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This study was undertaken to determine the incidence of undiagnosed apical disease in acute unilateral sinusitis and to evaluate the role of Orthopantomograms (OPGs). Our results, with an incidence of 10 per cent, are in agreement with the findings of Formby (1960) and we conclude that OPGs are not justified in the routine investigation of acute sinusitis.

Ear acupuncture followed by sepsis caused subacute bacterial endocarditis in a patient with rheumatic valve disease.

Depression of lymphocyte proliferative response occurs after trauma and hemorrhage. Because abnormalities in production or utilization of interleukin 2 (IL-2) can result in depression of mitogen-induced lymphocyte proliferation, we investigated the effects of unanesthetized hemorrhage on the generation of IL-2 by rat peripheral blood lymphocytes and the response of these cells to exogenous IL-2. Two hours after loss of 30% of total blood volume, IL-2 production was reduced by greater than 90%. Return to normal levels of IL-2 generation occurred by 48 hr after hemorrhage. Addition of purified rat IL-2 to cultures of phytohemagglutin-stimulated peripheral blood lymphocytes obtained from normal animals resulted in suppression of the proliferative response. Exogenous IL-2 produced a similar degree of suppression in the proliferation of cells obtained from hemorrhaged animals. These results show a profound hemorrhage-induced suppression of IL-2 generation, but no benefits of exogenous IL-2 in improving the depressed lymphocyte proliferative response that exists after hemorrhage.

Five different tests were used to evaluate oesophageal function in 22 patients who presented to a cardiac unit with acute chest pain but whose cardiological investigations were negative. Eight patients had an abnormality on oesophagoscopy, 10 had an abnormal pH monitoring study, six had a positive acid infusion test, 10 had an abnormal manometric study and six had an abnormal oseophageal transit scintiscan. Concordance for the three tests of gastro-oesophageal reflux disease was low at 28%, and for the two tests of oesophageal motility only 55%. Only two patients had normal results in all five tests.

Opiate receptor binding was studied in seizure sensitive (SS) and seizure resistant (SR) strains of the Mongolian gerbil. Cryostat sections of the brain were labeled with [3H]-dihydromorphine, subjected to autoradiography and analysed by microdensitometry. SS gerbils, prior to seizure induction, demonstrated overall greater brain opiate binding when compared to SR animals. Immediately following a seizure, binding in the interpeduncular nucleus fell to levels found in SR animals. The increased opiate binding in the SS (pre-seizure) compared to SR gerbils could reflect a deficit of endogenous ligand which could underlie the seizure diathesis in the gerbil.

Autoradiography was used to examine opioid receptor binding in the Mongolian gerbil, a genetic model of the epilepsies. Coronal brain sections of seizure-resistant (SR) and seizure-sensitive (SS) (both pre- and post-seizure conditions) gerbils were labeled with [3H]dihydromorphine. SS (pre-seizure) gerbils demonstrated overall greater brain opioid binding when compared to SR animals. The periaqueductal gray, substantia nigra and medial geniculate body were specific areas in SS (pre-seizure) gerbils which demonstrated highly significant increases in opioid binding compared to SR animals (% increase vs SR were 98%, 91.3% and 42.9%, respectively). Scatchard analysis demonstrated that the increase in opioid binding was due to an increase in the total number of receptors without a significant change in receptor affinity (i.e. periaqueductal gray area: total number of binding sites was 12.7 (SR) and 18.0 fmol/mg tissue (SS pre-seizure), while Kd values were 4.0 (SR) and 4.0 mM (SS pre-seizure). Opioid binding was also increased in the SS (post-seizure) animals when compared to SR animals, especially in the substantia nigra. However, when compared to SS (pre-seizure) gerbils, there was a general but not significant, decrease in opioid binding in SS post-seizure gerbils. The increased opioid binding in the SS (pre-seizure) gerbil compared to SR gerbils could reflect an up-regulation due to a deficit in endogenous ligand (e.g. a deficit in synthesis or decreased release) which could underlie the seizure diathesis in the gerbil.

The ability of propranolol to limit myocardial infarct size (IS) following coronary artery occlusion with and without reperfusion into a critical stenosis was assessed in the dog. IS was determined by the nitrobluetetrazolium staining method and expressed as percent of the left ventricle (free wall plus septum). In Series 1 dogs the left circumflex coronary artery (LCX) was ligated at its origin. IS at 6 h was similar in groups pretreated with saline (36.0 +/- 1.3%) or propranolol (0.2 mg . kg-1, 34.7 +/- 1.7%; 1.0 mg . kg-1, 36.7 +/- 1.5%; 4.4 mg . kg-1, 34.8 +/- 0.3%). In Series 2 dogs a relatively small infarction was produced by ligating the largest branch of the LCX between the left anterior descending and posterior descending arteries. IS at 6 h was not significantly different in dogs pretreated with saline (8.1 +/- 1.7%) or propranolol (0.2 mg . kg-1, 7.1 +/- 2.5%; 1.0 mg . kg-1, 4.6 +/- 1.2%). In Series 3 dogs the LCX was ligated approximately 10 mm from its origin for 60 min followed by reperfusion into a critical stenosis. IS determined at 24 h was significantly less in dogs treated with propranolol (1.0 mg . kg-1) before LCX occlusion (4.6 +/- 0.6%) or 5 min after LCX reperfusion (9.5 +/- 1.8%) than in dogs treated with saline (22.6 +/- 2.8%). In Series 4 dogs treatment was exactly as in Series 3 except that reperfusion was not instituted. IS was similar in dogs pretreated with saline (29.0 +/- 1.5%) or propranolol (31.1 +/- 3.0%). Thus, in the present study, propranolol limited IS in the presence but not in the absence of reperfusion. In the reperfusion model propranolol was effective when administered before coronary occlusion or after initiation of reperfusion.

The clinical findings, histopathology, and management of verrucous carcinoma of the larynx are discussed. Four cases are presented that demonstrate the efficacy of endoscopic removal of the tumor as a treatment modality. Complete endoscopic removal at the time of initial direct laryngoscopy with careful followup is recommended in cases of suspected verrucous carcinoma.

Recent reports suggest that arginine vasopressin (AVP) may be an endogenous antipyretic peptide and a mediator of febrile convulsions [10,12]. The spontaneously seizing Mongolian gerbil was used to investigate the thermoregulatory, behavioral and seizure modulatory effects of AVP. Injection of AVP (1.0 and 5.0 micrograms IV and 0.01-1.0 mg/kg SC) caused dose-related falls in body temperature. Stereotypic scratching, terminated by a body shake, was observed after AVP (1.0-5.0 micrograms IV). However, such behavior was not observed after subcutaneous injection of AVP. AVP did not potentiate seizure induction in the gerbils but rather reduced the seizure incidence. The data demonstrate that AVP can reduce body temperature and cause specific behaviors, but it does not appear to play a role in the pathogenesis of seizures in the seizure sensitive strain of Mongolian gerbil.

The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) acts through postsynaptic receptor sites which regulate membrane chloride ion channels. The GABA receptor-ionophore complex also contains modulatory receptor sites for two classes of centrally acting drugs, one for the benzodiazepines, and a second for both barbiturates and related depressants and for picrotoxin and related convulsants. The presence of these drug modulatory sites, directly on the GABA receptor protein, is consistent with other experimental observations; blocking GABA function can cause seizures, and augmenting GABA function can afford protection against seizures. This, and other circumstantial evidence, has suggested the possibility that a functional GABA deficit may be involved in some kinds of human epilepsy. Some neurochemical markers for GABA synapses have been reported to be altered in certain animal models as well as in human temporal lobe epilepsy. We have examined the postsynaptic GABA receptor complex using receptor binding assays for GABA, benzodiazepine (BZ), and barbiturate receptor sites in the seizure-susceptible gerbil, a genetic model of generalized epilepsy. A 30% deficit in BZ receptor binding was observed in the midbrain of seizure-sensitive animals relative to normal controls. This was shown by quantitative brain-slice binding autoradiography to involve a decrease in the number of binding sites in the substantia nigra (SN) and periaqueductal gray regions. A deficit in membrane receptors for BZs (which are linked to a subtype of postsynaptic GABA receptors) in a crucial region of brain might therefore contribute to seizure susceptibility in some kinds of epilepsy.

Injections of muscimol (12.5 or 25 ng bilaterally), a GABAA agonist, into the posterior nuclei of the thalamus suppressed generalized convulsive seizures in the spontaneously epileptic Mongolian gerbil. This anticonvulsant effect was dose-dependent and was reversed by picrotoxin (10 ng bilaterally), a GABAA antagonist. Bilateral intrathalamic injections of 1-baclofen (50 ng), an agonist of the GABAB receptor, were ineffective in suppressing seizures in this model. These results suggest that GABAergic transmission within the thalamus is involved in the control or the genesis of some generalized convulsive seizures.

Right atrial pacing at rapid heart rates induced ischemic S-T segment changes in 19 atherosclerotic, male rhesus monkeys. Prior administration of nitroglycerin (100 mug/kg, i.v.) prevented the S-T segment alteration at a given pacing rate in 5 animals, attenuated it in 12 others, and had no effect in the remaining 2. The results of these studies are similar to earlier ones in atherosclerotic rabbits.

Repeated pneumonia and hypogammaglobulinaemia was associated with long term low dose steroid therapy. Clinical improvement with restoration of antibody levels followed substitution of aerosol for oral therapy.

Sixty six patients with angina at rest were investigated by exercise electrocardiography, thallium scintigraphy, and coronary arteriography. A positive exercise electrocardiogram was highly predictive (93%) but poorly sensitive (52%) of coronary artery disease (greater than or equal to 50% stenosis). Thallium scintigraphy was as predictive of the presence of coronary artery disease (91%) but was also highly sensitive (91%). The diagnostic contribution of the thallium scan was greatest in those patients with an inconclusive exercise electrocardiogram without Q waves.

As more small peptidergic components of the central nervous system are isolated, their role in disease states is being investigated. Several of these neuropeptides, especially the opioidlike peptides, adrenocorticotropic hormone, and some hypothalamic releasing factors, have been found to alter neuronal excitability. This finding has led to the proposal that these peptides may play a role in the pathogenesis of the epilepsies. We tested this hypothesis in a genetic model of epilepsy. At nontoxic doses, several exogenously administered peptides had anticonvulsant properties, while others were proconvulsant. The most potent anticonvulsant was the opioidlike peptide beta-endorphin. Its effect was similar to that of the opioid alkaloids. Using the potent antagonist naloxone hydrochloride to block possible endogenous opioid-like peptides, we found no effects on seizures in naive animals. Naloxone did alter postictal events, however, by partially blocking the postictal refractoriness to further seizures. We speculate that one possible role for the endogenous opioid peptides may be to limit the spread of seizures or to modulate postictal susceptibility to further seizures. Naloxone was effective in this model only after stressful situations occurred that modified the seizures and presumably induced a release of endogenous opioidlike peptides. Support for this hypothesis from other epilepsy models is discussed. Other peptidergic systems may also be active in various epileptic models, and the current understanding of their roles is reviewed.

A microtiter assay for the detection of picomolar quantities of inorganic phosphate has been described. The assay, linear between 50 and 1000 pmol of inorganic phosphate, is simple and rapid, with results obtainable in several minutes. Results from 5'-nucleotidase and (Ca2+ + Mg2+)ATPase assays using this method were compared with conventional phosphate assays and showed a high degree of correlation. The high sensitivity of this assay and the small sample size needed allows its widespread use in biochemical studies involving the generation of inorganic phosphate.

The anti-arrhythmic action of 2,3-cis-1,2,3,4-tetrahydro-5-[(2-hydroxy-3-tert-butylamino)propoxy]2,3-naphthalenediol (nadolol) was evaluated and compared with that of propranolol in several experimental models of cardiac arrhythmias. Both nadolol and propranolol antagonized isoproterenol-induced tachycardia and ouabain-induced arrhythmias in cats, antagonized coronary artery ligation-induced ventricular fibrillation and suppressed ventricular ectopic activity during vagal stimulation in dogs. In contrast to propranolol, nadolol was considerably weaker in suppressing existing digoxin-induced arrhythmias, lacked local anesthetic activity and did not depress the heart in dogs. Because of these findings, it is concluded that the anti-arrhythmic activity of nadolol is apparently related to blockade of beta-adrenergic receptors.