Decreased Cesarean Birth Rates and Improved Perinatal Outcome: A Seven-Year Study

ABSTRACT: This study examined the decrease in cesarean section rates in relation to perinatal mortality between 1987 and 1993 at the primary referral hospital in north Jordan. Most of the population is at high risk and of low socioeconomic status. The cesarean section rate decreased from 15.5 percent in 1987 to 8.7 percent in 1993, and has remained at this low rate. During the same period the perinatal mortality dropped from 52 to 20.9 deaths per 1000 live births. These results do not include perinatal morbidity. The successful reduction of the cesarean section rate is attributed to active management of labor, trial of labor for women with a previous cesarean birth, and vaginal breech delivery in selected women. We conclude that the rate of cesarean delivery can be safely reduced in a developing country without adverse effects on birth outcomes.     

Incidence and relation to parity of pregnancy-induced hypertension in Iceland

A retrospective study was made to determine the incidence of pregnancy-induced hypertension (PIH, pre-eclampsia) in Iceland. One-fourth of all births in Iceland in 1985 were selected from the national birth registry files by random number allocation, a total of 904 women. Maternity records were found in 97.9% of the cases. The criteria used to define PIH were met in 17.4% of the women. There were 146 (16.5%) with mild PIH (blood pressure of greater than or equal to 140/90 mmHg with or without proteinuria after the 20th gestational week). Eight (0.9%) had severe PIH (blood pressure of greater than or equal to 160/110 mmHg with or without proteinuria after the 20th gestational week). Primigravid women formed one-third of the group and of these 20.9% had PIH compared with 15.4% of the parous women. The incidence in parous women was higher than usually reported.     

Genetic and familial predisposition to eclampsia and pre-eclampsia in a defined population

Familial predisposition and patterns of genetic inheritance of eclampsia and pre-eclampsia were investigated through three or four generations in 94 families from the homogenous island population of Iceland. The families descended from index women delivered in the years 1931-47 and who had either eclampsia (n = 38) or severe pre-eclampsia (n = 69). Inheritance was followed both through sons and daughters. The prevalence of pre-eclampsia and eclampsia in daughters was significantly higher (23%) than that in daughters-in-law (10%). No difference was noted in the prevalence of these diseases by whether the daughter was born of an eclamptic or pre-eclamptic mother or whether she was a first or later born daughter. There was a non-significantly higher occurrence of pre-eclampsia among grand-daughters than in grand-daughters-in-law. No difference was seen by whether grand-daughters descended through sons or daughters. With increasing numbers of affected daughters or grand-daughters the probability rose of finding more affected women in a family. Hypotheses of single recessive and dominant gene inheritance were compared and maximum likelihood estimates for gene frequency obtained. For a single recessive gene model this was 0.31 reflecting a population prevalence of 9.6%, whereas a dominant model with incomplete penetrance gave 0.14 at 48% gene penetrance, corresponding to a population prevalence of 0.9% homozygous expression of severe disease and 11% heterozygous expression of milder disease. Either genetic model could fit the data.     

Cytokine modulation and suppression of liver injury by a novel analogue of thalidomide

Thalidomide has been shown to reduce the production of tumor necrosis factor-alpha (TNF-alpha), a cytokine with deleterious pathophysiologic effects in various diseases. In search of thalidomide analogues with improved TNF-alpha inhibiting properties, 5-ethyl-1-phenyl-5-(3,4,5,6-tetrafluorophthalimido)barbituric acid (TFBA) was found to be superior to thalidomide. Besides TNF-alpha, TFBA also suppressed interleukin-6 and interleukin-10 production of isolated monocytes. The possibility that TFBA exerts its action by increasing levels of cAMP via inhibition of phosphodiesterase-4 activity was excluded. TFBA had no influence on T cell proliferation; neither did it inhibit TNF-alpha production in peripheral blood mononuclear cells stimulated by anti-CD3 monoclonal antibody. When applied to mice treated with D-galactosamine and lipopolysaccharide, TFBA prevented a rise in serum TNF-alpha, had no effect on interleukin-6 levels and led to an increase in interleukin-10 production. The changes in cytokine production observed in vitro and in vivo were reflected by similar changes in the mRNA expression. Moreover, TFBA significantly reduced liver transaminase levels in D-galactosamine/lipopolysaccharide-treated mice and thus efficiently protected the animals from liver injury. Thus, according to its properties, TFBA has the potential of modulating an immune response by acting as an anti-inflammatory agent.     

Copper, ceruloplasmin, superoxide dismutase and iron parameters in Parkinson's disease

In a previous study we found copper dyshomeostasis in patients with Alzheimer's disease. In this study, levels of copper in plasma, of ceruloplasmin in serum and ceruloplasmin oxidative activity as well as superoxide dismutase (SOD) activity in erythrocytes were determined in 40 patients with Parkinson's disease and their healthy age- and gender-matched controls. Copper concentrations did not differ significantly in the two groups, whereas both ceruloplasmin concentrations and ceruloplasmin oxidative activity were significantly lower in the patients, also relative to ceruloplasmin mass. SOD activity was not significantly different in the two groups but decreased significantly with the duration of disease. The same was found for ceruloplasmin oxidative activity. Ceruloplasmin oxidative activity and SOD activity did not decrease with age. Levels of serum iron, serum ferritin and total iron binding capacity were determined in about 30 of the patients and an equal number of controls and were not found to differ. Transferrin levels were significantly lower in the patients than in their controls but, conversely, the transferrin saturation was significantly higher in the patients. The results indicate that patients with Alzheimer's disease and Parkinson's disease have defective ceruloplasmin and SOD activities in common and that these defects are not necessarily associated with major disturbances in iron homeostasis.     

Low serum fetuin‐A concentration predicts poor outcome only in the presence of inflammation in prevalent haemodialysis patients

Background Fetuin‐A, a negative acute phase protein that inhibits vascular calcification, has a controversial association with mortality in chronic kidney disease (CKD) patients. Chronic inflammation, which is common in CKD, may promote vascular calcification. Materials and methods We investigated the impact of inflammation on the relationship between serum fetuin‐A and mortality (42 months) in 222 prevalent haemodialysis (HD) patients. Results Serum fetuin correlated negatively with comorbidity score (assessed by Davies score) and circulating inflammatory markers. Patients with low fetuin‐A levels (< median) had higher mortality (Hazard ratio ‘HR’ 2·2; CI 1·4–3·5, P < 0·001), but this association was lost after adjustment for age, gender, comorbidities score, dialysis vintage and inflammation (CRP > median). In inflamed patients with low fetuin a significantly independent association with mortality (HR 2·3; CI 1·2–4·5, P = 0·01) was observed compared to non‐inflamed patients with high fetuin‐A, after adjusting for the same variables. Non‐inflamed patients with low fetuin‐A and inflamed patients with high fetuin‐A did not have increased mortality compared to non‐inflamed patients with high fetuin‐A. Conclusions The results show that low levels of serum fetuin‐A are associated with increased mortality in HD patients only in the presence of inflammation. This suggests that coexistence of a low serum fetuin‐A level and low‐grade inflammation exerts an additive effect on the risk of death in HD patients.     

Renal cell carcinoma presenting as Garcin''s syndrome.

A 50 year old man presented with progressive unilateral cranial nerve palsies (Garcin's syndrome) for one year. Skull radiography and computed tomography (CT) showed intracranial extension of a soft tissue tumour from the right base of the skull. Necropsy revealed a papillary cell carcinoma of the right kidney and metastases in the base of the skull.     

Dual targeting of a single tRNA(Trp) requires two different tryptophanyl-tRNA synthetases in Trypanosoma brucei

The mitochondrion of Trypanosoma brucei does not encode any tRNAs. This deficiency is compensated for by the import of a small fraction of nearly all of its cytosolic tRNAs. Most trypanosomal aminoacyl-tRNA synthetases are encoded by single-copy genes, suggesting the use of the same enzyme in the cytosol and mitochondrion. However, the T. brucei genome contains two distinct genes for eukaryotic tryptophanyl-tRNA synthetase (TrpRS). RNA interference analysis established that both TrpRS1 and TrpRS2 are essential for growth and required for cytosolic and mitochondrial tryptophanyl-tRNA formation, respectively. Decoding the mitochondrial tryptophan codon UGA requires mitochondria-specific C-->U RNA editing in the anticodon of the imported tRNA(Trp). In vitro charging assays with recombinant TrpRS enzymes demonstrated that the edited anticodon and the mitochondria-specific thiolation of U33 in the imported tRNA(Trp) act as antideterminants for the cytosolic TrpRS1. The existence of two TrpRS enzymes, therefore, can be explained by the need for a mitochondrial synthetase with extended substrate specificity to achieve aminoacylation of the imported thiolated and edited tRNA(Trp). Thus, the notion that, in an organism, all nuclear-encoded tRNAs assigned to a given amino acid are charged by a single aminoacyl-tRNA synthetase, is not universally valid.