Beyond genetics: epigenetic code in chronic kidney disease

Beyond genetics: epigenetic code in chronic kidney disease: "

Beyond genetics: epigenetic code in chronic kidney disease

Kidney International 79,
23 (January (1) 2011). doi:10.1038/ki.2010.335

Authors: Rama S Dwivedi, James G Herman, Timothy A McCaffrey
& Dominic S C Raj

The best succinct review of epigenetics

Theory of gastric CO(2) ventilation and its control during respiratory acidosis: implications for central chemosensitivity, pH regulation, and diseases causing chronic CO(2) retention Gastric CO(2) ventilation during respiratory acidosis.

Theory of gastric CO(2) ventilation and its control during respiratory acidosis: implications for central chemosensitivity, pH regulation, and diseases causing chronic CO(2) retention Gastric CO(2) ventilation during respiratory acidosis.: "

Theory of gastric CO(2) ventilation and its control during respiratory acidosis: implications for central chemosensitivity, pH regulation, and diseases causing chronic CO(2) retention Gastric CO(2) ventilation during respiratory acidosis.

Respir Physiol Neurobiol. 2010 Dec 6;

Authors: Dean JB

The theory of gastric CO(2) ventilation describes a previously unrecognized reflex mechanism controlled by neurons in the caudal solitary complex (cSC) for non-alveolar elimination of systemic CO(2) during respiratory acidosis. Neurons in the cSC, which is a site of CO(2) chemosensitivity for cardiorespiratory control, also control various gastroesophageal reflexes that remove CO(2) from blood. CO(2) is consumed in the production of gastric acid and bicarbonate in the gastric epithelium and then reconstituted as CO(2) in the stomach lumen from the reaction between H(+) and HCO(3)(-). Respiratory acidosis and gastric CO(2) distension induce cSC/vagovagal mediated transient relaxations of the lower esophageal sphincter to vent gastric CO(2) upwards by bulk flow along an abdominal-to-esophageal (= intrapleural) pressure gradient the magnitude of which increases during abdominal (gastric) compression caused by increased contractions of respiratory muscles. Esophageal distension induces cSC/nucleus ambiguus/vagovagal reflex relaxation of the upper esophageal sphincter and CO(2) is vented into the pharynx and mixed with pulmonary gas during expiration or, alternatively, during eructation. It is proposed that gastric CO(2) ventilation provides explanations for 1) the postprandial increase in expired CO(2) and 2) the negative P(blood-expired)(CO)difference that occurs during increased metabolic CO(2) production. Furthermore, it is postulated that gastric CO(2) ventilation and alveolar CO(2) ventilation are coordinated under dual control by CO(2) chemosensitive neurons in the cSC. This new theory, therefore, presupposes a level of neural control and coordination between two previously presumed dissimilar organ systems and supports the notion that different sites of CO(2) chemosensitivity address different aspects of whole body pH regulation. Consequently, not all sites of central chemosensitivity are equal regarding the mechanism(s) activated for CO(2) elimination. A distributed CO(2) chemosensitive network-at least nine different areas in the CNS, including the cSC, have been reported to date-may reflect the complexity and dynamic nature of the fundamental neural circuitry required to achieve CO(2)/pH regulation across multiple organ systems under various states of arousal, oxygenation, pH status, and redox state. Moreover, coordination of respiratory and digestive control networks through the cSC could also account for the frequent co-expression of pulmonary diseases that cause chronic respiratory acidosis (and overstimulation of cSC neurons) with peptic ulcer disease or gastroesophageal reflux disease.

PMID: 21144912 [PubMed - as supplied by publisher]

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Evolutionary biology: Genomic hourglass

Evolutionary biology: Genomic hourglass: "

Evolutionary biology: Genomic hourglass

Nature 468, 7325 (2010). doi:10.1038/468768a

Authors: Benjamin Prud'homme & Nicolas Gompel

Comparative genomics studies reveal molecular signatures of the controversial 'phylotypic' stage — a time when embryos of members of an animal phylum all look more alike than at other embryonic stages. See Letters p.811 & p.815

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Developmental biology: Placenta key to fetal growth rate

Developmental biology: Placenta key to fetal growth rate: "

Developmental biology: Placenta key to fetal growth rate

Nature 468, 7324 (2010). doi:10.1038/468603d

Gestation period varies widely in the mammalian world, with some species developing twice as fast as others in the womb. This is largely because of differences in the arrangement of fetal and maternal tissues in the placenta.Isabella Capellini at Durham University, UK, and her

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Developmental biology: Placenta key to fetal growth rate

Developmental biology: Placenta key to fetal growth rate: "

Developmental biology: Placenta key to fetal growth rate

Nature 468, 7324 (2010). doi:10.1038/468603d

Gestation period varies widely in the mammalian world, with some species developing twice as fast as others in the womb. This is largely because of differences in the arrangement of fetal and maternal tissues in the placenta.Isabella Capellini at Durham University, UK, and her

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Placental microRNA expression in pregnancies complicated by preeclampsia.

Placental microRNA expression in pregnancies complicated by preeclampsia.: "

Placental microRNA expression in pregnancies complicated by preeclampsia.

Am J Obstet Gynecol. 2010 Nov 18;

Authors: Enquobahrie DA, Abetew DF, Sorensen TK, Willoughby D, Chidambaram K, Williams MA

OBJECTIVE:: The role of posttranscription regulation in preeclampsia is largely unknown. We investigated preeclampsia-related placental microRNA (miRNA) expression using microarray and confirmatory quantitative real-time polymerase chain reaction experiments. STUDY DESIGN:: Placental expressions of characterized and novel miRNAs (1295 probes) were measured in samples collected from 20 preeclampsia cases and 20 controls. Differential expression was evaluated using Student t test and fold change analyses. In pathway analysis, we examined functions/functional relationships of targets of differentially expressed miRNAs. RESULTS:: Eight miRNAs were differentially expressed (1 up-regulated and 7 down-regulated) among preeclampsia cases compared with controls. These included previously identified candidates (miR-210, miR-1, and a miRNA in the 14q32.31 cluster region) and others that are novel (miR-584 and miR-34c-5p). These miRNAs target genes that participate in organ/system development (cardiovascular and reproductive system), immunologic dysfunction, cell adhesion, cell cycle, and signaling. CONCLUSION:: Expression of miRNAs that target genes in diverse pathophysiological processes is altered in the setting of preeclampsia.

PMID: 21093846 [PubMed - as supplied by publisher]

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The "Great Obstetrical Syndromes" are associated with disorders of deep placentation.

The "Great Obstetrical Syndromes" are associated with disorders of deep placentation.: "

The 'Great Obstetrical Syndromes' are associated with disorders of deep placentation.

Am J Obstet Gynecol. 2010 Nov 20;

Authors: Brosens I, Pijnenborg R, Vercruysse L, Romero R

Defective deep placentation has been associated with a spectrum of complications of pregnancy including preeclampsia, intrauterine growth restriction, preterm labor, preterm premature rupture of membranes, late spontaneous abortion, and abruptio placentae. The disease of the placental vascular bed that underpins these complications is commonly investigated with targeted biopsies. In this review, we critically evaluate the biopsy technique to summarize the salient types of defective deep placentation, and propose criteria for the classification of defective deep placentation into 3 types based on the degree of restriction of remodeling and the presence of obstructive lesions in the myometrial segment of the spiral arteries.

PMID: 21094932 [PubMed - as supplied by publisher]

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