochondrial content in both legs; (7) perturb the energy production in the respiratory muscle; (8) change the nature of myosin in fast muscle; and (9) muscle weakness and hypoplasia. Finally, the disorders in the thyroid activity, TRs, Ds or MCTs may impact the myogenesis, the relaxation–contraction rates, metabolism and regeneration of the skeletal muscle. Additional considerations are necessary to confer the effect of thyroid disorders during the gestation on the fetal muscular physiological processes.

The aim of this study was to assess the effects of neonatal bisphenol A (BPA) administration on n... more The aim of this study was to assess the effects of neonatal bisphenol A (BPA) administration on neuroendocrine features (the thyroid-brain axis). BPA (20 or 40 µg/kg) was orally administered to juvenile male albino rats (Rattus norvegicus) from postnatal days (PNDs) 15 to 30. Both doses resulted in lower serum thyroxine (T4), triiodothyronine (T3), and growth hormone levels and higher thyrotropin level than the control levels at PND 30. In the neonatal cerebellum and cerebrum, vacuolation, pyknosis, edema, degenerative changes, and reductions in the size and number of the cells were observed in both treated groups. Alternatively, elevations in oxidative markers (lipid peroxidation, nitric oxide, and hydrogen peroxide [H 2 O 2 ]) at both dose levels were recorded at PND 30, along with decreased activities of antioxidant markers (ascorbic acid, total thiol [t-SH], glutathione, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and catalase) with respect to control levels. Thus, the BPA-induced hypothyroid state may disturb the neonatal thyroid-brain axis via production of free radicals, and this could damage the plasma membrane and cellular components, delaying cerebrum and cerebellum development.

Any disorders in the communications between the hypothalamus-pituitary-thyroid axis (HPTA) and th... more Any disorders in the communications between the hypothalamus-pituitary-thyroid axis (HPTA) and the hypothalamic-pituitary-adrenal axis (HPAA) during the gestation may cause a depression in both mothers and fetuses/neonates. The endocrine anomalies may increase the risk of morbidity and several developmental disorders. Dysfunction in the HPTA and HPAA can cause the major depressive disorders. Thus, additional studies are necessary to understand the potential associations between the fetal/perinatal adrenal-thyroid disorders and depression. Future examinations are wanted to discover whether the effect of maternal thyroid hormone replacement therapy on the developmental thyroid-adrenal axis play a role in modifying the signaling pathways to enhance the atypical, melancholic or severe depression during the perinatal period.

Thyroid hormones (THs) play an essential role during the fetal and neonatal development, particu... more Thyroid hormones (THs) play an essential role during the fetal and neonatal development, particularly the normal growth of bone cells. THs also induce the cellular proliferation of cartilage growth in the epiphyseal plate of long bones by stimulation the release of growth hormone (GH) and IGF (insulin-growth factor). In addition, thyroid receptors (TRs; α and β) were found in chondrocytes, growth plat, and osteoblasts. It has also been revealed that triiodothyronine (T3) can activate the terminal differentiation of growth plate chondrocytes, osteoclastic growth and the osteoblasts process. On the other hand, the maternal hypothyroidism delayed the body growth and ossification in rat. In addition, hypothyroidism can reduce the bone turnover, osteoclast bone reabsorption, osteoblast formation, and remodeling process. Alternatively, the hyperthyroidism can accelerate the development of skeletal bones and premature closure of the epiphyseal growth plates (EGPs), and subsequent diminish the longitudinal bone growth. During the early childhood, severe hyperthyroidism can induce the premature fusion of the sutures of the skull and craniosynostosis. More importantly, the disturbances in the TRα1 or TRβ can perturb and delay the development of epiphyseal growth plates and the ossification process. Thus, the maternal thyroid disorders may alter the general skeletal features during the prenatal and postnatal development. Additional examinations are desired to identify the gene expression and signaling of THs-bone axis during the development. Also, several experimental studies are required to test whether T3 can act directly or indirectly in osteoclasts.

It has been suggested that maternal HCV (chronic hepatitis C) may increase the risk of preterm de... more It has been suggested that maternal HCV (chronic hepatitis C) may increase the risk of preterm delivery, teratogenic consequences, child death, and neonatal thyroid disorders (thyroiditis or cancer). The presence of positive thyroid antibodies and macrophages is the prognostic factors of the thyroid disorders. In addition, these disorders may cause several brain disabilities and inflammatory-immune diseases in fetuses, neonates, and childhood. In general, these disturbances may delay the development and growth depending on the severity of HCV and time of its infection. However, the disruption mechanisms of HCV during the different periods of development are still uncertain. Thus, following the state of the pregnancy and the levels of maternal T3, T4, thyroid-stimulating hormone (TSH), thyroid antibodies, and serum fibrosis markers in the presence of HCV infection should be more significant to avoid or decrease the risk of teratogenic consequences and neonatal thyroid dysfunction. Hopefully, several pharmacogenomics methods will be used to recognize the activity of maternal thyroid gland during the gestation previous to the initiation of HCV treatments. Additional work is vital to determine the developmental (the metabolic pathways), molecular and biochemical disruption mechanisms of maternal HCV infection and its treatment during the fetal and neonatal development. Clinical examinations are still essential to understand the associations between the chronic HCV infection and the prevalence of maternofetal autoimmune thyroid disorders and thyroid cancer. As well, several studies are required to discover novel drugs for HCV treatment and new therapeutic approaches to improve the maternofetal and neonatal health consequences, and to decrease the morbidity and mortality in fetuses, neonates or child.

THs promote the general body growth and the development of fetal individual tissues and organs. I... more THs promote the general body growth and the development of fetal individual tissues and organs. In addition, any disorders in the levels of THs during intrauterine development may cause intrauterine and fetal growth restriction. Also, intrauterine growth restriction is a main and silent cause of fetal and neonatal morbidity and mortality. These disorders may disrupt the development and growth of fetus and neonates, and cause several lifelong consequences through permanent fluctuations in most biological systems. Thus, monitoring the activity of maternal THs may prevent any undesirable pathological state during intrauterine development. Additional studies should evaluate the relationship between the maternal thyroid disorders, thyroid autoantibodies, intrauterine and fetal growth restriction.

Any disorders in the activity of maternal thyroid gland during the gestation may increase the dem... more Any disorders in the activity of maternal thyroid gland during the gestation may increase the demyelination (hypomyelination) and decrease the thickness of the myelin sheath. These disruptions may increase the vulnerability of the CNS to multiple sclerosis and several inflammatory-immune impairments. As well, the gestational hypothyroidism associated with the multiple sclerosis may cause the following: (1) perturb the neural organization and synaptogenesis; (2) delay the development and progress of the fetal and neonatal neuroendocrine system (thyroid-brain axis); (3) increase the teratogenic consequences; (4) increase the risk of developing brain disorders (mental retardation or cognitive disorders); and (5) delay the fetal and neonatal development generally. Thus, both diseases may be a major avoidable health problem worldwide. These conditions may be depending on the severity, distribution and time of both diseases. Though, their molecular mechanisms are obscure. To date, it is not obvious whether the described effects of both diseases on the fetal or neonatal neuroendocrine system in experimental animal models might be fitted to human health. These observations strongly recommend assessing maternal THs and treating hypothyroidism before or during the gestation to avoid the vulnerability to any inflammatory diseases, in particular, multiple sclerosis in the fetal or neonatal CNS. Further experiments are influential to examine the impact of maternal hypothyroidism and multiple sclerosis on the fetal and neonatal neuroendocrine system (thyroid-brain axis). Moreover, the molecular and immunological variation due to both diseases during the gestation and lactation periods should be addressed. This could assist to understand the pathogenesis of both diseases and planning new therapeutic approaches.

Springer, 2022

Elsevier, 2022

Int. J. Dev. Neurosci. , 2020

Dose-Response: An International Journal, 1-12. , 2019

Toxicol. Res., 8, 196–205. , 2019

Toxicol. Res., 2019, 8, 196–205. , 2019

The objective of this examination was to explore the impact of gestational caffeine (1,3,7-trimet... more The objective of this examination was to explore the impact of gestational caffeine (1,3,7-trimethylxanthine) exposure on the maternofetal thyroid axis and fetal thyroid–cytokine communications during
gestation. Pregnant rats (Rattus norvegicus) were intraperitoneally administered caffeine (120 or
150 mg kg−1) from gestation day (GD) 1 to 20. Both doses of caffeine resulted in maternal hyperthyroidism, whereas the elevation in the concentration of serum free triiodothyronine (FT3) and free thyroxine
(FT4) was related to a depletion in the level of TSH at GD 20. Maternal body weight gain and food consumption were markedly increased, while fetal body weight was significantly reduced. These alterations
caused fetal hypothyroidism and several pathological lesions in the fetal thyroid gland including a vacuolar
colloid, destructive degeneration, atrophy and hyperplasia at embryonic day (ED) 20. The abnormalities in
the fetal thyroid gland seemed to depend on the activation of caspase-3, Bcl-2, BAX, Cox2, and NF-κB
mRNA expression. Both maternal caffeine doses caused a marked attenuation in the values of fetal serum
GH, IGF-II, VEGF, TGF-β, TNF-α, IL-1β, IL-6, leptin and MCP-1, and a noticeable elevation in the value of
fetal serum adiponectin at ED 20. Thus, gestational caffeine exposure might disrupt the fetal thyroid–
cytokine axis.

The BOOK aims to provide the student with: 1- A wide range of integrated knowledge and understand... more The BOOK aims to provide the student with:
1- A wide range of integrated knowledge and understanding of concepts and theories on the field of Vertebrates.
2- Skills necessary to analyze the relationship between the animal and the environment.

The BOOK aims to provide the student with: 1- A wide range of integrated knowledge and understand... more The BOOK aims to provide the student with:
1- A wide range of integrated knowledge and understanding of concepts and theories on the field of embryology.
2- Knowledge necessary for the embryonic culture, embryonic transplantation, folliculogenesis, and gene expression during development.
3- Skills necessary to analyze the relationship between the embryos and the environment.

Diabetes is a complex, progressive disease, which is accompanied by several complications. It is ... more Diabetes is a complex, progressive disease, which is accompanied by several complications. It is listed among the most common endocrine disorders and a global metabolic epidemic disease. This book focuses on the recent progress in diabetes research worldwide. This book has been written by extensively acknowledged experts, with each chapter providing unique data on developing features of diabetes. This book covers the interactions between diabetes and several disorders. Also, the book suggests some treatments for this disease offering us hope in prevention and successful improvement.

FUTURE BOOK: INTECHOPEN PUBLISHER BOOK EDITOR: Ahmed R. G. BOOK TITLE: Placenta ISBN: 978-953-51... more FUTURE BOOK: INTECHOPEN PUBLISHER
BOOK EDITOR: Ahmed R. G.
BOOK TITLE: Placenta
ISBN: 978-953-51-6651-1
Apply Proposal (before 10/04/2018): open online now
http://www.intechopen.com/welcome/447d49d62164c5437461f3b0aae7a67f/

Dear All Prof. Dr.
I write to you as the Editor of the eBook Series ‘Placenta ISBN: 978-953-51-6651-1’ will publish by INTECHOPEN Publishers. I am also the Founding Editor of several books such as also published by INTECHOPEN.
On account of the normal placentation is vital for maintaining the gestation and for the optimal fetal development; supply nutrients, exchange gases and eliminate the metabolic waste products, any disorders in the placental functions can cause several pregnancy complications. The current book will focus on nature, the developmental, biochemical, immunological and molecular basis of developing placenta (placental hemodynamics; invasion, proliferation, and migration). This book will review the factors that contribute to the fetoplacental axis including nutrients, exchange gases, oxygen concentration, human chronic gonadotropin, follicular stimulating hormone (FSH), luteinizing hormone (LH), thyroid hormones, growth hormone, insulin, steroid hormones, progesterone, estrogen, prolactin, prostaglandin, oxytocin, epidermal growth factor (EGF), vascular endothelial growth factor-A (VEGF-A)), inflammatory mediators, tumor necrosis factor alpha (TNF-α), and interleukin 10 (IL-10)), angiogenesis, angiopoietin 2 (Ang-2), angiogenin, expression of integrins and matrix metalloproteinases. Also, it will explore the associations between the placental dysfunctions, pregnancy complications, preeclampsia, premature delivery, fetal growth restriction, mortality, morbidity, hormonal disorders, hypothyroidism, hyperthyroidism, diabetes, hypertensive disorders, and autoimmunity diseases.
KEYWORDS:
Placenta, developmental, biochemical, immunological and molecular basis of placentation, placental hemodynamics, placental transporters, maternal decidua, endovascular trophoblast (EVT) invasion, trophoblast proliferation, intrauterine trophoblast migration kinetics, maternal spiral arteries, fetal trophoblast cells, fetoplacental unit, placental abruption, corpus luteum, human decidual cells, nutrients, exchange gases, oxygen concentration, metabolic waste products, placental dysfunctions, pregnancy complications, preeclampsia, premature delivery, fetal growth restriction, mortality, morbidity, human chronic gonadotropin, follicular stimulating hormone (FSH), luteinizing hormone (LH), thyroid hormones, growth hormone, insulin, steroid hormones, progesterone, estrogen, prolactin, prostaglandin, oxytocin, epidermal growth factor (EGF), vascular endothelial growth factor-A (VEGF-A)), inflammatory mediators, tumor necrosis factor alpha (TNF-α), and interleukin 10 (IL-10)), angiogenesis, angiopoietin 2 (Ang-2), angiogenin, expression of integrins and matrix metalloproteinases, hormonal disorders, hypothyroidism, hyperthyroidism, diabetes, hypertensive disorders, autoimmunity diseases, remodeling at the maternal-fetal interface, in vivo studies, in vitro studies.
These keywords are not definitive but can be used as the basis for the chapter content. We accept theoretical and applied scientific papers which can be presented as original research papers and review papers. The required length of the full chapters is 14 to 20 pages.

Please, if you like to submit a proposal before 10/04/2018, you can follow this link or attached file:
http://www.intechopen.com/welcome/447d49d62164c5437461f3b0aae7a67f/
I look forward to receiving your reply soon.
Thanks again
Regards
Ahmed RG

My Book: Germ Cell Book. Edited by Ahmed RG, ISBN 978-953-51-3759-7, Print ISBN 978-953-51-3758-... more My Book:
Germ Cell Book. Edited by Ahmed RG, ISBN 978-953-51-3759-7, Print ISBN 978-953-51-3758-0, 156 pages, Publisher: InTech, Chapters published January 31, 2018 under CC BY 3.0 license DOI: 10.5772/65614 Edited Volume. Germ Cell

Copy the following HTML and paste it in your blog post or your web page:

Germ Cell

Contents:
· Chapter 1 Germ Cell Specification: The Evolution of a Recipe to Make Germ Cellsby Pritesh Krishnakumar and Roland Dosch

· Chapter 2 The Regulation of Germline Stem Cells and Their Neighbouring Somatic Cells in the Fruit Fly (Drosophila melanogaster)by Sharon Wui Sing Tan, Yu Cai and Gyeong Hun Baeg

· Chapter 3 Primordial Germ Cell Reprogrammingby Maria P. De Miguel, Yago Alcaina and Diego Sainz de la Maza

· Chapter 4 Membrane Dynamics of Spermatozoa during Capacitation: New Insight in Germ Cells Signallingby Nicola Bernabò, Marina Ramal Sanchez, Luca Valbonetti, Luana Greco, Giulia Capacchietti, Mauro Mattioli and Barbara Barboni

· Chapter 5 Challenging the Paradigms on the Origin, Specification and Development of the Female Germ Line in Placental Mammalsby Noelia P. Leopardo, Pablo I.F. Inserra and Alfredo D. Vitullo

· Chapter 6 Germ Cell Tumors and their Association with Pregnancyby Mamta Gupta and Vandana Saini

Endocrine-disrupting compounds (EDCs) are able to imbalance hormone-driven processes in animals a... more Endocrine-disrupting compounds (EDCs) are able to imbalance hormone-driven processes in animals a humans (fish-eating populations). Disruption of maternal endocrine hormones during fetal development result in irreversible consequences in offspring. The book will focus on the nature and types of endocrine disruptors-including the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), bisphenol A (BPA), polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans (PCDFs), polychlorinated dibenzo-p-dioxins (PCDDs), triclosan, tributyltin (TBT) etc. In this book we will look at important interactions among EDCs, hormones receptors, protein expression, fat tissues, developmental dysfunction, cognitive behaviors and other phenotypic or physiological measures, to gain understanding of what factors—or groups of factors—are phenotypic changes in animals/human living in impacted environments. The book will not only to follow t effect of EDCs on endocrine hormones-dependent brain development but also to characterize the multip neuro-molecular mechanisms of EDCs, particularly the aryl hydrocarbon receptors. The book will provid information about the role of growth factors and antioxidant compounds against the neurotoxic effect of during the development. This book will be of interest to scientists, neuroendocrinologists, neurotoxicolog and physicians wishing to review recent developments in the field of EDCs.

Invite Colleagues/Peers for Research Contribution Dear Prof. Dr. I am an Ambassador in Bentham S... more Invite Colleagues/Peers for Research Contribution
Dear Prof. Dr.
I am an Ambassador in Bentham Science Publishers of Quality Research and I am encouraging you to submit your work (ARTICLES, REVIEW, Ebook program…ETC) in Bentham standard journals with fast and qualified reviewing.

Bentham Science Publishers (BSP) publishes over 100 scholarly journals, 38 of which have registered Impact factors as per the Journal Citation Reports 2018. You can learn about all of Bentham’s journals by visiting their website www.benthamscience.com
I would like to take this opportunity to recommend you to contribute your future article in Bentham Science journals. There are many journals indexed in renowned indexing agencies and their articles having a vast reach in the scientific community and the industry.
If you are interested in getting your article(s) published with Bentham Science Publishers, then please contact Bentham Sciences Marketing Manager Mr. Latif Ur Rehman at latif@benthamscience.net

Thanks
Regards
Ahmed RG

https://ahmedasd020.blogspot.com ملفات هامة عن الحياة والصحة العامة Important files about the lif... more https://ahmedasd020.blogspot.com
ملفات هامة عن الحياة والصحة العامة
Important files about the life and general health