OBJECTIVE: Because the survival rate has increased for extremely low birth weight neonates, many have raised the concern that the rate of developmental disability among survivors will also increase. To address this concern, we analyzed changes over time in survival and major neurosensory impairment in a sample of extremely low birth weight infants born between July 1, 1979, and June 30, 1994. METHODS: The study sample included 513 infants with birth weights of 501 to 800 g who were cared for in either of the two neonatal intensive care units that serve a 17-county region in northwest North Carolina and who were born to mothers residing in that region. At 1 year of age (corrected for gestation), survivors were examined by a pediatrician and were tested using the Bayley Scales of Infant Development. Major neurosensory impairment was defined as cerebral palsy, a Bayley Mental Developmental Index <68, or blindness. A total of 209/216 (97%) of survivors were examined at 1 year of age. Epoch of birth was defined as follows: epoch 1, July 1, 1979 to June 30, 1984; epoch 2, July 1, 1984 to June 30, 1989; and epoch 3, July 1, 1989 to June 30, 1994. RESULTS: Survival rates for epochs 1, 2, and 3 were, respectively, 24/120 (20%), 63/175 (36%), and 129/218 (59%). In contrast, the proportions with a major neurosensory impairment did not increase over time; rates for successive epochs were 6/24 (25%), 17/61 (28%), and 26/124 (21%). Rates of cerebral palsy were 3/24 (13%), 12/61 (20%), and 9/124 (7%); rates of delayed mental development were 4/24 (17%), 12/61 (20%), and 17/124 (14%); and rates of blindness were 2/24 (8%), 0/62, and 5/124 (4%), respectively. CONCLUSIONS: This analysis suggests that the increasing survival of extremely low birth weight neonates since the late 1970s has not resulted in an increased rate of major developmental problems identifiable at 1 year of age. 相似文献
The beta2 integrin (CD 18/CD 11 a, b, c) family of proteins mediate
adherence of leukocytes to vascular endothelium and the associated ligand,
intercellular adhesion molecule-1 (ICAM-1; CD 54), interacts with beta2
integrin proteins to allow transendothelial migration of leukocytes into
sites of inflammation. The present study examines the function of these
proteins in a murine model of acute cutaneous inflammation induced
following topical application of 12-O- tetradecanoylphorbol-13-acetate
(TPA) to the dorsal epidermis of SENCAR mice and in a model of skin
multistage carcinogenesis. At 24 h following topical application of TPA to
the dorsal epidermis of mice, dermal leukocytes expressed higher levels of
beta2 integrin protein compared with the lower levels of beta2 integrin
protein expression by peripheral blood leukocytes. ICAM-1 protein was
localized to epidermal keratinocytes and vascular endothelium in
TPA-treated skin and to proliferating papilloma cells. Intravenous (i.v.)
injection of either 50 microg anti-beta2 integrin antibody alone or in
combination with anti-ICAM-1 antibody significantly inhibited both
TPA-stimulated neutrophil infiltration into the dermis (P < 0.001) and
myeloperoxidase (MPO) activity (P < 0.03 anti-beta2 integrin antibody; P
< 0.01 anti- beta2 integrin + ICAM-1 adhesion molecule antibodies), but
had no effect on TPA-induced epidermal hyperplasia. In addition, injection
of either anti-ICAM-1 adhesion molecule antibody alone (P < 0.004) or in
combination with anti-beta2 integrin antibody (P < 0.001) significantly
inhibited TPA-induced production of 7,8-dihydroxy-2'-deoxyguanosine (8-
OHdG) immunoreactive proteins by epidermal keratinocytes. Beta2
integrin/ICAM-1 adhesion molecules work in concert to regulate migration,
retention and functional activation of leukocytes within the dermis during
TPA-induced skin inflammation and within stromal tissue of papillomas that
form during multi-stage carcinogenesis. Agents that inhibit these
receptor/ligand interactions may be useful in defining the roles of
specific cell populations in cutaneous inflammation and multistage
carcinogenesis and may also have potential as anti-promoting and
anti-progression agents.
相似文献
Interruption of the contrast column during inspiration can lead to non‐diagnostic CT pulmonary angiograms. The importance of this artefact will increase with more CT studies being performed for pulmonary embolism on multidetector row CT. We describe here an instance of such an artefact and discuss its aetiology. 相似文献
Abstract Gastroesophageal reflux disease (GERD) is a common disease in the West, which now appears to be also increasing in prevalence in the Asian Pacific region. The reasons for this changing epidemiology are two-fold: an increased awareness among doctors and patients, and/or a true increase in the prevalence of the disease. Prevalence rates of reflux esophagitis (RE) of up to 16% and prevalence of GERD symptoms of up to 9% have been reported in the Asian population. However, the frequency of strictures and Barrett's esophagus remain very low. Non-erosive reflux disease (NERD) appears to be the most common form of GERD among Asian patients accounting for 50–70% of cases with GERD. Among Asian patients differences can also be discerned among different ethnic groups. For example, in Malaysia where a multiracial society exists, RE is significantly more common among Indians compared to Chinese and Malays whereas NERD is more frequently seen in the Indian and Malays compared to the Chinese. The reasons for these differences are not known but may indicate both genetic factors and environmental factors peculiar to the particular racial group. GERD has also been increasing in the region demonstrating a time-lag phenomenon compared to the West. Differing predisposition to GERD among different ethnic groups would mean that such an increase would be more prominent among certain racial groups. 相似文献
Genetic predispositions and environmental influences both play an important role in adolescent externalizing behavior; however, they are not always independent. To elucidate gene–environment interplay, we examined the interrelationships between externalizing polygenic risk scores, parental knowledge, and peer substance use in impacting adolescent externalizing behavior across two time-points in a high-risk longitudinal sample of 1,200 adolescents (764 European and 436 African ancestry; Mage = 12.99) from the Collaborative Study on the Genetics of Alcoholism. Results from multivariate path analysis indicated that externalizing polygenic scores were directly associated with adolescent externalizing behavior but also indirectly via peer substance use, in the European ancestry sample. No significant polygenic association nor indirect effects of genetic risk were observed in the African ancestry group, likely due to more limited power. Our findings underscore the importance of gene–environment interplay and suggest peer substance use may be a mechanism through which genetic risk influences adolescent externalizing behavior.
Colorectal carcinoma is one of the commonest solid organ tumors in the world and its prevalence appears to be increasing in Asia. Recently, there has been much interest in various chemotherapeutic agents for the management of this condition, in particular nonsteroidal anti‐inflammatory drugs (NSAIDs). There is a large amount of data that suggest traditional NSAIDs, as well as the new cyclooxygenase (COX)‐2 selective inhibitors such as rofecoxib and celecoxib, have a role in the setting of primary and secondary prevention, and adjuvant therapy of both sporadic colorectal carcinoma and familial adenomatous polyposis. This review examines some of this data, as well as the potential problems and limitations of using these agents, particularly in light of the recent withdrawal of rofecoxib. 相似文献
Helicobacter pylori and Epstein–Barr virus (EBV) account for roughly 80% and 10%, respectively, of gastric carcinomas worldwide. Autophagy is an evolutionarily conserved and intricately regulated cellular process that involves the sequestration of cytoplasmic proteins and organelles into double‐membrane autophagosomes that eventually fuse with lysosomes for degradation of the engulfed content. Emerging evidence indicates that xenophagy, a form of selective autophagy, plays a crucial role in the pathogenesis of H. pylori‐ and EBV‐induced gastric cancer. Xenophagy specifically recognizes intracellular H. pylori and EBV and physically targets these pathogens to the autophagosomal–lysosomal pathway for degradation. In this connection, H. pylori or EBV‐induced dysregulation of autophagy may be causally linked to gastric tumourigenesis and therefore can be exploited as therapeutic targets. This review will discuss how H. pylori and EBV infection activate autophagy and how these pathogens evade recognition and degradation by the autophagic pathway. Elucidating the molecular aspects of H. pylori‐ and EBV‐induced autophagy will help us better understand the pathogenesis of gastric cancer and promote the development of autophagy modulators as antimicrobial agents. Published by John Wiley & Sons, Ltd 相似文献