General Practitioners in Public Obstetrics - an Underutilized Resource

Summary: We questioned 229 general practitioners (GPs), 288 women who had recently delivered babies in public hospitals, 26 public hospital doctors, and 33 midwives in South Brisbane. Shared antenatal care was undertaken by 84% of mothers, and recently provided by 88% GPs. Mothers valued having sufficient time with their antenatal clinician, continuity of care, and short waiting and travel times. They preferred a GP to provide antenatal care, and a hospital midwife to deliver them. GPs were interested in providing even more obstetric care - one third in providing intrapartum care - and in gaining continuing education in obstetrics. Hospital doctors and midwives were supportive of women choosing the personnel to deliver them, and of an increased GP and midwife role in public hospital obstetrics, but unenthusiastic about home deliveries. There is widespread support for an increased role for GPs in public obstetrics.     

Electrocardiographic findings in pulmonary arterial hypertension in children

Pulmonary hypertension (PH) induces high risk of cardiovascular morbidity and mortality, mainly in the primary or essential type. Invasive studies are needed to confirm the diagnosis; among the non- invasive approach, the electrocardiogram has been used to suspect such entity with poor results due to inadequate diagnostic criteria. Twelve children with pulmonary hypertension of the essential type (PPH) and ten children with PH due to interventricular septal defect (VSD) were studied haemodynamically and electrocardiographically and compared to electrocardiographic data of 53 normal children. PPH showed higher resistances than VSD (17.2 +/- 1.9 vs 6 +/- 0.6 u/m2 p less than 0.01) with the same pressure level (99.5 +/- 10.3 vs 101.5 +/- 4.8 mmHg). Right axis deviation, peaked P wave, increased ventricular activation time and prominent ST-T changes were seen in PPH patients whereas in VSD the electrical axis was within normal limits, without P wave changes and in some cases, less conspicuous ST-T abnormalities were observed (p less than 0.01). Such changes showed good sensitivity (80%) and specificity (81%) to suspect PH with resistances higher than 10 u/m2 with a predictive value of 75% (p less than 0.02). P wave and ST-T changes could be of use to suspect PPH with elevated resistances instead of right ventricular hypertrophy voltage criteria.     

Involvement of IL-1beta in acute stress-induced worsening of cerebral ischaemia in rats.

Stress is known to be one of the risk factors of stroke. Most of the knowledge on the effects of stress on cerebrovascular disease in humans is restricted to catecholamines and glucocorticoids effects on blood pressure and/or development of atherosclerosis. However, few experimental studies have examined the possible mechanisms by which stress may affect stroke outcome. We have used an acute stress protocol consisting of the exposure of male Fischer rats to an acute, single exposure immobilisation protocol (6 h) prior to permanent middle cerebral artery occlusion (MCAO), and we have found that stress worsens behavioural and neurological outcomes and increased infarct size after MCAO. The possible regulatory role of the TNFalpha and IL-1beta was studied by looking at the release of these cytokines in brain. The results of the present study showed an increase in IL-1beta release in cerebral cortex after exposure to acute stress. Brain levels of IL-1beta are also higher in previously stressed MCAO rats than in MCAO animals without stress. Pharmacological blockade of IL-1beta with an antibody anti-IL-1beta led to a decrease in the infarct size as well as in neurological and behavioural deficits after MCAO. In summary, our results indicate that IL-1beta, but not TNFalpha, accounts at least partly for the worsening of MCAO consequences in brain of rats exposed to acute stress.     

Determining the Alveolar Component of Nitric Oxide in Exhaled Air: Procedures and Reference Values for Healthy Persons

Nitric oxide (NO) production has been described using a 2-compartment model for the synthesis and movement of NO in both the alveoli and the airways. The alveolar concentration of NO (Ca_NO), an indirect marker of the inflammatory state of the distal portions of the lung, can be deduced through exhalation at multiple flow rates. Our objective was to determine reference values for Ca_NO. The fraction of exhaled NO (Fe_NO) was measured in 33 healthy individuals at a rate of 50 mL/s; the subjects then exhaled at 10, 30, 100, and 200 mL/s to calculate Ca_NO. A chemiluminescence analyzer (NIOX Aerocrine) was used to perform the measurements. The mean (SD) Fe_NO was 15 (6) ppb. The mean Ca_NO was 3.04 (1.30) ppb. These values of Ca_NO measured in healthy individuals will allow us to analyze alveolar inflammatory behavior in respiratory and systemic processes.     

Bilateral pleural effusion and ascites in the ovarian hyperstimulation syndrome.

We describe a pregnant woman with ovarian hyperstimulation syndrome with bilateral pleural effusion and ascites. Ovarian hyperstimulation syndrome is an iatrogenic complication of ovarian stimulation, characterized by a massive crossing of a protein-rich fluid from the vascular compartment into the peritoneal, pleural, or to a lesser extent, pericardial cavities. Management is usually conservative, with fluid and electrolytes correction and thromboprophylaxis. Prevention is very difficult, but an age younger than 35 years, low body mass index, polycystic ovarian disease, a high number of follicles, a high plasma oestradiol concentration, pregnancy, hyperandrogenism, and hypothyroidism are predisposing factors.     

Alterations in the ultrastructure of cardiac autonomic nervous system triggered by crotoxin from rattlesnake (Crotalus durissus cumanensis) venom.

This study explored the toxic effects of crotoxin isolated from Crotalus durissus cumanensis venom on the ultrastructure of mice cardiac autonomic nervous system. Mice were intravenously injected with saline (control group) and crotoxin diluted in saline venom (study group) at a dose of 0.107 mg/kg mouse body weight. Samples from the inter-ventricular septum were prepared for electron microscopy after 6 h (G1), 12 h (G2), 24 h (G3) and 48 h (G4). The G1 group showed some cardiomyocyte with pleomorphic mitochondria. Capillary swollen walls, nerve cholinergic endings with depleted acetylcholine vesicles in their interior and other depletions were observed. A space completely lacking in contractile elements was noticed. The G2 group demonstrated a myelinic figure, a subsarcolemic region with few myofibrils and nervous cholinergic terminal with scarce vacuoles in their interior. The G3 group demonstrated a structure with a depleted axonic terminal, mitochondrias varying in size and enhanced electron density. In addition, muscular fibers with myofibrillar structure disorganization, a depleted nervous structure surrounded by a Schwann cell along with an abundance of natriuretic peptides, were seen. An amyelinic terminal with depleted Schwann cell and with scarce vesicles was also observed. Finally, axonic lysis with autophagic vacuoles in their interior and condensed mitochondria was observed in the G4 group. This work describes the first report of ultrastructural damage caused by crotoxin on mice cardiac autonomic nervous system.     

A severe form of amyloidotic polyneuropathy in a Costa Rican family with a rare transthyretin mutation (Glu54Lys)

Four affected siblings in a Costa Rican family presented an aggressive polyneuropathy with widespread involvement of many visceral organs and onset during the third decade of life with rapid loss of muscle mass in the lower limbs and severe dysautonomy. The medical histories include vitreous opacity, cardiac enlargement, dermal and gastrointestinal infiltration, and autonomic dysfunction including circulatory compromise and gastrointestinal disturbances. Histological studies using Congo red stain and immunohistochemical assays with antibodies against the transthyretin (TTR) protein showed widespread deposition of amyloid in extracellular areas, including dermis and gastrointestinal lamina propia, endo- and perineural spaces, and vascular walls. A mutation search in the transthyretin (ttr) gene was performed seeking the cause of this severe form of familial amyloidotic polyneuropathy (FAP). We applied single-stranded conformational polymorphism (SSCP)-analyses followed by sequencing of the four exons of the ttr gene, revealing a point mutation in exon 3, a G to A transition that causes a Glu54Lys codon change. Western blots of plasma proteins incubated with anti-transthyretin antibodies after gel electrophoresis provided separation of wild-type and mutant TTR protein in affected family members.