[Care of premature infants and nursing--lessons from premature infant care: based on records of clinical training in premature infant care for midwifery students].
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Prematurity and premature rupture of the membranes present major obstetric problems. When associated with amnionitis, the result may be disastrous. A case of Haemophilus influenzae aminionitis in association with premature rupture of the membranes is presented. The rarity of this organism as a causative agent in amnionitis and its possible causative role in premature membrane rupture are considered in review of the scant relevant literature.
A study was made of the effect of a 3-hour incubation with inosine-pyruvate-phosphate (IPP) on the P50 values and 2,3-DPG contents of fresh blood and blood which had stood for 96 h, from healthy adults, term neonates, 1-2-week-old symptom-free premature infants and RDS premature infants. It was found that the P50 value and the 2,3-DPG content could be increased considerably by IPP treatment in both the fresh and the stood blood in the various groups of neonates. The question remains open as to whether the effect of IPP, in significantly improving the O2 transport in neonates, is a consequence of the 2,3-DPG alone or of some other metabolite. In RDS the stimulating effect of the IPP mixture is appreciably lower.
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In preparing a clinical study 14C-labelled bromhexine metabolite VIII was applied intraamnially in animal experiments. The distribution was measured in different maternal and fetal organs by thinlayer chromatography and autoradiography. A complete placental passage was found in both directions. An organspecific accumulation in the fetal lungs could not be demonstrated.
The characteristics of premature ventricular beats predisposing to ventricular tachycardia or fibrillation were assessed by 24-h ambulatory monitoring and maximal treadmill exercise testing in 339 cardiac patients with premature ventricular beats. Premature ventricular beats were divided into early (Q-premature ventricular beat less than QT), late (within the last 20% of the cardiac cycle), and midcycle. Ventricular tachycardia was recorded in 45 patients and ventricular fibrillation, in three. The frequency of ventricular tachycardia or fibrillation was 32% in patients with late, 16% in patients with early, and 7% in patients with midcycle premature ventricular beats (P less than 0.05). Patients with frequent (less than 10/min) multiformed premature ventricular beats had a frequency of ventricular tachycardia or fibrillation of 44%, while only 13% of patients with frequent uniformed premature ventricular beats had ventricular tachycardia (P less than 0.05). Ambulatory patients with ventricular tachycardia or fibrillation have frequent multiformed premature ventricular beats, and the ventricular tachycardia or fibrillation is usually triggered by late premature ventricular beats.
BACKGROUND: Rare damaging genetic variation accounts for a substantial proportion of the risk of rare developmental disorders (DDs), but common genetic variants as well as environmental factors, including prematurity, also contribute. Little is known about the interplay between prematurity and genetic variation in influencing phenotypic outcomes in DDs, nor about how genetic factors may contribute to risk of preterm birth in DDs. METHODS: We leveraged phenotypic and genetic data from 21,712 patients with DDs recruited for clinical sequencing, 16% of whom were born prematurely. Using multivariable regression models, we compared phenotypic features and the prevalence of diagnostic genetic variation in specific genes between preterm and term individuals with DDs. We tested whether the fraction of cases attributable to de novo mutations differed between term and preterm probands. Additionally, we assessed whether associations between common variant contributions to education-related traits and prematurity are explained by direct genetic effects. RESULTS: Prematurity was associated with more severe clinical phenotypes among these DD patients, including more affected organ systems and more delayed developmental milestones. Prematurity and the presence of a monogenic diagnosis contributed additively to severity. We found that genes associated with fetal anomalies were enriched for diagnostic mutations among preterm individuals (p = 7.83 × 10-5). We also demonstrated an exome-wide enrichment of de novo mutations (DNMs) in both term and preterm probands; the fraction of cases explained by DNMs in known DD-associated genes was higher in term than preterm cases (25% versus 20%) but DNMs in as-yet-undiscovered genes likely contribute approximately equally to both groups (14% versus 13%). Finally, we showed that the positive association between polygenic predisposition to education-related traits and gestational duration is likely to be the result of genetically influenced parental traits or confounders, rather than direct genetic effects in the child, and that a monogenic diagnosis modifies this association. CONCLUSIONS: Our findings emphasise the importance of considering environmental factors like prematurity in understanding outcomes in DDs suspected to have a genetic component, and motivate further exploration of the role that genetic variation plays in influencing prematurity.
To investigate the mechanism of postextrasystolic potentiation of contraction (PESP), the effects of extracellular K concentration, isoproterenol, verapamil and caffeine were examined in canine ventricular muscle. The muscles were driven at 1 Hz, then a premature stimulus was applied to elicit a premature action potential and after a compensatory pause postextrasystolic stimulus was applied to induce PESP. At 5.9 mM K the premature action potential had a longer plateau than the preceding control action potential. The prolongation was dependent on the proximity, i.e. the interval between the premature stimulus and the preceding control action potential; the maximal enhancement of about 25% was obtained with a proximity of 70 ms. In parallel with this prolongation the post-extrasystolic contraction was increased more than 5-fold. However, PESP was obtained without prolongation of the premature action potential when [K]0 was reduced to 1.2 mM. Similarly, PESP under the effect of 10(-6) g/ml isoproterenol or 10(-5) M verapamil was not accompanied by prolongation of the premature action potential. Thus it is difficult to explain the PESP solely by the increased Ca influx during the premature action potential. Since caffeine abolished PESP, some other effects of the premature beat on sarcoplasmic reticulum might be responsible for the PESP.
The activities of key gluconeogenic enzymes in the livers of newborn guinea pigs were monitored as a function of time following birth either vaginally at term or prematurely by cesarian section at 62 days of gestation. The activity of hepatic glucose-6-phosphatase rose dramatically from 1.40 +/- 0.26 mumol/min/g at birth to a maximum of 6.8 +/- 0.9 mumol/min/g at 24 hr in prematurely delivered animals although there was little significant change in activity in full term animals. The activity of hepatic fructose-1,6-diphosphatase and mitochondrial phosphoenolpyruvate carboxykinase changed little over the first 3 days of life in either full term or premature animals. Cytosolic phosphoenolpyruvate carboxykinase, on the other hand, had low activity at birth being 0.11 +/- 0.03 mumol/min/g in full term and 0.06 +/- 0.04 mumol in premature animals rising to values of 0.71 +/- 0.06 and 1.12 +/- 0.12 mumol/min/g, respectively, at 24 hr of life. Pyruvate carboxylase activities in the premature animals remained significantly lower than those in full term animals in the first 72 hr of life. Transient hypoglycemia was evident in the prematurely delivered animals, but not in the full term animals, the blood glucose values being 82 +/- 7 mg/100 ml for the full term animals and 20 +/- 8 mg/100 ml for the premature infants at 2 hr of life.
Neurological and psychological examinations have been conducted of prematurely born babies in good bodily condition and hypotrophic new-born infants (including control groups) as part of a not yet concluded longitudinal study. The hypoplastic premature infants showed a comparatively high proportion of statomotor retardation and neurological disturbances, which were also found in premature infants in good bodily condition with a pregnancy duration of 26-30 weeks. Cerebral motor disturbances were found primarily in hypoplastic new-born babies and especially in premature infants. The EQ (development quotient) for the premature infants in good bodily condition with a pregnancy duration between 26 and 30 weeks, and for the hypoplastic premature infants was lower than for other high-risk groups. These two groups were also responsible for the larger proportion of children showing light and medium psychic retardation. Behavioral peculiarities were, however, distributed also over other high-risk groups, and some were even more frequent there. It was also found that speech development was delayed. The study shows the necessity of following the development of high-risk babies and using individual therapies.
A cytogenetic investigation of two groups of prematurely born babies was carried out on the basis of the specialized department for prematurely born children in Moscow and in the Moscow Region. The material for this investigation was the culture of lymphocytes. In the first group comprising 607 prematurely born babies without any perceptible developmental defects abnormalities of the karyotype were observed in 15 probands (2.5%) which is 3.5 times higher than the frequency of karyotypic abnormalities among newborn babies from the same population born in proper time. In the second group comprising 70 prematurely born babies with various congenital malformations various karyotypic abnormalities were observed in 13 probands (18,6%), which is 8 times the frequency among babies from the same population born in proper time. The main type of abnormalities observed were those affecting the system of sex chromosomes and the cases of trisomy of the 21st pair of autosomes and structural abnormalities. The high proportion of X- and 21-trisomies among the chromosome abnormalities observed suggests their important role in the etiology of premature births and postnatal death-rate of mutant organisms having D- and E-trisomies and structurally unbalanced chromosomal aberrations.
Prematurity is by far the commonest cause of neonatal morbidity and mortality. The management of premature labour is empirical because little is understood about the mechanism of labour. Effective uterine relaxant drugs have an important, albeit minor role. Phototherapy has reduced the complications of neonatal hyperbilirubinemia, and the beneficial effect of antepartum corticosteroid therapy in minimizing the risk of respiratory distress syndrome is now convincing. Prophylactic antibiotic therapy in premature rupture of the membranes does not alter perinatal mortality, although postpartum maternal morbidity is reduced. The introduction of neonatal intensive care units has improved the survival rate of premature infants. Sound clinical judgement remains the mainstay in the management of premature labour.
In travenous magnesium sulfate and alcohol were compared as treatments for premature labor. A successful treatment was the absence of contractions for a 24 hour interval. Early treatment was found to be essential for successful management of premature labor. There is a significant correlation of cervical dilatation at the onset of treatment to success at controlling premature labor. There was no statistically significant relation to weeks of gestation or parity to success at controlling premature labor. In this study magnesium sulfate was the better agent for controlling premature labor.
Thyroid function was studied in healthy premature and term infants between 12 hours and 3 months of age. T4 and FT4I followed parallel courses in both groups; during the first 45 days, however, the values were significantly lower in premature infants under 34 weeks' EGA than in term infants (P less than 0.001). The post-delivery peak in TSH concentration (mean +/- SD) was 71.8 +/- 19.2 microunits/ml in the premature infants. In five premature infants, injection of TRH elicited a TSH increment of 29.4 +/- 20.7 microunits/ml at 30 minutes. T3 concentration was not significantly different in premature and term infants.
Because of clinical observations suggesting that nitroglycerin may suppress premature ventricular complexes during acute ischaemia, a study was undertaken to assess the effect of nitroglycerin on the incidence of premature ventricular complexes in patients with acute myocardial infarction. Forty patients with acute myocardial infarction were studied. Twenty-six patients received 0.4 mg nitroglycerin sublingually every 4 hours for the first 24 hours after admission to the coronary care unit. The total premature ventricular complex count for the 26 patients for 15 minutes before nitroglycerin was 592, and 276 for the 15 minutes after the drug (P less than 0.005). In the remaining 14 patients on the same nitroglycerin schedule, a single electrocardiographic lead was continuously recorded on tape. During the first hour after nitroglycerin, the premature ventricular complex count decreased by 58 per cent, and the second and third hours showed a decrease from control count of 71 and 65 per cent respectively. By the end of 4 hours the ectopic count was back to control level. The data indicate that nitroglycerin may decrease the number of premature ventricular complexes for up to 3 hours in patients with acute myocardial infarction. The mechanism of action of nitroglycerin is not elucidated by this study, but the observation may be of value in further studies of specific antiarrhythmic therapy and prevention of arrhythmias in patients with coronary artery disease.
Various drugs used to stop premature uterine contractions are discussed in the paper. Particular attention is paid to beta-mimetic drugs. The results of ming Partusisten, one of beta-mimetic drugs, is presented on the material of 104 patients with threatening immature and premature labour. Partusisten was administered in the form of intravenous drip infusion or tablets. During treatment monitoring of the uterine contractility and of foetal heart rate took place. Inhibition of the uterine contraction activity was successful in 100 per cent of cases. In 60,9 per cent in the group of threatening immature labour and in 38,1 per cent in the group threatening premature labour, the delay of delivery was more then 28 days. The delay of delivery by 48 hours was 87 per cent and 84 per cent in both groups respectively. Tachycardia was one of the first side effects observed in 15,2 per cent of cases. There is also presented an example of pregnancy when delivery was delayed by 21 days in spite of premature outflow of amniotic fluid (at a high rupture of membrane). The authors are of the opinion that Partusisten is very effective and gives little side effects, preventing premature uterine contractions. Dosage should be individualized according to the case and labour advancement, and should be based on topographic evaluation of uterine contraction. Negative influence of the drug on foetuses was not observed.
The authors described the effect of premature weaning on the fatty acid spectrum in the retroperintoneal fat of female rats during ontogenesis. Premature weaning reduced the lower fatty acid content [decanoic acid C 10:0, lauric acid C 12:0, myristic acid C 14:0] in 30- to 90-day-old rats, but in further development no differences between the amount of these fatty acids were observed in suckled and prematurely weaned animals. These changes concurred with the fatty acid composition of the relevant diet (rat milk and a standard laboratory diet). Changes induced in the amount of other acids by premature weaning were not permanent in character, with the exception of stearic acid C 18:0 and linoleic acid C 18:3, which were raised at 720 days in the retroperitoneal fat of prematurely weaned rats. The amount of lower saturated fatty acids fell with advancing age, whereas oleic C 18:1, linolic C 18:2 and linolenic C 18:3 acid rose.
Eukaryotic genomes are widely transcribed by RNA polymerase II (pol II) both within genes and in intergenic regions. POL II elongation complexes comprising the polymerase, the DNA template and nascent RNA transcript must be extremely processive in order to transcribe the longest genes which are over 1 megabase long and take many hours to traverse. Dedicated termination mechanisms are required to disrupt these highly stable complexes. Transcription termination occurs not only at the 3' ends of genes once a full length transcript has been made, but also within genes and in promiscuously transcribed intergenic regions. Termination at these latter positions is termed "premature" because it is not triggered in response to a specific signal that marks the 3' end of a gene, like a polyA site. One purpose of premature termination is to remove polymerases from intergenic regions where they are "not wanted" because they may interfere with transcription of overlapping genes or the progress of replication forks. Premature termination has recently been appreciated to occur at surprisingly high rates within genes where it is speculated to serve regulatory or quality control functions. In this review I summarize current understanding of the different mechanisms of premature termination and its potential functions.