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This paper examines sexual risk-taking within a sample of sexually active gay and bisexual men entering substance abuse treatment (n = 383), and identifies correlates of unprotected anal sex within this group. Sexual risk-taking was high, with 55% of these men engaging in anal intercourse without a condom within a 90-day period. Correlates of unprotected anal sex varied somewhat when looking at unprotected anal sex with a primary partner only and with non-primary partners; substance use variables (number of drugs used, use of inhalant nitrites or stimulant drugs with sex, length of time since use of alcohol/drugs, loss of control problems associated with alcohol/drug use) appear to play more of a role in unprotected anal sex with non-primary partners. Overall, logistic regression analyses indicated that sexual risk was greater for those who were more sexually active, enjoyed unprotected anal sex with withdrawal prior to ejaculation, did not approve of sex outside of a love relationship, and identified themselves as more risky. In addition, those who reported more social problems due to substance use had fewer expectations that substance use increased risk, had been HIV-tested, and used reappraisal/problem-solving coping strategies showed greater risk with a primary partner only. Sexual risk with non-primary partners was greater for those who used more drugs, reported more difficulty avoiding high-risk sex when aroused and were HIV+. The paper discusses the implications of these findings for the design of sexual risk-reduction interventions.

Background: Noxious stimulation-induced sensitization of the central nervous system has been proposed as a key element in the development of subsequent protracted pain. Accordingly, the authors used the formalin model of pain to test the hypothesis that general anesthesia can produce preemptive analgesia and thereby interfere with noxious stimulation-induced central sensitization., Methods: Rats received 0.9% or 1.8% halothane, 30% or 75% nitrous oxide (N2O), or 75% N2O plus 0.9% halothane (n = 4 or 5 per group). Control rats (n = 5) received only 100% oxygen. Fifteen minutes after the induction of anesthesia, formalin was injected subcutaneously into a hind paw of each rat, and anesthesia was maintained for 5 more min. Because the behavioral pain response to formalin (i.e., flinching of the injected paw) is biphasic, these treatment groups were anesthetized only during phase 1 (acute phase). Another group (n = 5) received 75% N2O only during phase 2 (delayed phase). Reversibility of the N2O effect was tested by the administration of naloxone before phase 1 or naltrexone during phase 2 (n = 5 per group). Finally, additional rats anesthetized as described above (n = 4 or 5 per group) underwent tail-flick testing during anesthesia., Results: All anesthetics reduced phase 1 pain behavior, but only N2O produced antinociception on tail-flick testing. Thirty percent and 75% N2O, administered during phase 1, suppressed phase 2 flinching 29% and 49%, respectively, whereas nitrous oxide administered after phase 1 did not suppress phase 2 pain behavior. This effect of nitrous oxide was reversed by an opioid antagonist given during phase 1 but not phase 2. Halothane administered during phase 1 had no effect on phase 2 flinching, and it antagonized the effect of 75% N2O., Conclusions: Nitrous oxide induces dose-dependent preemptive analgesia in this model that is reversed partially by naloxone, thus suggesting the involvement of endogenous opioids in this action. In contrast, halothane has no preemptive analgesic properties and even antagonizes the analgesic effect of nitrous oxide. Hence, the hypnotic potency of an anesthetic is a poor indication of its preemptive analgesic potential.

To test the hypothesis that acute subarachnoid hemorrhage is associated with abnormal myocardial perfusion, we assessed myocardial blood flow with thallium scintigraphy in 19 patients with a confirmed subarachnoid hemorrhage and an abnormal electrocardiogram. A thallium scan was performed at the bedside of each patient 3 +/- 2 days (mean +/- SD) after subarachnoid hemorrhage and subsequently was analyzed both qualitatively and quantitatively. Patients averaged 58 +/- 13 yr of age and 68% had one or more cardiac risk factors. The neurologic condition of patients on the day of the scan was II (median; range I-V) on the standard 5-point scale of Botterell. Abnormalities on a standard 12-lead electrocardiogram obtained on the same day as the scan consisted of repolarization changes in most patients; 10 had T wave inversions and 8 had nonspecific ST segment changes. Thirty-two percent (n = 6) of patients had an abnormal thallium scan. There were, however, no features of the clinical history, electrocardiogram pattern, or neurologic condition that were associated with a positive scan. For instance, 2 of 4 patients with diffuse deeply inverted T waves had a normal thallium scan, whereas the scan was abnormal in 2 of 8 patients with minor nonspecific electrocardiographic abnormalities. The thallium scan was also positive in neurologically intact (grade I) as well as severely injured (grade V) patients. Thus, abnormal myocardial perfusion and possibly myocardial ischemia occur frequently following subarachnoid hemorrhage, but no specific electrocardiographic characteristic identifies patients with a perfusion abnormality.

The effects of pentobarbital and halothane anesthesia on the expression in brain of the immediate-early genes c-fos and jun-B were investigated. Pentobarbital-anesthetized rats (n = 10) received a single intraperitoneal injection of pentobarbital 65 mg/kg in a vehicle of 40% propylene glycol and 10% ethanol and then were placed in a plexiglass box flushed continously with 100% oxygen at 5 l/min. Halothane-anesthetized rats (n = 10) received an intraperitoneal injection of vehicle only and were transferred to a box flushed continuously with oxygen plus 1.5% halothane. Unanesthetized control rats (n = 10) received an intraperitoneal injection of vehicle and were placed in a box flushed continuously with 100% oxygen. Four additional rats received no intraperitoneal injection but were handled and otherwise treated identically to the control group, and six others had a femoral arterial catheter inserted for blood pressure and blood gas measurements. Five animals from the control and both anesthetized groups were killed at 30 and 120 min postinjection and their brains rapidly removed and frozen. The messenger ribonucleic acid transcription products of the genes c-fos, jun-B, and beta-actin from whole cerebral hemispheres were analyzed autoradiographically after Northern blot hybridization with 32P-labeled deoxyribonucleic acid probes. Relative levels of c-fos and jun-B messenger ribonucleic acid were determined from optical density measurements of the autoradiographic bands, with beta-actin measurements being used to correct for sample-to-sample variation. Rats became immobile within minutes of drug administration and remained anesthetized until they were killed.(ABSTRACT TRUNCATED AT 250 WORDS)

This report describes complete airway obstruction following anterior cervical fusion caused by extreme, fixed flexion of the neck in a halo device. The causes and treatment of such an airway complication are reviewed.

SCH 39166 [(-)-trans-6,7,7a,8,9, 13b-hexahydro-3-chloro-2-hydroxy-N-methyl-5H-benzo-[d]naphtho[2, 1b]azepine] has recently been described as a selective D1 antagonist and has entered clinical trials for the treatment of schizophrenia. The tritiated analogue of this compound, [3H]SCH 39166, has now been synthesized and characterized for its in vitro and in vivo binding profiles. [3H]SCH 39166 binds to D1 receptors in a saturable, high-affinity fashion, with a KD of 0.79 nM. In competition studies, D1-selective antagonists like SCH 23390 displaced the binding of [3H]SCH 39166 with nanomolar affinities, whereas antagonists of other receptors exhibited poor affinity. In vivo, [3H]SCH 39166 bound to receptors in rat striatum in a fashion suggestive of D1 selectivity. Further, when the time course for the binding of [3H]SCH 39166 was compared with the behavioral time course of the unlabeled compound, the two durations of action were virtually indistinguishable. Similar studies were performed for SCH 23390 and its tritiated analogue, but the in vivo binding of this radioligand exhibited a duration of action far greater than the behavioral activity of the unlabeled drug. In concert, these data demonstrate that [3H]SCH 39166 selectively labels D1 receptors in vitro and in vivo, and that this drug is superior for in vivo imaging of the D1 receptor.

The authors investigated the spinal blood flow and metabolic effects of subarachnoid clonidine in conscious rats prepared with chronically implanted subarachnoid catheters. For the blood flow experiments, rats received saline (n = 7) or clonidine 20 nmol (7 micrograms; n = 6), 100 nmol (27 micrograms; n = 5), or 400 nmol (107 micrograms; n = 7) intrathecally. Another group of rats received clonidine 400 nmol intravenously (n = 4). Spinal glucose utilization was measured in rats that received either saline (n = 5) or clonidine 100 nmol (n = 5) intrathecally. Spinal cord blood flow (SCBF) and glucose utilization were measured in five gray and three white matter areas of lumbar spinal cord 15 min after drug administration with the autoradiographic iodo-[14C]-antipyrine and 2-[14C]-deoxyglucose methods, respectively. Physiologic differences between the groups were minor. Rats in the blood flow experiments that received clonidine 100 nmol had a slightly lower arterial PO2 level (70 +/- 1 vs. 82 +/- 3 mmHg; P less than 0.05), whereas those in the glucose utilization group were mildly hypocarbic (PCO2 27 +/- 1 vs. 32 +/- 2 mmHg; P less than 0.01) relative to control animals. Only animals that received 400 nmol clonidine intrathecally had significant analgesia, as assessed by the tail-flick test. One control animal for the metabolism experiments was technically unsatisfactory and was excluded from data analysis. Subarachnoid clonidine reduced both SCBF and glucose utilization. In spinal gray matter, the largest decreases in flow (32-44%; P less than 0.01) occurred with 20 nmol clonidine, whereas flow decreased least (12-27%) with the 400-nmol dose.(ABSTRACT TRUNCATED AT 250 WORDS)

To identify changes of ventricular performance and their relationship to myocardial glucose uptake in Sprague-Dawley rats exposed to hypobaric hypoxia, radionuclide angiocardiograms (n = 34) and 2-[14C]deoxyglucose (2-[14C]DG) autoradiography (n = 14) were performed on rats maintained either for two weeks in air at 380 mmHg (hypoxic group), two weeks in hypobaric hypoxia followed by two weeks of air (recovered group), or in air (control group). Right ventricular ejection fraction (RVEF) was 66% +/- 2% (mean +/- s.e.m.) in controls, 40% +/- 3% during hypoxia, and 60% +/- 2% in recovered rats. LVEF remained unchanged. In controls, RV 2-[14C]DG uptake was 77% +/- 3% of LV uptake. During hypoxia, 2-[14C]DG uptake increased. This increase was greater within the RV than the LV and septum (85 +/- 16% versus 51 +/- 10%, p less than 0.005). The alterations of RV 2-[14C]DG uptake correlated with systolic pulmonary artery pressure (r = 0.77, p = 0.002).

The negative results of assays for polarizing activity along the posterior border of the chick wing 24 and 48 hours after removal of the polarizing zone demonstrate that this zone is not regenerated following removal. These results, and the fact that normal wing development can occur after polarizing zone removal from stages 15 through 24 wing buds, indicate that during these stages the polarizing zone has no direct role in normal development of the limb bud. It is speculated that the polarizing zone is effective only during limb induction and that after this time it exists in latent or residual form.

Neohesperidin dihydrochalcone (NHDHC), known since 1963 as an intensely sweet compound, is determined to be 340 +/- 60 (p less than 0.05) times more potent than sucrose. The unusual temporal properties of this material are hypothesized as being due to the effects of metabolism, conformation, chelation, or hydrophobicity. Forty-four analogues are synthesized to test the four hypotheses, none of which are strongly supported. A method of quantitation of temporal characteristics of tastant molecules is developed so as to allow comparison of taste appearance time (AT) and extinction time (ET) of experimental compounds. Four of the new compounds, 40 and 43-45, exhibit high sweetness potencies, ranging from 280 and 440 times sucrose, and may be useful in selected food systems. The temporal taste characteristics remain unimproved over NHDHC, however.

Because of the physiologic and metabolic changes that occur during acclimatization, we hypothesized that LCGU may be normal during prolonged hypoxia. We exposed five Sprague-Dawley rats to hypoxia (air at 380 mm Hg) for 2 weeks (hypoxic group) and six rats to 2 weeks of hypoxia followed by 2 weeks of recovery in room air (recovered group). Six control rats breathed room air (control group). Regional brain glucose utilization was measured in awake animals by using 2-[C]deoxyglucose autoradiography. Glucose utilization was comparable in the control and recovered groups and in most brain regions of hypoxic animals. Glucose utilization was decreased slightly in 10 of 12 gray matter regions examined and was 20 to 25% lower (p <0.05) in the olfactory and auditory cortices, the caudate nucleus, and the superior olive of the hypoxic group. White matter glucose utilization was unchanged. Hypoxic rats, compared to controls, had a lower PaO2 (53 +/- 3 vs. 76 +/- 3 mm Hg, mean SEM, respectively), a lower PaCO2 (22 +/- 1 vs. 36 +/- 2 mm Hg), and a higher mean pulmonary artery pressure (46 +/- 3 vs. 14 +/- 3 mm Hg) and hematocrit (61 +/- 2% vs. 48 +/- 1%; p <0.005 for all comparisons). Pulmonary hypertension and polycythemia persisted in recovered rats. Arterial pressure, pH, and plasma glucose were unaffected. Therefore, while acute hypoxia may increase glucose utilization in most brain structures, prolonged exposure does not.

The [14C]deoxyglucose technique was used to measure brain glucose utilization in homozygous male Brattleboro and age-matched Long-Evans control rats. Brattleboro homozygotes had significantly higher daily water intakes and plasma osmolalities and significantly lower body weights than controls. Glucose utilization for the brain as a whole and for 46 discrete brain structures was not significantly different for the two strains. Our results indicate that vasopressin is not essential for the maintenance of overall brain glucose utilization in resting, awake rats.

A novel benzazepine, SCH 23390, has recently been described as a very potent and selective dopamine D-1 receptor antagonist based on its potent inhibition of dopamine sensitive adenylate cyclase and its selective displacement of 3H-piflutixol from rat striatal receptor sites. In the present study, the in vitro binding of 3H-SCH 23390 to specific striatal receptor sites has been characterized. Binding was saturable and stereospecific, and the results of both saturation and competition studies are consistent with the binding of 3H-SCH 23390 to a single striatal site. A KD of 0.53 nM was obtained through Scatchard analysis. Relative potencies of a variety of neuroleptics in competing with 3H-SCH 23390 and also 3H-spiperone support an interpretation that the single site to which 3H-SCH 23390 binds is the D-1 dopamine receptor. Also, the binding capacity of 3H-SCH 23390 (69 pmoles/gm wet weight) is in agreement with published values for the binding capacities of 3H-piflutixol and 3H-flupentixol. These data, coupled with the low level of non-specific binding encountered with this radioligand (4-8% of total binding at normally employed ligand concentration of 0.3 nM), its high specific activity and its negligible binding to plastic and glass surfaces make it ideally suited for studying interactions with this receptor.

A new test for sickling hemoglobin, SickleQuikTM, has been developed which has definitive advantages over existing turbidity tests. This test utilizes a biphasic liquid reagent system provided in individualized, ready-to-use reaction tubes which are stable at room temperature. The test differentiates homozygous from heterozygous S samples in less than eight minutes. Results are based on the color of a layer formed at the organic-aqueous interface and the color of the lower aqueous phase. Of more than 900 samples tested in independent laboratories, no false positive or false negative results occurred.

The effect of naloxone on gamma-hydroxybutyrate (GHB)-induced cerebral metabolic depression was studied in rats with the 2-[14C]deoxyglucose method. Naloxone pretreatment statistically significantly antagonized the cerebral metabolic effect of GHB in 10 of 38 structures examined. These results are consistent with previous data showing reversal of the dopaminergic, electroencephalographic, and behavioral effects of GHB by naloxone and suggest that some of the neuropharmacological effects of GHB are mediated by the endogenous opiate system.

The purpose of our study was to investigate the effect of hypermagnesemia on spinal metabolic rate. The 2-[14C]deoxyglucose technique was used to measure regional glucose utilization in the lumbar spinal cord of paralyzed, mechanically ventilated rats receiving 70% nitrous oxide and an intravenous infusion of either saline (n = 5) or magnesium sulfate (n = 5). Plasma magnesium concentrations were 6.75 +/- 0.5 and 0.9 +/- 0.5 mM (p less than 0.01) in hypermagnesemic and control rats, respectively. Hypermagnesemic rats were hypotensive (88 +/- 1 vs. 130 +/- 4 mm Hg, p less than 0.01) but blood pressure remained within the autoregulatory range. Glucose utilization was reduced 26-45% in spinal gray matter and 53-63% in spinal white matter during hypermagnesemia. We conclude that magnesium is a potent spinal metabolic depressant and that this action, which is unusually prominent in spinal white matter, is a plausible explanation for the recently reported beneficial effect of magnesium therapy during spinal cord ischemia.

Local rates of glucose utilization in the spinal cord and brain were measured with the 2-[14C]deoxyglucose method in conscious and in paralyzed and mechanically ventilated pentobarbital- or 70% nitrous oxide-treated rats. In conscious animal lumbar spinal cord glucose utilization is only 40-50% that of the cerebral cortex and shows little laminar heterogeneity. Pentobarbital reduces and nitrous oxide increases the cerebral glucose utilization of most structures. The effect of paralysis and nitrous oxide analgesia on lumbar spinal cord glucose utilization is quantitatively similar to that produced in brain; 15-25% increases occur in most spinal cord laminae and cerebral structures. In contrast, the 10-20% reduction in spinal cord gray matter metabolism in the paralyzed and pentobarbital-treated animals is considerably less than the 20-50% depression measured in most brain structures. From these data the authors conclude that, relative to that of most cerebral structures, spinal cord metabolism is less sensitive to depression by barbiturates and suggest that differences in the cell populations of these tissues may account partially for this observation.

The authors measured blood pressure changes non-invasively in 56 conscious, unpremedicated patients with cerebral arteriovenous malformations (AVMs) during preparation for proton beam therapy. The procedure requires six injections of local anesthetic and application of a stereotactic frame by fixation into the outer table of the skull, and has been used during the past 20 yr to treat over 1,000 patients with cerebral AVMs. No effort was made to control blood pressure. Blood pressure increased during administration of the local anesthetic and application of the frame. Maximum systolic and mean arterial pressures averaged 160 +/- 17 and 118 +/- 7 mmHg (mean +/- SD), respectively. This represented an average increase of 44 mmHg (38%) in systolic pressure and 32 mmHg (37%) in mean blood pressure at some point during the procedure (P less than 0.01 compared with pretreatment control pressures). Systolic pressure increased more than 60 mmHg in 21% of patients. Nevertheless, none of these 56 patients nor any of the more than 1,000 patients treated in similar fashion suffered a clinically evident AVM hemorrhage during the procedure. Since the treatment protocol has not changed materially during the past 20 yr, the authors assume that most patients treated in this fashion developed a similar degree of hypertension and conclude from this large clinical experience that moderate arterial hypertension does not precipitate spontaneous hemorrhage of intracranial AVMs.

Measurements of [1-14C]oleoyl CoA oxidation in homogenates and isolated mitochondria of skeletal muscles, hearts and livers from dystrophic C57BL/6J mice and unaffected litter-mates indicate that rates are lower in dystrophic mitochondria, but are comparable in whole homogenates. These findings are not due to differences in the endogenous concentrations of the fatty CoA esters. Qualitative and quantitative differences in the molecular weight distribution of the proteins in the mitochondria and post-mitochondrial supernatants are found in the skeletal muscles with increases in the post-mitochondrial supernatant and decreases in the mitochondria in dystrophic samples. We suggest that these results are due to increased leakiness of the mitochondrial membranes in dystrophic muscles. Such differences were not observed in preparations from normal animals.

The authors used the 2-[14C]deoxyglucose method to study local spinal and cerebral glucose utilization simultaneously during 1.2 per cent halothane anaesthesia in adult Sprague-Dawley rats. In conscious animals (n = 5) the rate of glucose utilization in lumbar spinal gray matter was about 50 per cent lower than that of cerebral cortex. Halothane anaesthesia (n = 6) reduced spinal cord and cerebral metabolic rate. Spinal glucose utilization was reduced 12-35 per cent, but this was less than the 45-70 per cent decrease halothane produced in 8 of 16 cerebral structures examined and was independent of the hypotension produced. These results indicate that halothane is a spinal metabolic depressant but that its effects on this tissue are substantially less than those it has on many cerebral structures.

The author studied in conscious rats the local spinal blood flow (SCBF) and metabolic effects of intrathecally administered bupivacaine. Fourteen rats received 0.75% bupivacaine, 15 microliters, through a chronically implanted lumbar subarachnoid catheter. Twelve control animals were treated identically, except that they received only an equal volume of saline intrathecally. Ten minutes after intrathecal drug injection, either local SCBF or glucose utilization was measured in the lumbar spinal cord of seven experimental and six control animals with the quantitative autoradiographic iodo-[14C]antipyrine or 2-[14C]deoxyglucose methods, respectively. Intrathecal bupivacaine produced a limp tail, absent hindlimb withdrawal to pinch, and 25-30 min of analgesia on the tail-flick test. Mean arterial blood pressure decreased 14% (P less than 0.01) after bupivacaine was administered, but there was no change in arterial blood gases, pH, or rectal temperature. Subarachnoid bupivacaine reduced both local SCBF and glucose utilization, but the SCBF effect was larger. Local SCBF decreased 27-34% (P less than 0.01) in all five spinal gray and three white matter areas measured, and there was little regional variability in the response. The reduction in spinal glucose utilization was regionally selective and less marked. For example, glucose utilization decreased 15% (P less than 0.05) and 21% (P less than 0.05) in lateral and anterior spinal white matter, respectively, but only decreased approximately 3% in laminae I-III and dorsal white matter (P greater than 0.1). A trend toward metabolic depression was also evident in laminae VIII (-15%, P = 0.06), VII (-13%, P = 0.09), and IV-VI (-11%, P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)

Ketamine produces both excitatory and depressant actions in the brain, but there have been conflicting results regarding which structures are affected and the magnitude of the alteration in cerebral metabolism produced. The authors applied the 2-[14C]deoxyglucose method quantitatively to a study of ketamine anesthesia (10 or 30 mg/kg intravenously) in the rat. Ketamine caused both increases and decreases in local cerebral glucose utilization. The areas with altered glucose utilization could be grouped into functional systems. Some structures of the limbic system showed large increases in glucose utilization; indeed the 70 per cent increases in cingulate gyrus and hippocampus were the largest of all regions examined. The extrapyramidal motor system and corpus callosum showed significant but less dramatic (20-40 per cent) increases. On the other hand, decreased metabolism occurred in the somatosensory and auditory systems, with the greatest reduction (40 per cent) in the inferior colliculus. Within some structures, such as the caudate nucleus and visual cortex, a striking redistribution of metabolism which is characterized by a change in the autoradiographic pattern of activity was noted. Reduced glucose utilization in the somatosensory and auditory systems suggests that a selective sensory deprivation occurs during ketamine anesthesia while the increased metabolism in the limbic system is consistent with neurophysiologic studies which have demonstrated seizure activity in this region. Compared with other anesthetics, which tend to produce a generalized decrease in metabolism, the cerebral metabolic effects of ketamine are unique and emphasize that it produces a state of "anesthesia" which is quite different from that of other commonly used drugs.

The simultaneous administration of B.C.G. vaccine, diphtheria-tetanus toxoid aluminium hydroxide adsorbed vaccine, and oral poliovaccine was studied in 628 children aged 13-14 years between 1966 and 1969 in Newham, London. The efficacy of these vaccines was unaffected by administering them at the same time; routine simultaneous administration is considered justified when organizational difficulties prevent the attainment of high immunization rates with the vaccines given separately. No adverse reactions to B.C.G. or oral poliomyelitis vaccines took place, but 8% of children had moderately severe local reactions after diphtheria-tetanus aluminium hydroxide adsorbed vaccine, which were attributed to diphtheria toxoid.Serological studies showed the need for immunization against diphtheria, tetanus, and poliomyelitis at 13-14 years of age. Because of the adverse reactions to diphtheria toxoid, however, simultaneous administration of tetanus toxoid aluminium hydroxide adsorbed, oral poliomyelitis, and B.C.G. vaccines only is recommended at present.An "adult type" diphtheria-tetanus toxoid might overcome the problem of reactions, though in two to three years' time most children aged 13-14 years will have received diphtheria-tetanus-pertussis vaccine in infancy and reinforcement might then be accomplished by a small intradermal dose of the currently available fluid diphtheria-tetanus vaccine.Continued serological studies of diphtheria and tetanus antitoxins and polio antibody are necessary to determine the future need for reinforcement of immunity; such studies should become an essential part of the surveillance of the community immunization programme.

The nature of the emission from central metal ions in complexes can be controlled by chemical alteration of the ligands. For iridium(III) species three types of emission have been observed, each originating from a different and orbitally identifiable excited state. Principles useful for designing new luminescent materials are formulated. They can be used for guiding photochemical research and for designing new analytical methods.

Recent developments in several areas of chemistry, laser technology, photodetector instrumentation, and calorimetry are surveyed, and their probable impact on the measurement of quantum yields is assessed. Chemical developments include: (a) synthesis and design of new luminescent molecules that could possibly serve as standards, (b) application of improved separation techniques to provide samples of extreme purity, and (c) advances in photochemistry that portend the development of wide-range chemical actinometers. The potential use of lasers in quantum-yield measurements and their advantages over conventional sources for application in both optical and calorimetric techniques are pointed out. New methods of quantum-yield measurements, based on the novel characteristics of laser pump sources, are suggested, including the feasibility of measuring yields under time-resolved conditions and of employing internal standards. The possible lifting of wavelength restrictions on both laser sources and detector devices and the implications of these developments for extending the spectral range of quantum-yield measurements are discussed. The current status of calorimetry for determining yields is surveyed, and the impact of recent technology on the feasibility of developing calorimetric methods competitive with optical methods is assessed.