Transition from open to robotic-assisted radical prostatectomy is associated with a reduction of positive surgical margins amongst private-practice-based urologists

Several recent studies have suggested that thought leaders in radical prostatectomy have decreased their own positive margin rates by switching from open to robot-assisted radical prostatectomy. Theoretically, this improvement is largely attributed to enhanced visualization of the deep pelvis and precision of dissection afforded by the instrumentation. To date, it has not been determined if this phenomenon exists amongst non-fellowship-trained urologists in private practice. Herein, we describe the positive margin rates of two non-fellowship-trained private-practice urologists who converted from open radical retropubic prostatectomy to robot-assisted radical prostatectomy. The margin positivity data from two non-fellowship-trained private-practice urologists (surgeon 1 and surgeon 2) were reviewed retrospectively. The last 50 cases of open radical retropubic prostatectomy from each surgeon were compared with the first 50 robotic prostatectomy cases of surgeons 1 and 2, respectively. A positive surgical margin was defined as tumor present at the inked margin of the prostate. There was a significant decrease in the overall and pT2 positive margin rates for both surgeons. The overall positive margin rate and pT2 positive margin rate for surgeon 1 dropped from 44 to 20% and from 37 to 5.7%, respectively, after changing from open to robotic prostatectomy. For surgeon 2, the overall positive margin rate changed from 26 to 18% and the pT2 positive margin rate changed from 27.5 to 7% after converting. Changing from open to robotic-assisted radical prostatectomy may improve the ability of urologists to obtain negative surgical margins. With proper training this phenomenon does seem to apply to non-fellowship-trained urologists in private practice and can be realized within the first 50 cases performed.     

Kritische und experimentelle Untersuchungen über die Nervennaht und Nervenregeneration

Ohne Zusammenfassung     

Impaired motor imagery in patients with essential tremor: a case control study.

Motor imagery (MI), which refers to the process of mental representation of movements, has not been studied in patients with essential tremor (ET). We investigated the presence of impaired MI in ET patients compared with healthy controls. A group of drug-naive and nondemented ET patients and age-matched controls were studied using transcranial magnetic stimulation, while they were specifically instructed to try and imagine themselves performing two motor tasks. The various clinical and electrophysiological variables were evaluated and compared. Repeated measures ANOVA demonstrated a significant difference between ET patients and controls with respect to mean motor-evoked potential (MEP) amplitudes (F(1,38) = 31.92, P < 0.005) during MI. The process of MI effectively facilitated MEP amplitude in controls but not in ET patients, regardless of side of stimulation or motor tasks. We provide evidence to demonstrate impairment of MI in a group of ET patients compared with healthy controls. The basis for this novel finding is unclear, and further studies are warranted to determine whether it is related to cerebellar or motor cortical dysfunction.     

Lead poisoning in six captive avian species

Red-winged blackbirds (Agelaius phoeniceus), brown-headed cowbirds (Molothrus ater), common grackles (Quiscalus quiscula), mallards (Anas platyrhynchos), northern bobwhites (Colinus virginianus), and eastern screech-owls (Otus asio) were poisoned with a concentration of lead (Pb) acetate in the diet which was increased by 60% each week until half of the birds in each treatment group died; surviving birds and all control birds except screech-owis were then killed by euthanasia. An additional group of mallards was poisoned with Pb shot. The gizzards of mallards poisoned either way usually were stained with bile; some of these birds also had proventricular impaction. Most poisoned birds of the other species were emaciated but lacked other gross lesions caused by Pb poisoning. In birds other than mallards, Pb poisoning could not be diagnosed without histological or hematological examinations or analysis of tissues. Poisoned birds of all six species could be reliably separated from control birds by an increase in the protoporphyrin concentrations in the blood and by a decrease in the activity of delta-aminolevulinic acid dehydratase (ALAD) in red blood cells. Hepatic iron (Fe) concentrations varied so much among individual birds that even though median hepatic Fe concentrations increased in poisoned birds, hepatic Fe concentrations were not useful in identifying poisoned birds. Renal intranuclear inclusion bodies occurred in 83% of all birds dying from Pb poisoning. Nephrosis, myocardial necrosis, and arterial fibrinoid necrosis were occasionally present. Median hepatic Pb concentrations varied from 20 ppm (wet wt) in male red-winged blackbirds to 111 ppm in female northern bobwhites. Median renal Pb concentrations varied from 22 ppm in redwinged blackbirds to 190 ppm in female northern bobwhites. Hepatic and renal Pb concentrations varied substantially among birds within each species. Median hepatic and renal Pb concentrations of birds that died were not statistically different (p > 0.05) from those of birds that were killed. Lead shot and Pb acetate affected mallards similarly.     

Changes in the Amphibian Antibody Repertoire are Correlated With Metamorphosis and not With Age or Size

Tadpole and adult Xenopus, manipulated to be of comparable size, exhibited stagespecific antibody expression. The production of adult-type higher-affinity anti-DNP antibodies proved to be independent of the age and size of the individual and is concomitant with the completion of metamorphosis. The appearance of new antibody specificities at such a time suggests that their expression occurs with the cell turnover and renewal during a period of morphological changes.     

Acute hemodynamic responses to electroconvulsive therapy are not related to the duration of seizure activity

Study Objective: To test the hypothesis that the magnitude of the acute hemodynamic response to electroconvulsive therapy (ECT) is related to the duration of the seizure activity in patients receiving different dosages of intravenous (IV) lidocaine.

Design: Randomized, double-blind, placebo-controlled, cross-over study.

Setting: University-affiliated hospital.

Patients: 21 ASA physical status I, II, and III patients undergoing four consecutive maintenance ECT treatments for chronic depression.

Interventions: Patients received lidocaine 50 mg, 100 mg, 200 mg IV, or saline prior to induction of anesthesia via a standardized anesthetic technique.

Measurements and Main Results: Noninvasive blood pressure (BP) and heart rate (HR), as well as the duration of motor and electroencephalographic (EEG) seizure, were measured. The duration of motor and EEG seizures (means ± SD) were 37 ± 13 sec and 64 ± 21 sec, 25 ± 11 sec and 52 ± 43 sec, 17 ± 12 sec and 32 ± 17 sec, 1 ± 3 sec and 18 ± 10 sec in the saline, lidocaine 50 mg, 100 mg, 200 mg groups, respectively. Although the duration of seizure activity was decreased in a dose-related fashion after lidocaine pretreatment, the peak increases in BP and HR were similar in the lidocaine and saline treatment groups.

Conclusions: Despite producing dose-related decreases in the duration of both motor and EEG seizure activity, lidocaine failed to attenuate the acute hemodynamic response to ECT. Thus, the acute hemodynamic response to ECT is not related to the duration of seizure activity.     

Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate

We observed that pretreatment of male F344 rats with benzyl selenocyanate, a versatile organoselenium chemopreventive agent in several animal model systems, decreases the levels of DNA and RNA modifications produced in the liver by the hepatocarcinogen 2- nitropropane. To clarify the mechanisms involved, we pretreated male F344 rats with either benzyl selenocyanate, its sulfur analog benzyl thiocyanate, phenobarbital or cobalt protoporphyrin IX; the latter is a depletor of P450. We then determined (1) the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on 2-nitropropane- induced liver DNA and RNA modifications and (3) amount of nitrate excreted in rat urine following administration of the carcinogen. Pretreatment with benzyl selenocyanate or phenobarbital increased the denitrification activity of liver microsomes by 217 and 765%, respectively, increased liver P4502B1 by 31- and 435-fold, respectively, decreased the levels of 2-nitropropane-induced modifications in liver DNA (29-70% and 17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and increased the 24-h urinary excretion of nitrate by 157 and 209%, respectively. Pretreatment with benzyl thiocyanate had no significant effect on any of these parameters. Pretreatment with cobalt protoporphyrin IX decreased liver P4502B 1 by 87%, decreased the denitrification activity of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic acid modifications by 17-67%. These results indicate that the metabolic sequence from 2-nitropropane to the reactive species causing DNA and RNA modifications does not involve the removal of the nitro group. Moreover, they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic acid modifications in part by increasing its detoxication through induction of denitrification, although it is evident that other mechanisms must also be involved.      

Effects of a specific benzodiazepine antagonist (RO 15-1788) on cerebral blood flow

RO 15-1788, a specific benzodiazepine antagonist, although it effectively antagonizes the clinical effects of benzodiazepines (i.e., sedation and amnesia), can also induce subjective agonist effects such as sedation or inverse agonist effects such as anxiety. The purpose of this study was to investigate in seven healthy volunteers the effect of RO 15-1788 on cerebral blood flow when intravenously injected alone or with midazolam and to compare its effects with midazolam administered alone. Cerebral blood flow was measured with the 133xenon inhalation technique and the drugs were administered simultaneously in a double-blind, randomized fashion during the four following sessions: placebo-placebo; midazolam-placebo; RO 15-1788-placebo; midazolam-RO 15-1788. No difference in cerebral blood flow was noted between the placebo-placebo, the RO 15-1788-placebo, and the RO 15-1788-midazolam sessions--although midazolam injected alone decreased cerebral blood flow by 30%. The sedation, amnesia, and the electroencephalograph (EEG) and muscle tone changes observed with midazolam-placebo were not present during the RO 15-1788-placebo and RO 15-1788-midazolam sessions. This study demonstrates the absence of effects of RO 15-1788 on cerebral blood flow when injected alone and the efficacy of this new drug in antagonizing the depressant effects of midazolam on cerebral hemodynamics.