Evidence of the inaccuracy of standard echocardiographic and angiographic criteria used for the recognition of true and "false" left ventricular inferior aneurysms

Diagnosis of so-called false aneurysms of the left ventricle after infarction is judged to be important because the risk of rupture is high and resection of aneurysms with a narrow orifice is usually successful. Aneurysms with larger communication orifices are less likely to rupture. Echocardiographic and angiographic criteria have been devised to classify left ventricular aneurysms into two distinct types. In four cases of inferior aneurysms the echocardiographic and angiographic criteria were typical of a "false aneurysm" but the defects were diagnosed as true aneurysms after intraoperative and histological examination. These aneurysms were characterised by their site in the inferior wall and by late diagnosis and treatment, which may have influenced their occurrence and determined the development of their characteristic shape. These findings suggest that the classic echocardiographic and angiographic diagnostic criteria for "false" aneurysms may have to be abandoned.     

Haemoglobin H disease in 2 Filipino families.

Haemoglobin H disease is described in successive generations of 2 Filipino families. The condition was asymptomatic. The inheritance pattern of haemoglobin H disease in these families appeared to be like that described for Thais.     

The acetyltransferase enzyme method for the assay of serum gentamicon concentrations and a comparison with other methods.

The adenylytransferase/acetyltransferase methods of gentamicin assay have been evaluated for accuracy, speed, and cost. For a comparable cost of materials the latter method is more accurate than that using the adenylytransferase enzyme. The acetyltransferase method is much quicker than the adenyltransferase due to the shorter time necessary for radioactive counting. Sonication is an easier method of enzyme preparation than the previously used osmotic shock technique. The acetyltransferase method is reproducible and there was a very good correlation between it and a microbiological agar-plate diffusion method.     

Lung vascular smooth muscle as a determinant of pulmonary hypertension at high altitude.

The pulmonary hypertensive response to chronic hypoxia varies markedly among mammalian species. An explanation for this variability was sought by exposing seven species to hypobaric hypoxia (PB equal to 435 mmHg) for 19-48 days. Control animals were studied at 1,600 m (PB equal to 630 mmHg). The pulmonary hypertension that developed varied in the following order of decreasing severity: calf and pig (severe); rat and rabbit (moderate); sheep, guinea pig, and dog (mild). Right ventricular hypertrophy developed in proportion to the elevation in right ventricular systolic pressure. These interspecies variations in response were not correlated with the degree of arterial hypoxemia, degree of polycythemia, elevation in heart rate, or postnatal age. However, the medial thickness of the small pulmonary arteries in control animals was highly correlated with the development of pulmonary hypertension and right ventricular hypertrophy in hypoxic animals. Thus, the amount of lung vascular smooth muscle inherent within each species is a major determinant of the pulmonary hypertensive response to high altitude and contributes to the interspecies variability in this response.     

Thermodilution method overestimates low cardiac output in humans

We compared 57 cardiac output measurements by the thermodilution and Fick methods in 26 patients and found that thermodilution values were higher in all 16 cases in which Fick outputs were less than 3.5 l/min. In 10 cases where Fick values were less than or equal to 2.5 l/min, thermodilution and Fick measurements differed by an average of 35%. When combined with the results of previous studies comparing the thermodilution, dye dilution, and Fick techniques, these findings suggest that the thermodilution method overestimates true cardiac output in the low output range. This overestimation probably is due to heat loss under conditions of low flow. Because the thermodilution method is used widely in patients with low output states, these findings have potentially important clinical implications.     

TonB is required for intracellular growth and virulence of Shigella dysenteriae

To assess the importance of TonB-dependent iron transport systems to growth of Shigella in vivo, a tonB mutant of Shigella dysenteriae was isolated and tested in cultured cells. The tonB mutant invaded epithelial cells, but did not form plaques in confluent monolayers of Henle cells, indicating an inability of this mutant to spread from cell to cell. The rate of intracellular multiplication of the tonB mutant was reduced significantly compared to that of the wild type. The loss of virulence in the tonB mutant was not due to loss of either Shu or Ent, the TonB-dependent systems which allow for transport of heme and ferrienterobactin, respectively. A shuA mutant lacking the outer membrane receptor for heme, an entB mutant defective in enterobactin synthesis, and a shuA entB double mutant each were able to invade cultured cells, multiply intracellularly, and form wild-type plaques. The ability of S. dysenteriae to access iron during intracellular growth was assessed by flow cytometric analysis of an iron- and Fur-regulated shuA-gfp reporter construct. Low levels of green fluorescent protein expression in the intracellular environment were observed in all strains, indicating that iron is available to intracellular bacteria, even in the absence of TonB-dependent iron transport. The failure of the tonB mutant to grow well in an iron-replete intracellular environment suggests that TonB plays a role in addition to heme- and siderophore-mediated iron acquisition in vivo, and this function is required for the intracellular growth and intercellular spread of S. dysenteriae.     

Increased multiclonal antibody-forming cell activity in the peripheral blood of patients with SLE

21 patients with criteria for systemic lupus erythematosus (SLE) and 12 normal controls were studied for their spontaneous circulating IgM and IgG plaque-forming cells (PFCs) reactive against sheep erythrocytes (SRBC) and against a panel of five haptens. Quantitatively defined active and mildly active SLE patients had significantly elevated IgM- and IgG-producing PFCs in their peripheral blood reactive with the panel of five chemically defined haptens. Those patients having inactive SLE also showed increased circulating IgM PFCs. Significant elevations in circulating hapten-reactive PFCs were found to correlate progressively with disease activity in the inactive, mildly active, and active SLE patient groups. Circulating IgM- and IgG-secreting PFC reactive against SRBC were both significantly elevated only in those patients with active SLE. The data support the concept that SLE patients have a generalized increase in B cell activity against a broad repertoire of determinants, even those ostensibly unrelated to natural tissue antigens.     

Do blood cultures need continuous monitoring so that clinical action can be taken outside normal working hours?

Many automated blood culture reading systems monitor bacterial growth 24 hours a day but it is unclear if reacting to prompts indicating bacterial growth outside normal laboratory hours is of clinical benefit. An analysis of 50 blood cultures from 43 patients which had organisms seen on Gram films and had triggered positive out-of-hours showed that examination of the Gram film altered management of seven patients and the results of culture or sensitivity testing altered that of a further four. However, after review, it was felt the clinical outcome would not have been influenced by earlier intervention in any of these patients. We therefore consider that an out-of-hours service for dealing with positive blood cultures is not justified in our hospital. This conclusion may not apply universally, especially in hospitals where potential pathogens show less predictable antimicrobial sensitivity patterns.     

Long-term potentiation deficits and excitability changes following traumatic brain injury

The effects of traumatic brain injury (TBI) on hippocampal long-term potentiation (LTP) and cellular excitability were assessed at postinjury days 2, 7, and 15. TBI was induced using a well-characterized central fluid-percussion model. LTP of the Schaffer collateral/commissural system was assessed in vivo in urethane-anesthetized rats. Significant LTP of the population excitatory postsynaptic potential (EPSP) slope was found only in controls, and no recovery to control levels was observed for any postinjury time point. Four measurement parameters reflecting pyramidal cell discharges (population spike) indicated that TBI significantly increased cellular excitability at postinjury day 2: (1) pretetanus baseline recording showed that TBI reduced population spike threshold and latency; (2) tetanic stimulation (400 Hz) increased population spike amplitudes to a greater degree in injured animals than in control animals; (3) tetanus-induced population spike latency shifts were greater in injured cases; and (4) tetanic stimulation elevated EPSP to spike ratios (E-S potentiation) to a greater degree in injured animals. These parameters returned to control levels, as measured on postinjury days 7 and 15. These results suggest that TBI-induced excitability changes persist at least through 2 days postinjury and involve a differential impairment of mechanisms subserving LTP of synaptic efficacy and mechanisms related to action potential generation