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Biomedical subjects

M Schwartz

Publications and source records attributed to M Schwartz.

At least 937 records · Page 52Linked to original sources
PubMedDate not supplied

Acute hemodynamic effects of tocainide in patients undergoing cardiac catheterization.

To characterize the acute hemodynamic effects of tocainide hydrochloride, a new antiarrhythmic agent, 11 patients undergoing diagnostic cardiac catheterization were given intravenous infusions of the drug for 15 minutes at rates of 0.50 (six patients) or 0.75 (five patients) mg/kg/min. The hemodynamic status of these subjects was determined before, during, and for 15 minutes after treatment, and blood levels of tocainide were followed during and after treatment. Tocainide blood levels at the end of the infusions were 14.9 +/- 1.6 microgram/ml (S.E.) and 15 minutes later were 6.0 +/- 0.7 microgram/ml. In these subjects treatment was not associated with significant changes in Ao or PCW, but it was associated with a statistically significant but small decrease in LV dp/dt. At the same time, LVED was not significantly elevated. Treatment was also accompanied by small increases in PA diastolic and mean pressures, but RA and RV were unchanged. Significant changes were not seen in HR, CO, CI, SV, SVR, or PVR. Thus, the intravenous infusion of 0.50 and 0.75 mg/kg/min of tocainide for 15 minutes produced small but statistically significant depression of left ventricular function without producing changes in CO or clinical evidence of congestive heart failure.

Adult↗
PubMedDate not supplied

Disaccharidase deficiency in amniotic fluid from cases of cystic fibrosis.

The activities of the disaccharidases maltase and sucrase in 4 amniotic fluid from cystic fibrosis (CF) pregnancies have been compared to those of 120 non CF-pregnancies. Very low levels were found in 3 of the CF-fluids. The fourth CF-fluid was normal in all measured microvillar enzyme activities. Elevated levels of disaccharidases in meconium from one of the patients born with CF, supports the idea that these enzymes are trapped in the intestinal cavity by sticky meconium.

Alkaline Phosphatase↗
PubMedDate not supplied

Ophthalmic effects of low-energy laser irradiation.

Laser irradiation at subthreshold energies exerts various effects on the eye and other parts of the body, mainly the skin and nervous system, through a mechanism that has yet to be adequately explained. The ocular bioeffects are manifested mostly in the retina, but also in other ocular tissues. This review outlines the reported effects of low-energy laser irradiation on nonophthalmological tissues and organs, including those of the nervous system, with special emphasis on the optic nerve. It also details the ophthalmic phenomena induced by low-energy laser irradiation and examines claims of its therapeutic efficacy in several eye diseases, such as keratitis, glaucoma and macular degeneration.

Animals↗
PubMedDate not supplied

A technique for integrating any DNA fragment into the chromosome of Escherichia coli.

We describe a technique that allows the insertion of any DNA fragment into the EcoRI-site-containing malPpa, the promoter of malPQ, one of the three maltose operons of Escherichia coli. DNA fragments were cloned into the unique EcoRI site of the pBR322-derived plasmid pOM40, which carries malPpa. In the next step these fragments were transposed into the chromosome by homologous recombination events occurring on both sides of malPp. Cells in which such insertion of the entire recombinant plasmid have occurred can be conveniently selected. Excision and curing of the vector plasmid could then occur spontaneously at a high frequency, leaving behind the inserted fragment that can be manipulated as any chromosomal marker. When the inserted fragment contains a properly positioned promoter, its promoting activity can be estimated by assaying amylomaltase, the product of malQ. When required, the inserted fragment can be easily transferred back onto pOM40. As examples of application we have transferred two different fragments into the chromosome of E. coli: one contained the ceaC-ceiC operon, which encodes colicin E3 and its immunity protein, and the other contained the lac promoter of E. coli.

Base Sequence↗
PubMedDate not supplied

A retrospective review of the relationship between facial fractures, head injuries, and cervical spine injuries.

Facial fractures are common in the multiply-traumatized patient, and the results of previous studies that have examined the relationship between facial fractures, cervical spine injuries, and head injuries have produced conflicting results. A retrospective review of 1,050 blunt-trauma patients during a 40-month period at a regional trauma unit revealed 168 patients with facial fractures. The average injury severity score (ISS) of these patients with facial fractures was 31 compared with an average ISS of 25.6 for the entire group. There were 266 facial fractures in these 168 patients: mandible (n = 72), maxilla (n = 74), zygoma (n = 52), orbital (n = 46), nasoethmoidal (n = 20), and frontal (n = 2). There were seven (4%) cervical spine injuries, three of which were atlanto-occipital subluxations in patients who ultimately died. Of the four surviving patients, one had a cord injury. In contrast, 145 (85%) showed evidence of head injuries; 64 (38%) of these head injuries were serious and 17 of these patients required craniotomy. The relationship of facial fractures and cervical spine injuries may be over emphasized; head injuries, although frequently minor, are much more commonly associated with facial fractures.

Adolescent↗
PubMedDate not supplied

Recognition and treatment of multifocal atrial tachycardia: a critical review.

Multifocal atrial tachycardia (MAT) is an uncommon but clinically important tachydysrhythmia that is usually seen in the setting of severe cardiopulmonary illness. Diagnostic criteria include the presence of at least three different, nonsinus P waves in the same lead; an atrial rate greater than 100 beats per minute; and an isoelectric baseline between P waves. MAT is often difficult to differentiate from atrial fibrillation. The pathogenesis of MAT is unknown; however, it is probably incited by "triggered" electrical activity, a form of abnormal automaticity. This electrophysiologic model has led to several small, uncontrolled clinical trials using calcium channel and beta-adrenergic blocking agents, specifically verapamil and metropolol. None of these trials meets rigorous methodologic standards, and all exclude unstable patients who are at greatest risk for hemodynamic compromise from the tachycardia. Treatment of MAT should first be directed at potential predisposing factors, such as hypoxia, congestive heart failure, and theophylline toxicity. Pharmacologic treatment includes intravenous metoprolol or verapamil; in published reports both agents have been well tolerated and have controlled the heart rate in a majority of patients.

Adult↗
PubMedDate not supplied

Potential neuroprotective therapy for glaucomatous optic neuropathy.

Accumulating evidence points to the existence of a mechanism that may explain why glaucomatous neuropathy continues to progress even after its primary cause, e.g., high intraocular pressure, has been alleviated or attenuated. We suggest that such a mechanism involves processes collectively termed secondary degeneration, an inevitable outcome of acute injury of the central nervous system. Secondary degeneration refers to the spread of degeneration to apparently healthy neurons that escaped the primary insult, but are adjacent to the injured neurons and are thus exposed to the degenerative milieu that the latter create. Neuroprotection, i.e., protection of undamaged neurons from secondary degeneration, would therefore require that the extracellular elements associated with the degeneration be neutralized, balanced off, or inhibited. In seeking an experimental framework for testing treatment modalities for neuroprotection, we have developed an animal model in which a well-calibrated, reproducible, partial lesion is inflicted on the optic nerve of the adult rat. Using this model, the extent of the primary damage can be quantified and the secondary degeneration demonstrated and assessed. Damage inflicted directly on the optic nerve fibers inevitably leads to their degeneration and the eventual death of their cell bodies. Over time, neurons that initially escaped the injury undergo self-perpetuating secondary degeneration, the extent of which is a function of the severity of the primary insult. We suggest that a similar mechanism may underlie the propagation of damage seen in glaucoma at any given time after alleviation of the primary cause of the disease, and might explain why patients with severe pre-existing damage are much more likely to deteriorate even if their intraocular pressure is the same or lower than that of patients without visual loss at the time of diagnosis. The model can be used to screen compounds for their efficacy in protecting initially spared neurons from undergoing secondary degeneration, thereby achieving a better functional outcome. The findings obtained using this model support the attempt to develop neuroprotective therapy for glaucoma. Such therapy would need to be applied in combination with treatment (e.g., antihypertensive therapy) directed against the primary cause of the neuropathy.

Animals↗