How tyrannical leadership relates to workplace bullying and turnover intention over time: The role of coworker support.

INTRODUCTION: In light of the deleterious consequences associated with workplace bullying, it is important to identify the work-related factors that can contribute to the presence of bullying behaviors over time. Up to now, most research on the topic has investigated job characteristics (presence of job demands, absence of job resources) as contributing factors of workplace bullying. Given the key role leadership plays in shaping employees' work environment, this study aims to better understand how harmful forms of leadership relate to bullying behaviors over time and, subsequently, to employee functioning. METHODS: More specifically, this longitudinal study (two data collections over a 3-month period) conducted among a sample of Canadian employees (T1 n = 600, T2 n = 422) assesses the temporal relationship between tyrannical leadership, exposure to bullying behaviors, and turnover intention, as well as the moderating role of perceived coworker support in the relationship between tyrannical leadership and bullying behaviors. RESULTS: Results from cross-lagged analyses show that, controlling for baseline effects, T1 tyrannical leadership positively predicts T2 exposure to bullying behaviors and that T1 bullying behaviors positively predict T2 turnover intention. T1 coworker support did not significantly buffer the relationship between T1 tyrannical leadership and T2 exposure to bullying behaviors, although it did significantly predict, negatively so, T2 turnover intention. CONCLUSION: The present study provides valuable insight into the social contextual determinants of bullying behaviors and highlights the destructive nature of tyrannical leadership. Furthermore, this study illustrates the importance of fostering supportive behaviors between colleagues, as this important social resource can play a key role in reducing turnover intention over time.

Single-cell RNA sequencing reveals immunosuppressive myeloid cell diversity during malignant progression in a murine model of glioma.

Recent studies have shown the importance of the dynamic tumor microenvironment (TME) in high-grade gliomas (HGGs). In particular, myeloid cells are known to mediate immunosuppression in glioma; however, it is still unclear if myeloid cells play a role in low-grade glioma (LGG) malignant progression. Here, we investigate the cellular heterogeneity of the TME using single-cell RNA sequencing in a murine glioma model that recapitulates the malignant progression of LGG to HGG. LGGs show increased infiltrating CD4+ and CD8+ T cells and natural killer (NK) cells in the TME, whereas HGGs abrogate this infiltration. Our study identifies distinct macrophage clusters in the TME that show an immune-activated phenotype in LGG but then evolve to an immunosuppressive state in HGG. We identify CD74 and macrophage migration inhibition factor (MIF) as potential targets for these distinct macrophage populations. Targeting these intra-tumoral macrophages in the LGG stage may attenuate their immunosuppressive properties and impair malignant progression.

When does exposure to daily negative acts frustrate employees' psychological needs? A within-person approach.

Based on self-determination theory, this two-sample study investigates the effects of negative acts on psychological need frustration in greater depth using a within-person perspective. More specifically, through two distinct diary studies, we aim to contribute to the dearth of research on the daily effects of bullying by investigating the daily relationship between exposure to negative acts and need frustration as well as the moderating role of perceived emotional support at work in this relationship. Overall, results from both studies show that employees experience greater need frustration (perceptions of rejection, oppression, and incompetence) on days they are confronted with negative acts and that daily emotional support buffers the impact of direct negative acts (humiliation, physical intimidation) on frustration of the needs for competence and relatedness at the daily level. As such, the results of the present two-sample study provide a better understanding of the boundary conditions under which exposure to negative acts may result in psychological costs by identifying emotional support as a key resource in the workplace that can offset the immediate harmful effects of certain negative behaviors. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

When workload predicts exposure to bullying behaviours in nurses: The protective role of social support and job recognition.

AIMS: This study examined the moderating role of two resources (social support and recognition) in the longitudinal relationship between workload and bullying behaviours in nurses. DESIGN: A two-wave (12-month) longitudinal study was conducted. METHOD: French-Canadian nurses (n = 279) completed an online survey (October 2014 and October 2015) assessing their perceptions of job characteristics within the work environment (workload, social support, job recognition) as well as exposure to negative behaviours at work. RESULTS: Workload positively predicted exposure to bullying behaviours over time, but only when job recognition and social support were low. Workload was unrelated to bullying when social support was high and was negatively related to bullying when job recognition was high. CONCLUSION: This study aligns with the work environment hypothesis, showing that poorly designed and stressful job environments provide fertile ground for bullying behaviours. IMPACT: Bullying is a growing concern in the nursing profession that not only undermines nurses' well-being but also compromises patient safety and care. It is thus important to identify work-related factors that can contribute to the presence of bullying behaviours in nurses in the hopes of reducing their occurrence and repercussions. This study contributes to this endeavour and identifies two key social coping resources that can help manage the stress associated with workload, resulting in less perceived bullying behaviour among nurses.

Job resources and burnout: Work motivation as a moderator.

This longitudinal study (T1 n = 399; T2 n = 279) investigated the moderating role of work motivation in the relationship between job resources (control and recognition) and burnout. Overall, job recognition and control resulted in more burnout for employees with poor-quality work motivation (high controlled or low autonomous motivation). These results suggest that poor-quality motivation renders employees more vulnerable to certain resources in their work environment, as these job characteristics stimulate compensatory behaviours (e.g., overinvesting in one's job to boost one's sense of self-worth or to obtain others' approval), leading to energy depletion over time.

Contribution of High School Sport Participation to Young Adult Bone Strength.

INTRODUCTION: Nearly 8 million American adolescents participate in sports. Participation declines in young adulthood. PURPOSE: This study assessed longitudinal effects of high school sport participation and muscle power on young adult bone strength. METHODS: Two hundred twenty-eight young adults from the Iowa Bone Development Study completed an interscholastic sport participation questionnaire. Current physical activity (PA) behaviors were assessed via questionnaire. Dual x-ray absorptiometry assessed hip areal bone mineral density and was used with hip structure analysis to estimate femoral neck section modulus and hip cross-sectional area. Peripheral quantitative computed tomography provided strength-strain index and bone strength index at 38% and 4% midshaft tibial sites, respectively. Vertical jump estimated muscle power at 17 yr. Sex-specific multiple linear regression predicted young adult bone outcomes based on sport participation groups. Mediation analysis analyzed the effects of muscle power on relationships between sport participation and bone strength. RESULTS: At follow-up, males participating in any interscholastic sport had greater bone strength than males who did not participate in sport. The explained variability in bone outcomes was 2% to 16%. Females who participated in sports requiring muscle power had greater bone strength than females who did not participate in sports or females who participated in nonpower sports (explained variability was 4%-10%). Muscle power mediated 24.7% to 41% of the effect of sport participation on bone outcomes in males and 19.4% to 30% in females. CONCLUSIONS: Former male interscholastic sport participants and female interscholastic power sport participants have stronger bones than peers even when adjusting for current PA. Muscle power did not fully explain differences in all bone outcomes, suggesting that sport participation has additional bone health benefits.

A20 Haploinsufficiency Aggravates Transplant Arteriosclerosis in Mouse Vascular Allografts: Implications for Clinical Transplantation.

BACKGROUND: Inflammation is central to the pathogenesis of transplant arteriosclerosis (TA). We questioned whether physiologic levels of anti-inflammatory A20 influence TA severity. METHODS: We performed major histocompatibility complex mismatched aorta to carotid artery interposition grafts, using wild type (WT) or A20 heterozygote (HET) C57BL/6 (H-2) donors and BALB/c (H-2) recipients, and conversely BALB/c donors and WT/HET recipients. We analyzed aortic allografts by histology, immunohistochemistry, immunofluorescence, and gene profiling (quantitative real-time reverse-transcriptase polymerase chain reaction). We validated select in vivo A20 targets in human and mouse smooth muscle cell (SMC) cultures. RESULTS: We noted significantly greater intimal hyperplasia in HET versus WT allografts, indicating aggravated TA. Inadequate upregulation of A20 in HET allografts after transplantation was associated with excessive NF-кB activation, gauged by higher levels of IkBα, p65, VCAM-1, ICAM-1, CXCL10, CCL2, TNF, and IL-6 (mostly localized to SMC). Correspondingly, cytokine-induced upregulation of TNF and IL-6 in human and mouse SMC cultures inversely correlated with A20 expression. Aggravated TA in HET versus WT allografts correlated with increased intimal SMC proliferation, and a higher number of infiltrating IFNγ and Granzyme B CD4 T cells and natural killer cells, and lower number of FoxP3 regulatory T cells. A20 haploinsufficiency in allograft recipients did not influence TA. CONCLUSIONS: A20 haploinsufficiency in vascular allografts aggravates lesions of TA by exacerbating inflammation, SMC proliferation, and infiltration of pathogenic T cells. A20 single nucleotide polymorphisms associating with lower A20 expression or function in donors of vascularized allografts may inform risk and severity of TA, highlighting the clinical implications of our findings.

The C-terminal domain of A1/Bfl-1 regulates its anti-inflammatory function in human endothelial cells.

A1/Bfl-1 is a NF-κB dependent, anti-apoptotic Bcl-2 family member that contains four Bcl-2 homology domains (BH) and an amphipathic C-terminal domain, and is expressed in endothelial cells (EC). Based on NF-κB reporter assays in bovine aortic EC, we have previously demonstrated that A1, like Bcl-2 and Bcl-xL, inhibits NF-κB activation. These results, however, do not fully translate when evaluating the cell's own NF-κB machinery in human EC overexpressing A1 by means of recombinant adenovirus (rAd.) mediated gene transfer. Indeed, overexpression of full-length A1 in human umbilical vein EC (HUVEC), and human dermal microvascular EC (HDMEC) failed to inhibit NF-κB activation. However, overexpression of a mutant lacking the C-terminal domain of A1 (A1ΔC) demonstrated a potent NF-κB inhibitory effect in these cells. Disparate effects of A1 and A1ΔC on NF-κB inhibition in human EC correlated with mitochondrial (A1) versus non-mitochondrial (A1ΔC) localization. In contrast, both full-length A1 and A1ΔC protected EC from staurosporine (STS)-induced cell death, indicating that mitochondrial localization was not necessary for A1's cytoprotective function in human EC. In conclusion, our data uncover a regulatory role for the C-terminal domain of A1 in human EC: anchoring A1 to the mitochondrion, which conserves but is not necessary for its cytoprotective function, or by its absence freeing A1 from the mitochondrion and uncovering an additional anti-inflammatory effect.

A20 promotes liver regeneration by decreasing SOCS3 expression to enhance IL-6/STAT3 proliferative signals.

UNLABELLED: Liver regeneration is of major clinical importance in the setting of liver injury, resection, and transplantation. A20, a potent antiinflammatory and nuclear factor kappa B (NF-κB) inhibitory protein, has established pro-proliferative properties in hepatocytes, in part through decreasing expression of the cyclin dependent kinase inhibitor, p21. Both C-terminal (7-zinc fingers; 7Zn) and N-terminal (Nter) domains of A20 were required to decrease p21 and inhibit NF-κB. However, both independently increased hepatocyte proliferation, suggesting that additional mechanisms contributed to the pro-proliferative function of A20 in hepatocytes. We ascribed one of A20's pro-proliferative mechanisms to increased and sustained interleukin (IL)-6-induced signal transducer and activator of transcription 3 (STAT3) phosphorylation, as a result of decreased hepatocyte expression of the negative regulator of IL-6 signaling, suppressor of cytokine signaling 3 (SOCS3). This novel A20 function segregates with its 7Zn not Nter domain. Conversely, total and partial loss of A20 in hepatocytes increased SOCS3 expression, hampering IL-6-induced STAT3 phosphorylation. Following liver resection in mice pro-proliferative targets downstream of IL-6/STAT3 signaling were increased by A20 overexpression and decreased by A20 knockdown. In contrast, IL-6/STAT3 proinflammatory targets were increased in A20-deficient livers, and decreased or unchanged in A20 overexpressing livers. Upstream of SOCS3, levels of its microRNA regulator miR203 were significantly decreased in A20-deficient livers. CONCLUSION: A20 enhances IL-6/STAT3 pro-proliferative signals in hepatocytes by down-regulating SOCS3, likely through a miR203-dependent manner. This finding together with A20 reducing the levels of the potent cell cycle brake p21 establishes its pro-proliferative properties in hepatocytes and prompts the pursuit of A20-based therapies to promote liver regeneration and repair.

A20-mediated modulation of inflammatory and immune responses in aortic allografts and development of transplant arteriosclerosis.

BACKGROUND: Transplant arteriosclerosis (TA) is the pathognomonic feature of chronic rejection, the primary cause of allograft failure. We have shown that the NF-κB inhibitory protein A20 exerts vasculoprotective effects in endothelial and smooth muscle cells (SMC), and hence is a candidate to prevent TA. We sought direct proof for this hypothesis. METHODS: Fully mismatched, C57BL/6 (H2) into BALB/c (H2), aorta to carotid allografts were preperfused with saline, recombinant A20 adenovirus (rAd.A20) or rAd.ß-galactosidase (ß-gal), implanted, harvested 4 weeks after transplantation, and analyzed by histology, immunohistochemistry, and immunofluorescence staining. We measured indoleamine 2,3-dioxygenase, interleukin-6, and transforming growth factor-ß mRNA and protein levels in nontransduced, and rAd.A20 or rAd.ß-gal-transduced human SMC cultures after cytokine treatment. RESULTS: Vascular overexpression of A20 significantly reduced TA lesions. This correlated with decreased graft inflammation and increased apoptosis of neointimal SMC. Paradoxically, T-cell infiltrates increased in A20-expressing allografts, including the immunoprivileged media, which related to A20 preventing indoleamine 2,3-dioxygenase upregulation in SMC. However, infiltrating T cells were predominantly T-regulatory cells (CD25+/Forkhead Box P3 [FoxP3+]). This agrees with A20 inhibiting interleukin-6 and promoting transforming growth factor-ß production by medial SMC and in SMC cultures exposed to cytokines, which favors differentiation of regulatory over pathogenic T cells. CONCLUSIONS: In summary, A20 prevents immune-mediated remodeling of vascular allografts, therefore reduces TA lesions by affecting apoptotic and inflammatory signals and modifying the local cytokine milieu to promote an immunoregulatory response within the vessel wall. This highlights a novel function for A20 in local immunosurveillance, which added to its vasculoprotective effects, supports its therapeutic promise in TA.

Hepatocyte growth factor preferentially activates the anti-inflammatory arm of NF-κB signaling to induce A20 and protect renal proximal tubular epithelial cells from inflammation.

Inflammation induces the NF-κB dependent protein A20 in human renal proximal tubular epithelial cells (RPTEC), which secondarily contains inflammation by shutting down NF-κB activation. We surmised that inducing A20 without engaging the pro-inflammatory arm of NF-κB could improve outcomes in kidney disease. We showed that hepatocyte growth factor (HGF) increases A20 mRNA and protein levels in RPTEC without causing inflammation. Upregulation of A20 by HGF was NF-κB/RelA dependent as it was abolished by overexpressing IκBα or silencing p65/RelA. Unlike TNFα, HGF caused minimal IκBα and p65/RelA phosphorylation, with moderate IκBα degradation. Upstream, HGF led to robust and sustained AKT activation, which was required for p65 phosphorylation and A20 upregulation. While HGF treatment of RPTEC significantly increased A20 mRNA, it failed to induce NF-κB dependent, pro-inflammatory MCP-1, VCAM-1, and ICAM-1 mRNA. This indicates that HGF preferentially upregulates protective (A20) over pro-inflammatory NF-κB dependent genes. Upregulation of A20 supported the anti-inflammatory effects of HGF in RPTEC. HGF pretreatment significantly attenuated TNFα-mediated increase of ICAM-1, a finding partially reversed by silencing A20. In conclusion, this is the first demonstration that HGF activates an AKT-p65/RelA pathway to preferentially induce A20 but not inflammatory molecules. This could be highly desirable in acute and chronic renal injury where A20-based anti-inflammatory therapies are beneficial.

O-glycosylation regulates ubiquitination and degradation of the anti-inflammatory protein A20 to accelerate atherosclerosis in diabetic ApoE-null mice.

BACKGROUND: Accelerated atherosclerosis is the leading cause of morbidity and mortality in diabetic patients. Hyperglycemia is a recognized independent risk factor for heightened atherogenesis in diabetes mellitus (DM). However, our understanding of the mechanisms underlying glucose damage to the vasculature remains incomplete. METHODOLOGY/PRINCIPAL FINDINGS: High glucose and hyperglycemia reduced upregulation of the NF-κB inhibitory and atheroprotective protein A20 in human coronary endothelial (EC) and smooth muscle cell (SMC) cultures challenged with Tumor Necrosis Factor alpha (TNF), aortae of diabetic mice following Lipopolysaccharide (LPS) injection used as an inflammatory insult and in failed vein-grafts of diabetic patients. Decreased vascular expression of A20 did not relate to defective transcription, as A20 mRNA levels were similar or even higher in EC/SMC cultured in high glucose, in vessels of diabetic C57BL/6 and FBV/N mice, and in failed vein grafts of diabetic patients, when compared to controls. Rather, decreased A20 expression correlated with post-translational O-Glucosamine-N-Acetylation (O-GlcNAcylation) and ubiquitination of A20, targeting it for proteasomal degradation. Restoring A20 levels by inhibiting O-GlcNAcylation, blocking proteasome activity, or overexpressing A20, blocked upregulation of the receptor for advanced glycation end-products (RAGE) and phosphorylation of PKCßII, two prime atherogenic signals triggered by high glucose in EC/SMC. A20 gene transfer to the aortic arch of diabetic ApoE null mice that develop accelerated atherosclerosis, attenuated vascular expression of RAGE and phospho-PKCßII, significantly reducing atherosclerosis. CONCLUSIONS: High glucose/hyperglycemia regulate vascular A20 expression via O-GlcNAcylation-dependent ubiquitination and proteasomal degradation. This could be key to the pathogenesis of accelerated atherosclerosis in diabetes.

Volumetric effects of motor cortex injury on recovery of dexterous movements.

Due to the heterogeneous nature of most brain injuries, the contributions of gray and white matter involvement to motor deficits and recovery potential remain obscure. We tested the hypothesis that duration of hand motor impairment and recovery of skilled arm and hand motor function depends on the volume of gray and white matter damage of the frontal lobe. Lesions of the primary motor cortex (M1), M1 + lateral premotor cortex (LPMC), M1 + LPMC + supplementary motor cortex (M2) or multifocal lesions affecting motor areas and medial prefrontal cortex were evaluated in rhesus monkeys. Fine hand motor function was quantitatively assessed pre-lesion and for 3-12 months post-lesion using two motor tests. White and gray matter lesion volumes were determined using histological and quantitative methods. Regression analyses showed that duration of fine hand motor impairment was strongly correlated (R(2)>0.8) with the volume of gray and white matter lesions, with white matter lesion volume being the primary predictor of impairment duration. Level of recovery of fine hand motor skill was also well correlated (R(2)>0.5) with gray and white matter lesion volume. In some monkeys post-lesion skill exceeded pre-lesion skill in one or both motor tasks demonstrating that continued post-injury task practice can improve motor performance after localized loss of frontal motor cortex. These findings will assist in interpreting acute motor deficits, predicting the time course and expected level of functional recovery, and designing therapeutic strategies in patients with localized frontal lobe injury or neurosurgical resection.

Perception of hand motion direction uses a gravitational reference.

We studied possible frames of reference for kinesthetic perception of imposed hand motion direction in the frontal plane in ten young adult subjects with no history of neuromuscular disease. In one experiment, subjects were instructed to set unseen hand motion imposed by a motorized linear slide device parallel to the trunk-fixed longitudinal axis, seven visually specified axes and vertical (gravitational axis) while in a standard erect head/trunk posture and with head/trunk orientation varied. The visually specified axes were presented on a head-mounted display that also blocked vision of the external environment. In a second experiment using the same device, subjects set unseen hand motion parallel to vertical and to subjective oblique directions of 45 degrees clockwise (cw) and counter clockwise (ccw) from vertical in erect and varied head/trunk postures. Errors for setting hand motion to vertical and to verbally specified oblique axes (45 degrees cw and ccw from vertical) were lower than to the trunk longitudinal axis and visually specified axes. There were clear oblique effects in setting hand motion to visually specified axes and to subjective oblique (45 degrees cw and ccw) axes. When head and trunk orientation were varied, variable errors were higher for all axes, but remained lowest for vertical and subjective oblique axes. Moreover, errors for setting hand motion to all axes depended on head/trunk orientation. Overall, these results show that kinesthetic perception of imposed hand motion uses a subjective gravitational frame of reference that varies somewhat with head/trunk orientation.

Location memory biases reveal the challenges of coordinating visual and kinesthetic reference frames.

Five experiments explored the influence of visual and kinesthetic/proprioceptive reference frames on location memory. Experiments 1 and 2 compared visual and kinesthetic reference frames in a memory task using visually-specified locations and a visually-guided response. When the environment was visible, results replicated previous findings of biases away from the midline symmetry axis of the task space, with stability for targets aligned with this axis. When the environment was not visible, results showed some evidence of bias away from a kinesthetically-specified midline (trunk anterior-posterior [a-p] axis), but there was little evidence of stability when targets were aligned with body midline. This lack of stability may reflect the challenges of coordinating visual and kinesthetic information in the absence of an environmental reference frame. Thus, Experiments 3-5 examined kinesthetic guidance of hand movement to kinesthetically-defined targets. Performance in these experiments was generally accurate with no evidence of consistent biases away from the trunk a-p axis. We discuss these results in the context of the challenges of coordinating reference frames within versus between multiple sensori-motor systems.

Failure to disrupt the 'sensorimotor' memory for lifting objects with a precision grip.

When repetitively lifting an object with mechanical properties that vary from lift-to-lift, the fingertip forces for gripping and lifting are influenced strongly by the previous lift, revealing a 'sensorimotor' memory. Two recent reports indicate that the sensorimotor memory for grip force is easily disrupted by an unrelated task like a strong pinch or vibration, even when the lift was performed with the hand contralateral to the vibration or preceding pinch. These findings indicate that this memory may reflect sensory input or muscle contraction levels, rather than object properties or the specific task of gripping and lifting. Here we report that the predictive scaling of lift force was not disrupted by conditioning tasks that featured exerting a vertical isometric force with the upper extremity. When subjects lifted a 2 N object repetitively the peak lift force rate was 26.4 N/s. The lift force rate increased to 36.1 N/s when the 2 N object was lifted (regardless of hand) after lifting the 8 N object with the right hand, which reveals the expected 'sensorimotor' memory. The lift force rate did not increase (24.8 vs. 26.4 N/s for the control condition) when a bout of isometric exertion (9.8 N) in the vertical direction with the distal right forearm preceded lifts of the 2 N object. This finding was confirmed with another isometric task designed to more closely mimic lifting an object with a precision grip. This difference in the sensitivity of grip versus lift force to a preceding isometric contraction indicates that separate sensorimotor memories contribute to the predictive scaling of the commands for gripping and lifting an object.

Measurement of coordination of object manipulation in non-human primates.

We present a modification of the automated movement assessment panel [Gash DM, Zhang Z, Umberger G, Mahood K, Smith M, Smith C, et al. An automated movement assessment panel for upper limb motor functions in rhesus monkeys and humans. J Neurosci Methods 1999;89:111-7] that incorporates a three-dimensional load cell to record forces applied by monkeys while manipulating food targets. The absolute force-time integral (total absolute impulse) is used to characterize the total of the applied forces over time as the food (carrot chip with a hole punched through the center) is manipulated and lifted from a flat surface (easiest task) and threaded over a straight rod (medium difficulty) or curved rod (highest difficulty). The total impulse can be measured even on unsuccessful attempts to acquire the food. Thus, it can be used to evaluate changes in performance even before successful acquisition occurs as in learning or recovery following a nervous system insult. We show from tests in three rhesus monkeys that the total absolute impulse measure is sensitive to task complexity, learning and lesion of frontal lobe motor areas (in one case) and that there is good reliability in day-to-day performance (even with long periods between performances) after the monkey has learned the task. Importantly, the task requires minimal training as the monkeys can be successful on even the most difficult of these tasks with one or two training sessions, yet performance improvements continue to occur over several testing sessions. Furthermore, the three levels of task difficulty permit analysis of a progression of ability.

Sensorimotor memory for fingertip forces: evidence for a task-independent motor memory.

When repetitively lifting an object with randomly varying mechanical properties, the fingertip forces reflect the previous lift. We examined the specificity of this "sensorimotor memory" by observing the effects of an isolated pinch on the subsequent lift of a known object. In this case, the pinch force was unrelated to the fingertip forces necessary to grip the object efficiently. The peak grip force used to lift the test object (4 N weight) depended on the preceding task. Compared with repetitively lifting the 4 N test object, the peak grip force was 2 N greater when a lift of the same object was preceded by a lift in which a hidden mass was attached to the object to increase the weight to 8 N. This 2 N increase in grip force also occurred when subjects lifted the 4 N test object after pinching a force transducer with a force of 8 N. Thus, similar grip forces were stored in sensorimotor memory for both tasks, and reflected subjects' use of 7.9 +/- 1.1 N to lift the 8 N object. Similar effects occurred when the preceding pinch or lift was performed with the opposite hand. The peak lift force was unaffected by the isolated pinch, suggesting that a generalized increase in fingertip and limb forces did not occur. We conclude that the sensorimotor memory is not specific for lifting an object. It is doubtful that this particular memory stores the physical properties of objects or reflects a forward internal model for predictively controlling fingertip forces.