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Biomedical subjects

R L Volle

Publications and source records attributed to R L Volle.

At least 19 recordsLinked to original sources
PubMed1992

Impact of the USMLE step 1 on teaching and learning of the basic biomedical sciences. United States Medical Licensing Examination.

Medical licensure in the United States is in transition. In June 1991, the National Board of Medical Examiners (NBME) made major modifications in the content, format, pass/fail standards, and score reports of the NBME Part I examination. This year, Part I became Step 1, the first of three components of the United States Medical Licensing Examination (USMLE), which will shortly be the sole examination pathway to initial licensure for allopathic physicians. This essay describes Step 1, reviews the phase-in plans for the USMLE, and discusses the potential impact of both on medical schools' teaching and students' learning of the basic biomedical sciences. The authors recommend that medical schools (1) abandon the use of Step 1 as a sole criterion for student promotion to the third year and (2) carefully review other examination-related requirements for promotion and graduation.

Curriculum↗
PubMed1990

Score reporting on NBME examinations.

Because the National Board of Medical Examiners (NBME) will introduce new comprehensive Part I and Part II examinations in 1991, a review has been made of score reporting methods to be used in the new examinations. The review was conducted also because of concern expressed by some that NBME examination scores are misused in medical schools and in resident selection. In this paper, selected aspects of score reporting are defined, the uses of score reports outlined, and the potential for misuse described. It should be noted that the NBME is obliged to make available numerical scores to state medical boards and to examinees. Individual scores are reported to others only with the permission of the examinee. The results of an opinion poll conducted by the NBME of medical educators and medical students are presented. The range of opinion is broad but favors numerical score reporting and a designated pass/fail score.

Attitude of Health Personnel↗
PubMed1990

Standardized testing of patient management skills. A computer-based method.

Clinical cases can be simulated by using computers with programs designed to provide all of the information required to make a diagnosis and initiate a treatment plan. The cases are uncued, simulate time, and require sound clinical judgment for management. All transactions between the physician and case are recorded so that each action can be evaluated from the standpoint of timeliness, sequence, appropriateness, risk, and cost. Results from field studies indicate that the performance by residents in the management of clinical case simulations measures more than knowledge.

Clinical Competence↗
PubMed1984

Muscarinic receptors and [3H]inositol incorporation in a rat sympathetic ganglion.

[3H]Inositol incorporation into phosphatidylinositol was accelerated in rat superior cervical ganglia treated with 4-aminopyridine or Bethanechol. The inositol response to these drugs occurred in intact and denervated ganglia and was prevented by atropine. The possibility that muscarinic receptor subtypes are present in the ganglia is considered because bethanechol, but not 4-aminopyridine, is known to increase cGMP in rat superior cervical ganglia by an atropine-sensitive process.

4-Aminopyridine↗
PubMed1983

Regulation of cyclic GMP levels in nerve tissue.

In rat superior cervical ganglia the regulation of cyclic GMP (cGMP) formation does not involve muscarinic or adrenergic transmitters or receptors. Marked increases in cGMP content during preganglionic axonal stimulation by electric currents, elevated K+, or drugs that cause transmitter release are unaffected by muscarinic and adrenergic receptor blockade. However, the cGMP response does require Ca2+ and intact preganglionic axonal terminals. Two possibilities exist: either cGMP accumulates in the preganglionic nerves or a noncholinergic, nonadrenergic transmitter activates guanylate cyclase in postsynaptic structures. Sodium azide and nitroprusside cause cGMP accumulation in denervated ganglia, which indicates that postsynaptic structures are capable of forming cGMP. In pineal glands elevated [K+]o releases [3H]norepinephrine and causes cGMP accumulation, which suggests a relationship between the two responses and the possibility that cGMP accumulation is involved in autoinhibition of transmitter release. The finding that phentolamine, alpha-adrenergic receptor antagonists, prevent the cGMP response to K+ is compatible with this review. However, clonidine, an alpha-receptor agonist, depresses norepinephrine release but has no effect on pineal gland cGMP. Conversely, large increases in pineal gland cGMP produced by nitroprusside do not affect K+-evoked norepinephrine release. For these reasons it is not possible to relate cGMP to the auto-inhibition of [3H]norepinephrine release that is mediated by prejunctional alpha-adrenergic receptors.

Animals↗
PubMed1982

The regulation of cyclic nucleotides in a sympathetic ganglion.

Preganglionic nerve terminal stimulation in rat superior cervical ganglia causes marked increases in the levels of cyclic nucleotides. Results are similar when preganglionic nerve stimulation is compared with elevated [K+]0 or 4-aminopyridine. Although intact nerve terminals and Ca2+ are required for the response to occur, pharmacological studies indicate that acetylcholine and adrenergic transmitters are not involved in the cyclic nucleotide response. It is suggested that cyclic nucleotide accumulation occurs in the nerve terminals or an unknown transmitter or substance participates in the postsynaptic accumulation of the cyclic nucleotides. Polypeptides tested thus far do not seem to be implicated. Interrelationships among phospholipid turnover, Ca2+-exchange and cyclic nucleotide accumulation in rat sympathetic ganglia are considered, but are difficult to establish.

4-Aminopyridine↗
PubMed1982

Ketamine and ditran block end-plate ion conductance and [3H]phencyclidine binding to electric organ membrane.

Alterations by ketamine (10-100 microM) and ditran (50-100 microM) of end-plate currents were studied using transected cutaneous pectoris muscles. Both drugs reduced peak current and shortened the time constant for end-plate current decay (tau). Ketamine was more effective at pH 5.3 than at 7.4 or 9.1. Recovery from blockade was asymmetrical in that tau recovered more quickly than did peak current when the drugs were removed from the bath. By contrast, 4-aminopyridine antagonized the depression of peak current by ketamine, but not the reduction of tau. Both ketamine and ditran disrupted the voltage dependence of tau. The binding to microsacs prepared from electric organs of [3H]phencyclidine ([3H]PCP) was blocked by ketamine and ditran. In microsacs treated with carbachol, the IC50 for ketamine block of [3H]PCP binding was 6.6 X 10(-6) M. For ditran, the IC50 for block of [3H]PCP binding in the presence of carbachol was 1.7 X 10(-6) M. The binding of [alpha-125I]bungarotoxin to the microsacs or to the cultured chick myotubes was reduced only slightly by ketamine. Because ketamine has no effect on transmitter release and little effect on [alpha-125I]bungarotoxin binding, it is concluded that, like PCP, ketamine and ditran block open channels in the end-plate. In addition, the asymmetrical recovery of end-plate current parameters suggests that ketamine may block closed channels. The recovery from block of closed channels (caused by either a direct action on closed channels or a very slow channel unblocking rate) proceeds more slowly than does the block of open channels.

Animals↗
PubMed1981

Cyclic guanosine 3':5'-monophosphate accumulation and 45Ca-uptake by rat superior cervical ganglia during preganglionic stimulation.

Repetitive preganglionic nerve stimulation increases cyclic guanosine 3':5'-monophosphate (cGMP) content in rat superior cervical ganglia by a mechanism requiring Ca++ but resistant to blockade by cholinergic receptor antagonists. Similarly, 45Ca-uptake during prolonged preganglionic nerve stimulation is unaffected by hexamethonium or atropine. These findings indicate that nerve stimulation increases cGMP accumulation and 45Ca-uptake by a noncholinergic mechanism Substance P, met-enkephalin and luteinizing hormone-releasing factor have little or no effect on cGMP content. By contrast, bethanechol causes a 3-fold increase in cGMP content and postganglionic cell firing. Thus, as reported by others, muscarinic receptor activation increases ganglionic cGMP[. 4-Aminopyridine causes an increase in cGMP of resting ganglia that requires Ca++ and the nerve terminal is blocked by tetrodotoxin but unaffected by atropine or hexamethonium. Ouabain also increases ganglionic cGMP content by a process that requires Ca++ and the nerve terminals. Like preganglionic nerve stimulation, 4-aminopyridine and ouabain cause cGMP accumulation in the nerve terminals or in the ganglion cells as a consequence of releasing a noncholinergic transmitter. The uptake of Ca++ by ganglion cells is not an adequate stimulus for cGMP accumulation because the nicotinic receptor agonist dimethylphenylpiperazinium increases 45Ca-uptake but has no effect on cGMP formation in ganglia.

4-Aminopyridine↗
PubMed1980

Effects of McN-A-343, a cholinomimetic drug, on endplate currents in the frog.

The muscarinic ganglion stimulating agent, McN-A-343 has unusual blocking actions on endplate currents (EPCs) at frog neuromuscular junctions. McN-A-343 caused depolarization by a curare-sensitive process, blocked neuromuscular transmission, depressed EPCs and reduced the time for EPC decay. These results are explained best by a nicotinic agonist action of McN-A-343 on the acetylcholine receptor to cause ion flow and the blockade by McN-A-343 of the open ion channels. The actions of McN-A-343 are similar to those of decamethonium (C-10) described by others. Unlike C-10, however, McN-A-343 did not alter the exponential character of the EPC or alter the voltage dependency of the EPC. The prototypical nicotinic agonist, dimethylphenylpiperazinium had no effect on EPC parameters of endplate clamped at -90mV.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1979

Transmission blockade and stimulation of ganglionic adenylate cyclase by catecholamines.

Isolated rat superior cervical ganglia treated with isoproterenol and related drugs show an increase in ganglionic cyclic adenosine 3':5'-monophosphate (cAMP) and a block of transmission. For isoproterenol, the maximum increase in cAMP occurred at 1 X 10(-6) M, a concentration without effect on transmission. Approximately 5 X 10(-4) M isoproterenol was required to reduce the ganglionic compound action potential by 50%. Dopamine, in contrast to isoproterenol, had no effect on the content of cAMP but depressed transmission. The maximum increase in cAMP produced by norepinephrine occurred with 5 X 10(-4) M, a concentration that reduced transmission by approximately 35%. The effects of isoproterenol on adenylate cyclase and transmission were prevented either by practolol (10(-4) M) or phentolamine (10(-5) M). Dopamine-induced blockade of transmission was antagonized by phentolamine (10(-5) M). Whereas the blockade of transmission by norepinephrine was antagonized by practolol (10(-5) M) or phentolamine (10(-5) M), the stimulation of adenylate cyclase by norepinephrine was prevented by practolol (10(-4) M) but not by phentolamine (10(-5) M). These results show that the blockade of transmission and stimulation of adenylate cyclase are unrelated in rat ganglia and that adrenergic receptor classification is ambiguous. The role of adenylate cyclase in ganglia is unclear.

Adenylyl Cyclases↗
PubMed1979

Nicotinic, muscarinic and adrenergic receptors in a parasympathetic ganglion.

Transmission in submandibular ganglia of hamsters was blocked by hexamethonium and dimethylphenylpiperazinium. Dimethylphenylpiperazinium caused depolarization and decreased membrane resistance (Rm). The muscarinic agonist, bethanechol (BCh) caused depolarization of some cells and hyperpolarization of others. Regardless of the change in membrane potential, BCh always increased Rm. Since the responses to BCh persisted in the absence of [Ca++]0, it was concluded that BCh acted directly on the ganglion cells and did not depend upon a transsynaptic process. All responses to BCh were prevented by atropine. The evidence suggests that the ganglion cells possess muscarinic receptors. Like BCh, norepinephrine (NE) either depolarized or hyperpolarized the ganglion cells. There was no relationship between the blockade of transmission by NE and the effect of NE on the membrane potential. The responses to NE were prevented by dihydroergotamine, suggesting the presence of alpha adrenergic receptors on the ganglion cells.

Acetylcholine↗
PubMed1978

Responses of the rat superior cervical ganglion in vitro to isoprenaline and bethanechol.

The effects of isoprenaline were studied in isolated rat superior cervical ganglia. Intracellularly recorded excitatory postsynaptic potentials were depressed by isoprenaline in concentrations of 10(-5) to 10(-4)M. In 13 out of 17 cells, isoprenaline caused ganglionic hyperpolarization (mean, 4mV). Changes in the amplitude and contour of antidromic action potentials caused by isoprenaline could be accounted for by the increased membrane potential. A slight increase in membrane input resistance from 44--50.2 megohms (mean values) occurred in about half of the cells. Activation of an ion pump by isoprenaline was suggested by the finding that the hyperpolarization did not occur when the bathing solution contained ouabain (10(-5)M) or lacked Na+ or K+. Characterization of the isoprenaline effects by the use of alpha and beta adrenergic blocking drugs was not possible because of the direct depressant effects of the antagonists. The muscarinic agonist bethanechol (2.5 X 10(-5) to 2.5 X 10(-4)M) caused ganglionic depolarization and increased input membrane resistance (42--52 megohms) during depolarization in each of the cells tested. The ganglionic responses to bethanechol were prevented by atropine.

Action Potentials↗
PubMed1978

The increase in spontaneous transmitter release produced by beta-bungarotoxin and its modification by inorganic ions.

The excitatory phase of the biphasic action on transmitter release of the neurotoxin, beta-bungarotoxin (beta-BuTX; 0.5 microgram ml-1), was studied on miniature end-plate potentials (MEPPs) at frog sciatic nerve-sartorius muscle junctions. The most common type of excitatory response was characterized by a continuous increase in MEPP frequency that reached a plateau; a less common form was characterized by irregular episodic bursts of firing. There was a direct relationship between toxin activity and [K+]O (2.5-10.0 mM) with virtually no effect of the toxin at normal [K]O+ at the concentration of toxin used. In the absence of Mg++, there was a paradoxical inverse relationship between toxin activity and [Ca++]O (0.5-4.0 mM) at higher [K+]O. However, in the presence of 1.0 mM Mg++ the increased MEPP frequency produced by beta-BuTX was independent of [Ca++]O. The action of beta-BuTX was very sensitive to blockade by Mg++. Toxin activity was demonstrated in a Sr++-containing, Ca++-free solution, but not in a Mg++-containing, Ca++-free solution. It is probable that beta-BuTX causes a slight depolarization of the nerve terminals by a mechanism not sensitive to blockade by tetrodotoxin and that the ability of beta-BuTX to depolarize the terminals can account for the enhancement of the response by raising [K+]O and the depression of the response by Mg++. Alternatively, beta-BuTX could be producing its effects by some, as yet undefined, direct action on the release process.

Action Potentials↗