Effect of expiratory resistive loading on inspiratory and expiratory muscle fatigue

Inspiratory and expiratory pressures are increased during expiratory resistive loading (ERL). We asked whether ERL elicits inspiratory as well as expiratory muscle fatigue. On four separate days, seven male subjects underwent ERL to task failure. Subjects maintained respiratory frequency at 15 breaths min⁻¹, expiratory gastric pressure at 40% or 60% of maximum, and expiratory duty cycle at 0.4 or 0.7 (ERL_40%0.4, ERL_40%0.7, ERL_60%0.4, ERL_60%0.7). Inspiratory and abdominal muscle contractility was assessed before and up to 30 min after ERL by measuring transdiaphragmatic twitch pressure (P_di,tw) and gastric twitch pressure (P_ga,tw) in response to magnetic nerve stimulation. After each trial, P_di,tw and P_ga,tw were reduced below baseline values (−9 to −15% for P_di,tw and −15 to −22% for P_ga,tw; P < 0.05). The severity of diaphragm fatigue was unaffected by expiratory pressure production or expiratory duty cycle, whereas extending the expiratory duty cycle increased the severity of abdominal muscle fatigue. In conclusion, ERL elicits contractile fatigue of the diaphragm and the abdominal muscles.     

Acute effects of inspiratory pressure threshold loading upon airway resistance in people with asthma

Large inspiratory pressures may impart stretch to airway smooth muscle and modify the response to deep inspiration (DI) in asthmatics. Respiratory system resistance (Rrs) was assessed in response to 5 inspiratory manoeuvres using the forced oscillation technique: (a) single unloaded DI; (b) single DI at 25 cmH₂O; (c) single DI at 50% maximum inspiratory mouth pressure [MIP]; (d) 30 DIs at 50% MIP; and (e) 30 DIs at 50% MIP with maintenance of normocapnia. Rrs increased after the unloaded DI and the DI at 25 cmH₂O but not after a DI at 50% MIP (3.6 ± 1.6 hPa L s⁻¹ vs. 3.6 ± 1.5 hPa L s⁻¹; p = 0.95), 30 DIs at 50% MIP (3.9 ± 1.5 hPa L s⁻¹ vs. 4.2 ± 2.0 hPa L s⁻¹; p = 0.16) or 30 DIs at 50% MIP under normocapnic conditions (3.9 ± 1.5 hPa L s⁻¹ vs. 3.9 ± 1.5 hPa L s⁻¹; p = 0.55). Increases in Rrs in response to DI were attenuated after single and multiple loaded breaths at 50% MIP.     

Dynamics of T cell activation accompanying CD4 recovery in antiretroviral treated HIV-infected Ugandan children

Africans have elevated T cell activation compared to residents of Europe or the USA. Levels of T cell activation also correlate with disease progression in HIV-infected individuals. We sought to determine if treatment with antiretroviral therapy (ART) would reduce levels of T cell activation (CD38 and HLADR co-expression) in HIV-infected Ugandan children. The median CD8+ T cell activation level among 199 ART-treated children (30%) was lower than in 57 ART-naïve children (45%, p < 0.001), but remained higher than in 30 HIV-uninfected children (18%, p < 0.001). Among ART-treated children, CD4% was inversely correlated with both CD8− (ρ = − 0.61, p < 0.001) and CD8+ (ρ = − 0.38, p < 0.001) T cell activation. Prospectively, CD4 recovery correlated with post-treatment CD8+ T cell activation level (p = 0.008). Our data suggest that significant decreases in T cell activation accompany CD4 recovery in ART-treated HIV-infected African children, to levels that approach but do not reach those of uninfected children.     

Pulmonary blood flow generates cardiogenic oscillations

Cardiogenic oscillations are small waves produced by heartbeats, which are superimposed on the pressure and flow signals at the airway opening. The aim of this study was to investigate the role of the two main factors believed to generate these oscillations: (1) contact between heart and lungs and (2) pulmonary blood flow. We studied 15 heart surgery patients on cardiopulmonary bypass so both factors could be manipulated independently.At minimal heart–lung contact pressure and flow oscillations were larger than during maximal contact (1.20 ± 0.17 cmH₂O and 2.36 ± 0.08 L min⁻¹ vs 0.92 ± 0.15 cmH₂O and 1.78 ± 0.26 L min⁻¹, mean ± SD, p < 0.05). Cardiogenic oscillations for pressure and flow were smaller at 50% compared to 100% pulmonary blood flow (0.80 ± 0.12 cmH₂O and 1.56 ± 0.34 L min⁻¹ vs 1.19 ± 0.14 cmH₂O and 2.38 ± 0.19 L min⁻¹). We conclude that the amount of pulmonary blood flow and not the contact between heart and lungs is the main factor determining the amplitude of cardiogenic oscillations.     

Effects of obesity on breathing pattern, ventilatory neural drive and mechanics

The purpose of this study was to assess whether obesity induces changes in breathing pattern and ventilatory neural drive and mechanics. Measurements performed in 34 male obese subjects (BMI, 39 ± 6 kg/m²) and 18 controls (BMI, 23 ± 3 kg/m²) included anthropometric parameters, spirometry, breathing patterns, mouth occlusion pressure, maximal inspiratory pressure and work of breathing. The results show that spirometric flow (FEV₁% pred, FVC% pred) and maximal inspiratory pressure (P_Imax) were significantly lowers (p < 0.001) in obese subjects compared to controls. The (fR/VT) ratio was higher in obese subjects than in controls (p < 0.001). The increase in (fR/VT) was associated with an increase in the ratio of mean inspiratory pressure to maximal inspiratory pressure (P_I/P_Imax) and the duty cycle (T_I/T_TOT) (p < 0.001). The energy cost of breathing (W_rest/W_crit), which reflects the oxygen consumed by the respiratory muscle was greater in obese subject than in controls (p < 0.001) inducing an increase in the effective inspiratory impedance on the respiratory muscles. It is concluded that obese subjects show impairment in breathing pattern and respiratory mechanics as assessed by rapid shallow breathing leading to ventilatory failure.     

Surplus dietary tryptophan inhibits stress hormone kinetics and induces insulin resistance in pigs

Recently we have shown that surplus dietary tryptophan (TRP) reduced the plasma concentrations of cortisol and noradrenaline in pigs. Stress hormones are known to affect insulin sensitivity and metabolism. We now investigated the long-term effects of surplus dietary TRP on 1) plasma and urinary stress hormone kinetics, 2) insulin sensitivity for glucose and amino acid clearance, and 3) whole body nitrogen balance. Pigs were fed for 3 weeks a high (13.2%) vs normal (3.4%) TRP to large neutral amino acids (LNAA) diet, leading to reduced fasting (14 h) plasma cortisol (17.1 ± 3.0 vs 28.9 ± 4.3 ng/mL, p < 0.05) and noradrenaline (138 ± 14 vs 225 ± 21 pg/mL, p < 0.005) concentrations, lower daily urinary noradrenaline (313 ± 32 vs 674 ± 102 ng/kg day, p < 0.001) and adrenaline (124 ± 13 vs 297 ± 42 ng/kg day, p < 0.001) but higher dopamine (5.8 ± 0.5 vs 1.5 ± 0.2 µg/kg day, p < 0.001) excretions, respectively. Insulin sensitivities for both glucose and amino acid clearance, (as measured by the intraportal hyperinsulinaemic (1 mU/kg min) euglycaemic euaminoacidaemic clamp technique), were lower by 22% in pigs on the high vs normal TRP/LNAA diet (14.8 ± 1.4 vs 18.9 ± 0.9, p < 0.05 and 69.7 ± 4.3 vs 89.7 ± 6.8 mL/kg min, p < 0.05, respectively) without affecting urinary nitrogen excretion (35.5 ± 1.0 vs 36.6 ± 1.0% of dietary nitrogen intake, p = ns). In conclusion, long-term feeding of surplus dietary TRP inhibits both baseline adrenocortical and sympathetic nervous system activity, it induces insulin resistance for both glucose and amino acid clearance but it does not affect whole body protein catabolism. This indicates that the bioactive amino acid TRP contributes to homeostasis in neuroendocrinology and insulin action and that low baseline adrenocortical and sympatho-adrenal axis activity are associated with insulin resistance.     

Impact of pregnancy and obesity on cardiorespiratory responses during weight-bearing exercise

The present study is the first to compare the cardiorespiratory responses during progressive weight-bearing treadmill exercise in normal-weight non-pregnant (NP, n = 14), normal-weight pregnant (PG, n = 20) and obese pregnant (PGOB, n = 20) women. Exercise duration and peak treadmill speed were lower in PG (23.9 ± 4.9 min; 1.6 ± 0.2 m/s; P < 0.001) compared to NP (33.7 ± 4.9 min; 2.0 ± 0.2 m/s) and were further reduced in PGOB (19.6 ± 2.8 min; 1.4 ± 0.1 m/s; P < 0.001) indicating a performance limitation to exercise. Ventilation in response to exercise was increased in PG (49.4 ± 6.6 L/min) compared to NP (39.8 ± 5.4 L/min, at 100 W; p < 0.05) women, and was further augmented by obesity (56.7 ± 9.3 L/min, at 100 W; p < 0.05 versus PG) secondary to an elevated metabolic cost of exercise as indicated by no further increase in and in PGOB compared to PG women. The normal augmentation of heart rate observed in PG during exercise was not further increased by obesity at standardized sub-maximal work rates.     

Neuroprotection (and lack of neuroprotection) afforded by a series of noble gases in an in vitro model of neuronal injury

Xenon-induced neuroprotection has been well studied both in vivo and in vitro. In this study, the neuroprotective properties of the other noble gases, namely, krypton, argon, neon and helium, were explored in an in vitro model of neuronal injury. Pure neuronal cultures, derived from foetal BALB/c mice cortices, were provoked into injury by oxygen and glucose deprivation (OGD). Cultures were exposed to either nitrogen hypoxia or noble gas hypoxia in balanced salt solution devoid of glucose for 90 min. The cultures were allowed to recover in normal culture medium for a further 24 h in nitrogen or noble gas. The effect of noble gases on cell reducing ability in the absence of OGD was also investigated. Cell reducing ability was quantified via an MTT assay and expressed as a ratio of the control. The OGD caused a reduction in cell reducing ability to 0.56 ± 0.04 of the control in the absence of noble gas (p < 0.001). Like xenon (0.92 ± 0.10; p < 0.001), neuroprotection was afforded by argon (0.71 ± 0.05; p < 0.01). Neon and krypton did not have a protective effect under our experimental conditions. Helium had a detrimental effect on the cells. In the absence of OGD, krypton reduced the reducing ability of uninjured cells to 0.84 ± 0.09 (p < 0.01), but argon showed an improvement in reducing ability to 1.15 ± 0.11 (p < 0.05). Our data suggest that the cheap and widely available noble gas argon may have potential as a neuroprotectant for the future.     

A novel nanocomposite polymer for development of synthetic heart valve leaflets

A novel nanocomposite polymer with a polycarbonate soft segment (PCU) and polyhedral oligomeric silsesquioxanes (POSS) nanoparticle (POSS–PCU) has been selected for a synthetic heart valve due to its superior biocompatibility and in vivo biostability. However, the development of synthetic heart valves from polymeric materials requires an understanding of the basic mechanical and surface properties of the polymer. In this study, the mechanical properties of POSS–PCU, including tensile strength, tear strength and hardness, were tested and compared to control (PCU). The surface property was analyzed using contact angle measurement and the resistance to platelet adhesion was also investigated. POSS–PCU (hardness 84 ± 0.8 Shore A) demonstrated significantly higher tensile strength 53.6 ± 3.4 and 55.9 ± 3.9 N mm⁻² at 25 and 37 °C, respectively) than PCU (33.8 ± 2.1 and 28.8 ± 3.4 N mm⁻² at 25 and 37 °C, respectively). Tensile strength and elongation at break of POSS–PCU was significantly higher than PCU at both 25 and 37 °C (P < 0.001). POSS–PCU showed a relatively low Young’s modulus (25.9 ± 1.9 and 26.2 ± 2.0 N mm⁻²) which was significantly greater in comparison with control PCU (9.1 ± 0.9 and 8.4 ± 0.5 N mm⁻²) at 25 and 37 °C, respectively, with 100 μm thickness. There was no significant difference (P > 0.05) in tear strength between POSS–PCU and PCU at 25 °C. However, tear strength increased significantly (P < 0.001) (at 37 °C) as the thickness increased from 100 μm (51.0 ± 3.3 N mm⁻¹) to 200 μm (63 ± 1.5 N mm⁻¹). The surface of POSS–PCU was significantly less hydrophilic than that of PCU.     

Continuous positive airway pressure reduces loop gain and resolves periodic central apneas in the lamb

Continous positive airway pressure (CPAP) is used to treat infant respiratory distress syndrome and apnea of prematurity, but its mode of action is not fully understood. We hypothesised that CPAP increases lung volume and stabilises respiratory control by decreasing loop gain (LG). Experimentally induced periodic breathing (PB) in the lamb was terminated early by CPAP in a dose-dependent manner, with a control epoch of 45.4 ± 5.1 s at zero CPAP falling to 32.9 ± 5.4, 13.2 ± 4.2 and 9.8 ± 3.1 s at 2.5, 5 and 10 cmH₂O, respectively (p < 0.001); corresponding duty ratios (duration of the ventilatory phase of PB divided by its cycle duration) increased from 0.50 ± 0.02 to 0.62 ± 0.05, 0.76 ± 0.06 and 0.68 ± 0.08, respectively (p < 0.001). Since epoch duration and duty ratio are surrogate measures of LG, we conclude that CPAP ameliorates the effects of recurrent central apneas, and perhaps mixed and obstructive apneas, by decreasing LG via increases in lung volume.     

Graded unilateral cervical spinal cord injury and respiratory motor recovery

We examined the potential contribution of ventromedial (VM) tissue sparing to respiratory recovery following chronic (1 mo) unilateral C2 spinal cord injury (SCI) in rats. Preserved white matter ipsilateral to the injury was quantitatively expressed relative to contralateral white matter. The ipsilateral-to-contralateral white matter ratio was 0 after complete C2 hemisection (C2HS) and 0.23 ± 0.04 with minimal VM sparing. Inspiratory (breath min⁻¹) and phrenic frequency (burst min⁻¹), measured by plethysmography (conscious rats) and phrenic neurograms (anesthetized rats) respectively, were both lower with minimal VM sparing (p < 0.05 vs. C2HS). Tidal volume also was greater in minimal VM sparing rats during a hypercapnic challenge (p < 0.05 vs. C2HS). In other C2 hemilesioned rats with more extensive VM matter sparing (ipsilateral-to-contralateral white matter ratio = 0.55 ± 0.05), respiratory deficits were indicated at 1 mo post-injury by reduced ventilation during hypercapnic challenge (p < 0.05 vs. uninjured). Anterograde (ventral respiratory column-to-spinal cord) neuroanatomical tracing studies showed that descending respiratory projections from the brainstem are present in VM tissue. We conclude that even relatively minimal sparing of VM tissue after C2 hemilesion can alter respiratory outcomes. In addition, respiratory deficits can emerge in the adult rat after high cervical SCI even when relatively extensive VM sparing occurs.     

Regulation of local sweating in sleep-deprived exercising humans

Summary Thermoregulatory sweating [total body (m _sw,b), chest (m _sw,c) and thigh (m _sw,t) sweating], body temperatures [oesophageal (T _oes) and mean skin temperature (T _sk)] and heart rate were investigated in five sleep-deprived subjects (kept awake for 27 h) while exercising on a cycle (45 min at approximately 50% maximal oxygen consumption) in moderate heat (T _air andT _wall at 35° C. Them _sw,c andm _sw,t were measured under local thermal clamp (T _sk,1), set at 35.5° C. After sleep deprivation, neither the levels of body temperatures (T _oes,T _sk) nor the levels ofm _{sw, b},m _{sw, c} orm _{sw, t} differed from control at rest or during exercise steady state. During the transient phase of exercise (whenT _sk andT _sk,1 were unvarying), them _{sw, c} andm _{sw, t} changes were positively correlated with those ofT _oes. The slopes of them _{sw, c} versusT _oes, orm _{sw, t} versusT _oes relationships remained unchanged between control and sleep-loss experiments. Thus the slopes of the local sweating versusT _oes, relationships (m _{sw, c} andm _{sw, t} sweating data pooled which reached 1.05 (SEM 0.14) mg·cm^–2·min^–1°C^–1 and 1.14 (SEM 0.18) mg·cm^–2·min^–1·°C^–1 before and after sleep deprivation) respectively did not differ. However, in our experiment, sleep deprivation significantly increased theT _oes threshold for the onset of bothm _{sw, c} andm _{sw, t} (+0.3° C,P<0.001). From our investigations it would seem that the delayed core temperature for sweating onset in sleep-deprived humans, while exercising moderately in the heat, is likely to have been due to alterations occurring at the central level.     

Ventilation in Pacific hagfish (Eptatretus stoutii) during exposure to acute hypoxia or hypercapnia

A technique was developed to measure ventilation in unrestrained Pacific hagfish (Eptatretus stoutii) by inserting and fastening into the nostril a flexible tube fitted with an ultrasonic flow probe. This technique permitted the continuous measurement of ventilation (respiratory) frequency (fR), stroke volume and minute ventilation () in real time in fish exposed to acute hypoxia or hypercapnia. Exposing fish to acute hypoxia (final Pw_O2=21.0±3.4 mm Hg) caused hypoxaemia and a marked increase in of 350 ± 71 ml min⁻¹ kg⁻¹ (from 235 to 585 ml min⁻¹ kg⁻¹) owing exclusively to an increase in fR of 44 ± 7 min⁻¹ (from 19 to 63 min⁻¹). Because O₂ consumption (0.4 mmol kg⁻¹ h⁻¹) was unaltered during hypoxia, there was an associated marked increased in the ventilation convection requirement from 36.7 to 81.8 l mmol⁻¹. Injecting the O₂ chemoreceptor stimulant NaCN into inspired water (external CN⁻) or pre-branchial blood (internal CN⁻) evoked ventilatory responses that were similar to those observed during hypoxia although of a lesser magnitude. With external CN⁻, increased maximally by 146 ± 46 ml min⁻¹ kg⁻¹ and fR increased by 20 ± 2 min⁻¹. With internal CN⁻, the maximal increase in was 93 ± 30 ml min⁻¹ kg⁻¹ and fR increased maximally by 19 ± 6 min⁻¹. Exposure to acute hypercapnia (final PwC = 7.0 ± 0.2 mm Hg) caused an increase in of 169 ± 60 ml min⁻¹ kg⁻¹. These results provide compelling evidence for chemoreceptor-mediated control of breathing in hagfish and suggest that ventilatory responses to environmental hypoxia and hypercapnia in the vertebrates arose in the myxine lineage.     

Effects of stress on heart rate complexity—A comparison between short-term and chronic stress

This study examined chronic and short-term stress effects on heart rate variability (HRV), comparing time, frequency and phase domain (complexity) measures in 50 healthy adults. The hassles frequency subscale of the combined hassles and uplifts scale (CHUS) was used to measure chronic stress. Short-term stressor reactivity was assessed with a speech task. HRV measures were determined via surface electrocardiogram (ECG). Because respiration rate decreased during the speech task (p < .001), this study assessed the influence of respiration rate changes on the effects of interest. A series of repeated-measures analyses of covariance (ANCOVA) with Bonferroni adjustment revealed that short-term stress decreased HR D2 (calculated via the pointwise correlation dimension PD2) (p < .001), but increased HR mean (p < .001), standard deviation of R–R (SD_RR) intervals (p < .001), low (LF) (p < .001) and high frequency band power (HF) (p = .009). Respiratory sinus arrhythmia (RSA) and LF/HF ratio did not change under short-term stress. Partial correlation adjusting for respiration rate showed that HR D2 was associated with chronic stress (r = −.35, p = .019). Differential effects of chronic and short-term stress were observed on several HRV measures. HR D2 decreased under both stress conditions reflecting lowered functionality of the cardiac pacemaker. The results confirm the importance of complexity metrics in modern stress research on HRV.     

Comparaison de deux techniques de monitorage du débit cardiaque : méthode du contour de pouls et thermodilution artérielle pulmonaire continueComparison of two methods of cardiac output monitoring : systemic arterial pressure and thermodilution curves

Two devices for continuous cardiac output (CO) monitoring at patient bedside were evaluated. Vigilance™ monitor (Baxter Lab.) provides CO measurements by intermittent bolus (TDCO Vig) and continuous thermodilution (CCO Vig) methods, curves are both collected using a pulmonary artery catheter ; PICCO™ monitor (Pulsion Lab.) also provides continuous CO by pulse contour analysis (CCO Pic) and intermittent trans-thoracic thermodilution CO measurements (TDCO Pic), which is used to calculate a calibration factor for further beat-to-beat estimations of CCO Pic. Both systemic arterial pressure and thermodilution curves are collected using a femoral arterial catheter. The objectives of the study were : 1) to compare both methods, 2) to identify the situations possibly responsible for a poor reliability of the pulse contour method. CO measurements (n=301) were recorded simultaneously with both devices in 10 ICU patients : 44 conflicting data pairs, measured after vaso-active drugs initiation or following a calibration procedure performed during cardiac arythmia, were excluded. 257 data pairs for continuous CO measurements were compared using linear regressions and Bland-Altman plots method. Mean values for CCO Vig and CCO Pic were 7,3±2,63 and 7,8±3,04 l.min⁻¹ respectively, and the correlation was significant (r=0,94, p<10⁻⁴). The average difference (bias) was 0,5± 1,06 l.min⁻¹, i.e 7 % overestimation of CO by CCO Pic, and the 95 % confidence interval was large. For 9 among 10 patients the correlation between CCO Vig and CCO Pic was good (Spearman test). For CO values less than 8 l.min⁻¹, the bias and 95 % confidence interval were smaller (0,2±0,66 l.min⁻¹, n=180). Moreover, 108 data pairs for intermittent CO measurements were collected. The correlation between TDCO Vig (7,4±2,7 l.min⁻¹) and TDCO Pic (8,1±1,06 l.min⁻¹) was significant (r=0,97, p<10⁻⁴). The bias was 0,76±0,86 l.min⁻¹ and could be related to a thermal loss between pulmonary and femoral arterial collection. On the whole, the agrement between both continuous CO measurments is acceptable. Since TDCO Pic is used for CCO Pic calibration, the difference between the two CO continuous methods could be partly explained by an overestimation of TDCO Pic. Consequently, the software calibration process should be refined. Moreover, we identified two situations that are responsible for erroneous values of CCO Pic and require a new calibration : cardiac arythmia during PICCO™ calibration, vaso-active drugs initiation.     

Recombinant C3adesArg/acylation stimulating protein (ASP) is highly bioactive: A critical evaluation of C5L2 binding and 3T3-L1 adipocyte activation

C5L2 is a recently identified receptor for C5a/C5adesArg, C3a and C3adesArg (ASP). C5a/C5adesArg bind with high affinity, with no identified activation. By contrast, some studies demonstrate C3a/ASP binding/activation to C5L2; others do not. Our aim is to critically evaluate ASP/C3adesArg-C5L2 binding and bioactivity.Cell-associated fluorescent-ASP (Fl-ASP) binding to C5L2 increased from transiently transfected < stably transfected < Fl-ASP-sorted C5L2-HEK for both human C5L2 and mouse C5L2. Transfected C5L2-CHO cells had similar results. Endogenous C5L2 expression increased from 3T3-L1 preadipocytes < 3T3-L1 adipocytes < primary mouse adipocytes. Non-transfected cells ± Fl-ASP demonstrated background fluorescence only.In adherent C5L2-HEK (Fl-ASP sorted) and 3T3-L1 cells, blocking with 10% fetal calf serum, protamine sulfate or ovalbumin prevented ¹²⁵I-ASP non-specific binding (NSB, no cells), while albumin increased NSB. Binding to non-transfected HEK was comparable to NSB. Optimal specific binding was obtained at 20 °C (vs. 4 °C) in PBS or serum-free medium with K_d 83.7 ± 23.7 nM (C5L2-HEK), 66 ± 15 nM (C5L2-CHO) and 76 ± 14.3 nM (3T3-L1 preadipocytes); ¹²⁵I-C5a binding had greater affinity. Fl-ASP-C5L2 binding was comparable and concentration dependent (K_d 31 nM (direct binding) and IC₅₀ 35 nM (competition binding) regardless of conditions).Recombinant ASP (rASP) produced in modified Escherichia coli Origami (DE3) (allowing folding and disulphide bridge formation), purified under non-denaturing conditions demonstrated 10× greater bioactivity vs. proteolytically derived plasma ASP for triglyceride synthesis and fatty acid uptake in 3T3-L1 adipocytes and preadipocytes while adipose tissue from C5L2 KO mice was non-responsive. rASP stimulation of adipocyte BODIPY-fatty acid uptake demonstrated EC₅₀ 115 ± 93 nM and maximal stimulation of 413 ± 33%, p < 0.001. ASP binding has distinct characteristics that lead to C5L2 activation and increased bioactivity.     

Assessment of isometricity before and after total knee arthroplasty: A cadaver study

Total knee arthroplasty (TKA) relies on soft tissue to regulate joint stability after surgery. In practice, the exact balance of the gaps can be difficult to measure, and various methods including intra-operative spreaders or distraction devices have been proposed. While individual ligament strain patterns have been measured, no data exist on the isometricity of the soft tissue envelope as a whole. In this study, a novel device was developed and validated to compare isometricity in the entire soft tissue envelope for both the intact and TKA knee.A spring-loaded rod was inserted in six cadaver knee joints between the tibial shaft and the tibial plateau or tibial tray after removing a 7 mm slice of bone. The displacement of the rod during passive flexion represented variation in tissue tension around the joint. The rod position in the intact knee remained within 1 mm of its initial position between 15° and 135° of flexion, and within 2 mm (± 1.2 mm) throughout the entire range of motion (0–150°). After insertion of a mobile-bearing TKA, the rod was displaced a mean of 6 mm at 150° (p < 0.001). The results were validated using a force transducer implanted in the tibial baseplate of the TKA, which showed increased tibiofemoral force in the parts of the flexion range where the rod was most displaced. The force measurements were highly correlated with the displacement pattern of the spring-loaded rod (r = − 0.338; p = 0.006).A simple device has been validated to measure isometricity in the soft tissue envelope around the knee joint. Isometricity measurements may be used in the future to improve implantation techniques during TKA surgery.     

Mechanical properties of arteries cryopreserved at −80 °C and −150 °C

A new protocol for cryopreservation of arteries frozen at −80 °C was compared to the reference protocol for cryopreservation at −150 °C and to freshly harvested arteries. The aim of the study is to evaluate both protocols as global procedures to freeze and thaw arteries commonly used in tissue banks. Changes in mechanical properties of rabbit common carotid arteries were studied. Vascular segments were tested in vitro under dynamics loading conditions. Pressure and diameter were recorded simultaneously by a high fidelity transducer and an echotracking device, respectively. The pressure–diameter relationship was fitted by the arctangent Langewouters’ model and the arterial thickness was derived from histological measurements. Histological sections showed that the fresh and −80 °C groups were less damaged by hemodynamic load and histological preparation than the −150 °C group (p < 0.05). No differences between fresh and cryopreserved arteries regarding the structural (diameter, intimal-media thickness) and mechanical parameters (distensibility, circumferential stress, elastic modulus) were found. The isobaric circumferential stress was reduced in frozen arteries. These results demonstrate that the cryopreservation at −80 °C preserves the histological structure and mechanical properties better than the cryopreservation at −150 °C, suggesting that the new cryopreservation protocol at −80 °C is a method of choice for treating vessel replacement in vascular surgery.     

Quantification of single-breath underestimation of lung volume in emphysema

The extent to which a single breath measurement represents available gas dilutional as well as compressible thoracic volume in emphysema patients has not been quantified. We therefore measured single breath (TLC_SB) and rebreathe helium dilution (TLC_RB), and plethysmographic lung volume (TLC_pleth), in fifty-five outpatients with clinical and radiographic emphysema, and in twenty-one normal controls. Among emphysema patients, TLC_SB increasingly underestimated both TLC_pleth and TLC_RB as FEV₁% predicted decreased (p for interaction = 0.001 for both) by a mean of 1.7 l for TLC_RB (p < 0.001) and 2.2 l for TLC_pleth (p < 0.001). In contrast, TLC_RB underestimated TLC_pleth by a mean of 0.5 l (p < 0.001) regardless of FEV1% (p for interaction = 0.25). TLC_SB, TLC_RB, and TLC_pleth showed strong agreement among normal subjects. We conclude that TLC_SB underestimates available gas dilutional and compressible lung volume as physiologic emphysema severity increases. In contrast, TLC_RB and TLC_pleth show closer agreement which is unaffected by physiologic emphysema severity.