Electrocautery Induced Damage of Total Knee Implants.

BACKGROUND: Pitting damage on implants has been reported and attributed to the use of electrocautery. This study aimed to determine how different total knee arthroplasty bearing surfaces are susceptible to this type of damage and whether surgeons are aware that this damage can occur. METHODS: A survey was sent to Hip and Knee Society members to determine what percentage of adult reconstructive surgeons use electrocautery after implantation of components. Three bearing surfaces for total knee arthroplasty were selected: cobalt chromium, Oxinium, and zirconium nitride to be damaged by electrocautery with a monopolar (MP) and bipolar (BP) electrocautery with 3 different energy settings. A comparison of surface damage using scanning electron microscopy and elemental differences using energy dispersion spectroscopy was performed. Average roughness (Ra), maximal peak-to-valley height (Rz), kurtosis (Rk), and skewness (Rsk) were recorded for comparison using a profilometer was performed. RESULTS: Median Rz and Ra measurements were larger for BP damaged areas compared to MP for all bearing surfaces. The Oxinium surface had the greatest increase in roughness parameters. Survey results indicate that a significant percentage of adult reconstructive surgeons use the electrocautery after implants are in place and are not aware of this type of damage. Backscatter scanning electron microscopy analysis found significant changes for BP damage compared to MP. CONCLUSION: Surface damage caused by electrocautery can have significant effects on the bearing surfaces of implants but further study needs to be performed to determine if this is a clinical issue. Our survey determined that many arthroplasty experts are unaware that this damage can occur.

Comparison of Inflammatory Cell-Induced Corrosion and Electrocautery-Induced Damage of Total Knee Implants.

Recently, inflammatory cell-induced corrosion (ICIC), a unique type of damage, has been reported in cobalt-chromium (CoCr) implants, but the mechanism remains poorly understood and controversial because electrocautery damage has also been shown to produce similar findings. This study aimed to distinguish between these two damage mechanisms. Forty-one CoCr primary total knee arthroplasty specimens were collected at time of necropsy. After removal and cleaning, light microscopy was used to identify areas of ICIC-like damage scars. A CoCr knee implant was intentionally damaged by electrocautery from both Bovie and Aquamantys sources using a 3-second hover method with 3 different energy settings for comparison to necropsy findings. Average roughness (Ra), max peak-to-valley height (Rmax), kurtosis (Rk), and skewness (Rsk) measurements were collected to represent the topography on the damaged areas for the CoCr implants. Necropsy implants showed signs of ICIC in 7 of 41 implants (17%) examined. Fe/C ratios of the Bovie electrocautery-damaged knee implant were shown to be statistically higher than those of necropsy-retrieved implants. Median Ra measurements were statistically less (P = 0.008) for Bovie-damaged areas compared to ICIC-dam-aged areas on CoCr. Median Rmax and Ra measurements were statistically less (P = 0.012, P < 0.001, respectively) for Aquamantys-damaged areas compared to ICIC-damaged areas on CoCr. While the visual patterns seen in necropsy-retrieved implants appeared similar to those with the intentionally damaged CoCrMo implant, the contents of the corroded regions are unique. The difference in roughness found on ICIC-damaged and electrocautery-damaged regions also indicates examination of surface topography as another distinguishing feature between the two mechanisms.

Prenatal nicotine exposure enhances the trigeminocardiac reflex via serotonin receptor facilitation in brainstem pathways.

In this study we used a rat model for prenatal nicotine exposure to test whether clinically relevant concentrations of brain nicotine and cotinine are passed from dams exposed to nicotine to her pups, whether this changes the trigeminocardiac reflex (TCR), and whether serotonergic function in the TCR brainstem circuitry is altered. Pregnant Sprague-Dawley dams were exposed to 6 mg·kg(-1)·day(-1) of nicotine via osmotic minipumps for the duration of pregnancy. Following birth dams and pups were killed, blood was collected, and brain nicotine and cotinine levels were measured. A separate group of prenatal nicotine-exposed pups was used for electrophysiological recordings. A horizontal brainstem slice was obtained by carefully preserving the trigeminal nerve with fluorescent identification of cardiac vagal neurons (CVNs) in the nucleus ambiguus. Stimulation of the trigeminal nerve evoked excitatory postsynaptic current in CVNs. Our data demonstrate that prenatal nicotine exposure significantly exaggerates both the TCR-evoked changes in heart rate in conscious unrestrained pups, and the excitatory neurotransmission to CVNs upon trigeminal afferent nerve stimulation within this brainstem reflex circuit. Application of the 5-HT1A receptor antagonist WAY 100635 (100 µM) and 5-HT2A/C receptor antagonist ketanserin (10 µM)significantly decreased neurotransmission, indicating an increased facilitation of 5-HT function in prenatal nicotine-exposed animals. Prenatal nicotine exposure enhances activation of 5-HT receptors and exaggerates the trigeminocardiac reflex.

5-HT2 receptors modulate excitatory neurotransmission to cardiac vagal neurons within the nucleus ambiguus evoked during and after hypoxia.

To examine the role of 5-HT2 receptors in the central cardiorespiratory network, and in particular the respiratory modulation of parasympathetic activity to the heart, we used an in vitro medullary slice that allowed simultaneous examination of rhythmic inspiratory-related activity recorded from hypoglossal rootlet and excitatory inspiratory-related neurotransmission to cardioinhibitory vagal neurons (CVNs) within the nucleus ambiguus (NA). Focal application of ketanserin, a 5-HT2 receptor antagonist, did not significantly alter the frequency of spontaneous excitatory postsynaptic excitatory currents (EPSCs) in CVNs in control conditions. However, ketanserin diminished spontaneous excitatory neurotransmission to CVNs during hypoxia. The inhibitory action of ketanserin was on 5-HT3 mediated EPSCs during hypoxia since these responses were blocked by the 5-HT3 receptor antagonist ondansetron. In addition, a robust inspiratory-related excitatory neurotransmission was recruited during recovery from hypoxia. Focal application of ketanserin during this posthypoxia period evoked a significant augmentation of the frequency of inspiratory-related, but not spontaneous EPSCs in CVNs. This excitatory effect of ketanserin was prevented by application of the purinergic receptor blocker pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS). These results demonstrate 5-HT2 receptors differentially modulate excitatory neurotransmission to CVNs during and after hypoxia. Activation of 5-HT2 receptors acts to maintain excitatory neurotransmission to CVNs during hypoxia, likely via presynaptic facilitation of 5-HT3 receptor-mediated neurotransmission to CVNs. However, activation of 5HT2 receptors diminishes the subsequent inspiratory-related excitatory neurotransmission to CVNs that is recruited during the recovery from hypoxia likely exerting an inhibitory action on inspiratory-related purinergic signaling.

Serotonergic modulation of the trigeminocardiac reflex neurotransmission to cardiac vagal neurons in the nucleus ambiguus.

Stimulation of the trigeminal nerve evokes a dramatic decrease in heart rate and blood pressure, and this reflex has generally been termed the trigeminocardiac reflex. A subset of the trigeminocardiac reflex is the diving reflex in which the nasal mucosa is stimulated with water or air-borne chemical irritants. Activation of the diving reflex evokes a pronounced bradycardia, mediated by increased parasympathetic cardiac activity, and is the most powerful autonomic reflex. However, exaggeration of this protective response could be detrimental and has been implicated in Sudden Infant Death Syndrome (SIDS). Despite the importance and strength of the trigeminocardiac reflex, there is little information about the cellular mechanisms and brain stem pathways that constitute this reflex. To address these issues, stimulation of trigeminal afferent fibers and the evoked excitatory postsynaptic currents were recorded in cardiac vagal neurons (CVNs) in an in vitro brain stem slice preparation. This synaptic pathway is robust and activation of the trigeminal pathway often evoked action potentials in CVNs. Application of the serotonin (5-HT) reuptake inhibitor citalopram significantly enhanced these responses. Consistent with the hypothesis this pathway is endogenously modulated by 5-HT receptors the 5-HT1A receptor antagonist, WAY 100635 inhibited, whereas the 5-HT2A/C receptor antagonist, ketanserin facilitated the excitatory neurotransmission to CVNs. The 5-HT1A receptor agonist 8-hydroxy-2-(dipropylamino)tetralin hydrobromide increased, whereas the 5-HT2 receptor agonist, alpha-methylserotonin maleate salt inhibited this reflex pathway. These results indicate stimulation of trigeminal fibers evokes a powerful excitatory and polysynaptic pathway to CVNs, and this pathway is endogenously modulated and differentially enhanced and depressed, by 5-HT1A and 5-HT2 receptors, respectively.

Mapping and identification of GABAergic neurons in transgenic mice projecting to cardiac vagal neurons in the nucleus ambiguus using photo-uncaging.

The neural control of heart rate is determined primarily by the activity of preganglionic parasympathetic cardiac vagal neurons (CVNs) originating in the nucleus ambiguus (NA) in the brain stem. GABAergic inputs to CVNs play an essential role in determining the activity of these neurons including a robust inhibition during each inspiratory burst. The origin of GABAergic innervation has yet to be determined however. A transgenic mouse line expressing green florescent protein (GFP) in GABAergic cells was used in conjunction with caged glutamate to identify both clusters and individual GABAergic neurons that evoke inhibitory GABAergic synaptic responses in CVNs. Transverse slices were taken with CVNs patch-clamped in the whole cell configuration. Sections containing both the pre-Botzinger complex as well as the calamus scriptorius were divided into approximately 90 quadrants, each 200 x 200 microm and were sequentially photostimulated. Inhibitory post synaptic currents (IPSCs) were recorded in CVNs after a 5-ms photostimulation of 50 microM caged glutamate. The four areas that contained GABAergic cells projecting to CVNs were 200 microm medial, 400 microm medial, 200 microm ventral, and 1,200 microm dorsal and 1,000 microm medial to patched CVNs. Once foci of GABAergic cells projecting to CVNs were determined, photostimulation of individual GABAergic neurons was conducted. The results from this study suggest that GABAergic cells located in four specific areas project to CVNs, and that these cells can be individually identified and stimulated using photouncaging to recruit GABAergic neurotransmission to CVNs.

Abolishment of serotonergic neurotransmission to cardiac vagal neurons during and after hypoxia and hypercapnia with prenatal nicotine exposure.

Cardioinhibitory cardiac vagal neurons (CVNs) do not receive inspiratory-related excitatory inputs under normal conditions. However, excitatory purinergic and serotonergic pathways are recruited during inspiratory activity after episodes of hypoxia and hypercapnia (H/H). Prenatal nicotine (PNN) exposure is known to dramatically change cardiorespiratory responses and decrease the ability to resuscitate from H/H. This study tested whether PNN exposure alters excitatory neurotransmission to CVNs in the nucleus ambiguus during and after H/H. Spontaneous and inspiratory evoked excitatory postsynaptic currents were recorded in CVNs from rats that were exposed to nicotine (6 mg x kg(-1) x d(-1)) throughout the prenatal period. In contrast to unexposed animals, in PNN animals H/H recruited excitatory neurotransmission to CVNs during inspiratory-related activity that was blocked by the alpha3beta4 nicotinic acetylcholine receptor (nAChR) blocker alpha-conotoxin AuIB (alpha-CTX AuIB, 100 microM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 50 microM) and d(-)-2-amino-5-phosphonopentanoic acid (AP5, 50 microM), selective AMPA/kainate and N-methyl-d-aspartate receptor blockers, respectively. Following H/H, there was a significant increase in inspiratory-related excitatory postsynaptic currents that were unaltered by alpha-CTX AuIB or ondansetron, a 5-HT3 receptor blocker, but were subsequently inhibited by pyridoxalphosphate-6-azophenyl-2', 4'-disulphonic acid (100 microM), a purinergic receptor blocker and CNQX and AP5. The results from this study demonstrate that with PNN exposure, an excitatory neurotransmission to CVNs is recruited during H/H that is glutamatergic and dependent on activation of alpha3beta4-containing nAChRs. Furthermore, exposure to PNN abolishes a serotonergic long-lasting inspiratory-related excitation of CVNs that is replaced by recruitment of a glutamatergic pathway to CVNs post H/H.

Recruitment of excitatory serotonergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus post hypoxia and hypercapnia.

Inhibitory GABAergic and glycinergic neurotransmission to cardioinhibitory cardiac vagal neurons (CVNs) increase during inspiratory activity and likely mediate respiratory sinus arrhythmia, while the frequency of excitatory postsynaptic currents (EPSCs) in CVNs are unaltered during the different phases of respiration. However, following hypoxia and hypercapnia (H/H), the parasympathetic activity to the heart increases and thus far, identification of the pathways and neurotransmitters that are responsible for exciting CVNs post H/H are unclear. This study identifies different excitatory pathways to CVNs recruited post H/H. Spontaneous and inspiratory-related EPSCs were recorded in CVNs before, during, and after 10 min of H/H in an in vitro slice preparation that retains rhythmic respiratory activity. Before and during H/H, EPSCs in CVNs were completely blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and d(-)-2-amino-5-phosphonopentanoic acid (AP5), selective AMPA/kainate and N-methyl-d-apartate (NMDA) receptor blockers, respectively. However, after H/H, there was a significant increase in EPSCs during each inspiratory burst. While some of the inspiratory-related EPSCs were blocked by the broad purinergic receptor antagonist pyridoxalphosphate-6-azophenyl-2', 4'-disulphonic acid (PPADS) and the specific P2X receptor antagonist 2',3'-O-(2,4,6-trinitrophenyl) adenosine 5'-triphosphate monolithium trisodium salt (TNP-ATP) a P2X receptor blocker, most of the recruited excitatory neurotransmission to CVNs is serotonergic because odansetron, a selective 5-HT3 antagonist, abolished the majority of the spontaneous and inspiratory-related EPSCs evoked during recovery from H/H. The results from this study suggest that following episodes of H/H, two nonglutamatergic excitatory pathways, purinergic and serotonergic, activating P2X and 5-HT3 receptors, respectively, are recruited to excite CVNs in the post H/H recovery period.

Nerve growth factor induces the expression of the LIM homeodomain transcription factor Isl-1 with the kinetics of an immediate early gene in adult rat dorsal root ganglion.

LIM-homeodomain genes encode a major class of transcription factors which play a critical role in regulating tissue specific gene expression. In this report, we have shown that three members of the LIM-homeodomain gene family - Isl-1, Rlim and Lim-3 are expressed in adult rat sensory neurons. Furthermore, we show that the addition of nerve growth factor (NGF) to cultures of primary dorsal root ganglion neurons leads to the induction of Isl-1, Rlim and Lim-3 mRNA expression. The increase in Isl-1 mRNA levels upon NGF addition was rapid and occurred even in the presence of cycloheximide. These findings place Isl-1 as a novel member of the immediate early class of genes. In contrast, Rlim and Lim-3mRNA induction by NGF required protein synthesis. The role of LIM-homeodomain genes in mediating responses to NGF in adult sensory neurons is discussed.

cGMP stimulates bile acid-independent bile formation and biliary bicarbonate excretion.

The effect of guanosine 3',5'-cyclic monophosphate (cGMP) on hepatic bile formation was studied in isolated perfused rat livers and rat hepatocytes. Studies in isolated perfused rat livers showed that infusion of 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP, 3 micromol/min or 100 microM) 1) increased bile flow without affecting biliary excretion of simultaneously infused taurocholate, 2) increased biliary concentration and excretion of HCO3(-) but did not affect biliary excretion of glutathione, and 3) increased net perfusate H+ efflux without affecting hepatic O2 uptake. Studies in isolated rat hepatocytes showed that 1) 8-BrcGMP increased intracellular pH in the presence (but not in the absence) of extracellular HCO-3, and effect inhibited by 4,4' -diisothiocyanostilbene-2,2'-disulfonic acid and Na+ replacement, 2) 8-BrcGMP did not affect taurocholate uptake and intracellular [Ca2+], and 3) bile acids, like ursodeoxycholate and cholate, did not increase cellular cGMP. Taken together, these results indicate that cGMP stimulates bile acid-independent bile formation, in part by stimulating biliary HCO3- excretion. cGMP may increase HCO3- excretion by stimulating sinusoidal Na+ - HCO3- cotransport, but not Na+/H+ exchange. cGMP, unlike adenosine 3',5'-cyclic monophosphate, may not regulate hepatic taurocholate transport, and bile acid-induced HCO3- rich choleresis may not be mediated via cGMP.

Recruiting and retaining phlebotomists.

The phlebotomy team is receiving greater recognition than ever before for its contribution to the service image of the laboratory. Laboratory managers must recognize that phlebotomists are the laboratory's goodwill ambassadors. Because phlebotomists work on the front line, their technical skills and professional demeanor are prime factors in getting physician referrals and attracting patients to the facility. To recruit and retain a skilled professional phlebotomy team, laboratory managers must assess their operations and determine the skills, personal attributes, and education needed to perform the phlebotomy duties. To keep your best employees, try to continually upgrade your training, continuing education, and career advancement opportunities. To learn what makes a successful phlebotomy team, CLMR surveyed several CLMA members to find out how they are recruiting and developing their phlebotomists. Our special thanks go to all our respondents for sharing their expertise and experiences with us.

Effects on nurse retention. An experiment with scheduling.

Four randomly selected nursing groups were assigned to three experimental groups and one control group to test the relative impact of three experimental nursing schedules, using a before-after design. The three experimental treatments were straight shifts; regular schedule but with unlimited requests for changes; and individual station-designed schedules. Before treatment, score differences between the experimental and control groups were limited to one of 36 highly reliable scales specifically constructed and pretested to gauge effects of scheduling. This single difference was judged not to be significantly related to experimental outcomes. Because of a poor job market situation, retention was not affected significantly by any of the three treatments, but root causes of turnover were. Results of the experiment showed that individual station-designed schedules triggered the most changes that favor retention. In contrast, the other two treatments unexpectedly increased nurses' own sense of marketability and reduced teamwork among nurses. Reasons accounting for the results are discussed in the text.

Radiation-induced hemopoietic death in mice as a function of photon energy and dose rate.

Radiation-induced hemopoietic death was measured in mice exposed to photons of four different energies: 250-kVp X rays, 60Co gamma rays (1.25 MeV), and 6- and 25-MV photons from a linear accelerator. For each radiation source, the lethal dose which killed 50% of the population in 30 days (LD50/30) associated with the hemopoietic syndrome was determined in groups of mice exposed to graded doses from 600 to 1150 cGy at dose rates of 20, 40, and 80 cGy/min. The calculated LD50/30 values for 25 and 6 MV were significantly different from each other at all exposure rates while no difference was observed between 6 MV and 60Co. Using 60Co gamma rays as the standard, the relative biologic effectiveness was as follows: 250 kVp greater than 25 MV greater than 6 MV = 60Co. The data suggest that there may be a greater damage to tissue within the marrow cavities following exposure to very high megavoltage radiation, a factor which must be considered with the increasing utilization of linear accelerators in the clinic and laboratory.

Nicotine exposure and Parkinson disease.

The observed inverse relationship between smoking and Parkinson disease has prompted suggestions that nicotine, a centrally active agent, might protect against the disease. In this case-control study, cases were found to have ever regularly smoked cigarettes significantly less frequently than sex-, race-, and age-matched neighbors. This report analyzes the detailed smoking histories of cases and neighbors to see if these histories support the nicotine protection hypothesis. Estimated nicotine exposure before age at onset of symptoms for smoking cases was 186.1 g; for smoking controls it was 208.3 g (p = 0.34). Among the cases, severity of disease was not related to the extent of nicotine exposure before disease onset. Age at onset of symptoms for smoking cases (52.7 years) was not delayed (57.8 years for nonsmoking cases). Since the study was unable th find further support for the nicotine protection hypothesis, it is concluded that the observed inverse relationship between smoking and Parkinson disease is likely explainable by other factors, such as selective mortality or pre-morbid behavioral and/or constitutional changes.

Cigarette smoking and Parkinson disease: 1. Comparison of cases with matched neighbors.

In previous studies, there were fewer cigarette smokers among persons with Parkinson disease than among other patients. We reinvestigated this phenomenon, using nonpatient controls. In home interviews with 237 Parkinson patients and 474 age-, sex-, and race-matched neighbors, we inquired about consumption of tobacco, coffee, tea, and alcohol. All Parkinson patients were diagnosed by a neurologist, had two or more cardinal features of parkinsonism, and had not received chronic phenothiazine therapy. One hundred fifty (63%) of 237 cases and 224 (47%) of 474 controls never smoked cigarettes (p < 0.0001). Significantly different smoking rates were also preset at 10 and 20 years before the onset of parkinsonism.