Revisiting the sternocleidomastoid flap as a reconstructive option in head and neck surgery.

BACKGROUND: The sternocleidomastoid can be used as a pedicled flap in head and neck reconstruction. It has previously been associated with high complication rates, likely due in part to the variable nature of its blood supply. OBJECTIVE: To provide clinicians with an up-to-date review of clinical outcomes of sternocleidomastoid flap surgery in head and neck reconstruction, integrated with a review of vascular anatomical studies of the sternocleidomastoid. METHODS: A literature search of the Medline and Web of Science databases was conducted. Complications were analysed for each study. The trend in success rates was analysed by date of the study. RESULTS: Reported complication rates have improved over time. The preservation of two vascular pedicles rather than one may have contributed to improved outcomes. CONCLUSION: The sternocleidomastoid flap is a versatile option for patients where prolonged free flap surgery is inappropriate. Modern vascular imaging techniques could optimise pre-operative planning.

Effectiveness of behavioural interventions to reduce urinary tract infections and Escherichia coli bacteraemia for older adults across all care settings: a systematic review.

BACKGROUND: Escherichia coli bacteraemia rates in the UK have risen; rates are highest among older adults. Previous urinary tract infections (UTIs) and catheterization are risk factors. AIM: To examine effectiveness of behavioural interventions to reduce E. coli bacteraemia and/or symptomatic UTIs for older adults. METHODS: Sixteen databases, grey literature, and reference lists were searched. Titles and/or abstracts were scanned and selected papers were read fully to confirm suitability. Quality was assessed using Critical Appraisal Skills Programme guidelines and Scottish Intercollegiate Guidelines Network grading. FINDINGS: Twenty-one studies were reviewed, and all lacked methodological quality. Six multi-faceted hospital interventions including education, with audit and feedback or reminders reduced UTIs but only three supplied statements of significance. One study reported decreasing catheter-associated UTI (CAUTI) by 88% (F (1,20) = 7.25). Another study reported reductions in CAUTI from 11.17 to 10.53 during Phase I and by 0.39 during Phase II (χ2 = 254). A third study reported fewer UTIs per patient week (risk ratio = 0.39). Two hospital studies of online training and catheter insertion and care simulations decreased CAUTIs from 33 to 14 and from 10.40 to 0. Increasing nursing staff, community continence nurses, and catheter removal reminder stickers reduced infection. There were no studies examining prevention of E. coli bacteraemias. CONCLUSION: The heterogeneity of studies means that one effective intervention cannot be recommended. We suggest that feedback should be considered because it facilitated reductions in UTI when used alone or in multi-faceted interventions including education, audit or catheter removal protocols. Multi-faceted education is likely to be effective. Catheter removal protocols, increased staffing, and patient education require further evaluation.

Grafting derivatives of Mn6 single-molecule magnets with high anisotropy energy barrier on Au111 surface.

We study the magnetic properties of two new functionalized single-molecule magnets belonging to the Mn 6 family (general formula [Mn (III)6O2(R-sao)6(O2C-th)2L(4-6)], where R=H (1) or Et (2), HO2C-th=3-thiophene carboxylic acid, L=EtOH, H2O and saoH2 is salicylaldoxime) and their grafting on the Au(111) surface. Complex 1 exhibits spin ground-state S=4, as the result of ferromagnetic coupling between the two antiferromagnetic Mn (III) 3 triangles, while slight structural changes in complex 2, switch the dominant magnetic exchange interactions from anti- to ferromagnetic, enhancing the spin ground-state to S=12 and, consequently, the effective energy barrier for the relaxation of magnetization. Direct-current and alternating-current magnetic susceptibility measurements show that the functionalized complexes preserve the main magnetic properties of the corresponding not-functionalized Mn 6 clusters (i.e., total spin value and magnetic behavior as a function of temperature), though a reduction of the anisotropy barrier is observed in complex 2. For both complexes, the -O2C-th functionalization allows the direct grafting on Au(111) surface by liquid-phase deposition. X-ray photoemission spectroscopy demonstrates that the stoichiometry of the molecular cores is preserved after grafting. Scanning tunneling microscopy (STM) reveals a sub-monolayer distribution of isolated clusters with a slightly higher coverage for complex 1. The cluster stability in the STM images and the S-2p energy positions demonstrate, for both derivatives, the strength of the grafting with the gold surface.

Muscular torque generation during imposed joint rotation: torque-angle relationships when subjects' only goal is to make a constant effort.

It is a reasonable expectation that voluntarily activated spinal motoneurons will be further excited by increases in spindle afferent activity produced by muscle stretch. Human motor behavior attributed to tonic stretch reflexes and to reflexes recruited by relatively slow joint rotation has been reported from several laboratories. We reinvestigated this issue by rotating the elbow joint over the central portion of its range while subjects focused on keeping their elbow flexion effort constant at one of three different levels and made no attempt to control the position, speed or direction of movement of their forearm. There is evidence that subjects' voluntary motor status is constant under these conditions so that any change in torque would be of involuntary origin. On average, torques rose somewhat and then fell as the elbow was flexed through a range of 80 degrees at 10, 20 and 60 degrees/s and a similar pattern occurred during elbow extension; i.e., both concentric and eccentric torque-angle profiles had roughly similar shapes and neither produced consistent stabilizing cross-range stiffness. The negative stiffness (rising torque) during the early part of a concentric movement and the negative stiffness (falling torque) during the later part of an eccentric movement would not have occurred if a stabilizing stretch reflex had been present. Positive stiffness rarely gave rise to torque changes greater than 20% in either individual or cross-subject averaged data. When angular regions of negative stiffness are combined with regions of low positive stiffness (torque change 10% or less), much of the range of motion was not well stabilized, especially during eccentric movements. The sum of the EMGs from biceps brachii, brachioradialis and brachialis showed a pattern opposite to that expected for a stretch reflex; there was an upward trend in the EMG as the elbow was flexed and a downward trend as the elbow was extended. There was little change in the shape of this EMG-angle relationship with either direction or velocity. The individual EMG-angle relationships were distinctive for each of these three elbow flexor muscles in four of the six subjects; in the remaining two, biceps was distinctive, but brachioradialis and brachialis appeared to be coupled. Although the EMGs of individual muscles were modulated over the angular range, no consistent stretch reflexes could be seen in the individual records. Thus, we could find no clear evidence for stretch reflex stabilization of human subjects maintaining a constant effort. Rather, muscle torque appears to be reflexly modulated across a much used portion of the elbow's angular range so that any appreciable stabilizing stiffness that is sustained for more than fractions of a second is associated with a change in effort.

Neural gain changes subserving perceptual acuity.

When small and large objects of equal weight are lifted, the small object feels heavier than the large one (the size-weight illusion) and requires more effort to lift (the size-effort illusion). It has been suggested that these illusions result from neural gain changes designed to maintain acuity under different working conditions. If this suggestion is correct, a given mass should produce a larger increase in perceived weight or effort when added to the small object. This was found to be the case.

Perceptions of effort and heaviness during fatigue and during the size-weight illusion.

Previous work has shown that force perception and the sense of motor effort are different attributes of sensorimotor function. This study explores the hypothesis that one reason force and effort perceptions are distinct is to inform an individual of impaired motor function when muscular force lags effort. This hypothesis predicts that effort and force perceptions will dissociate when motor function is impaired by fatigue but not during the size-weight illusion. All subjects reported a distinct increase in effort when lifting a standard test weight as fatigue developed. When fatigue was sufficiently marked so that they could barely lift the test weight, they rated their effort as similar to that required to lift a maximal weight in the unfatigued state. The perceived heaviness of the test weight also increased as fatigue developed, but this fatigue-weight illusion was smaller than the increase in effort for all subjects and displayed greater variability. In contrast, both the perceived weight of a small object and the effort required to lift it increased in parallel when small and large objects were lifted sequentially. The size-weight and size-effort illusions appear to be examples of a common phenomenon in which perceptual experience is rescaled to maintain acuity under different working conditions. The fatigue-weight illusion also has the effect of increasing perceptual acuity as the subject's weight lifting range decreases due to fatigue.

Association between eye dominance and training for rifle marksmanship: a pilot study.

BACKGROUND: This pilot study was performed to determine the effect, if any, exerted by crossed dominance (contralateral hand and eye dominance) on the ability of novice riflemen to learn how to accurately shoot a rifle. METHODS: Sighting dominance was used to determine the dominant eye. Hand dominance was determined by the arm used to shoulder the rifle in the shooting position. Subjects were 308 military recruits at the Fort Benning Army Base in Columbus, Georgia, who had undergone basic training in rifle marksmanship. Qualification scores obtained at the base rifle range were used to measure the subjects' ability to learn marksmanship skills. RESULTS: The subjects with right-hand/right-eye and left-hand/left-eye (uncrossed) dominance had qualification scores that were significantly higher (p = .009) than the subjects with right hand/left-eye and left-hand/right-eye (crossed) dominance. A significantly higher percentage of subjects with uncrossed dominance achieved rifle qualification (86.1 percent) than subjects with crossed dominance (56.5 percent) (p = .000). CONCLUSIONS: The learning of rifle marksmanship is influenced by eye dominance. Individuals who shoot right handed and are left-eye dominant or who shoot left handed and are right-eye dominant do not learn marksmanship skills as readily as individuals who have matched eye and hand dominance. Since crossed hand and eye dominance can be easily determined, it should be possible to identify cross dominant individuals and provide them with special training so that they can perform at a higher level of skill.

Measurement of coronary blood flow velocity in conscious rats.

This study describes a technique for the continuous recording of coronary blood flow velocity (CBV) in conscious unrestrained rats. A pulsed Doppler flow probe consisting of a 1-mm2 crystal mounted in a 4-mm suction cup was positioned over the left coronary artery of pentobarbital sodium-anesthetized rats. The probe was held in place with mild suction and sutured to the surface of the myocardium. Probes were connected to a pulsed Doppler flowmeter, which measures Doppler shift and provides an index of blood flow velocity. While rats were still anesthetized, the measurement of CBV was validated by determining that CBV peaked during diastole and increased in parallel with arterial pressure. Phasic CBV signals obtained in conscious rats were similar to those observed in anesthetized animals. Intravenous infusion of dipyridamole (0.5-3 mg.kg-1 x mg-1) produced a dose-dependent increase in CBV and decrease in coronary vascular resistance in conscious unrestrained rats 7 days after placement of the probe. Light microscopic review of cardiac tissue from instrumented rats revealed minimal epicardial reaction (fibrin deposition) restricted to the immediate area of the probe without distortion of the coronary architecture, edema, inflammation, or necrosis compared with controls. Heart weight-to-body weight ratios of instrumented rats were also not different from those of control rats. This study describes the first technique by which CBV can be measured continuously in chronically instrumented rats.

Coronary blood flow in rats is dependent on the release of vascular nitric oxide.

The present study evaluated the role of nitric oxide (NO) in determining basal coronary vascular tone and the mechanism by which NO regulates coronary blood flow. Sprague-Dawley rats were anesthetized and instrumented for recording arterial pressure (AP), heart rate (HR) and coronary blood flow (CBF; Doppler). In rats without ventricular pacing, N-nitro-L-arginine methyl ester (LNAME) (10 mumol/kg, i.v.), an inhibitor of NO synthesis, produced an increase in AP and a decrease in HR. The LNAME-induced bradycardia was inhibited by sinoaortic denervation. LNAME also produced a reduction in left anterior descending (LAD) CBF. When the same dose of LNAME was administered to a separate group of rats measuring CBF in the right coronary artery (RCA), the decrease in CBF was found to be more prominent in the LAD compared to the RCA. Removal of the sympathetic innervation to the heart and adrenal demedullation did not alter the decrease in CBF, indicating that the effects of LNAME were not centrally mediated. To determine if the effect of LNAME on CBF was due to a direct action on the coronary vasculature or was secondary to the change in HR, dose-response curves were performed for LNAME (0.3-300 mumol/kg, i.v.) in rats with ventricular pacing. Under these conditions, LNAME still produced an increase in AP and a decrease in CBF, resulting in an increase in coronary vascular resistance. Administration of L-arginine (100-300 mg/kg, i.v.) resulted in a reversal of the cardiovascular effects of LNAME with the reversal being sustained for 1 to 5 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of coronary vasoconstriction produced by rostral ventrolateral medulla stimulation in rats.

Previous studies have demonstrated that coronary vasoconstriction can be produced by activation of specific central nervous system sites in the cat. The present study was undertaken 1) to develop a rat model for studying central influences on coronary circulation and 2) to utilize this model for characterization of the changes in coronary blood flow (CBF) produced by stimulation of rostral ventrolateral medulla (RVLM). Electrical stimulation of right RVLM in chloralose-anesthetized rats with bilateral vagotomy produced a transient decrease in CBF followed by an increase in CBF concomitant with a decrease in hindquarter blood flow, a pressor response, and tachycardia. After atenolol the tachycardia and increase in CBF were abolished, whereas the decrease in CBF was enhanced and prolonged. Phentolamine (1 mg/kg iv) or removal of the stellate ganglia inhibited the decrease in CBF but did not totally abolish the increase in coronary vascular resistance. Inhibition of nitric oxide synthesis with N-nitro-L-arginine (10 microM/kg iv) enhanced the decrease in CBF produced by stimulation in RVLM. These results indicate that, in rat model, the centrally induced decrease in CBF is 1) mediated by cardiac sympathetic innervation but only partially through alpha-adrenoceptors and 2) enhanced by removal of the inhibitory effect of the endothelium.

Patterns of hemodynamic responses associated with central activation of coronary vasoconstriction.

Previous studies in our laboratory have identified several central sites from which coronary vasoconstriction can be elicited by electrical stimulation. The present study was conducted to determine if specific patterns of hemodynamic responses are associated with activation of the coronary vasoconstrictor pathway in the hypothalamus, pons, and medulla. Cats anesthetized with chloralose were instrumented for recording arterial pressure, heart rate, and coronary, femoral, renal, and mesenteric blood flow velocities. After vagotomy and atenolol (1 mg/kg iv), anterior hypothalamus (AHA), parabrachial nucleus (PBN), a site very close to the ventral surface of the pons lateral to the pyramidal tract, and rostral ventrolateral medulla (RVLM) were stimulated electrically. Stimulation produced a decrease in coronary blood flow that was associated with all of the cardiovascular components of the defense reaction, an integrated response that included a decrease in hindquarter vascular resistance (blocked by methyl atropine), increases in renal and mesenteric vascular resistances, and a pressor response, except no change in renal vascular resistance from RVLM. Different patterns of hemodynamic responses were obtained from sites outside the coronary vasoconstrictor areas. From these results we conclude that coronary vasoconstriction is a frequent component of the defense reaction.

Differential routes of cocaine administration indicate a peripheral cardiotoxic action.

The present study utilized different routes of administration in unanesthetized Wistar Kyoto (WKY) rats to determine whether cocaine-induced death was mediated through a peripheral or central site of action. Administration of cocaine via a route that resulted in high concentrations of cocaine reaching the heart produced arrhythmias, convulsions, a decrease in heart rate and mean arterial pressure, and death. However, administration of the same dose via a route that resulted in passage of cocaine through the liver before reaching the heart produced only a pressor response. Additionally, administration of the same dose via a route that resulted in high levels of cocaine reaching the brain did produce a pressor response that was followed by a decrease in blood pressure and heart rate, arrhythmias, convulsions and death. However, these effects were delayed in comparison to the response when high concentrations of cocaine reached the heart immediately. These results support a peripheral site of action for cocaine-induced death.

Chronic cocaine treatment enhances the responsiveness of the left anterior descending coronary artery and the femoral artery to vasoactive substances.

The mechanism by which cocaine produces sudden cardiac death has not been elucidated, but clinical evidence indicates that it may be due to a direct or indirect action on coronary vessels. The present study was designed to compare the responses of the isolated left anterior descending (LAD) coronary artery and femoral artery taken from untreated dogs with the response of these vessels taken from dogs administered cocaine (1 mg/kg i.v.) daily for 4 weeks. The actions of norepinephrine, U-46619 (a thromboxane A2 analog) and serotonin (5-HT) were evaluated. The direct vascular action of cocaine was also determined. Morphology of the blood vessels was evaluated by scanning electron microscopy. Chronic cocaine treatment significantly increased the sensitivity and maximum response of the femoral artery to norepinephrine, U-46619 and 5-HT. The sensitivity of the LAD coronary artery to U-46619 and 5-HT and the maximum response to U-46619 and 5-HT were also enhanced. Vasoconstriction produced by cocaine was not dose dependent and only occurred at high concentrations (10(-5)-10(-4) M). Morphology of the vessels was evaluated by scanning electron microscopy. Femoral arteries from cocaine-treated dogs exhibited loss of endothelial integrity, areas of excessive endothelial cell sloughing and thrombus formation. LAD coronary arteries exhibited only areas of enhanced endothelial cell sloughing. The results of this study indicate that the femoral artery and the LAD coronary artery are more sensitive to endogenous vasoactive substances after chronic cocaine use, which may result in enhanced peripheral vasoconstriction and cardiac ischemia. Morphological results demonstrate femoral arterial thrombosis associated with cocaine use.

Central mechanisms of action involved in cocaine-induced tachycardia.

The present study was designed to determine the central effects of cocaine on heart rate and blood pressure in Wistar Kyoto rats (WKY) and to evaluate mechanisms involved in the response. Cocaine (0.025-4 mg/kg) was administered to unanesthetized, unrestrained rats via a cannula placed into the lateral ventricle. Procaine (0.1 and 4 mg/kg) was also administered centrally. Cocaine did not significantly alter blood pressure at doses of 0.025, 0.1, or 0.5 mg/kg, icv. Only the highest dose, 4 mg/kg, icv produced a significant pressor response. Cocaine produced significant dose-dependent tachycardia, with the maximum increase in heart rate occurring within 5 min. Procaine (4 mg/kg, icv) produced tachycardia, but the effect was significantly less than that produced by cocaine (4 mg/kg, icv). Cocaine also produced tachycardia at a dose of 0.1 mg/kg, but procaine did not significantly alter heart rate at the same dose. Central phentolamine pretreatment (0.1 mg/kg, icv) significantly attenuated the increase in heart rate produced by cocaine. These results indicate that the centrally mediated tachycardia produced by cocaine is partly due to its local anesthetic activity and to indirect stimulation of alpha receptors.

Catecholaminergic and opioidergic mechanisms involved in the hypotensive response of pindolol.

The present study evaluated the involvement of opioidergic and catecholaminergic mechanisms in the hypotensive action of pindolol. Pindolol (1 mg/kg i.a.) was administered to unanesthetized spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats instrumented for direct arterial pressure monitoring. Peripheral administration of pindolol produced a significant decrease in blood pressure in both SHR and WKY rats with SHR animals having a greater response. Heart rate was reduced in SHR; however, a tachycardia was observed in WKY rats. Pretreatment with naloxone (100 micrograms/kg i.a.) 10 min prior to pindolol administration prevented the hypotensive response. Similar pretreatment with yohimbine, an alpha 2-receptor antagonist, also prevented the pindolol-induced hypotensive response in both SHR and WKY rats. Neither naloxone nor yohimbine alone significantly affected blood pressure or heart rate. These results suggest that opioidergic and catecholaminergic mechanisms are involved in the hypotensive action of pindolol.

Naloxone pretreatment blocks the hypotensive effects of atenolol in SHR and WKY rats.

The present study examined the interaction of opioidergic systems in the hypotensive action of atenolol. Anesthetized, adult spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats were instrumented to monitor blood pressure and heart rate. Atenolol (100 micrograms/kg, i.v.) produced a decrease in blood pressure of similar magnitude in both SHR and WKY rats. However, the bradycardia was greater in SHR. Pretreatment with naloxone (0.1 mg/kg, i.v.) 15 min prior to the administration of atenolol completely prevented the hypotensive response in SHR and decreased the maximum hypotensive response by approximately 50% in WKY rats. The atenolol-induced bradycardia was unaffected in both groups of animals. Additionally, pretreatment with yohimbine, an alpha 2-receptor antagonist, inhibited the hypotensive response of atenolol in SHR. Collectively, these results suggest an interaction between opioidergic and catecholaminergic systems as a possible site of action of antihypertensive drugs.