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Purpose: The purpose of this study was to determine the learning curve for total operative time using a novel cutting guide positioning robotic assistant for total knee arthroplasty (raTKA). Additionally, we compared complications and final limb alignment between raTKA and manual TKA (mTKA), as well as accuracy to plan for raTKA cases., Methods: We performed a retrospective cohort study on a series of patients (n = 180) that underwent raTKA (n = 90) using the ROSA Total Knee System or mTKA (n = 90) by one of three high-volume (> 200 cases per year) orthopaedic surgeons between December 2019 and September 2020, with minimum three-month follow-up. To evaluate the learning curve surgical times and postoperative complications were reviewed., Results: The cumulative summation analysis for total operative time revealed a change point of 10, 6, and 11 cases for each of three surgeons, suggesting a rapid learning curve. There was a significant difference in total operative times between the learning raTKA and both the mastered raTKA and mTKA groups (p = 0.001) for all three surgeons combined. Postoperative complications were minimal in all groups. The proportion of outliers for the final hip-knee-ankle angle compared to planned was 5.2% (3/58) for the mastered raTKA compared to 24.1% (19/79) for mTKA (p = 0.003). The absolute mean difference between the validated and planned resections for all angles evaluated was < 1 degree for the mastered raTKA cases., Conclusion: As the digital age of medicine continues to develop, advanced technologies may disrupt the industry, but should not disrupt the care provided. This cutting guide positioning robotic system can be integrated relatively quickly with a rapid initial learning curve (6-11 cases) for operative times, similar 90-day complication rates, and improved component positioning compared to mTKA. Proficiency of the system requires additional analysis, but it can be expected to improve over time., Level of Evidence: Level III Retrospective Therapeutic Cohort Study., (© 2021. The Author(s).)

Background: Apart from biomechanical alterations in movement patterns, it is known that movement limitations in persons with knee osteoarthritis (PwKOA) are related to an individual's perception and belief regarding pain and disability. To gain more insights into the functional movement behaviour of PwKOA in a clinical setting, inertial sensor technology can be applied. This study first aims to evaluate the ability of inertial sensors to discriminate between healthy controls (HC) and PwKOA. Secondly, this study aims to determine the relationship between movement behaviour, pain-related factors and disability scores., Methods: Twelve HC and 19 PwKOA were included. Five repetitions of six functional movement tasks (walking, forward lunge, sideward lunge, ascent and descent stairs, single leg squat and sit-to-stand) were simultaneously recorded by the inertial sensor system and a camera-based motion analysis system. Statistically significant differences in angular waveforms of the trunk, pelvis and lower limb joints between HC and PwKOA were determined using one-dimensional statistical parametric mapping (SPM1D). The Knee injury and Osteoarthritis Outcome Score and TAMPA scale for Kinesiophobia were used to evaluate the relationship between discriminating joint motion, pain-related factors and disability using spearman's correlation coefficients., Results: PwKOA had significantly less trunk rotation, internal pelvis rotation and knee flexion ROM during walking. Additionally, the reduced knee flexion (i.e. at the end of the stance phase and swing phase) was related to increased level of perceived pain. During the sideward lunge, PwKOA had significantly less knee flexion, ankle plantarflexion and hip abduction. This decreased hip abduction (i.e. during stance) was related to higher fear of movement. Finally, PwKOA had significantly less knee flexion during the forward lunge, single leg squat and during ascent and descent stairs. No significant correlations were observed with disability., Conclusions: Inertial sensors were able to discriminate between movement characteristics of PwKOA and HC. Additionally, significant relationships were found between joint motion, perceived pain and fear of movement. Since inertial sensors can be used outside the laboratory setting, these results are promising as they indicate the ability to evaluate movement deviations. Further research is required to enable measurements of small movement deviations in clinically relevant tasks.

Blood pressure (BP) decreases in the first weeks after Roux-and-Y gastric bypass surgery. Yet the pathophysiology of the BP-lowering effects observed after gastric bypass surgery is incompletely understood. We evaluated BP, systemic hemodynamics, and baroreflex sensitivity in 15 obese women[mean age 42 ± 7 standard deviation (SD) yr, body mass index 45 ± 6 kg/m 2 ] 2 wk before and 6 wk following Roux-and-Y gastric bypass surgery. Six weeks after gastric bypass surgery, mean body weight decreased by 13 ± 5 kg (10%, P < 0.001). Office BP decreased from 137 ± 10/86 ± 6 to 128 ± 12/81 ± 9 mmHg (P < 0.001, P < 0.01), while daytime ambulatory BP decreased from 128 ± 14/80 ± 9 to 114 ± 10/73 ± 6 mmHg (P = 0.01, P = 0.05), whereas nighttime BP decreased from 111 ± 13/66 ± 7 to 102 ± 9/62 ± 7 mmHg (P = 0.04, P < 0.01). The decrease in BP was associated with a 1.6 ± 1.2 l/min (20%, P < 0.01) decrease in cardiac output (CO), while systemic vascular resistance increased (153 ± 189 dyn·s·cm -5 , 15%, P < 0.01). The maximal ascending slope in systolic blood pressure decreased (192 mmHg/s, 19%, P = 0.01), suggesting a reduction in left ventricular contractility. Baroreflex sensitivity increased from 9.0 [6.4-14.3] to 13.8 [8.5-19.0] ms/mmHg (median [interquartile range]; P < 0.01) and was inversely correlated with the reductions in heart rate (R = -0.64, P = 0.02) and CO (R = -0.61, P = 0.03). In contrast, changes in body weight were not correlated with changes in either BP or CO. The BP reduction following Roux-and-Y gastric bypass surgery is correlated with a decrease in CO independent of changes in body weight. The contribution of heart rate to the reduction in CO together with enhanced baroreflex sensitivity suggests a shift toward increased parasympathetic cardiovascular control., New & Noteworthy: The reason for the decrease in blood pressure (BP) in the first weeks after gastric bypass surgery remains to be elucidated. We show that the reduction in BP following surgery is caused by a decrease in cardiac output. In addition, the maximal ascending slope in systolic blood pressure decreased suggesting a reduction in left ventricular contractility and cardiac workload. These findings help to understand the physiological changes following gastric bypass surgery and are relevant in light of the increased risk of heart failure in these patients., (Copyright © 2017 the American Physiological Society.)

Type 2 diabetes mellitus is associated with microvascular complications, hypertension, and impaired dynamic cerebral autoregulation. Intensive blood pressure (BP) control in hypertensive type 2 diabetic patients reduces their risk of stroke but may affect cerebral perfusion. Systemic hemodynamic variables and transcranial Doppler-determined cerebral blood flow velocity (CBFV), cerebral CO2 responsiveness, and cognitive function were determined after 3 and 6 months of intensive BP control in 17 type 2 diabetic patients with microvascular complications (T2DM+), in 18 diabetic patients without (T2DM-) microvascular complications, and in 16 nondiabetic hypertensive patients. Cerebrovascular reserve capacity was lower in T2DM+ versus T2DM- and nondiabetic hypertensive patients (4.6±1.1 versus 6.0±1.6 [P<0.05] and 6.6±1.7 [P<0.01], Δ%mean CBFV/mm Hg). After 6 months, the attained BP was comparable among the 3 groups. However, in contrast to nondiabetic hypertensive patients, intensive BP control reduced CBFV in T2DM- (58±9 to 54±12 cm·s(-1)) and T2DM+ (57±13 to 52±11 cm·s(-1)) at 3 months, but CBFV returned to baseline at 6 months only in T2DM-, whereas the reduction in CBFV progressed in T2DM+ (to 48±8 cm·s(-1)). Cognitive function did not change during the 6 months. Static cerebrovascular autoregulation appears to be impaired in type 2 diabetes mellitus, with a transient reduction in CBFV in uncomplicated diabetic patients on tight BP control, but with a progressive reduction in CBFV in diabetic patients with microvascular complications, indicating that maintenance of cerebral perfusion during BP treatment depends on the progression of microvascular disease. We suggest that BP treatment should be individualized, aiming at a balance between BP reduction and maintenance of CBFV.

Although a relation between diminished human immunity and stress is well recognized both within the general public and the scientific literature, the molecular mechanisms by which stress alters immunity remain poorly understood. We explored a novel model for acute human stress involving volunteers performing a first-time bungee jump from an altitude of 60 m and exploited this model to characterize the effects of acute stress in the peripheral blood compartment. Twenty volunteers were included in the study; half of this group was pretreated for 3 d with the β-receptor blocking agent propranolol. Blood was drawn 2 h before, right before, immediately after and 2 h after the jump. Plasma catecholamine and cortisol levels increased significantly during jumping, which was accompanied by significantly reduced ex vivo inducibility of proinflammatory cytokines as well as activation of coagulation and vascular endothelium. Kinome profiles obtained from the peripheral blood leukocyte fraction contained a strong noncanonical glucocorticoid receptor signal transduction signature after jumping. In apparent agreement, jumping down-regulated Lck/Fyn and cellular innate immune effector function (phagocytosis). Pretreatment of volunteers with propranolol abolished the effects of jumping on coagulation and endothelial activation but left the inhibitory effects on innate immune function intact. Taken together, these results indicate that bungee jumping leads to a catecholamine-independent immune suppressive phenotype and implicate noncanonical glucocorticoid receptor signal transduction as a major pathway linking human stress to impaired functioning of the human innate immune system.

Sickle cell disease (SCD) is associated with a high incidence of ischemic stroke. SCD is characterized by hemolytic anemia, resulting in reduced nitric oxide-bioavailability, and by impaired cerebrovascular hemodynamics. Cerebrovascular CO2 responsiveness is nitric oxide dependent and has been related to an increased stroke risk in microvascular diseases. We questioned whether cerebrovascular CO2 responsiveness is impaired in SCD and related to hemolytic anemia. Transcranial Doppler-determined mean cerebral blood flow velocity (V(mean)), near-infrared spectroscopy-determined cerebral oxygenation, and end-tidal CO2 tension were monitored during normocapnia and hypercapnia in 23 patients and 16 control subjects. Cerebrovascular CO2 responsiveness was quantified as Delta% V(mean) and Deltamicromol/L cerebral oxyhemoglobin, deoxyhemoglobin, and total hemoglobin per mm Hg change in end-tidal CO2 tension. Both ways of measurements revealed lower cerebrovascular CO2 responsiveness in SCD patients versus controls (V(mean), 3.7, 3.1-4.7 vs 5.9, 4.6-6.7 Delta% V(mean) per mm Hg, P < .001; oxyhemoglobin, 0.36, 0.14-0.82 vs 0.78, 0.61-1.22 Deltamicromol/L per mm Hg, P = .025; deoxyhemoglobin, 0.35, 0.14-0.67 vs 0.58, 0.41-0.86 Deltamicromol/L per mm Hg, P = .033; total-hemoglobin, 0.13, 0.02-0.18 vs 0.23, 0.13-0.38 Deltamicromol/L per mm Hg, P = .038). Cerebrovascular CO2 responsiveness was not related to markers of hemolytic anemia. In SCD patients, impaired cerebrovascular CO2 responsiveness reflects reduced cerebrovascular reserve capacity, which may play a role in pathophysiology of stroke.

In the upright position, cerebral blood flow is reduced, maybe because arterial carbon dioxide partial pressure (Pa(CO(2))) decreases. We evaluated the time-dependent influence of a reduction in Pa(CO(2)), as indicated by the end-tidal Pco(2) tension (Pet(CO(2))), on cerebral perfusion during head-up tilt. Mean arterial pressure, cardiac output, middle cerebral artery mean flow velocity (MCA V(mean)), and dynamic cerebral autoregulation at supine rest and 70 degrees head-up tilt were determined during free breathing and with Pet(CO(2)) clamped to the supine level. The postural changes in central hemodynamic variables were equivalent, and the cerebrovascular autoregulatory capacity was not significantly affected by tilt or by clamping Pet(CO(2)). In the first minute of tilt, the decline in MCA V(mean) (10 +/- 4 vs. 3 +/- 4 cm/s; mean +/- SE; P < 0.05) and Pet(CO(2)) (6.8 +/- 4.3 vs. 1.7 +/- 1.6 Torr; P < 0.05) was larger during spontaneous breathing than during isocapnic tilt. However, after 2 min in the head-up position, the reduction in MCA V(mean) was similar (7 +/- 5 vs. 6 +/- 3 cm/s), although the spontaneous decline in Pet(CO(2)) was maintained (P < 0.05 vs. isocapnic tilt). These results suggest that the potential contribution of Pa(CO(2)) to the postural reduction in MCA V(mean) is transient, leaving the mechanisms for the sustained restrain in MCA V(mean) to be identified.