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Biomedical subjects

C G Gillies

Publications and source records attributed to C G Gillies.

12 recordsLinked to original sources
PubMed1988

Pulmonary histopathology of rats following parenteral injections of nickel chloride.

To elucidate the subacute toxic reactions to parenteral administration of Ni2+, male F-344 rats were given daily injections of NiCl2 (62.5 or 125 mumol/kg, sc) for 3 to 6 weeks. Nickel accumulation was greater in lung than in the other major organs, based upon tissue analyses by electrothermal atomic absorption spectrometry. After 5 or 6 weeks of NiCl2 treatment, severe pathological changes developed in the lungs, including a) prominent hydropic and degenerative changes of the endothelium of pulmonary arteries and veins; b) marked proliferation of alveolar lining cells, affecting Type II (granular)pneumocytes; c) thickening of alveolar walls, with proteinaceous alveolar exudate; d) hyperplasia of bronchial epithelium, with cellular atypia and mitoses; and e) focal bronchial pneumonia with intrabronchial exudates. These pulmonary responses to repeated daily injections of NiCl2 were substantially different from the pathological lesions seen 24 to 72 hours after a single sc injection of NiCl2 (500 or 750 mumol/kg), which included perivascular edema, karyorrhexis and pyknosis of mononuclear cells in focal perivascular infiltrates, and mild pulmonary congestion. This study shows that the lung is a primary site of toxicity in rats following parenteral administration of NiCl2; vascular endothelial cells, Type II pneumocytes, bronchial epithelial cells, and mononuclear cells constitute the principal cellular targets for pulmonary toxicity of Ni2+.

Animals↗
PubMed1985

Embolic tubular epithelial cells in percutaneous renal biopsies.

Four percutaneous renal biopsies with intravascular embolic tubular epithelial cells are presented. This unusual finding is presumably the result of the needle biopsy procedure and can be a puzzling and misleading artifact. It is postulated that dislodged tubular epithelial cells are pushed forward into or pulled back into punctured intrarenal arteries and subsequently transported to distant glomeruli.

Biopsy↗
PubMed1984

Spontaneous in vitro transformation of human fibroblasts.

The establishment of a spontaneously transformed tumorigenic human fibroblast line, VIP-F:T, is described. This line was developed from a primary culture of normal skin from a donor from whom a separate nontransformed fibroblast line, Pen-F2, also was established. The transformed line VIP-F:T exhibited aneuploid karyotype with a marker chromosome, showed anchorage-independent growth, and produced progressively growing tumors with morphologic characteristics of sarcoma in CD-1 (nu/nu) nude mice. The normal fibroblast line Pen-F2 exhibited diploid karyotype, showed no anchorage-independent growth, and produced no tumors in the nude mice. The spontaneously transformed fibroblast line VIP-F:T and its normal counterpart Pen-F2 will be valuable in studies of oncogene expression and in other investigations relevant to neoplasia.

Cell Division↗
PubMed1982

Erythrocytosis, glomerulomegaly, mesangial hyperplasia, sialyl hyperplasia, and arteriosclerosis induced in rats by nickel subsulfide.

Histopathological examinations were performed upon groups of male Fischer rats killed at intervals from 1 h to 18 weeks after unilateral intrarenal (ir) injection of nickel subsulfide (2.5 or 5 mg of Ni3S2/rat). Consistent with previous findings, erythroid hyperplasia of bone marrow and spleen occurred from 2 to 18 weeks after Ni3S2-treatment, resulting in pronounced erythrocytosis. Hitherto unreported effects of Ni3S2-treatment include: (a) marked glomerulomegaly and hyperplasia of mesangial cells in both kidneys; (b) hyperplasia of submandibular salivary glands, and (c) widespread arteriosclerotic lesions. The present study suggests that mesangial cells of renal glomeruli produce erythropoietin. Discovery that ir injection of Ni3S2 induces arteriosclerotic lesions in rats furnishes a new experimental model to investigate the pathogenesis of arteriosclerosis.

Animals↗
PubMedDate not supplied

Tubular inclusions in macrophages in the brain of a patient with acute hemorrhagic leukoencephalitis (Weston-Hurst syndrome).

A case history, biopsy findings, and autopsy findings of an unusually long-lasting case of acute hemorrhagic leukoencephalitis in a young woman are presented. Diagnosis by stereotactic biopsy of brain lesions seen on computed tomography and magnetic resonance imaging scans had been attempted previously. On histologic examination the biopsy showed sheets of macrophages, which were found to contain unusual tubular inclusions on electron microscopy. The nature of these inclusions is discussed.

Acute Disease↗
PubMedDate not supplied

Transmission electron microscopy: evaluation of damage in human oviducts caused by different surgical instruments.

Different wave length lasers (CO2, Nd-YAG, KTP-532), electrocautery and radiofrequency instruments were used to assess the degree of tissue damage in human oviducts. Excision of the human fallopian tube for tuboplasty is achieved most often by electrocautery, scalpel and, more recently, the Carbon Dioxide (CO2) Laser. There is not enough evidence at the present time to scientifically justify using one particular mode of incision which would show minimal damage to surrounding healthy tissue, especially heat lateral damage. The present study compares the tissue damage produced by the microelectrocautery, the CO2, the KTP-532, the Nd-YAG lasers and the radiofrequency surgical instrument, utilizing different power densities on the fallopian tubes freshly removed at the isthmic portion, taken from healthy women ages 30-42. Transmission electron microscopy sections at the cellular level show that the electrosurgical radiofrequency surgical instrument produces the least damage to surrounding healthy tissue. The CO2 laser with intermittent superpulse mode showed the second lowest amount of damage. The most damage was observed with the Nd-YAG laser at high power densities.

Adult↗
PubMedDate not supplied

Hepatic toxicity of nickel chloride in rats.

Enhanced lipid peroxidation was observed in livers of rats killed 24 hr after sc injection of nickel chloride (NiCl2) (750 mumol per kg), as evidenced by 13-fold increase of conjugated dienes in microsomal lipids and 4-fold increase of thiobarbituric acid (TBA) chromogens in hepatic cytosol. Histologic examination of livers from rats killed one to three days after NiCl2 injection (500 mumol per kg) showed microvesicular fatty metamorphosis, mild hydropic degeneration, and foci of inflammation. Microvesicular steatosis of hepatocytes was confirmed by electron microscopy. Dose-related increases of serum aspartate aminotransferase (ALT) activity (up to 7-fold vs controls) and alanine aminotransferase (ALT) activity (up to 3-fold vs controls) were observed 24 hr after injection of NiCl2 (125 to 750 mumol per kg); diminished serum alkaline phosphatase activity (up to 72 percent reduction vs controls) was seen at NiCl2 dosages from 375 to 750 mumol per kg. Diethyldithiocarbamate did not influence the effects of NiCl2 on TBA-chromogens in liver homogenates or on serum AST and ALT activities but acted synergistically with NiCl2 to diminish serum alkaline phosphatase activity and to increase serum bilirubin concentration. This study demonstrates that parenteral administration of NiCl2 to rats produces acute hepatic toxicity, with enhanced lipid peroxidation, microvesicular steatosis, and increased serum AST and ALT activities.

Alanine Transaminase↗