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1.
S Afr Med J ; 92(12): 986-90, 2002 Dec.
Article in English | MEDLINE | ID: mdl-12561416

ABSTRACT

INTRODUCTION: Retinopathy of prematurity (ROP) is a complication of prematurity, is diagnosed by ophthalmological screening of infants at risk (birth weight < or = 1,500 g), and may lead to blindness. The incidence of ROP is under-reported in developing countries, including South Africa. Published data from the USA (CRYO-ROP) show that black infants have a lower incidence of threshold ROP than their white counterparts (3.2% v. 7.4%). Preliminary results of a screening programme initiated at Kalafong Hospital in 1999 are reported. AIM: To determine the incidence of ROP in infants with a birth weight of < or = 1,500 g born at Kalafong Hospital. PATIENTS AND METHODS: Consecutive infants were enrolled at birth and screened for ROP 4-6 weeks later by indirect ophthalmoscopy. Repeat examinations were performed until vascularisation was complete or until the infant reached a postconceptional age of 40 weeks. Infants with stage 3 ROP who developed threshold disease were treated with cryotherapy or laser therapy. RESULTS: One hundred and forty-five infants were enrolled over 10 months (15 February 1999-25 December 1999); of these 94 were screened. Of the remaining 51 infants, 24 died before screening and 27 were discharged before screening and were lost to follow-up. ROP was diagnosed in 23 of the 94 infants screened (24.5%). Stage 1 and 2 ROP occurred in 17 of the infants screened (18.1%) and stage 3 ROP in 6 (6.4%), of whom 4 (median birth weight 995 g, range 900-1,450 g) developed threshold ROP and were treated. CONCLUSIONS: The incidence of ROP in black very-low-birth-weight infants born at Kalafong Hospital is 24.5%. The incidence of threshold ROP is 4.3% (3.2% in infants < or = 1,250 g) and correlates with published data from the USA. Infants with a birth weight < or = 1,500 g should receive ophthalmological screening to diagnose stage 3 ROP timeously.


Subject(s)
Infant, Very Low Birth Weight , Retinopathy of Prematurity/diagnosis , Retinopathy of Prematurity/epidemiology , Black or African American/statistics & numerical data , Birth Weight , Black People , Cryotherapy , Developing Countries , Follow-Up Studies , Gestational Age , Humans , Incidence , Infant, Newborn , Laser Therapy , Neonatal Screening/methods , Ophthalmoscopy/methods , Oxygen Inhalation Therapy/adverse effects , Population Surveillance , Retinopathy of Prematurity/classification , Retinopathy of Prematurity/therapy , Severity of Illness Index , South Africa/epidemiology , Twins/statistics & numerical data , Vision Screening/methods
2.
Am J Physiol Lung Cell Mol Physiol ; 281(4): L816-23, 2001 Oct.
Article in English | MEDLINE | ID: mdl-11557585

ABSTRACT

Interleukin (IL)-1beta is an important early mediator of inflammation in pulmonary artery smooth muscle cells. We previously reported that a geranylgeranyltransferase inhibitor elevated basal levels of inducible nitric oxide synthase (iNOS) and enhanced IL-1beta-mediated induction, suggesting that Rac or Rho small G proteins are candidates for antagonism of such induction. In this study, overexpression of constitutively active Rac1 or its dominant negative mutant did not affect IL-1beta induction of iNOS. Alternatively, treatment with Clostridium botulinum C3 exoenzyme, which ADP-ribosylates Rho, was associated with superinduction of iNOS, suggesting an inhibitory role for Rho. IL-1beta activated the three mitogen-activated protein kinase (extracellular signal-regulated kinases 1 and 2, c-Jun NH2-terminal kinase/stress-activated protein kinase, and p38) and the Janus kinase (JAK)-signal transducer and activator of transcription pathways. The former two pathways were not associated with IL-1beta-mediated iNOS induction, whereas the latter two appeared to have inhibitory roles in iNOS expression. These data suggest that a broad intracellular signaling response to IL-1beta in rat pulmonary artery smooth muscle cells results in elevated levels of iNOS that is opposed by the geranylgeranylated small G protein Rho as well as the p38 and JAK2 pathways.


Subject(s)
Interleukin-1/pharmacology , JNK Mitogen-Activated Protein Kinases , MAP Kinase Signaling System/physiology , Muscle, Smooth, Vascular/enzymology , Nitric Oxide Synthase/metabolism , Pulmonary Artery/cytology , Animals , Botulinum Toxins/pharmacology , Cells, Cultured , DNA-Binding Proteins/metabolism , Enzyme Activation/drug effects , Enzyme Activation/physiology , Enzyme Inhibitors/pharmacology , Flavonoids/pharmacology , MAP Kinase Kinase 4 , MAP Kinase Signaling System/drug effects , Male , Mitogen-Activated Protein Kinase 1/metabolism , Mitogen-Activated Protein Kinase 3 , Mitogen-Activated Protein Kinase Kinases/metabolism , Mitogen-Activated Protein Kinases/metabolism , Muscle, Smooth, Vascular/cytology , Nitric Oxide Synthase Type II , Phosphotransferases (Phosphate Group Acceptor)/antagonists & inhibitors , Phosphotransferases (Phosphate Group Acceptor)/metabolism , Rats , Rats, Sprague-Dawley , STAT3 Transcription Factor , Trans-Activators/metabolism , p38 Mitogen-Activated Protein Kinases , rac1 GTP-Binding Protein/metabolism , rho GTP-Binding Proteins/metabolism
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