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Cell Cycle Regulation and Cytoskeletal Remodelling Are Critical Processes in the Nutritional Programming of Embryonic Development  [PDF]
Angelina Swali, Sarah McMullen, Helen Hayes, Lorraine Gambling, Harry J. McArdle, Simon C. Langley-Evans
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0023189
Abstract: Many mechanisms purport to explain how nutritional signals during early development are manifested as disease in the adult offspring. While these describe processes leading from nutritional insult to development of the actual pathology, the initial underlying cause of the programming effect remains elusive. To establish the primary drivers of programming, this study aimed to capture embryonic gene and protein changes in the whole embryo at the time of nutritional insult rather than downstream phenotypic effects. By using a cross-over design of two well established models of maternal protein and iron restriction we aimed to identify putative common “gatekeepers” which may drive nutritional programming. Both protein and iron deficiency in utero reduced the nephron complement in adult male Wistar and Rowett Hooded Lister rats (P<0.05). This occurred in the absence of damage to the glomerular ultrastructure. Microarray, proteomic and pathway analyses identified diet-specific and strain-specific gatekeeper genes, proteins and processes which shared a common association with the regulation of the cell cycle, especially the G1/S and G2/M checkpoints, and cytoskeletal remodelling. A cell cycle-specific PCR array confirmed the down-regulation of cyclins with protein restriction and the up-regulation of apoptotic genes with iron deficiency. The timing and experimental design of this study have been carefully controlled to isolate the common molecular mechanisms which may initiate the sequelae of events involved in nutritional programming of embryonic development. We propose that despite differences in the individual genes and proteins affected in each strain and with each diet, the general response to nutrient deficiency in utero is perturbation of the cell cycle, at the level of interaction with the cytoskeleton and the mitotic checkpoints, thereby diminishing control over the integrity of DNA which is allowed to replicate. These findings offer novel insight into the primary causes and mechanisms leading to the pathologies which have been identified by previous programming studies.
Myeloid Neoplasms in the Guise of Nutritional Deficiency
Veda Parthasarathy
Case Reports in Hematology , 2012, DOI: 10.1155/2012/826939
Abstract: The classic BCR-ABL-negative myeloproliferative neoplasms (MPNs) which include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) are among the most frequent hematologic neoplasms. Because of their relatively smooth clinical course, it is likely that many of these MPNs actually go undetected. Considering the high prevalence of iron, folic-acid, and vitamin B12 deficiencies in developing countries, their coexistence with MPN can be expected frequently. In such situations where both disorders coexist, MPN is often overlooked. This causes considerable diagnostic delay. In this paper, two cases of PMF and one case of PV where the diagnosis of MPN was delayed for about 3 years are discussed. Presence of concomitant vitamin B12, folate, and iron deficiencies perhaps camouflaged the underlying MPN. Bearing in mind the possibility of MPN, even in the setting of apparent nutritional deficiency and performing a bone marrow evaluation, is the crucial step in unveiling the hidden MPN.
Myeloid Neoplasms in the Guise of Nutritional Deficiency  [PDF]
Veda Parthasarathy
Case Reports in Hematology , 2012, DOI: 10.1155/2012/826939
Abstract: The classic BCR-ABL-negative myeloproliferative neoplasms (MPNs) which include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) are among the most frequent hematologic neoplasms. Because of their relatively smooth clinical course, it is likely that many of these MPNs actually go undetected. Considering the high prevalence of iron, folic-acid, and vitamin B12 deficiencies in developing countries, their coexistence with MPN can be expected frequently. In such situations where both disorders coexist, MPN is often overlooked. This causes considerable diagnostic delay. In this paper, two cases of PMF and one case of PV where the diagnosis of MPN was delayed for about 3 years are discussed. Presence of concomitant vitamin B12, folate, and iron deficiencies perhaps camouflaged the underlying MPN. Bearing in mind the possibility of MPN, even in the setting of apparent nutritional deficiency and performing a bone marrow evaluation, is the crucial step in unveiling the hidden MPN. 1. Introduction Myeloproliferative neoplasms (MPNs) are among the most frequent hematologic neoplasms, usually affecting the middle aged and elderly [1]. “Classic BCR-ABL-negative (Philadelphia negative) MPN” is an operational subcategory [2, 3] which includes polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). Because of their relatively smooth clinical course, it is likely that many classic BCR-ABL negative MPN cases actually go undetected. Deficiencies of iron, folic acid, and Vitamin B12 are known to occur in association with BCR-ABL-negative MPNs [4–6]. These deficiencies may be coincident, secondary, or perhaps a manifestation of the underlying MPN. In developing countries where nutritional deficiencies are prevalent, their coexistence with MPN can be expected more often. In such situations where both disorders coexist, MPN often goes unnoticed. This paper illustrates three cases of BCR-ABL-negative MPN which went unnoticed for few years owing to concurrent nutritional deficiencies. 2. Case 1 A 24-year-old female was referred with six months history of weakness and anorexia. Her records revealed that she had received hematinics and red cell concentrates several times in the past two years. She had undergone upper GI endoscopy and colonoscopy which were unremarkable. She was moderately built, had mild icterus, and spleen was palpable 4?cms below left costal margin. Her blood counts: Hb 9.3?g/dL, hematocrit 33.1%, WBC 8.8 × 109/L, platelets 682 × 109/L, MCV 103.8?fl, MCH 29.2?pg, mean platelet volume (MPV)
Nutritional programming of pancreatic β-cell plasticity  [cached]
David J Hill
World Journal of Diabetes , 2011, DOI: 10.4239/wjd.v2.i8.119
Abstract: Nutritional insufficiency during pregnancy has been shown to alter the metabolism of the offspring and can increase the risk of type 2 diabetes. The phenotype in the offspring involves changes to the morphology and functional capacity of the endocrine pancreas, and in the supporting islet microvasculature. Pancreatic β-cells possess a plastic potential and can partially recover from catastrophic loss. This is partly due to the existence of progenitors within the islets and the ability to generate new islets by neogenesis from the pancreatic ducts. This regenerative capacity is induced by bone marrow-derived stem cells, including endothelial cell progenitors and is associated with increased angiogenesis within the islets. Nutritional insults in early life, such as feeding a low protein diet to the mother, impair the regenerative capacity of the β-cells. The mechanisms underlying this include a reduced ability of β-cells to differentiate from the progenitor population, changes in the inductive signals from the microvasculature and an altered presence of endothelial progenitors. Statin treatment within animal models was associated with angiogenesis in the islet microvasculature, improved vascular function and an increase in β-cell mass. This demonstrates that reversal of the impaired β-cell phenotype observed following nutritional insult in early life is potentially possible.
Systematic Screening of Drosophila Deficiency Mutations for Embryonic Phenotypes and Orphan Receptor Ligands  [PDF]
Ashley P. Wright,A. Nicole Fox,Karl G. Johnson,Kai Zinn
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012288
Abstract: This paper defines a collection of Drosophila deletion mutations (deficiencies) that can be systematically screened for embryonic phenotypes, orphan receptor ligands, and genes affecting protein localization. It reports the results of deficiency screens we have conducted that have revealed new axon guidance phenotypes in the central nervous system and neuromuscular system and permitted a quantitative assessment of the number of potential genes involved in regulating guidance of specific motor axon branches. Deficiency “kits” that cover the genome with a minimum number of lines have been established to facilitate gene mapping. These kits cannot be systematically analyzed for phenotypes, however, since embryos homozygous for many deficiencies in these kits fail to develop due to the loss of key gene products encoded within the deficiency. To create new kits that can be screened for phenotype, we have examined the development of the nervous system in embryos homozygous for more than 700 distinct deficiency mutations. A kit of ~400 deficiency lines for which homozygotes have a recognizable nervous system and intact body walls encompasses >80% of the genome. Here we show examples of screens of this kit for orphan receptor ligands and neuronal antigen expression. It can also be used to find genes involved in expression, patterning, and subcellular localization of any protein that can be visualized by antibody staining. A subset kit of 233 deficiency lines, for which homozygotes develop relatively normally to late stage 16, covers ~50% of the genome. We have screened it for axon guidance phenotypes, and we present examples of new phenotypes we have identified. The subset kit can be used to screen for phenotypes affecting all embryonic organs. In the future, these deficiency kits will allow Drosophila researchers to rapidly and efficiently execute genome-wide anatomical screens that require examination of individual embryos at high magnification.
Telomere DNA Deficiency Is Associated with Development of Human Embryonic Aneuploidy  [PDF]
Nathan R. Treff ,Jing Su,Deanne Taylor,Richard T. Scott Jr
PLOS Genetics , 2011, DOI: 10.1371/journal.pgen.1002161
Abstract: Aneuploidy represents the most prevalent form of genetic instability found in human embryos and is the leading genetic cause of miscarriage and developmental delay in newborns. Telomere DNA deficiency is associated with genomic instability in somatic cells and may play a role in development of aneuploidy commonly found in female germ cells and human embryos. To test this hypothesis, we developed a method capable of quantifying telomere DNA in parallel with 24-chromosome aneuploidy screening from the same oocyte or embryo biopsy. Aneuploid human polar bodies possessed significantly less telomere DNA than euploid polar bodies from sibling oocytes (?3.07 fold, P = 0.016). This indicates that oocytes with telomere DNA deficiency are prone to aneuploidy development during meiosis. Aneuploid embryonic cells also possessed significantly less telomere DNA than euploid embryonic cells at the cleavage stage (?2.60 fold, P = 0.002) but not at the blastocyst stage (?1.18 fold, P = 0.340). The lack of a significant difference at the blastocyst stage was found to be due to telomere DNA normalization between the cleavage and blastocyst stage of embryogenesis and not due to developmental arrest of embryos with short telomeres. Heterogeneity in telomere length within oocytes may provide an opportunity to improve the treatment of infertility through telomere-based selection of oocytes and embryos with reproductive competence.
A Program of Nutritional Education in Schools Reduced the Prevalence of Iron Deficiency in Students  [PDF]
María Nieves García-Casal,Maritza Landaeta-Jiménez,Rafael Puche,Irene Leets,Zoila Carvajal,Elijú Pati o,Carlos Ibarra
Anemia , 2011, DOI: 10.1155/2011/284050
Abstract: The objective was to determine the prevalence of iron, folates and retinol deficiencies in school children and to evaluate the changes after an intervention of nutritional education. The project was developed in 17 schools. The sample included 1,301 children (678 males and 623 females). A subsample of 480 individuals, was randomly selected for drawing blood for biochemical determinations before and after the intervention of nutritional education, which included in each school: written pre and post-intervention tests, 6 workshops, 2 participative talks, 5 game activities, 1 cooking course and 1 recipe contest. Anthropometrical and biochemical determinations included weight, height, body-mass index, nutritional status, hematocrit, serum ferritin, retinol and folate concentrations. There was high prevalence of iron (25%), folates (75%) and vitamin A (43%) deficiencies in school children, with a low consumption of fruit and vegetables, high consumption of soft drinks and snacks and almost no physical activity. The nutritional education intervention produced a significant reduction in iron deficiency prevalence (25 to 14%), and showed no effect on vitamin A and folates deficiencies. There was a slight improvement in nutritional status. This study shows, through biochemical determinations, that nutritional education initiatives and programs have an impact improving nutritional health in school children.
The Neurological Complications of Nutritional Deficiency following Bariatric Surgery  [PDF]
Danielle A. Becker,Laura J. Balcer,Steven L. Galetta
Journal of Obesity , 2012, DOI: 10.1155/2012/608534
Abstract: Neurologic complications of bariatric surgery have become increasingly recognized with the rising numbers of procedures and the increasing prevalence of obesity in the US. Deficits are most commonly seen with thiamine, vitamin B12, folate, vitamin D, vitamin E, and copper deficiencies. The neurological findings observed with these nutritional deficiencies are variable and include encephalopathy, optic neuropathy, myelopathy, polyradiculoneuropathy, and polyneuropathy. We review the neurological complications of bariatric surgery and emphasize that these findings may vary based on the specific type of bariatric surgery and time elapsed from the procedure.
The Neurological Complications of Nutritional Deficiency following Bariatric Surgery  [PDF]
Danielle A. Becker,Laura J. Balcer,Steven L. Galetta
Journal of Obesity , 2012, DOI: 10.1155/2012/608534
Abstract: Neurologic complications of bariatric surgery have become increasingly recognized with the rising numbers of procedures and the increasing prevalence of obesity in the US. Deficits are most commonly seen with thiamine, vitamin B12, folate, vitamin D, vitamin E, and copper deficiencies. The neurological findings observed with these nutritional deficiencies are variable and include encephalopathy, optic neuropathy, myelopathy, polyradiculoneuropathy, and polyneuropathy. We review the neurological complications of bariatric surgery and emphasize that these findings may vary based on the specific type of bariatric surgery and time elapsed from the procedure. 1. Introduction The rate of obesity continues to rise and affects more than one-third of the US adult population (over 72 million people) [1]. One of the most effective treatments for obesity and its associated comorbidities is bariatric surgery because of its dramatic and durable results. According to the American Society for Metabolic and Bariatric Surgery, the number of bariatric surgeries has increased more than 10-fold, from 16,000 in the early 1990s to approximately 220,000 in 2008 [2]. However, as the prevalence of obesity and the numbers of patients undergoing bariatric surgeries rise, the incidence and recognition of neurologic complications from bariatric surgery also continues to increase. There is a growing literature to support the effectiveness of bariatric surgery in reducing morbidity and mortality for those with BMI >40 and for patients with BMI >35 and obesity-related complications [3]. Further growth of this surgical field is supported by the recent FDA approval for the expanded use of the lap-band system to include patients with a minimum BMI of 35?kg/m2 without comorbidities and 30 with comorbidities. Associated bariatric procedures contribute to nutritional deficiencies by restricting food intake and/or limiting intestinal absorption. The forms of surgery that are solely restrictive include gastric banding and vertical banding. The procedures that are restrictive and produce malabsorption include the Roux-en-Y gastric bypass procedure and the biliopancreatic diversion with duodenal switch. After these surgeries, patients should remain on high protein and low-fat diets with vitamin supplementation and have nutritional and metabolic blood tests performed on a frequent basis. In addition, it is important to note that nutritional recommendations and complications tend to be associated with the specific type of bariatric surgical procedure performed (Tables 1 and 2) [4–6]. Table 1:
A Program of Nutritional Education in Schools Reduced the Prevalence of Iron Deficiency in Students  [PDF]
María Nieves García-Casal,Maritza Landaeta-Jiménez,Rafael Puche,Irene Leets,Zoila Carvajal,Elijú Pati?o,Carlos Ibarra
Anemia , 2011, DOI: 10.1155/2011/284050
Abstract: The objective was to determine the prevalence of iron, folates and retinol deficiencies in school children and to evaluate the changes after an intervention of nutritional education. The project was developed in 17 schools. The sample included 1,301 children (678 males and 623 females). A subsample of 480 individuals, was randomly selected for drawing blood for biochemical determinations before and after the intervention of nutritional education, which included in each school: written pre and post-intervention tests, 6 workshops, 2 participative talks, 5 game activities, 1 cooking course and 1 recipe contest. Anthropometrical and biochemical determinations included weight, height, body-mass index, nutritional status, hematocrit, serum ferritin, retinol and folate concentrations. There was high prevalence of iron (25%), folates (75%) and vitamin A (43%) deficiencies in school children, with a low consumption of fruit and vegetables, high consumption of soft drinks and snacks and almost no physical activity. The nutritional education intervention produced a significant reduction in iron deficiency prevalence (25 to 14%), and showed no effect on vitamin A and folates deficiencies. There was a slight improvement in nutritional status. This study shows, through biochemical determinations, that nutritional education initiatives and programs have an impact improving nutritional health in school children. 1. Introduction Programs on nutritional education have been widely used for teaching or reinforcing knowledge on food habits or healthy life styles in children and are considered a useful strategy to prevent the appearance of nontransmissible chronic diseases at early ages. The implementation of nutritional education programs in schools may help to inculcate in children the ability of identifying a healthy food choice for themselves [1]. It has been established that the triangulation of information amongst the teacher, the children, and the family is a useful strategy for modifying negative feeding behaviors that are contributing to the recent increase in the prevalence of overweight, obesity, hypertension, diabetes, and metabolic syndrome in children, while in the opposite extreme of the spectrum, nutritional deficits persist as important nutritional problems, especially regarding micronutrient, and vitamin deficiencies such as iron, calcium, folic acid, and vitamin A, among others [2, 3]. The inclusion of nutritional education into formal education programs is one of the most used and recommended strategies, mainly because the children obtain and fix the
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