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Biomedical subjects

F M Robertson

Publications and source records attributed to F M Robertson.

At least 37 records · Page 2Linked to original sources
PubMed1996

Renal cell carcinoma in association with tuberous sclerosis in children.

Tuberous sclerosis, a genetically transmitted multisystem neurocutaneous disorder, is associated with renal lesions in 50% of cases. The expected lesions are angiomyolipomas or renal cysts; renal cell carcinoma has been encountered in adults who have tuberous sclerosis, but is very rare in children. The authors report the case of a 5-year-old girl with tuberous sclerosis for whom atypical computed tomography findings led to the diagnosis of renal carcinoma at an early age. This experience suggests that children with tuberous sclerosis may need earlier screening.

Adult↗
PubMed1996

Inhibition of pro-inflammatory cytokine gene expression and papilloma growth during murine multistage carcinogenesis by pentoxifylline.

Topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA) to the dorsal epidermis of Sencar mice induces synthesis of pro-inflammatory cytokines, including interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-alpha (TNF-alpha). These proteins differentially regulate proliferation of epidermal keratinocytes, as well as stimulate chemotaxis, migration and production of reactive oxygen and nitrogen intermediates by leukocytes. Studies over the past several years have demonstrated that pentoxifylline ([1-(5-oxohexyl)-3,7-dimethyl-xanthine], oxpentifylline), which is a methylxanthine derivative used clinically for treatment of vascular insufficiency, has the unique ability to inhibit synthesis of pro-inflammatory cytokines. The present studies were performed to examine the effects of acute and chronic administration of pentoxifylline on TPA-induced cutaneous inflammation in female Sencar mice treated once with 10 micrograms TPA and also to determine the ability of pentoxifylline to inhibit the tumor promotion process in mice treated with a single application of 25 nmol 7,12-dimethylbenz[a]anthracene (DMBA) followed for 8 weeks by twice weekly topical application of TPA. Intraperitoneal injection of 50 micrograms/g pentoxifylline at 30 min prior to topical application of 10 micrograms TPA to the dorsal epidermis of Sencar mice inhibited TPA-induced IL-1 alpha and TNF-alpha gene expression 24 h after TPA treatment. Administration of pentoxifylline also significantly inhibited all parameters of acute TPA-induced inflammatory response examined 24 h later, including skin thickening (P < 0.005), infiltration of neutrophils into the dermis (P < 0.001), the corresponding dermal myeloperoxidase activity (P < 0.01) and epidermal hyperplasia (P < 0.001). Injection of 50 micrograms/g pentoxifylline over an 8 week time period significantly inhibited DMBA/TPA-induced papilloma growth (P < 0.05). These results indicate that administration of pentoxifylline is an effective means of inhibiting acute TPA-induced cutaneous inflammation and pro-inflammatory cytokine gene expression, as well as is effective as an antipromoter that inhibits papilloma growth.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

Gene expression and cellular sources of inducible nitric oxide synthase during tumor promotion.

The present studies examined the temporal sequence of inducible nitric oxide synthase (iNOS) gene expression and the cellular sources of iNOS protein and of 3-nitrotyrosine, as a marker of production of nitric oxide-derived reactive nitrogen intermediates during murine multi-stage carcinogenesis. Levels of iNOS mRNA in dorsal skin isolated from acetone-treated female Sencar mice were 2.5-fold higher than iNOS gene expression detected in cutaneous tissue isolated from Sencar mice at 1, 3, 6, 10, 16 and 22 weeks after exposure to a single topical application of 25 nmol 7,12-dimethylbenz[a]anthracene (DMBA) followed by repetitive applications of 2 microgram 17-O-tetradecanoylphorbol-13-acetate (TPA). Papillomas isolated at 16 and 22 weeks of a tumor promotion protocol also had low levels of iNOS mRNA. The diminished levels of iNOS mRNA inversely correlated with the extent of TPA-induced epidermal hyperplasia. In acetone-treated mouse skin, iNOS immunospecific antibody binding was localized to the stratum corneum and suprabasal keratinocytes. In contrast, iNOS protein was present in lower amounts and was localized to the upper-most suprabasal keratinocytes in cutaneous tissue isolated at 22 weeks following a single exposure to either 25 nmol DMBA or acetone and repetitive applications of 2 microgram TPA. At all time points examined over the 22 week time period of papilloma growth, infiltrating neutrophils within the dermis bound significant levels of anti-iNOS antibodies. The production of iNOS by neutrophils within the dermis correlated with the formation of protein nitrotyrosination within the dermal tissue, as detected by 3-nitrotyrosine-specific antibodies. The present studies indicate that NOS and reactive nitrogen intermediates, including peroxynitrite, are produced specifically by dermal neutrophils during the tumor promotion process at time points that correspond to simultaneous production of reactive oxygen intermediates. Conversely, iNOS is simultaneously down-regulated in hyperplastic epidermis and in papillomas.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

Modification of the "push" technique for percutaneous endoscopic gastrostomy in infants and children.

BACKGROUND: Percutaneous endoscopic gastrostomy (PEG) by the "push" technique avoids peri-catheter infection, repeated insertion of the endoscope, potential esophageal injury from the catheter, and the possible need for another endoscopy for catheter removal associated with the "pull" technique. In small infants, however, the "push" technique could result in loss of gastric insufflation and pneumoperitoneum during tract dilatation. A simple modification of the "push" technique has eliminated this problem. STUDY DESIGN: During a 16-month period, 22 infants and children underwent PEG insertion using our modified "push" technique. These cases were reviewed for patient characteristics including age, weight, indication for the procedure, duration of the procedure, cost, conversion to open technique, and complications. RESULTS: We have used the modified "push" technique to place PEG tubes in 20 infants and children aged four weeks to 15 years (mean, 13 months), weighing 2.7 to 36 kg (median, 6.0 kg), indicated for failure to thrive due to cystic fibrosis (n=3) or neurologic impairment (n=10). These patients have had follow-up examination from nine to 30 months after the procedure. Operative time averaged 15 minutes. The "push" technique was successful in 95 percent of patients with one failure caused by loss of gastric insufflation when Fogarty balloons failed. All PEGs were used within 24 hours. There were no deaths and no peri-catheter infections. CONCLUSIONS: A simple modification of the "push" technique of PEG insertion eliminated problems with loss of gastric insufflation previously encountered in small infants. The modified "push" technique is safe, simple, and quick, obviating potential risks inherent in the "pull" technique when applied in infants.

Adolescent↗
PubMed1995

Temporal sequence of pulmonary cytokine gene expression in response to endotoxin in C3H/HeN endotoxin-sensitive and C3H/HeJ endotoxin-resistant mice.

Although previous studies suggested that tumor necrosis factor alpha (TNF-alpha) was a critical cytokine responsible for the inflammation observed after exposure to endotoxin, other mediators may also play an important role in the regulation of systemic inflammatory responses independent of TNF-alpha. The present study compared the temporal sequence of endotoxin-induced TNF-alpha, interleukin-1 alpha (IL-1 alpha), and interleukin-10 (IL-10) gene expression and cellular localization of cytokine proteins in pulmonary tissue of two strains of mice that have a genetically based differential sensitivity to endotoxin. Lung tissue and plasma were harvested from endotoxin-sensitive C3H/HeN and endotoxin-resistant C3H/HeJ mice at 15 min, 30 min, 1 h, 2 h, 4 h, 6 h, 12 h, and 24 h after intraperitoneal (i.p.) injection of 5 mg/kg endotoxin (Escherichia coli-derived lipopolysaccharide, serotype 0111:B4). There were significant elevations in both TNF-alpha gene and IL-1 alpha expression immediately (15 min) after endotoxin injection in C3H/HeN mice. Although levels of TNF-alpha mRNA in the two mouse strains were similar at 1-2 h, the IL-1 alpha gene expression in pulmonary tissue isolated from endotoxin-resistant mice was not comparable to the levels detected in C3H/HeN endotoxin-sensitive mice at the same times. The most dramatic difference in endotoxin-induced cytokine gene expression between the two strains of mice was in IL-10 mRNA levels in pulmonary tissue isolated from endotoxin-sensitive mice, compared to the lack of detectable increase in IL-10 gene expression in C3H/HeJ endotoxin-resistant mice above baseline at any time point examined. Quantitation of neutrophil infiltration into pulmonary tissue using immunochemical detection of GR-1, a myeloid differentiation-specific antibody, demonstrated that there was a significantly decreased inflammatory infiltrate in pulmonary tissue isolated from C3H/HeJ mice following endotoxin administration, which correlated with decreased levels of proinflammatory cytokine immunoreactive protein within pulmonary cells. Pulmonary cytokine synthesis and immunoreactive protein production did not directly correlate with either the magnitude or the temporal sequence of increases in plasma cytokine levels, suggesting that systemic levels of cytokines may not accurately reflect the cytokine response within the local tissue milieu. The present observations demonstrate that the differential synthesis and production of immunosuppressive cytokines as well as proinflammatory cytokines may be important variables in the determination of the extent of infiltration of inflammatory cells into the local pulmonary site in response to endotoxin and may significantly contribute to the determination of sensitivity or resistance to endotoxin in this murine model.

Animals↗
PubMed1995

Devascularization and staged resection of giant sacrococcygeal teratoma in the premature infant.

Sacrococcygeal teratoma identified in utero is associated with 50% fetal demise, which is caused by hyperdynamic cardiac failure, hemorrhage, and polyhydramnios-induced preterm labor. A premature infant (26 weeks' gestation) with prenatally diagnosed sacrococcygeal teratoma was managed successfully with initial devascularization to control the hyperdynamic state, followed by staged resection.

Arteries↗
PubMed1995

Effects of nitric oxide synthase inhibition on regional blood flow in a porcine model of endotoxic shock.

The results of early studies suggest that nitric oxide (NO) synthesis inhibition may be therapeutic in sepsis, but recent data indicate that NO inhibition may be harmful. This study investigates the effects of NO synthesis inhibition with N-nitro-L-arginine methyl ester (NAME) on regional blood flow following endotoxemia. Anesthetized, instrumented swine were randomly divided into four groups. Controls received normal saline resuscitation (NSR) at 1 cc/kg/min beginning at T0. The lipopolysaccharide group (LPS) received NSR and Escherichia coli LPS, 200 micrograms/kg at T0. The LPS+NAME group received NSR and LPS at T0, plus NAME (50 micrograms/kg/min) starting at T1. The NAME group received only NSR and NAME. Hemodynamic data, regional blood flow, and gastric intramucosal pH (pHi) were measured hourly. LPS increased renal and carotid blood flow consistent with a hyperdynamic state. Mesenteric blood flow was decreased. Treatment of endotoxic animals with NAME decreased renal and carotid blood flow. Mesenteric blood flow and gastric pHi were improved by NAME. NO inhibition in endotoxic shock results in decreased carotid and renal blood flow, by decreasing cardiac output. Mesenteric blood flow and perfusion were improved; however, this requires further study for validation.

Amino Acid Oxidoreductases↗
PubMed1994

Detrimental hemodynamic effects of nitric oxide synthase inhibition in septic shock.

OBJECTIVE: To investigate the physiologic effects of nitric oxide synthase inhibition with N-nitro-L-arginine methyl ester in an acute resuscitated model of porcine septic shock. DESIGN: Randomized control trial. SETTING: Animal research facility. STUDY SUBJECTS: Domestic Yorkshire swine. INTERVENTIONS: Twenty-four animals were randomly divided into one of four treatment groups as follows: normal saline resuscitation (NSR) (control group); NSR plus 200 micrograms/kg of lipopolysaccharide (LPS) at 1 hour after baseline (LPS group); NSR, LPS, and a continuous infusion of 50 micrograms/kg per minute of N-nitro-L-arginine methyl ester (NAME) at 1 hour after baseline (LPS/NAME group); and NSR and NAME (NAME group). All animals received NSR at 1 mL/kg per minute starting at baseline. MAIN OUTCOME MEASURES: Mean arterial pressure (MAP), systemic vascular resistance index (SVRI), mean pulmonary arterial pressure (MPAP), and pulmonary vascular resistance index (PVRI) were measured at baseline and hourly for 4 hours. Values at baseline and 3 hours are given below as mean (+/- SE). RESULTS: All variables remained unchanged in the control group. The administration of LPS produced a systemic hyperdynamic response characterized by a decrease in MAP and SVRI from 66.0 +/- 3.9 to 55.0 +/- 2.8 mm Hg (P < .05) and from 422.0 +/- 22.0 to 272.0 +/- 29.0 mm Hg.min.kg/L (P < .05), respectively. The administration of LPS produced an increase in MPAP and PVRI from 16.3 +/- 0.8 to 30.0 +/- 1.3 mm Hg (P < .05) and from 37.0 +/- 5.3 to 119.0 +/- 13.0 mm Hg.min.kg/L (P < .05), respectively. In the LPS/NAME group, NAME infusion normalized MAP and increased SVRI from 506.0 +/- 40.0 to 642.0 +/- 72.0 mm Hg.min.kg/L (P < .05). Infusion of NAME potentiated LPS-induced pulmonary hypertension, increasing MPAP and PVRI from 16.8 +/- 0.6 to 36.0 +/- 2.8 mm Hg (P < .05) and from 59.0 +/- 3.5 to 319.0 +/- 64.0 mm Hg.min.kg/L (P < .05), respectively. Infusion of NAME alone increased MAP from 74.0 +/- 1.3 to 100.0 +/- 4.1 mm Hg (P < .05) and had no significant effect on MPAP and PVRI. CONCLUSIONS: The potentiation of LPS-induced pulmonary hypertension following NAME infusion suggests that inhibition of nitric oxide synthase may have a limited role in the treatment of septic shock.

Amino Acid Oxidoreductases↗
PubMed1994

Granulocyte-macrophage colony stimulating factor gene expression and function during tumor promotion.

Although recent evidence suggests that granulocyte-macrophage colony stimulating factor (GM-CSF) plays a role in cutaneous inflammation induced by topical exposure of phorbol ester tumor promoters to murine epidermis, there is little information available on the temporal sequence of gene expression of this cytokine over the time course of tumor promotion or about its function in this process. The goal of the present studies was to examine the potential role of GM-CSF in tumor promotion in SENCAR mice. Competitive reverse transcriptase polymerase chain reaction (RT-PCR) studies demonstrated that a single topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA; 2 micrograms, 10 micrograms) to the dorsal epidermis of SENCAR mouse skin stimulated a dose and time dependent GM-CSF gene expression that was upregulated at 1 h after TPA exposure, peaked at 3 h and declined at 12 h. Although treatment with 7',12'-dimethylbenz[a]anthracene (DMBA) did not stimulate GM-CSF gene expression, GM-CSF gene expression was elevated in epidermal tissue isolated from SENCAR mice treated with a single application of 10 nmol DMBA followed by multiple applications of 2 micrograms TPA over a 1-22 week time course. Immunochemical and autoradiographic studies demonstrated that GM-CSF protein was produced by suprabasal keratinocytes, interfollicular cells, nonproliferating papilloma cells and leukocytes within the dermis. Intraperitoneal injection of recombinant (r) GM-CSF into SENCAR mice at 2 h prior to topical application of 10 micrograms TPA induced a significant increase in epidermal keratinocyte proliferation, leukocyte infiltration into the dermis, hydroperoxide production by circulating neutrophils and chemotactic activity present within the plasma at 24 h compared to treatment with only 10 micrograms TPA. Intravenous injection of anti-GM-CSF antibodies significantly inhibited both local and systemic inflammatory events induced by topical application of TPA. The present studies suggest that GM-CSF has a broad spectrum of activity with at least two target cell populations, epidermal keratinocytes within the proliferative compartment and leukocytes. This cytokine is actively transcribed during the tumor promotion process, acts as a signal peptide that stimulates epidermal proliferation, primes circulating neutrophils to produce hydroperoxide and regulates leukocyte migration.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1994

Prenatal diagnosis and management of gastrointestinal anomalies.

The increased use of prenatal sonography has led to earlier and more frequent diagnosis of a wide range of gastrointestinal anomalies. Many of these anomalies are associated with other severe cardiac, renal, and genetic abnormalities that may impact on decisions regarding timing and site of delivery. The majority of these patients should be referred to a center that provides perinatal, neonatal, and pediatric surgical expertise. After a complete prenatal evaluation, a decision regarding the site of delivery and the need for subspecialty referral can be made. Prenatal diagnosis of the conditions discussed in this article does not influence the mode of delivery, but subsequent management of the newborn is improved by delivery in a tertiary care center.

Digestive System Abnormalities↗
PubMed1994

Prenatal diagnosis and management of the fetus with an abdominal wall defect.

Prenatal ultrasound has advanced our understanding of congenital abdominal wall defects. In addition to providing insights into the divergent embryological origins and natural history of abdominal wall defects, ultrasound has had an important impact on the management of these anomalies. For fetuses with gastroschisis, the changes in appearance of the bowel may suggest expeditious delivery. In cases of omphalocele, the presence of additional anomalies is significantly associated with the ultimate prognosis for these fetuses. Giant omphalocele may preclude vaginal delivery secondary to dystocia. Exstrophies of the cloaca and bladder are rare congenital abnormalities that often present complex management issues, including gender reassignment in cases of cloacal exstrophy, for those couples wishing to continue the pregnancy. We believe that the optimal management of a fetus diagnosed with an abdominal wall defect requires a coordinated effort among specialists from maternal fetal medicine, pediatric surgery, and pediatrics.

Abdominal Muscles↗
PubMed1993

Adenosine diphosphate stimulation of cultured hematopoietic cell lines.

Adenosine diphosphate (ADP) plays a critical role in platelet activation both by exogenous stimulation and the release of endogenous intracellular stores. As the platelet ADP receptor is not well defined, we have chosen to identify and characterize several cell lines that possess functional receptors for this nucleotide. Rat promegakaryoblasts (RPM), human erythroleukemia cells (HEL), U937, and K562 leukemia cells responded to ADP, as measured by a rapid increase in intracellular calcium. In the case of RPM cells, ADP was the only naturally occurring platelet agonist capable of eliciting this response. Binding studies with [3H]ADP and fixed cells showed 3.99 +/- 1.77 x 10(5) binding sites/cell for RPM cells (apparent dissociation constant [kd] = 7.75 +/- 2.3 x 10(-8) mol/L), 8.19 +/- 3.25 x 10(5) sites/cell for HEL cells (kd = 2.15 +/- 0.84 x 10(-7) mol/L, 1.15 +/- 0.23 x 10(6) sites/cell for U937 cells (kd = 2.20 +/- 0.53 x 10(-7) mol/L) and 5.39 +/- 2.80 x 10(5) sites/cell for K562 cells (kd = 1.37 +/- 0.39 x 10(-7) mol/L), Inhibition studies with unlabeled nucleotides and analogues showed that binding was approximately 85% specific and the inhibitory pattern was similar to that seen with mature platelets. The purine base adenosine resulted in little or no inhibition. These studies indicate that both human and rat hematopoietic cell lines possess intact ADP receptors and may be useful tools in future studies of the structure and function of this important platelet-activation system.

Adenosine Diphosphate↗
PubMed1993

Measurement of intracellular hydrogen peroxide induced by biomaterials implanted in a rodent air pouch.

Biomaterials elicit an inflammatory response that is undoubtedly a factor in their healing and in the complications associated with their use. Herein, we report the modification of a rat air pouch in which we measured the production of intracellular hydrogen peroxide by inflammatory cells adherent to the surfaces of silicone elastomer (SE) and expanded polytetrafluoroethylene (ePTFE). We used the fluorescent probe dichlorofluorescein diacetate (DCFH-DA) to measure the intracellular production of hydrogen peroxide 2 and 7 days after implantation. After 2 days, host cells adherent to ePTFE produced almost 3.5 times more hydrogen peroxide than did cells adherent to SE (P < .001). By 7 days, the H2O2 production of cells adherent to ePTFE had decreased while that on cells adherent to SE was unchanged. These data indicate that the air pouch is a good alternative to other in vivo models for studies of the biological reactions induced by biomaterials.

Air↗
PubMed1993

Differential induction of stromelysin mRNA by bovine articular chondrocytes treated with interferon-gamma and interleukin-1 alpha.

Articular chondrocytes from rheumatoid joints have been shown to express class II major histocompatibility (MHC) antigens that were correlated with the presence of interferon-gamma (IFN-gamma) in the inflamed joint. Chondrocytes expressing MHC antigens function as antigen presenting cells and thus stimulate lymphocyte proliferation. These responses suggest a powerful role for the IFN-gamma stimulation of chondrocytes. The present studies were designed to examine the functional role of chondrocytes exposed to IFN-gamma during cartilage degradation that occurs in synovial disease. Destruction of cartilage in arthritis is partially attributable to metalloproteinases released by the chondrocytes in response to interleukin-1 (IL-1). Bovine articular chondrocytes treated with interleukin-1 alpha (IL-1 alpha) produced enhanced levels of stromelysin mRNA, however, Northern blots could not determine the percentage of cells responding. Exposure of bovine articular chondrocytes to IFN-gamma induced the expression of bovine HLA-DR (boHLA-DR) antigen in 50% of the cells. Using a modified cell sorting technique, chondrocytes that expressed class II MHC antigens produced two fold greater stromelysin mRNA than chondrocytes that did not express this antigen. In contrast, collagen type II mRNA levels were similar in chondrocytes, regardless of the expression of class II MHC antigens. In situ hybridization studies showed that less than half of all cartilage chondrocytes were induced to synthesize stromelysin mRNA. These observations suggest that IFN-gamma stimulates specific subpopulations of chondrocytes to be functionally active in inflammation-induced metalloprotease secretion.

Animals↗
PubMed1993

Interleukin-1 alpha gene expression and localization of interleukin-1 alpha protein during tumor promotion.

Treatment of the dorsal epidermis of SENCAR mice with 12-O-tetradecanoylphorbol-13-acetate (TPA) induced a time- and dose-dependent stimulation of interleukin-1 alpha (IL-1 alpha) gene expression. Levels of IL-1 alpha mRNA were elevated as early as 15 min and peaked at 3-4 h after a single application of TPA (2 micrograms or 10 micrograms). IL-1 alpha gene expression increased in epidermal tissue isolated from SENCAR mice at 1, 3, 6, 10, 16, and 22 wk after a single treatment with 10 nmol 7,12-dimethylbenz[a]anthracene (DMBA) and subsequent twice-weekly application of 2 micrograms TPA. IL-1 alpha-immunoreactive protein was specifically localized within suprabasal keratinocytes in cutaneous tissue isolated from mice treated with DMBA-TPA for 1-22 wk and in nonproliferating cells located within papilloma tissue isolated from SENCAR mice at 22 wk after initiation and promotion. Basal cells within hyperplastic epidermis did not produce IL-1 alpha-immunoreactive protein. DMBA treatment alone did not induce IL-1 alpha gene expression. Injection of IL-1 alpha-specific antibodies (50 micrograms) into SENCAR mice via the tail vein 2 h before treatment with TPA (2 micrograms or 10 micrograms) significantly (P < 0.05) inhibited the skin thickening usually observed 24 h after treatment with TPA. Autoradiography studies showed that injection of anti-IL-1 alpha antibodies inhibited incorporation of [methyl-3H]thymidine by keratinocytes within the epidermis and by cells within hair follicles. It also inhibited neutrophil infiltration into the dermis, which usually results from topical application of TPA. These data suggest that IL-1 alpha is a pivotal cytokine produced by specific subpopulations of epidermal keratinocytes and that IL-1 alpha primarily regulates the epidermal proliferative response of a distinctly separate population of keratinocytes after topical exposure of murine epidermis to TPA and secondarily modulates neutrophil migration into the dermis. Consequently, manipulation of IL-1 alpha may be a way to attenuate or abrogate the cutaneous response to TPA by altering keratinocyte proliferation, the resultant hyperplasia, and a portion of the inflammatory response characterized by dermal infiltration of neutrophils.

Acetone↗
PubMed1993

Amplified expression of intercellular adhesion molecule-1 (ICAM-1) and M(r) 40K protein by DLD-1 colon tumor cells by interferon-gamma.

Inflammatory bowel disease, in particular ulcerative colitis, is characterized by localization of leukocytes in close proximity to the colonic epithelium, which may be mediated by the expression of intercellular adhesion molecules (ICAM-1; CD 54). We previously reported the presence of an organ-specific M(r) 40K colonic protein that acts as an autoantigen in ulcerative colitis and is present on the surface of colonic epithelial cells and also in DLD-1 colon cancer cells. Using the colon tumor cell line DLD-1 and flow cytometry, ICAM-1 antibody binding by untreated cultured DLD-1 cells was similar to background antibody binding (mean channel number, MCN = 9.77 +/- 2.13). Interferon-gamma (100 U) induced a 1-2 log increase in anti-ICAM-1 antibody binding from as early as 12 hr after exposure up to 72 hr and a moderate increase (up to about 100%) in the binding of anti-M(r) 40K antibody. Additional studies showed that anti-ICAM-1 and anti-M(r) 40K antibodies bound to DLD-1 cells regardless of the presence of the other antibody. Taken together, the present observations suggest that the epitopes of ICAM-1 and M(r) 40K molecules are coexpressed by colonic epithelial cells, regardless of the presence of the other molecule. Furthermore, lymphocytes in the colonic mucosa that are activated to produce interferon-gamma may upregulate the expression of both of these molecules.

Autoantigens↗
PubMed1993

Inguinal-scrotal suppuration following treatment of perforated appendicitis.

Suppuration of a congenital hernia or communicating hydrocele following generalized peritonitis is rare. The lack of reported cases in the recent literature may indicate a decreasing incidence of this unusual complication. We report a case of suppuration of a communicating hydrocele with testicular loss 2 days after treatment of perforated appendicitis in a 10-year-old boy.

Appendicitis↗