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This prospective study examined the effects of prismatic adaptation on visual exploration strategies in patients with left unilateral spatial neglect (USN). Photo-oculographic gaze recordings were obtained, as the subjects (28 brain-damaged; 15 control) performed a free visual exploration task before and after a session of prismatic adaptation. (i) Before prismatic adaptation, the pattern of visual exploration described two subgroups of patients (symmetrical exploration of hemispaces – similar to the control subjects, deficient exploration of left hemispace). Twelve of 20 patients failed to describe significant elements in the left part of the displayed image. Several visuoverbal patterns were observed, some dissociating visual exploration and verbal description. (ii) Immediately after prismatic adaptation, patients with asymmetrical visual exploration presented a significant increase in the number of point fixations and saccades in the left hemispace. Patients with symmetrical exploration presented the opposite pattern. Improved pattern of visual exploration contrasted with an absence of improved verbal description. Eye movements and visuoverbal descriptions exhibit heterogeneous and dissociated patterns before and after prismatic adaptation. This results demonstrate that prismatic adaptation has no effect in certain patients, suggesting that therapeutic indications and evaluation of prismatic test results should take into consideration the heterogeneous nature of USN. [ABSTRACT FROM AUTHOR]

Human urotensin-II (hU-II) is a cyclic peptide recently cloned in humans and present in human cardiac tissue and human arteries. The effects of hU-II were studied on human coronary bypass grafts in vitro. In three out of eight human mammary arteries, and two out of three human radial arteries, hU-II caused contraction; human saphenous veins did not respond to hU-II. When it exists, the contraction slowly develops and has a low-to-moderate intensity. All radial arteries obtained from young healthy non-human primates contracted strongly to hU-II. [ABSTRACT FROM AUTHOR]

Objective: Sustained return to work after surgery for work-related rotator cuff syndrome (WRRCS) remains quite difficult. The main purpose of the present study was to identify predictive factors of a return-to-work (RTW) trajectory., Methods: A total of 96 workers with WRRCS were identified by 4 surgeons. They were followed prospectively before and after the surgery, until 1 year after RTW, or for 20 months after surgery when they did not. Participants completed a series of standardized questionnaires related to working conditions, health, and beliefs, and performed functional tests at the inclusion time. During the follow-up period, they were regularly asked about their working conditions (present or not at work), activity (normal or lightened physical duties) and schedules (full- or part-time job). Statistical analysis was based on single- and multiple-factor models of prediction of the workers' trajectory., Results: Three trajectories of RTW were distinguished, considering RTW and absenteeism that occurred during the follow-up: stable, unstable, and non-RTW. The median age of the sample was 49.5 [45.0-54.0], with 67.7% of workers employed in highly physically demanding jobs. In the multiple factor model, three factors were highly predictive of the trajectory: perceived health before surgery, having had a repaired ruptured-rotator-cuff tendinopathy, and the level of physical demand of the job., Conclusion: Three easy-to-collect predictive factors of RTW trajectory have been identified. They may be useful for healthcare professionals and care givers to identify vulnerable workers' risk of occupational dropout after arthroscopic surgery for rotator cuff tendinopathy., (© 2023 Wiley Periodicals LLC.)

Background: Return to work (RTW) after surgery for a work-related rotator cuff disorder (WRRCD) is often difficult. The study's purpose was to identify preoperative factors predicting RTW., Methods: Ninety-two workers with a WRRCD were identified by four surgeons. Before surgery, the workers completed a series of standardized questionnaires related to working conditions, health, and health beliefs. They were followed up prospectively for 20 months. Statistical analysis was based on single and multiple-factor Cox models of the duration of absence from the time of surgery until RTW., Results: The median age at inclusion was 49 years (27-62), with 52 women included (57%). Sixty-one subjects (66%) were employed in highly physically demanding jobs. Forty-two (46%) stayed at work until their surgery, whereas preoperative sick leave exceeded 100 days in 20 subjects (21%). Twenty months after surgery, 14 were still not back at work. For the other participants, the mean duration until RTW was 225 days (SD 156). In the fully adjusted model, variables that were significantly predictive of the duration until RTW were: work physical demand levels, preoperative sick leave, the number of body parts causing pain or discomfort in the last 12 months, self-assessed 2-year workability, and the Readiness for RTW (RRTW) Scale., Conclusions: Several physical, psychological, and work-related factors, easily recorded, can be identified preoperatively. They may be predictive of delayed return, loss of employment, or employability as a result of shoulder surgery., (© 2021 Wiley Periodicals LLC.)

Monocytes can be induced to express both tissue factor (TF) and its inhibitor, TF pathway inhibitor-1 (TFPI-1). A short incubation (<6 h) with interleukin (IL)-4 and IL-10, two potent deactivators of monocyte functions, has been shown to modulate the synthesis and expression of TF by monocytes activated by lipopolysaccharide, but the consequences of longer incubations (up to 96 h) on both TF and TFPI-1 are unknown. The results of this study showed that adherent monocytes in culture spontaneously expressed TF and TFPI and that prolonged incubation with IL-10 induced a time- and dose-dependent decrease of monocyte TF synthesis, and an accumulation of TF/TFPI-1 complexes at the moncyte surface, suggesting a decreased clearance of these complexes. In contrast, IL-4 induced a time- and dose-dependent increase in TF synthesis, which remained intracytoplasmic, as shown by confocal microscopy. Surprisingly, TF:antigen (Ag) was decreased at the monocyte surface, but the procoagulant activity (PCA) of IL-4-treated monocytes was increased, as a result of more pronounced decrease of TFPI-1:Ag expression than that of TF. In conclusion, prolonged incubation with IL-4 and IL-10 oppositely modified PCA of cultured monocytes, and altered TF and TFPI trafficking and clearance. These data explain the respective deleterious or benefit effects of IL-4 or IL-10 in atherothrombosis.

Interleukin-12 (IL-12) or natural killer cell stimulatory factor (NKSF), has multiple effects on T lymphocytes and natural killer cells. In this study, the effect of IL-12 on human hematopoiesis was studied by analyzing the growth of CD34+ peripheral blood stem cells (PBSC), in steady state. In the presence of Epo, IL-12 alone or in combination with IL-3 or SCF had no effect on the formation of colonies from CD34+ cells. In culture with Epo, G-CSF, and IL-3, the effect of Flt3-ligand (FL) on CD34+ PBSC was investigated in the presence or absence of IL-12. No additional effect of IL-12 was observed when combined with FL. We evaluated 5-FU-treated human CD34+ PBSC proliferation in cultures with Epo, G-CSF, and IL-3, in the presence or absence of IL-12. No cytokine combination enhanced colony formation from 5-FU-treated CD34+ cells. However, in cultures of 5-FU-treated human CD34+ cells, the most efficient combination was IL-3 + Epo + G-CSF + Accessory cells (CD34-). Furthermore, IL-12 enhanced this colony formation significantly. To investigate whether immature CD34+ cells were responsible for FL or SCF, 5-FU-treated human CD34+ cells were cultured with or without IL-12. Whereas no synergistic effect was observed in combination with IL-12, SCF alone significantly enhanced colony formation. However, the colony number was found to be smaller than with the potent combination of accessory cells in the presence of IL-12. These results indicate that accessory cells, lost in CD34+ cell purification, could be partly responsible for an IL-12 effect on immature human PBSC proliferation.

Urokinase (uPA) and its receptor (uPAR) have been proposed to be involved in monocyte migration by inducing degradation of matrix proteins. In addition, uPAR is also implicated in cell adhesion to the vascular wall. The adhesive function of uPAR depends on a direct interaction with vitronectin which is increased by uPA and by modification of cell surface integrin (such as CD11b-CD18) when associated to uPAR. In this study we analysed the role of three deactivating cytokines, IL-4, IL-10 and IL-13, on the surface expression of uPA, uPAR and CD11b by monocytes and their consequences on monocyte adhesion to immobilized fibrinogen and vitronectin. IL-10 induced a decrease in uPA and CD11b after 18 h incubation and a delayed decrease in uPAR which was only significant after 48 h incubation. These results may explain the decrease in monocyte adhesion, which was observed after an 18 h incubation with IL-10, on immobilized vitronectin and fibrinogen. In contrast, IL-4 and IL-13 induced a decrease in uPAR after 18 h and a significant increase in uPA both in the cell lysates and at the cell surface, as well as an increase in cell surface associated CD11b. These cytokines did not modify cell adhesiveness to vitronectin or fibrinogen despite the increase in CD11b-CD18. This could be due to the decrease in uPAR because CD11b-CD18/uPAR forms a cell adhesion complex. In addition, the increase in uPA induced by IL-4 could counterbalance the direct interaction of uPAR with vitronectin. The increase in uPA suggests that IL-4 and IL-13 could induce plaque fissuring by monocytes, whereas IL-10 may induce protection against matrix protein degradation by decreasing uPA.