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Genetically engineered bacteria can be used for a wide range of applications, from monitoring environmental toxins to studying complex communication networks in the human digestive system. Although great strides have been made in studying single strains of bacteria in well-controlled microfluidic environments, there remains a need for tools to reliably control and measure communication between multiple discrete bacterial populations. Stable long-term experiments (e.g., days) with controlled population sizes and regulated input (e.g., concentration) and output measurements can reveal fundamental limits of cell-to-cell communication. In this work, we developed a microfluidic platform that utilizes a porous monolith to reliably and stably partition adjacent strains of bacteria while allowing molecular communication between them for several days. We measured small molecule production by the bacterial populations in response to stimuli using analytical chemistry methods and measured fluorescent output. The results are compared with communication and diffusion delay models. This porous monolith microfluidic system enables bacterial cell-to-cell communication assays with dynamic control of inputs, relatively long-term experimentation with no cross contamination, and stable bacterial population size. This system can serve as a valuable tool in understanding bacterial communication and improving biosensor design capabilities.

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The case of a 40-year-old woman with mitral valve prolapse and severe atypical chest pain is presented. The diagnosis was confirmed by phonocardiographic, echocardiographic, and angiocardiographic studies. The electrocardiogram revealed an ischemic pattern of ST-T on the anterior and inferior wall. Coronary angiographic studies showed normal coronary arteries. The patient's long-standing, prolonged, disabling atypical chest pain could not be relieved with medical therapy, despite the administration of beta-adrenergic blocking agents, calcium antagonists, and short-acting nitrites during a 30-month period. Thus, the prolapsed mitral valve was replaced with a Hancock xenograft. After 12 months the patient is totally free of symptoms, without any treatment and with a normal ECG. This excellent surgical result could be explained on the basis of the valvular theory of chest pain in mitral valve prolapse, suggesting that pain is promoted probably by a regional imbalance between oxygen availability and consumption, because of the excessive papillary muscular stretching produced by the prolapse. To our knowledge, this is the first published report of successful surgical treatment of chest pain in mitral valve prolapse.

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An experimental study of the production of cardiogenic shock together with the results of its treatment by means of the intraaortic balloon was carried out. Cardiogenic shock was produced in dogs with closed thorax and spontaneous respiration. In 13 of the 21 dogs studied, the production of acute myocardial infarction by means of selective embolism of the left circumflex artery permitted the reproduction of a model of cardiogenic shock. Embolism was produced by injecting metalic mercury through a double catheter. Six of the 8 remaining dogs died due to accidental introduction of mercury in the anterior descending coronary artery which produced irreversible ventricular fibrillation. The other 2 died due to rupture of the ascending aorta during the maneuveres to place the coronarygraphy catheter. The 13 dogs with cardiogenic shock were treated with intraaortic balloon pumping during 3-4 hours. The left ventricular systolic pressure fell from 128 +/- 12.07 to 124 +/- 4.65 mm. Hg. The cardiac index increased by 42%. These findings confirm the fact that intraaortic balloon pumping lessens the after load. The fall of the telediastolic pressure by 20% was an index of the lessening or the preload. The aortic telediastolic pressure rose by a mean value of 32.21 mm. Hg. This raises the coronary perfusion pressure thus limiting the extension or reducing the size of the infarction. A frank reduction of the electrographic subepicardiac lesion was observed after using intraaortic balloon pumping. The mean aortic pressure only rose by 8%, the central venous pressure remained unchanged and the increase in diuresis was not estimable. The maximum dP/dt was unaltered and the Vmax. rose 17%. Two dogs were left alive after the experiment and lived for 3 and 12 days respectively. To conclude the results obtained permit us to indicate that intraaortic balloon pumping when used in dogs with this standard type of cardiogenic shock produces an important reduction of the after load, a discrete reduction of the preload and a significative increase in coronary blood flow. There were no changes in cardiac frequency and although the results of myocardial contractility were not definite, they seem to indicate a moderate improvement.

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