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R M Gallucci

Publications and source records attributed to R M Gallucci.

12 recordsLinked to original sources
PubMed1999

Functional asymmetries in the quality of handwriting movements: a kinematic analysis.

Writing hand preference is a prominent functional asymmetry, but biomechanical factors may also contribute to any kinematic differences in the quality of handwriting movements performed by either hand. Eighteen dextral participants used a noninking pen with their right or left hand to write cursive letter ls, inverted ls, and their mirror images (to control for biomechanical differences) on a graphics tablet. Kinematic analysis of the scaling, consistency, efficiency, and shape of writing stroke trajectories revealed functional asymmetries between hands. The right hand was faster and produced more efficient strokes, which were of more consistent length, duration, and peak velocity. Differences between hands do not simply reflect biomechanical factors; therefore, the documentation of any functional asymmetries may allow their subsequent use as markers of underlying pathology in conditions such as schizophrenia.

Adolescent↗
PubMed1998

Response (re-)programming in aging: a kinematic analysis.

BACKGROUND: Age-related motor slowing may reflect either motor programming deficits, poorer movement execution, or mere strategic preferences for online guidance of movement. We controlled such preferences, limiting the extent to which movements could be programmed. METHODS: Twenty-four young and 24 older adults performed a line drawing task that allowed movements to be prepared in advance in one case (i.e., cue initially available indicating target location) and not in another (i.e., no cue initially available as to target location). Participants connected large or small targets illuminated by light-emitting diodes upon a graphics tablet that sampled pen tip position at 200 Hz. RESULTS: Older adults had a disproportionate difficulty initiating movement when prevented from programming in advance. Older adults produced slower, less efficient movements, particularly when prevented from programming under greater precision requirements. CONCLUSIONS: The slower movements of older adults do not simply reflect a preference for online control, as older adults have less efficient movements when forced to reprogram their movements. Age-related motor slowing kinematically resembles that seen in patients with cerebellar dysfunction.

Adult↗
PubMed1997

Antibodies to tumor necrosis factor alfa attenuate hepatic necrosis and inflammation caused by chronic exposure to ethanol in the rat.

Tumor necrosis factor (TNF)alpha, a pivotal cytokine involved in inflammation, is produced primarily by Kupffer cells in the liver. It has been shown that inactivation of Kupffer cells prevents alcohol-induced liver injury; therefore, the purpose of this study was to determine if neutralizing anti-TNF-alpha antibody is also effective. Male Wistar rats were exposed to ethanol (11 to 12 g x kg(-1) x d[-1]) continuously for up to 4 weeks via intragastric feeding using an enteral feeding model. Before ethanol exposure, polyclonal anti-mouse TNF-alpha rabbit serum was injected (2.0 mg/kg intravenously). There were no significant differences in body weight, mean ethanol concentration, or cyclic patterns of ethanol in urine when ethanol- and ethanol plus antibody-treated groups were compared. Expression of TNF-alpha and macrophage inflammatory protein 2 (MIP-2) messenger RNA (mRNA), determined using reverse transcription-polymerase chain reaction, was three- to four-fold higher in livers of ethanol-treated rats than in those of rats fed an ethanol-free, high-fat control diet. In addition, MIP-2 levels were also elevated when detected by Northern blot analysis. Anti-TNF-alpha antibody did not affect expression of mRNA for interleukin (IL) 1alpha, IL-6, transforming growth factor beta1, or TNF-alpha. However, MIP-2 mRNA expression, which is regulated by TNF-alpha, was decreased significantly by anti-TNF-alpha antibody treatment. Serum aspartate transaminase levels were elevated in ethanol-treated rats to 136 +/- 12 IU/L after 4 weeks but only reached 90 +/- 5 IU/L (P < .05) in rats treated with anti-TNF-alpha antibody. The hepatic inflammation and necrosis observed in ethanol-fed rats were attenuated significantly by antibody treatment, and steatosis was not. These results support the hypothesis that TNF-alpha plays an important role in inflammation and necrosis in alcohol-induced liver injury and that treatment with anti-TNF-alpha antibody may be therapeutically useful in this disease.

Animals↗
PubMed1997

Modulation of NK cell cytolytic activity by macrophages in chronically exercise-stressed mice.

This study was designed to investigate the effects of moderate-intensity endurance training on basal natural killer (NK) cell cytolytic activity in murine splenocytes that were enriched for 1) NK1.1+ cells or 2) macrophages and NK1.1+ cells. Mice were assigned to sedentary (Sed), treadmill control (TM), or treadmill-trained (Trn) groups. Splenocyte number, the percentages of NK1.1+, large granular lymphocytes (NK1.1+, LGL-1+), and other subpopulations did not change in Trn mice. Approximately 70% of cells enriched for NK1.1+ expressed this surface antigen. Lytic units (LU) expressed per LGL-1+ cell were significantly lower in Trn [83.9 +/- 3.2 (SE)] compared with Sed (109.5 +/- 7.5) and TM (101.3 +/- 6.4) groups. When macrophages remained in the in vitro assay, LU per LGL-1(+) cell did not differ across groups. The results indicate that highly enriched NK1.1+ cells from Trn mice had lower NK cell activity compared with Sed mice. No differences in NK cell activity were observed when cells were enriched for NK1.1+ cells and macrophages. These findings support the hypothesis that macrophage modulation of NK cells may be one mechanism contributing to augmented basal NK cell activity in endurance-trained individuals.

Animals↗
PubMed1996

Ethanol consumption suppresses the IL2-induced proliferation of NK cells.

Ethanol (20% w/v) given to female, C57BL/6 mice in their drinking water suppresses natural killer (NK) and lymphokine activated killer cell cytolytic activity in mixed splenocytes and in splenocytes highly enriched for NK cells. The present study examined the effects of ethanol consumption on rIL2-induced proliferation of enriched NK cells. Mice were given 20% w/v ethanol in the drinking water for 2 weeks. Splenic NK cells were harvested and enriched up to 88% based on surface expression of NK1.1. The enriched NK cells were cultured in the presence of 1000 IU/ml (20 pg/ml) murine recombinant interleukin 2 (rIL2). There were fewer cells (p < 0.02) from ethanol-consuming mice compared to cells from water-drinking control mice after incubation with IL2 at 2, 4, and 6 days of culture. Ethanol consumption was associated with significantly lower [3H]thymidine uptake (p < 0.05). Ethanol consumption did not affect apoptosis or intracellular levels of interferon-gamma, tumor necrosis factor-alpha, or granulocyte macrophage colony-stimulating factor in NK cells. Ethanol consumption did not affect the expression of c-myc mRNA in NK cells that were cultured for 10 min or 4, 8, and 18 hr in rIL2. Suppression of IL2-induced NK cell proliferation is associated with ethanol consumption, and suppression is not due to altered IL2 receptor expression, increased apoptosis, intracellular cytokine levels, or c-myc expression.

Animals↗
PubMed1995

Ethanol consumption reduces the cytolytic activity of lymphokine-activated killer cells.

Ethanol (20% w/v) given to female C57BL/6 mice in their drinking water reduces splenic natural killer (NK) cell cytolytic activity after 2, 4, and 10 weeks of consumption. This reduction is transient because the levels of NK cell cytotoxicity from ethanol-consuming mice are nearly equal to those of water-drinking mice after splenocytes were incubated in 1000 IU/ml of recombinant interleukin-2 (rIL2) for 16-18 hr. In this study, mice were given 20% w/v ethanol in the drinking water for 2 weeks. Splenic NK cells were enriched up to 88% by negative selection based on surface expression of NK1.1. Enriched NK cells were expanded in rIL2 for 6 days. Lymphokine-activated killer (LAK) cells from both ethanol-consuming and water-drinking mice were > 95% NK1.1+. LAK cell cytolytic activity was significantly lower against NK-insensitive P815 mastocytoma [6.67 +/- 2.18 vs. 17.21 +/- 1.8 lytic units (LUs), p < 0.01], moderately NK-sensitive B16 melanoma (25.3 +/- 6.6 vs. 66.2 +/- 14.2 LU, p < 0.05), and NK-sensitive YAC-1 lymphoma targets (80.5 +/- 34.7 vs. 177.0 +/- 43.6 LU, p < 0.005) in cells from ethanol-consuming mice compared with water-drinking controls. Ethanol consumption did not affect the morphology or phenotype of LAK cells with respect to surface expression of NK1.1, B220, CD3, CD25, CD11a, CD54, CD45RB, or class I major histocompatibility complex.

Alcohol Drinking↗
PubMed1994

Effects of ethanol consumption on enriched natural killer cells from C57BL/6 mice.

Ethanol (20% w/v) given to female, C57BL/6 mice in their drinking water was previously shown to suppress natural killer (NK) cell cytolytic activity in a mixed splenocyte population. The present study was designed to examine the hypothesis that ethanol consumption independently results in inhibition of NK cell cytolytic activity. Mice were given 20% w/v ethanol in the drinking water for 2 weeks, and splenic NK cells were enriched up to 88% based on surface expression of NK1.1. Cytolytic activity of these freshly enriched NK cells from ethanol-consuming mice against YAC-1 lymphoma cells was inhibited an average of 41% relative to water-drinking controls. Cytolytic activity of enriched NK cells from ethanol-consuming mice was stimulated to levels equal to control water-drinking mice after 16- to 18-hr incubation in 1000 units/ml recombinant interleukin 2. These data indicate that in vitro cytolytic activity of NK cells from ethanol-consuming mice is inhibited in the absence of other modulatory leukocytes.

Alcoholism↗
PubMed1994

Mechanistic differences in NK cell cytolytic activity in treadmill-trained and chronic ethanol-consuming mice.

The present study was undertaken to investigate mechanisms contributing to differences in natural killer (NK) cell activity in moderately endurance-trained and ethanol-consuming mice. Independent of ethanol exposure, NK cell activity in nylon wool-nonadherent (NWNA) splenocytes is lower in trained than in sedentary control mice (Blank et al. J. Appl. Physiol. 72: 8-14, 1992). Reduced activity may result from a generalized loss of cytolytically active cells, redistribution of NK cells from the spleen to other body compartments, or disruption of paracrine regulation of NK cells after removal of nylon wool-adherent cells. To examine these possibilities, NK cell cytolytic activity was determined in nonenriched splenocytes from treadmill-trained and ethanol-consuming mice. Lymphocyte subpopulations in nonenriched splenocytes and NWNA splenocytes were also compared. Peripheral blood lymphocyte subpopulations were determined to examine combined effects of training and ethanol intake on regional distribution of lymphocytes in blood and spleen. NK cell activity in nonenriched splenocytes from trained water-drinking mice was not reduced compared with that in sedentary mice; rather, cytolytic activity was moderately enhanced (17% increase in lytic units, P < 0.05). Training did not change percentages of T-cells, B-cells, and NK [NK1.1+ and large granular lymphocytes (LGL-1+)] cells or the LGL/NK ratio in the spleen and blood. NK cell cytolytic activity was significantly reduced in nonenriched splenocytes from ethanol-consuming mice, independent of training. These findings support the hypothesis that moderate-intensity endurance training influences splenic NK cell function by modulating paracrine regulation of NK cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗
PubMed1994

Factors involved in modulation of NK cell activity by ethanol consumption.

Natural killer (NK) cells are large granular lymphocytes (LGL) whose functional characteristics play an important immunological role in tumor surveillance, bacterial and viral infections, baematopoiesis, and tissue transplantation. NK cell cytotoxicity is mediated through non-MHC-restricted lysis and by antibody-dependent cellular lysis against NK-sensitive and insensitive targets. Non-MHC restricted lysis of targets can occur when NK cells are in a non-activated state (inherent NK cell cytolytic activity) and following activation by interleukin 2 (IL-2).

Alcohol Drinking↗
PubMed1993

Alcohol consumption suppresses metastasis of B16-BL6 melanoma in mice.

Female C57BL/6 mice were fed a defined, pelleted diet and given 10% w/v or 20% w/v ethanol in their drinking water. Natural killer (NK) cell cytolytic activity was compared between water-drinking and ethanol-consuming mice and in mice that were also treated with polyinosinic-polycytidylic acid (poly I:C) to augment NK cell activity or with anti-NK1.1 antibody to decrease activity. NK cell cytolytic activity was not altered in mice given 10% ethanol, but was decreased in mice given 20% ethanol compared to water-drinking mice. Poly I:C treatment increased and anti-NK1.1 antibody treatment decreased NK cell activity in both water-drinking and 20% ethanol-consuming mice. Experimental and spontaneous metastases of B16-BL6 melanoma were evaluated as a function of the duration of ethanol consumption before tumor inoculation and as a function of altered NK cell activity. Experimental metastasis was inhibited after 4 and also after 6.5 weeks of ethanol exposure. Poly I:C treatment inhibited tumor lung colonization irrespective of ethanol consumption. Anti-NK1.1 antibody treatment increased metastasis, although to a lesser degree in mice consuming 10% ethanol. Spontaneous metastasis was inhibited in mice consuming 10% ethanol for 4 weeks, and in mice consuming 20% ethanol for 1 and 4 weeks before melanoma inoculation.

Alcohol Drinking↗
PubMed1993

Ethanol-induced changes in peripheral blood and splenic natural killer cells.

Previous work demonstrated that splenic natural killer (NK) cell cytolytic activity was suppressed in ethanol-consuming mice within 1 week and for as long as 10 weeks concurrent with ethanol intake. However, it is unknown if suppression of NK cell activity with ethanol consumption results from regional losses in NK cells. The present experiments were designed to examine the effects of ethanol on the percentage and total number of NK cells in the spleen and blood. Data indicate that, after 4 weeks of ethanol intake, NK cell activity of peripheral blood lymphocytes was also suppressed (50% of controls). With short-term (2-week) exposure, the percentage of NK cells in the blood and the spleen remained relatively constant. In the spleen, changes in the number of NK cells reflected generalized fluctuations in lymphocyte numbers rather than variation in the percentage of NK cells. NK cells were most sensitive to the effects of ethanol during long-term (8-week) ethanol intake, as demonstrated by significant reductions in the total percentage of NK1.1+ cells in the blood, and the LGL-1+ subset in the blood and spleen. These results provide insight into the mechanism of NK modulation by ethanol. Because NK cells were not selectively depleted after 2-4 weeks of ethanol intake, loss of cytolytically active NK cells cannot explain the suppression of in vitro cytolytic activity of cells from ethanol-consuming mice. However, with prolonged ethanol intake (8 weeks), the depletion of NK cells, specifically the LGL-1+ subset, may contribute to the overall suppression of NK cell cytolytic function.

Alcoholism↗