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K B Quattrocchi

Publications and source records attributed to K B Quattrocchi.

15 recordsLinked to original sources
PubMed2000

Effect of leukocyte-endothelial adhesion antagonism on neutrophil migration and neurologic outcome after cortical trauma.

BACKGROUND: Administration of anti-CD11B, a monoclonal antibody directed against the leukocyte adhesion molecule CD11B, results in decreased neutrophil infiltration into injured tissue after experimental ischemia. We determined the effect of anti-CD11B administration on neutrophil migration and neurologic functioning after experimental cortical trauma. METHODS: Injuries were produced by a pneumatic impactor. Treatment animals received anti-CD11B after injury. Neurologic functioning was quantitated at 1, 12, and 24 hours after injury. Neutrophil migration was assessed with the myeloperoxidase assay. RESULTS: Neutrophil influx was increased in injured cortex after trauma. Anti-CD11B significantly reduced neutrophil influx. There was no significant improvement in neurologic functioning after MAb administration. CONCLUSIONS: These results show there is marked neutrophil response to injury as produced with the pneumatic contusion model. This migration may be significantly attenuated by administration of a anti-CD11B.

Analysis of Variance↗
PubMed1999

Pilot study of local autologous tumor infiltrating lymphocytes for the treatment of recurrent malignant gliomas.

A prospective pilot study was performed in order to assess the safety of treating recurrent malignant gliomas (MGs) with locally infused autologous tumor infiltrating lymphocytes (TILs) and recombinant interleukin-2 (rIL-2). Six patients were entered between June 27, 1994 and June 2, 1995 and followed until July 1, 1998. At surgery an Ommaya reservoir was placed for later infusion of TILs and rIL-2. Following surgery, autologous TILs were expanded in vitro in the presence of rIL-2 and infused on treatment days 1 and 14, with concurrent rIL-2 infusions performed three times each week for one month. Following completion of immunotherapy all patients were offered chemotherapy. Phenotypic analysis demonstrated TILs to be T-lymphocytes (87-99% CD3+). Of these, 4 of 6 cases (67%) phenotyped as cytotoxic/suppressor T-lymphocytes (CD8+) and 2 of 6 cases (33%) phenotyped as helper/inducer T-lymphocytes (CD4+). TILs demonstrated limited selective cytotoxicity, with dose dependent cytotoxicity against autologous tumor, allogenic tumor and long term MG cell lines. There were no significant (Grade 3 or 4) complications. One patient developed transient low grade fevers, and 2 developed asymptomatic hydrocephalus. All patients developed transient and asymptomatic cerebral swelling, noted on the immediate post-treatment imaging studies. At three and six month follow-up, 3 patients responded with partial response, 2 demonstrated stable disease and 1 patient progressed. At long term follow-up, 1 patient had a complete response (45 month follow-up), 2 had a partial response (48 and 47 month follow-up) and 3 patients expired as a result of progressive disease (at 12, 12 and 18 months following immunotherapy). A relationship between subsequent chemotherapy or extent of resection to outcome was not apparent but could not be excluded. This pilot study demonstrated that locally infused autologous TILs and rIL-2 could be delivered without serious toxicity. Further studies are indicated to determine the safety and long term efficacy of TIL immunotherapy.

Adult↗
PubMed1992

Lymphocyte function in patients with interstitial cystitis.

To determine whether there is a primary immunological disorder involved in the etiology of interstitial cystitis, we compared the in vitro function of peripheral blood lymphocytes from 10 patients with interstitial cystitis to those from 10 healthy female controls. The lymphocytes were isolated and incubated in either cell culture medium alone, cell culture medium supplemented with the mitogen phytohemagglutinin or cell culture medium with autologous sterile filtered urine, the latter to detect any immunogenic potential of urine in this disease. We studied the relative proliferation of the phenotypes CD2, CD4, CD8, CD19, CD14 and CD56 by immunofluorescence and flow cytometry. To detect activation of T lymphocytes we also studied expression of HLA-Dr and interleukin-2 receptors. There was no difference in the rate of proliferation of the various lymphocyte phenotypes between the 2 groups in any of the culture media. Similarly, there was no difference between the 2 groups in the degree of lymphocytic activation after incubation. Furthermore, incubation in the presence of autologous urine caused no increase in activation above that seen in control cultures. We also assessed the production of the lymphokines interleukin-1, interleukin-2 and interferon-gamma in the supernatant fluid of the cell cultures. There was no difference in the production of these immunoregulatory cytokines between the control and patient groups, and again urine did not act as a mitogen in either group. We conclude from this study that there is no primary immunological disorder evident in patients with interstitial cystitis, and that the urine does not act as a stimulant to the immune system. This finding casts severe doubt on any theory suggesting that interstitial cystitis is an autoimmune disease or that urine contains an autoantigen causing the disease.

Adult↗
PubMed1992

Impairment of helper T-cell function following severe head injury.

Major infections, such as sepsis and pneumonia, occur in 50-75% of patients following isolated severe head injury. Previous studies have demonstrated that this high incidence of infection following severe head injury may be related to a decrease in helper T-cell activation and function. The present study was designed to investigate the effect of severe head injury on specific subgroups of helper T cells known to enhance or suppress cellular immune function. Specifically, peripheral blood lymphocytes (PBLs) from 10 head-injured patients and 10 matched controls were evaluated following in vitro stimulation with the T-cell mitogen, phytohemagglutinin (PHA). Subsets of helper T cells evaluated included activated helper (CD4+/CD25+) T cells; helper/inducer (CD4+/CDw29+) T cells, which enhance cellular immune activity; and suppressor/inducer (CD4+/CD45R+) T-cells, which induce suppressor (CD8+) T-cells. In addition, the effect of intraventricular fluid (IVF) on PHA-stimulated in vitro CD4 and CD25 expression was investigated to determine whether severe head injury results in the production of mediators within the central nervous system capable of affecting T-cell activation. The results of this study indicate that isolated severe head injury selectively reduces the ability of PHA-stimulated PBLs to express the helper/inducer (CD4+/CDw29+) T-cell (p = 0.023) and activated helper (CD4+/CD25+) T-cell (P = 0.041) phenotypes. There was no significant change in PHA-stimulated CD4 or CD25 expression following incubation of PBLs with intraventricular fluid (IVF) from head-injured patients. The relationship between these changes in specific helper T-cell subpopulations and the infectious complications of severe head injury are discussed.

Adolescent↗
PubMed1992

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors.

Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factor(s) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

Adolescent↗
PubMed1991

An adapter for stereotactic insertion of unitized shunt systems.

When ventricles are small or distorted, or when a cyst is located deep within the brain, positioning of the proximal catheter of a shunt system may be difficult. An adapter that allows for insertion of a unitized shunt system using the Brown Roberts Wells stereotactic system is described. Using this adapter, the proximal catheter tip of the shunt system is inserted to a defined stereotactic location, eliminating the need for multiple passes when attempting to cannulate small ventricles or deep cystic lesions.

Cerebrospinal Fluid Shunts↗
PubMed1991

Quantification of midline shift as a predictor of poor outcome following head injury.

A retrospective study of patient outcome, based on admission computed tomography, was carried out in 75 consecutive patients with head injury. Computed tomography data collected included the type and extent of intracranial hemorrhage, the extent of midline shift, and the ratio of midline shift compared with the extent of intracranial hemorrhage. Midline shift was considered to be out of proportion to intracranial hemorrhage when the midline shift of the septum pellucidum exceeded the extent of the hemorrhage as measured radially from the inner table of the skull. When computed tomography data were analyzed by logistic regression, significant predictive factors for poor outcome were intracranial hemorrhage (34%), intracranial hemorrhage with midline shift (61%), and midline shift out of proportion to the extent of intracranial hemorrhage (88%). When patient outcome and mortality rates are considered, our study indicates that midline shift out of proportion to the extent of intracranial hemorrhage is a highly useful predictor of poor patient outcome following head injury.

Adult↗
PubMed1991

Severe head injury: effect upon cellular immune function.

Infection is a major cause of morbidity following severe head injury. Although investigations have demonstrated central nervous system modulation of immune function, the effects of severe head injury on immune activity have not been well documented. This study prospectively investigated cellular immune function in 20 patients with isolated severe head injury. In vivo cellular immune status was determined by responses to delayed-type hypersensitivity (DTH) skin tests. In vitro studies included the effect of the lymphocyte mitogen, phytohaemagglutinin (PHA), on peripheral blood lymphocyte (PBL) phenotype expression and PBL blastogenesis. DTH skin testing demonstrated anergy to all antigens used during the first two weeks following head injury. Analysis of PBLs incubated with PHA demonstrated a decrease in the percent of PBL blastogenesis (p = 0.002), the percentage of cells marking as T-cells (p = 0.018), helper T-cells (p less than 0.001) and those expressing interleukin-2 receptors (p less than 0.001). There was a significant increase in the percentage of cells that marked as monocytes (p = 0.030), whereas there was no significant change in the percentage of B-cells, suppressor/cytotoxic T-cells, natural killer cells or in cells expressing the HLA-DR antigen. The infection rate was 55% with most occurring within 5 days of injury. The results of this study suggest that isolated severe head injury causes suppression of cellular immunity. The decrease in PHA stimulated PBL blastogenesis, helper T-cell phenotypic and interleukin-2 receptor expression, suggests suppression in early helper T-cell activation may be responsible for the high incidence of infection following severe head injury. The possible significance of increased monocyte phenotypic expression is discussed.

Adolescent↗
PubMed1991

Humoral and cellular immunity following severe head injury: review and current investigations.

Infection is a common and serious complication of severe head injury. Immunocompetence in 25 severely head injured patients was investigated by measuring: (1) delayed-type hypersensitivity (DTH) skin test responses to common antigens; (2) phytohaemagglutinin (PHA) stimulated peripheral blood lymphocyte (PBL): blastogenesis, phenotype expression, and lymphokine production; (3) lymphokine-activated killer (LAK) cytotoxicity, antibody dependent cellular cytotoxicity (ADCC) and natural killer (NK) cytotoxicity; and (4) immunoglobulin and complement levels. The incidence of anergy to DTH skin testing was 100%. There was a decrease in PHA stimulated: PBL blastogenesis (p = 0.002), T-cell expression (p = 0.018), helper T-cell expression (p less than 0.001), interleukin-2 receptor expression (p less than 0.001), interleukin-2 production (p = 0.035) and gamma-interferon production (p less than 0.001). LAK cytotoxicity was depressed following incubation with IL-2 (p less than 0.001). There was no significant decrease in immunoglobulin levels and all acute phase reactants tested increased. The results of this study indicate that the cellular arm of immune response, including lymphocyte activation and cytokine production, is suppressed following severe head injury. The lack of enhancement in LAK cytotoxicity following incubation of PBLs with interleukin-2 suggests that factors other than decreased interleukin-2 production, such as the inherent lymphocyte dysfunction, other soluble mediators or suppressor cells, may be responsible for the reduction in cellular immunity observed following severe head injury.

Adolescent↗
PubMed1991

Impairment of helper T-cell function and lymphokine-activated killer cytotoxicity following severe head injury.

Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-gamma), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-gamma and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p less than 0.001 for INF-gamma, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p less than 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-gamma production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggest that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

Adolescent↗
PubMed1990

Suppression of cellular immune activity following severe head injury.

Infection is a major cause of morbidity following multiple traumatic and head injury. Although immunosuppression has been demonstrated after multiple traumatic injury, the effects of head injury on immune function have not been thoroughly investigated. In a prospective study of 10 severely head-injured patients, in vitro and in vivo parameters of cellular immune activity were assessed. In vitro measurements of lymphocyte surface antigen expression following mitogen stimulation were made serially over a 3-week period in 10 patients with severe head injury. The control group consisted of 20 healthy subjects. Phenotyping of peripheral blood lymphocytes (PBLs) was performed following incubation with and without mitogens. Phenotypes were determined by flow cytometry using monoclonal antibodies (MABs) to T lymphocyte subsets and the alpha subunit of interleukin 2 (IL-2) receptors. In vivo cellular immune function was determined by measuring patient responses to delayed-type hypersensitivity (DTH) skin testing within 24 h of injury. When head-injured patients were compared to controls, PBLs incubated in the presence of phytohemagglutinin (PHA) demonstrated a decrease in cells marking as T cells (p = 0.005), helper-inducer T cells (p = 0.001), and in the number of IL-2 receptor-bearing cells (p = 0.001). The functional ability of these lymphocyte subpopulations to proliferate in the presence of PHA was significantly suppressed within 24 h of injury and normalized within 3 weeks of injury. DTH skin testing to Candida, mumps, trichophyton, and PPD antigens was performed within 24 h of injury and resulted in anergic responses in all 10 patients when measured at 24, 48, and 72 h following administration. The overall infection rate was 60%, with the majority of infections occurring within the first 4 days following injury. The results of this study indicate that severe head injury results in suppression of cellular immune function with a corresponding high rate of infection. The possible significance of the decrease in the percentage of helper-inducer T cells and in the number of cells bearing IL-2 receptors following mitogen stimulation is discussed.

Adolescent↗
PubMed1990

Traumatic aneurysm of the superior cerebellar artery: case report and review of the literature.

Less than 10% of the 250 reported cases of traumatic intracranial aneurysms have involved the posterior circulation. Traumatic aneurysms of the superior cerebellar artery are extremely rare, with only three cases previously reported. This is the first report of a traumatic superior cerebellar artery aneurysm in which the diagnosis was suggested by computed tomographic scan. The potential for a good outcome suggests the value of early angiography when the history and diagnostic imaging studies suggest the possibility of a traumatic aneurysm.

Adult↗
PubMed1989

Cavernous angioma of the tentorium cerebelli. Case report.

The case of a cavernous angioma of the tentorium cerebelli is described. This is the seventh reported case of a cavernous angioma in this unusual location and the first of a dural cavernous angioma demonstrated by magnetic resonance imaging. The clinical presentation, radiographic features, and surgical treatment of these rare tumors are discussed, along with a review of the literature.

Cerebellar Neoplasms↗
PubMedDate not supplied

MR of recurrent high-grade astrocytomas after intralesional immunotherapy.

PURPOSE: To describe the MR findings in six patients with recurrent cerebral astrocytomas before, immediately after, and 3 months after local immunotherapy with tumor-infiltrating lymphocytes and interleukin-2. METHODS: Contrast-enhanced MR studies were obtained in six patients (three with anaplastic astrocytoma and three with glioblastoma multiforme) at the time of tumor recurrence, after a second resection and placement of an Ommaya catheter, at the end of immunotherapy, and thereafter at 3-month intervals. These MR studies were reviewed with special attention to pattern and degree of enhancement, edema, and mass effect. RESULTS: In three patients, gross total removal of recurrent tumor was achieved and postimmunotherapy MR studies showed a flare phenomenon characterized by increased nodular enhancement, increased edema, and mass effect. On the 3-month follow-up examination, these findings had resolved, and no further tumor recurrence was seen during the following 12-month period. Neither of the two patients who had subtotal resection had a flare phenomenon. In one of these patients, the tumor was stable at the 12-month follow-up; the other patient had recurrent tumor at the 6-month follow-up. In the last patient, who also had subtotal tumor resection and progressive enhancement after immunotherapy, tumor progression was rapid. CONCLUSION: After local immunotherapy, increased enhancement, edema, and mass effect are most likely the result of a flare phenomenon, but because rapid tumor progression may produce similar features, follow-up MR studies are indispensable. The flare phenomenon resolved by 3 months in all patients.

Adult↗