Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to ensure the higher effectiveness, more stability and sustainability of Protective plantations, the definition of phase-directional management (PDM) of protective plantations was brought forward on the basis of management researches and practices for protective plantations. The basics of PDM is protective maturity, which is defined as the time when the protective plantations attain to the state that the protective plantations can provide effective and complete protection to the objects needed to be protected. Protective maturity has two points, initial protective maturity age (IPMA), the age of protective maturity started, and terminal protective maturity age (TPMA), the age of protective maturity ended. Three management phases of protective plantation, i.e., prematurity phase, the period from sapling or establishment to initial protective maturity, protective maturity phase, the period of protective maturity lasting, and regeneration phase, the period during regeneration and before the establishment, are divided based on the fundamental of protective maturity. Directional management of protective plantation means that all of the management techniques in each phase are directed at the aim of protective maturity, i.e., protective maturity is the direction of management of protective forests, and protective maturity is the final objective for the management of protective forests. In order to sustain the protective maturity state, corresponding measures should be conducted in each phase, according to the classification of protective plantations. In pre-maturity phase, the purpose of managing is to accelerate the protective maturity, therefore, the measures such as weed clearing, soil cultivation, irrigation, fertilization, intercropping and branch cutting etc. should be conducted in protective plantations. In maturity phase, the aim of managing is to sustain the protective maturity, i.e., the techniques (tending and thinning) of controlling the structure of protective plantations should be paid emphases. In the period of regeneration, the objective of managing is to recover the protective maturity, accordingly, the regeneration patterns and ways should be determined reasonably. Additionally, the methods of determining protective maturity, i.e., the core of the phase-directional management, are also given corresponding to farmland shelterbelt, sand-fixation forest and water and soil conservation forest. For farmland shelterbelt, IPMA can be determined according to the growth pattern of tree height under the suitable structure (porosity). For sand-fixation forest, it can be determined by the cover degree of the forest, i.e., the age when cover degree gets to pi/4 can be considered as IPMA. In the case of water and soil conservation forest, IPMA is determined by the canopy closure at the height of 1m above forest ground, which can be obtained from the hemispherical silhouettes in vertical direction. As for the TPMA, it can be described by the natural age of trees for all of above-mentioned three kinds of protective plantations, but the concrete methods for estimating the natural age of trees in each kind of forests are different.
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PMID:[Phase-directional management of protective plantations. I. Fundamentals]. 1255 90

Hyperoxia is closely linked with the development of chronic lung disease of prematurity (CLD), but the exact mechanisms whereby hyperoxia alters the lung architecture in the developing lung remain largely unknown. We developed a fetal human lung organ culture model to investigate (a) the morphologic changes induced by hyperoxia and (b) whether hyperoxia resulted in differential cellular responses in the epithelium and interstitium. The effects of hyperoxia on lung morphometry were analyzed using computer-assisted image analysis. The lung architecture remained largely unchanged in normoxia lasting as long as 4 d. In contrast, hyperoxic culture of pseudoglandular fetal lungs resulted in significant dilatation of airways, thinning of the epithelium, and regression of the interstitium including the pulmonary vasculature. Although there were no significant differences in Ki67 between normoxic and hyperoxic lungs, activated caspase-3 was significantly increased in interstitial cells, but not epithelial cells, under hyperoxic conditions. These changes show that exposure of pseudoglandular lungs to hyperoxia modulates the lung architecture to resemble saccular lungs.
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PMID:Differential response of the epithelium and interstitium in developing human fetal lung explants to hyperoxia. 1649 76

Prematurity is associated with cerebral abnormalities that might account for poorer cognitive performance. The aim of our study was to investigate the correlations between corpus callosum reductions and neuropsychologic performance in adolescents who were born preterm. Twenty-five subjects born before 33 weeks' gestation were compared with 25 subjects born at term and of similar age, gender, and sociocultural status. All subjects underwent magnetic resonance imaging and neuropsychologic examinations. Premature subjects performed worse than controls in global cognitive functioning, verbal memory, and verbal fluency. Corpus callosum measurements showed a global reduction owing mainly to thinning in the splenium, posterior midbody, and genu. Corpus callosum size significantly correlated with gestational age, Wechsler Performance IQ, and memory performance. These results suggest that cerebral growth during infancy does not compensate for corpus callosum reduction and that this reduction reflects neuropsychologic deficit. The cognitive impairment can arise from the paucity of the complex interneuronal connections owing to fiber damage, particularly myelinated fibers.
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PMID:Corpus callosum size and neuropsychologic impairment in adolescents who were born preterm. 1690 46

Spontaneous intestinal perforation (SIP) occurs commonly in extremely low birth weight (ELBW) infants. Our understanding of its etiologies has improved dramatically over the last decade. Included in this comprehension is an ongoing reconciliation of the iatrogenic risk factors, the microbiology, and the histopathology. The latter shows focal perforations with necrosis of the muscularis externa and no sign of ischemic damage (typically characterized by mucosal necrosis in the preterm bowel). Associations include extreme prematurity, early postnatal steroids (EPS), early use of indomethacin (EUI), and two common pathogens (Candida and Staphylococcus epidermis). Animal models of SIP suggest that all risk factors converge on a common collection of signaling pathways: those of nitric oxide synthases (NOS), insulin-like growth factors (IGFs), and epidermal growth factors (EGFs). Many of these factors skew trophism of the ileum (defined as thinning of the submucosa concomitant with hyperplasia of the muscosa). Global depletion of NOS is associated with disturbed intestinal motility and diminished transforming growth factor-alpha (TGF-alpha) in the muscularis externa. This constellation of insults seems to make the distal intestine vulnerable to perforation during recovery of motility.
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PMID:Understanding intestinal vulnerability to perforation in the extremely low birth weight infant. 1878 6

Cortical development in the first years of age for children with very low birth weight is not well characterized. We obtained high-resolution structural magnetic resonance images from children aged 18-22 months (16 very low birth weight/7 term) and 3-4 years (12 very low birth weight/8 term). Cortical surface area and thickness of the brain were assessed using the FreeSurfer data analysis program, and manually inspected for accuracy. For children with very low birth weight, a negative correlation was evident between birth weight and cortical thickness at 18-22 months (P = 0.04), and a positive correlation with cortical surface area at 3-4 years (P = 0.02). Between groups, children with very low birth weight demonstrated a consistent trend for thicker cortices and reduced surface area, compared with control term children (18-22 month surface area, P = 0.08; thickness, P = 0.11; 3-4 year surface area, P = 0.73; thickness, P = 0.14). The normal processes of cortical thinning and surface area expansion in the first several years of age may be delayed by premature delivery, a potentially more prominent effect with greater degrees of prematurity.
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PMID:Prematurity affects cortical maturation in early childhood. 2190 80

Thickening of the corpus callosum is an important feature of development, whereas thinning of the corpus callosum can be the result of a number of diseases that affect development or cause destruction of the corpus callosum. Corpus callosum thickness reflects the volume of the hemispheres and responds to changes through direct effects or through Wallerian degeneration. It is therefore not only important to evaluate the morphology of the corpus callosum for congenital anomalies but also to evaluate the thickness of specific components or the whole corpus callosum in association with other findings. The goal of this pictorial review is raise awareness that the thickness of the corpus callosum can be a useful feature of pathology in pediatric central nervous system disease and must be considered in the context of the stage of development of a child. Thinning of the corpus callosum can be primary or secondary, and generalized or focal. Primary thinning is caused by abnormal or failed myelination related to the hypomyelinating leukoencephalopathies, metabolic disorders affecting white matter, and microcephaly. Secondary thinning of the corpus callosum can be caused by diffuse injury such as hypoxic-ischemic encephalopathy, human immunodeficiency virus (HIV) encephalopathy, hydrocephalus, dysmyelinating conditions and demyelinating conditions. Focal disturbance of formation or focal injury also causes localized thinning, e.g., callosal dysgenesis, metabolic disorders with localized effects, hypoglycemia, white matter injury of prematurity, HIV-related atrophy, infarction and vasculitis, trauma and toxins. The corpus callosum might be too thick because of a primary disorder in which the corpus callosum finding is essential to diagnosis; abnormal thickening can also be secondary to inflammation, infection and trauma.
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PMID:Corpus callosum thickness in children: an MR pattern-recognition approach on the midsagittal image. 2517 5

This narrative review based on a literature search in PubMed and PsycInfo on the two terms prenatal and antenatal depression includes empirical studies, reviews and meta-analyses that have been published during the last 5 years on risk factors, developmental effects and interventions for prenatal depression. Risk factor studies that met criteria feature demographic measures (lower socioeconomic status, less education, non-marital status, non-employment, less social support and health locus of control, unintended pregnancy, partner violence and history of child abuse) and physiological variables (cortisol, amylase, and pro-inflammatory cytokines and intrauterine artery resistance). The negative effects include postpartum depression, paternal depression, and prematurity and low birth weight. Negative effects on infants include greater right frontal EEG, amygdala connectivity, cortical thinning and more difficult temperament. In childhood, externalizing and internalizing problems have been reported. The data on prenatal antidepressants (specifically SSRIs) reveal negative effects including internalizing problems as well as a greater risk for autism spectrum disorder. Prenatal interventions that have been effective include interpersonal psychotherapy, peer support, massage therapy, yoga, tai chi, and aerobic exercise. Potential underlying mechanisms are discussed as well as methodological limitations including homogeneity of samples and lack of randomization to intervention groups. Despite these limitations, the literature highlights the need for prenatal depression screening and intervention.
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PMID:Prenatal Depression Risk Factors, Developmental Effects and Interventions: A Review. 2870 6

There is an ongoing need for relevant animal models in which to test therapeutic interventions for infants with neurological sequelae of prematurity. The ferret is an attractive model species as it has a gyrified brain with a white-to-gray matter ratio similar to that in the human brain. A model of encephalopathy of prematurity was developed in postnatal day 10 (P10) ferret kits, considered to be developmentally equivalent to infants of 24-26 weeks' gestation. Cross-fostered P10 ferret kits received 5 mg/kg of lipopolysaccharide (LPS) before undergoing consecutive hypoxia-hyperoxia-hypoxia (60 min at 9%, 120 min at 60%, and 30 min at 9%). Control animals received saline vehicle followed by normoxia. The development of basic reflexes (negative geotaxis, cliff aversion, and righting) as well as gait coordination on an automated catwalk were assessed between P28 and P70, followed by ex vivo magnetic resonance imaging (MRI) and immunohistochemical analysis. Compared to controls, injured animals had slower overall reflex development between P28 and P40, as well as smaller hind-paw areas consistent with "toe walking" at P42. Injured animals also displayed significantly greater lateral movement during CatWalk assessment as a result of reduced gait coordination. Ex vivo MRI showed widespread white-matter hyperintensity on T2-weighted imaging as well as altered connectivity patterns. This coincided with white-matter dysmaturation characterized by increased intensity of myelin basic protein staining, white-matter thinning, and loss of oligodendrocyte transcription factor 2 (OLIG2)-positive cells. These results suggest both pathological and motor deficits consistent with premature white-matter injury. This newborn ferret model can therefore provide an additional platform to assess potential therapies before translation to human clinical trials.
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PMID:A Ferret Model of Encephalopathy of Prematurity. 3107 96

The involvement of the choroid in ocular growth regulation has been postulated in studies showing that refractive errors correlate with alterations in choroidal thickness (ChT). The advent of optical coherence tomography imaging has enabled qualitative and quantitative assessment of the choroid. In children, ChT changes correlate with a number of ocular pathologies, including myopia, retinopathy of prematurity, and amblyopia. We synthesize mechanisms and evidence regarding choroidal thickness variation during childhood. Subfoveal ChT is influenced by a number of factors including age, ethnicity, gender, axial length, and intraocular pressure. Myopic eyes have thinner choroids compared to emmetropic and hyperopic eyes. ChT may in fact serve as a marker of myopic progression, as ChT thinning occurs early during myopic development, but this association has not been established quantitatively. In addition, subfoveal ChT appears thicker in amblyopic eyes, while prematurity and retinopathy of prematurity may be associated with thinner ChT. Overall, both animal models and clinical research indicate that ChT induces or reflects physiological changes in the eye pertaining to ocular growth or maturation.
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PMID:Choroidal thickness and ocular growth in childhood. 3263 43