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Biomedical subjects

K G Smith

Publications and source records attributed to K G Smith.

At least 19 recordsLinked to original sources
PubMed1992

Augmentin-induced jaundice with a fatal outcome.

OBJECTIVE: To report a case of death due to Augmentin-induced cholestatic hepatitis and discuss a possible drug interaction between Augmentin and oestrogenic steroids. CLINICAL FEATURES, INTERVENTION AND OUTCOME: An 81-year-old man, on oestrogen therapy for prostatic malignancy, presented with obstructive jaundice one week after completing a four-week course of Augmentin for recurrent urinary tract infection. Liver biopsy showed features of a drug-induced cholestatic hepatitis with bile duct injury. His clinical course was marked by progressive deterioration with increasing jaundice and the development of hepatic encephalopathy. A course of prednisolone did not result in any improvement and he died nine weeks after the onset of jaundice. CONCLUSIONS: The cholestatic hepatitis induced by Augmentin is usually reversible but may be progressive, leading to death. The concurrent administration of ethinyloestradiol, a potentially cholestatic agent, may have altered the susceptibility and/or course of the reaction in this patient.

Aged↗
PubMed1992

Equipment and methods for simple sensory testing.

Four simple tests which can be used for routine sensory testing following trigeminal nerve injuries are suggested. The methods for constructing the equipment needed for these tests are described.

Differential Threshold↗
PubMed1990

A fluoridation campaign: the Phoenix experience.

On January 31, 1989, the city council of Phoenix, Arizona, voted to approve water fluoridation. Despite a small number of campaign participants and a limited budget, profluoridationists launched a successful 16-month effort that included novel marketing techniques, intensive collaboration with media representatives, and an aggressive challenge of the antifluoridation movement. Public support was garnered through an advisory petition effort and positive media coverage; political support resulted from a carefully orchestrated educational strategy that included expert testimony and comprehensive reference materials. With a population of approximately 1 million people, Phoenix is the ninth largest city in the country and, until the measure was implemented, the third largest nonfluoridated city.

Arizona↗
PubMed1987

T cell activation by anti-CD3 antibodies: function of Fc receptors on B cell blasts, but not resting B cells, and CD18 on the responding T cells.

Mouse anti-human CD3 (T3) antibodies can induce T cell proliferation in the presence of Fc receptor (FcR)-bearing accessory cells. Depending on whether the particular antibody can interact with the FcR, it can be mitogenic or otherwise. Previously, some of us (Smith, K. G. C. et al., Eur. J. Immunol. 1986. 16:478) examined human T cell responses to the murine anti-CD3 antibody switch variants UCHT1 (IgG1) and UCHT1B (IgG2b). Using a novel xenogeneic system with mouse macrophages (M phi) and an anti-FcR antibody, 2.4G2, we obtained direct evidence for accessory function of FcR in these responses. However, mouse B cells which also possess FcR were not accessory cells. Here we show that resting B cells do not inhibit anti-CD3 responses in the presence of other accessory cells, and they do not synergize with them. They appear to be inert in these responses but this is not simply because of their radiosensitivity. In contrast, B cell blasts proved to be potent stimulators of responses with UCHT1, UCHT1B and OKT3 (IgG2a). All three responses were inhibited by 2.4G2, whereas we have shown previously that the OKT3 response with M phi was not, in keeping with the known specificities of B cell and M phi FcR. These findings are discussed in relation to the molecular cloning of FcR, and we consider the possibility that distinct FcR could be expressed on resting and activated B cells. A report that anti-CD18 (LFA-1) antibodies blocked the UCHT1 response with human monocytes raised the possibility that this molecule might also be involved in accessory function. However, we show that this inhibition is in fact at the level of the T cell, since anti-human, but not anti-mouse CD18 antibodies, inhibited proliferative responses and clustering with both human and mouse accessory cells. Our results demonstrate that the principal contribution of accessory cells to anti-CD3 responses may be the provision of an FcR, and that CD18 is most probably required at the level of the T cell.

Animals↗
PubMed1986

T cell activation by anti-T3 antibodies: comparison of IgG1 and IgG2b switch variants and direct evidence for accessory function of macrophage Fc receptors.

The human T3 antigen is closely associated with the T cell receptor. Some anti-T3 antibodies cause T cell proliferation in the presence of monocytes which have Fc receptors (FcR) that bind particular antibody subclasses. Such an interaction is thought to determine whether or not an anti-T3 antibody is mitogenic. We examined the mitogenicity of an IgG1 antibody, UCHT1, and an IgG2b switch variant of identical specificity, UCHT1B. With autologous monocytes, 76% of individuals responded to UCHT1 and 9% to UCHT1B, falling into three patterns of responsiveness. Both antibodies in the absence of monocytes induced responsiveness to recombinant interleukin 2, even for UCHT1B nonresponder T cells. The proliferation induced by UCHT1B, however, was always less than that induced by UCHT1. These findings demonstrate the critical role played by the Fc region for mitogenesis, and suggest a possible role for the hinge region. We then obtained direct evidence that mitogenicity can be mediated exclusively via FcR. Mouse macrophages have distinct FcR: FcRI binds IgG2a but FcRII binds IgG1 and IgG2b and its function can be inhibited by the specific antibody 2.4G2. Because UCHT1 and UCHT1B were of the correct subclass to interact with FcRII we examined the accessory function of mouse peritoneal macrophages. Without exception, human T cells now responded to both antibodies. Proliferation was drastically inhibited by 2.4G2 but not by an irrelevant anti-macrophage antibody, F4/80, nor by an anti-human neutrophil FcR antibody, 3G8. Furthermore, 2.4G2 did not inhibit the accessory function of mouse macrophages for OKT3, an IgG2a antibody that presumably interacts with FcRI, and did not inhibit the function of human monocytes for UCHT1 and UCHT1B. Mouse B cells, in contrast to macrophages, have an FcR which binds all three subclasses, but which can be inhibited by 2.4G2. B cells, however, were not accessory cells for mitogenesis with UCHT1, UCHT1B or OKT3. These findings are discussed in relation to other requirements for T cell activation by anti-T3 antibodies.

Antibodies, Monoclonal↗
PubMed1986

Phenyl isopropyl adenosine alters fetal electrocorticogram, breathing and heart rate.

Six fetal sheep were equipped with intratracheal, amniotic and vascular catheters and electrocorticogram electrodes to study the effect of phenyl isopropyl adenosine (PIA) on electrocorticogram and fetal breathing movements. Three animals had functioning electrocardiogram electrodes. During 1,000-min control periods, low-voltage high-frequency (LVHF) electrocorticogram predominated 60 +/- 1% (mean +/- SEM) of total time. Fetal breathing movements occurred 34 +/- 1% of total time and only during LVHF electrocorticogram. PIA 0.125 mg was given intravenously to the fetus during established LVHF electrocorticogram and fetal breathing movements. LVHF electrocorticogram converted in 58 +/- 16 s to high-voltage low-frequency (HVLF) electrocorticogram which persisted for 10 +/- 3 min. This was followed by a third electrocorticogram pattern for 119 +/- 12 min. Fetal breathing movements ceased in 47 +/- 25 s and did not recur for 150 +/- 20 min. An increase in fetal breathing movements (59 +/- 2% of total time) occurred between 300 and 800 min (control 34 +/- 1%, p less than 0.05). Electrocardiogram demonstrated a decrease in heart rate from 170 +/- 6 to 90 +/- 6 beats per min with return to baseline in 113 +/- 49 min. No significant changes occurred in blood gases. We conclude that fetal electrocorticogram, fetal breathing movements and heart rate are influenced by adenosine.

Adenosine↗
PubMed1985

Cerebrocostomandibular syndrome. Case report and literature review.

Cerebrocostomandibular syndrome (CCM) is characterized by micrognathia, cleft palate, rib defects, and frequently, mental deficiency. Death from respiratory complications occurs in 40 percent of cases before they reach 1 year of age. We describe a case of CCM with the previously unreported findings of large for gestational age at birth, radiologic evidence of bilaterally displaced radial heads, and development of brachycephaly.

Birth Weight↗