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A C Harris

Publications and source records attributed to A C Harris.

At least 19 recordsLinked to original sources

The imaging features of gastrointestinal stromal tumours.

Gastrointestinal stromal tumours (GISTs) are a rare group of mesenchymal neoplasms that occur predominantly in the gastrointestinal tract. Previously GISTs were classified as smooth muscle tumours referred to as leiomyomas, leiomyosacromas or leiomyoblastomas. However, with the advent of immunohistochemistry, GISTs are now defined by the identification of cKit positivity. This is now used to select patients with metastatic disease who may respond to chemotherapeutic agents such as the tyrosine kinase inhibitor, STI-571. In this pictorial essay we have attemped to describe the range of imaging findings of GISTs that can suggest a pre-biopsy diagnosis.

Contrast Media↗

Double dissociation in the neural substrates of acute opiate dependence as measured by withdrawal-potentiated startle.

The basolateral amygdala and portions of the "extended" amygdala (i.e. central nucleus of the amygdala, bed nucleus of the stria terminalis and shell of the nucleus accumbens) have been implicated in the aversive aspects of withdrawal from chronic opiate administration. Given that similar withdrawal signs are observed following a single opiate exposure, these structures may also play a role in "acute opiate dependence." In the current study, drug-naïve rats underwent naloxone-precipitated withdrawal from acute morphine (10 mg/kg) exposure on two successive days. On either the first or second day of testing, the basolateral amygdala, central nucleus of the amygdala, bed nucleus of the stria terminalis, or nucleus accumbens was temporarily inactivated immediately prior to naloxone injection by microinfusion of the glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo(f)quinoxaline-7-sulfonamide (3 microg/0.5 microl). On the first day, inactivation of the basolateral amygdala, central nucleus of the amygdala, or bed nucleus of the stria terminalis, but not the nucleus accumbens blocked withdrawal-potentiated startle, a behavioral measure of the anxiogenic effects of withdrawal. On the second day, inactivation of the nucleus accumbens, but not the basolateral amygdala, central nucleus of the amygdala, or bed nucleus of the stria terminalis disrupted the withdrawal effect. Effects of structural inactivations on withdrawal-potentiated startle were not influenced by differences in withdrawal severity on the two days of testing. A fear-potentiated startle procedure provided functional confirmation of correct cannulae placement in basolateral amygdale- and central nucleus of the amygdala-implanted animals. Our findings indicate a double dissociation in the neural substrates of withdrawal-potentiated startle following a first versus second morphine exposure, and may reflect a reorganization of the neural circuitry underlying the expression of withdrawal-induced negative affect during the earliest stages of opiate dependence.

Acoustic Stimulation↗

Synovial osteochondromatosis: the spectrum of imaging findings.

Imaging plays a vital role in the diagnosis and management of synovial osteochondromatosis, a proliferative disorder of the synovium with associated loose body formation. The aim of this pictorial review is to illustrate the radiographic, computed tomographic and magnetic resonance appearances of various stages of the disease.

Chondromatosis, Synovial↗

Leiomyosarcoma of the distal femur in a patient with a history of bilateral retinoblastoma: a case report and review of the literature.

We report a case of primary leiomyosarcoma of the distal femoral shaft arising in a patient who had undergone bilateral orbital enucleation for bilateral retinoblastoma several years previously. Radiography demonstrated an osteolytic, expansive lesion with cortical destruction anteriorly in the distal femoral shaft, and these findings were confirmed on CT. MR imaging revealed an expansive intramedullary lesion with cortical breakthrough and soft tissue extension. The occurrence of a second malignancy in patients with a history of bilateral retinoblastoma is well documented. Many different histological types have been described, with osteosarcoma and leiomyosarcoma occurring with the greatest frequency.

Eye Enucleation↗

Odontoid fracture following an epileptic seizure.

Fractures of the thoracic and lumber spine are well recognized following an epileptic seizure. Fractures of the cervical spine are not. The rare occurrence of a displaced odontoid fracture type 2, secondary to a grand mal seizure is presented. To our knowledge, this association has not been described previously in the English literature.

Aged↗

Ct findings in blunt renal trauma.

Computed tomography (CT) can provide essential anatomic and physiologic information required to determine management of intraabdominal and retroperitoneal injuries sustained during blunt abdominal trauma. It can help in evaluation of the type and severity of parenchymal injury, the extent of perirenal hemorrhage and parenchymal devascularization, and the presence of urinary extravasation. CT can help confirm the presence of major injuries to the vascular pedicle and depict occult renal pathologic conditions. Principal indications for the use of CT in the evaluation of blunt renal trauma include (a) the presence of gross hematuria, (b) microscopic hematuria associated with shock (systolic blood pressure <90 mm Hg), and (c) microscopic hematuria associated with a positive result of diagnostic peritoneal lavage. The majority of renal injuries sustained during blunt abdominal trauma are contusions and minor parenchymal lacerations amenable to nonoperative management. Deep parenchymal lacerations, urinary extravasation, and mild to moderate degrees of parenchymal devascularization may also be treated conservatively. Radiologists should look for coexisting renal lesions such as tumors and traumatic false aneurysms that may alter management.

Abdominal Injuries↗

The white chest.

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Adult↗

Enhanced intestinal adenomatous polyp formation in Pms2-/-;Min mice.

Analysis of two human familial cancer syndromes, hereditary nonpolyposis colorectal cancer and familial adenomatous polyposis, indicates that mutations in either one of four DNA mismatch repair gene homologues or the adenomatous polyposis coli (APC) gene, respectively, are important for the development of colorectal cancer. To further investigate the role of DNA mismatch repair in intestinal tumorigenesis, we generated mice with mutations in both Apc and the DNA mismatch repair gene, Pms2. Whereas Pms2-deficient mice do not develop intestinal tumors, mice deficient in Pms2 and heterozygous for Min, an allele of Apc, develop approximately three times the number of small intestinal adenomas and four times the number of colon adenomas relative to Min and Pms2+/-;Min mice. Although Pms2 deficiency clearly increases adenoma formation in the Min background, histological analysis indicated no clear evidence for progression to carcinoma.

Adenoma↗

Tumour susceptibility and spontaneous mutation in mice deficient in Mlh1, Pms1 and Pms2 DNA mismatch repair.

Germline mutations in the human MSH2, MLH1, PMS2 and PMS1 DNA mismatch repair (MMR) gene homologues appear to be responsible for most cases of hereditary non-polyposis colorectal cancer (HNPCC; refs 1-5). An important role for DNA replication errors in colorectal tumorigenesis has been suggested by the finding of frequent alterations in the length of specific mononucleotide tracts within genes controlling cell growth, including TGF-beta receptor type II (ref. 6), BAX (ref. 7) and APC (ref. 8). A broader role for MMR deficiency in human tumorigenesis is implicated by microsatellite instability in a fraction of sporadic tumours, including gastric, endometrial and colorectal malignancies. To better define the role of individual MMR genes in cancer susceptibility and MMR functions, we have generated mice deficient for the murine homologues of the human genes MLH1, PMS1 and PMS2. Surprisingly, we find that these mice show different tumour susceptibilities, most notably, to intestinal adenomas and adenocarcinomas, and different mutational spectra. Our results suggest that a general increase in replication errors may not be sufficient for intestinal tumour formation and that these genes share overlapping, but not identical functions.

Adaptor Proteins, Signal Transducing↗

Malignant lymphoma can present as hepatobiliary disease.

BACKGROUND: Liver involvement by non Hodgkin's lymphoma usually represents systemic progression of a low grade lymphoma. Sixteen patients without palpable lymphadenopathy who presented with features suggesting hepatic inflammation were found to have non Hodgkin's lymphoma involving the liver. METHODS: Tissue sections stained with hematoxylin and eosin were examined by light microscopy. Immunohistochemical studies were performed on formalin-fixed paraffin embedded tissue to determine phenotype. Patients' medical records were reviewed for clinical details. RESULTS: Clinical presentation included fever, jaundice, and elevated liver enzymes. Peripheral lymphadenopathy was absent. Hepatomegaly and splenomegaly were common. Imaging studies revealed a homogeneous pattern of liver involvement without a discrete mass. Histologically, infiltration of the liver was predominantly portal consisting of large, atypical cells scattered within a background of small lymphoid cells. By immunohistochemistry, it was determined that eight were T-cell and eight were B-cell lymphomas. Of the eight patients who had lymph node sampling, three showed involvement by diffuse mixed, small cleaved, and large cell lymphomas. Each of these three involved lymph nodes was located near the liver. Bone marrow infiltration was demonstrated in 10 of the 11 patients in whom it was sampled. Eleven of the 16 patients died 2 days to 31 months after diagnosis, and at last follow-up, 5 patients were alive 2 weeks to 13 months after diagnosis. CONCLUSIONS: Patients with non-Hodgkin's lymphoma can present with hepatic dysfunction and without peripheral lymphadenopathy. This presentation of lymphoma is associated with extensive disease and an aggressive course.

Adolescent↗

Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over.

Mice that are deficient in either the Pms2 or Msh2 DNA mismatch repair genes have microsatellite instability and a predisposition to tumours. Interestingly, Pms2-deficient males display sterility associated with abnormal chromosome pairing in meiosis. Here mice deficient in another mismatch repair gene, Mlh1, possess not only microsatellite instability but are also infertile (both males and females). Mlh1-deficient spermatocytes exhibit high levels of prematurely separated chromosomes and arrest in first division meiosis. We also show that Mlh1 appears to localize to sites of crossing over on meiotic chromosomes. Together these findings suggest that Mlh1 is involved in DNA mismatch repair and meiotic crossing over.

Adaptor Proteins, Signal Transducing↗

Comparison of the clinic microscopy laboratory with the cytopathology laboratory in the detection of malignant cells in body fluids.

The clinical microscopy (fluids) laboratory evaluates almost every body fluid that is obtained in the hospital. Because the fluids laboratory functions at all hours, it is often the first laboratory to receive a body fluid. In addition to its primary purpose of quantitating categories of cells, the medical technologist in this laboratory has an opportunity to identify malignant cells. To our knowledge, no formal study has ever been undertaken to evaluate the performance of the fluids laboratory in detecting malignancy. The authors therefore retrospectively identified 928 body fluids (pleural, peritoneal, cerebrospinal, and miscellaneous) over a 2-year period that had undergone simultaneous cytologic examination in our cytopathology laboratory and body fluid analysis in our fluids laboratory. Of these, a cytologic diagnosis of malignancy was made by the cytopathology laboratory in 107 cases; 821 were considered to be benign. No false-positive results were rendered by the fluids laboratory (100% specificity), but only 26 of the 107 malignant cases were identified (24% sensitivity); the overall accuracy was 93%. Factors contributing to the inability of the fluids laboratory to identify malignant cells included (1) too few cells to warrant a cytocentrifuge preparation, especially in cerebrospinal fluid specimens; (2) differences in the processing of specimens; (3) differences in staining procedures; and (4) differences in the training of personnel. The authors conclude that although the fluids laboratory correctly identifies neoplastic cells in approximately one fourth of the cases in which they are present, it should not be expected to detect malignant cells in every cytologically malignant case.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Fluids↗

Bone marrow changes associated with recombinant granulocyte-macrophage and granulocyte colony-stimulating factors. Discrimination of granulocytic regeneration.

The hematopoietic growth factors recombinant human granulocyte-macrophage colony-stimulating factor and recombinant human granulocyte colony-stimulating factor are associated with changes of the bone marrow. To evaluate the morphologic features and to differentiate them from leukemia, bone marrow specimens from 12 patients who had been treated with one of these agents were evaluated. The bone marrow displayed marked promyelocytic hyperplasia and a less striking increased percentage of myeloblasts. In each of the 11 patients without leukemia at the time of bone marrow biopsy, the percentage of promyelocytes in the bone marrow was greater than that of myeloblasts. Cytologic features of stimulated regeneration included diffuse cytoplasmic hypergranulation of immature neutrophilic precursors that had prominent perinuclear spherical clear areas representing the Golgi zones. With consideration of bone marrow composition and careful attention to cytologic detail, the distinction of bone marrow regeneration from acute leukemia can be made in most patients who are being treated with recombinant hematopoietic growth factors.

Adolescent↗