Allergic reaction to hyaluronidase after a peribulbar injection.
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Adjuvants, Anesthesia↗
Biomedical subjects
A Agrawal
Publications and source records attributed to A Agrawal.
Oesophageal stricturing secondary to adult Stevens-Johnson syndrome: similarities in presentation and management to corrosive injury.
Clinical decisions often have to be made in the absence of evidence. In some cases, it is appropriate to use evidence from similar but more common conditions for which studies have resulted in evidence-based practice. This report describes a case of oesophageal stricture following Stevens-Johnson syndrome illustrating this concept, although it is likely that there are many other conditions in which the same principle will stand the clinician in good stead. Dilatation led to long-standing relief of dysphagia in our case.
Barium Sulfate↗
Visual symptoms in patients on cyclophosphamide may herald sight threatening disease.
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Adult↗
Transient third nerve palsy in a young patient with intracranial arteriovenous malformation.
PURPOSE: To describe a patient with transient third nerve palsy as the possible presenting sign of intracranial arteriovenous malformation. METHOD: Case report. RESULT: A 24-year-old female presented to ophthalmic casualty with sudden onset binocular diplopia and was diagnosed to have right sided partial third nerve palsy. Within 30 hours the third nerve palsy had recovered completely. A MRI scan and subsequent carotid angiogram revealed a large, high flow, trans-cortical Spetzler-Martin grade 4 arteriovenous malformation. The feeder vessel of the AVM originated from the right middle cerebral artery. Superficial venous drainage was via the superficial middle cerebral vein to the right transverse sinus. The deep venous drainage was via thalamostriate veins into markedly dilated internal cerebral vein and vein of Galen (Great cerebral vein). Venous reflux was noted around the midbrain from the vein of Galen. CONCLUSIONS: Transient third nerve palsy may rarely occur secondary to intracranial arteriovenous malformation. Ophthalmologists should consider neuroimaging in the investigations for transient cases of III nerve palsy in young patients.
Adult↗
Fate of chronically infected onlay mesh in groin wound.
This case report throws some light on the way in which the body handles an infected onlay mesh following groin hernia repair. It describes the case of a 73-year-old man who developed this rare complication and demonstrates the mechanism by which this complication occurred.
Aged↗
A twin study of sex differences in social support.
BACKGROUND: Social support may reduce the risk of psychiatric illness. Though perceived as an environmental measure, genetic factors may influence levels of social support. A relationship between social roles and personality with social support suggests possible sex effects on the sources of individual differences in social support. METHOD: We used the responses of MZ and DZ same and opposite sex twins to 16 questions regarding their social life. Six factors--friend support, relative support, friend problem, relative problem, confidants and social integration were used for structural equation modelling. Factor derived scales were analysed for genetic, shared and unique environmental influences. Quantitative and qualitative gender differences were analysed using the software package Mx. RESULTS: Except for relative support and confidants, no qualitative sex differences were seen. Genetic and individual specific environmental influences accounted for the variance for friend support, friend problems, relative problems and social integration and no quantitative gender differences were seen. For relative support genetic factors were detected in females but not males, while for confidants, the shared environment was important in females but not males. CONCLUSIONS: Except for relative support in males, genetic factors influence variation in all dimensions of social support. Shared environmental factors influence relative support and relative problems in both sexes. Sex differences were detected for confidants and relative support.
Adult↗
Preclinical studies of gene transfer for the treatment of desmoid disease in familial adenomatous polyposis.
BACKGROUND: Familial adenomatous polyposis (FAP) arises following mutation or loss of the adenomatous polyposis coli (APC) gene. Desmoid tumours are proliferations of fibroblasts and occur as an extracolonic manifestation of FAP. They are a leading cause of death after colectomy. The aim of this study was to assess the potential for APC gene transfer into fibroblasts in vitro and in vivo as a basis for consideration of gene therapy in the prevention or treatment of desmoid tumours. METHODS: The APC gene was transferred by lipofection into fibroblasts in tissue culture and into peritoneum and small bowel mesentery in vivo. Reverse transcriptase-polymerase chain reaction was used to determine whether or not transfection was successful. RESULTS: Transgene expression was recorded in vitro to 7 days after transfection. High levels of transgene expression were also seen in samples of peritoneum (all eight mice), small bowel mesentery (seven of eight), liver (seven of eight) and intestinal tissues (five to six of eight) following intraperitoneal treatment. Interestingly, transgene expression in gonadal tissues was occasionally noted. CONCLUSION: Liposomal transfection of APC gave prolonged high-level expression of the transgene, an important basis for gene therapy. No adverse effects were recorded. Further work is needed in animal models of desmoid disease to assess the clinical effects of gene therapy.
Adenomatous Polyposis Coli↗
Superior chemotherapeutic efficacy of amphotericin B in tuftsin-bearing liposomes against Leishmania donovani infection in hamsters.
Chemotherapeutic efficacy of the amphotericin B (Amp B), which is the drug of choice for treatment of the leishmanial infections (kala-azar) that become resistant to the conventional chemotherapy using antimonials, has been examined in the Leishmania donovani infected hamsters after encapsulating the drug in tuftsin-free as well as tuftsin-bearing liposomes. The activity was significantly increased (p < 0.05) by delivering Amp B in tuftsin-free liposomes. This antileishmanial effect of the liposomized Amp B was further increased (p < 0.05) by grafting the natural macrophage-activator tetrapeptide, tuftsin (Thr-Lys-Pro-Arg), on the liposome's surface. This could possibly be attributed to both the enhanced drug tolerance after liposomization as well as to the increased uptake of tuftsin-bearing Amp B-laden liposomes by the macrophages. In addition to the increased efficacy, encapsulation of Amp B in the tuftsin-bearing liposomes also enhanced the drug accessibility to areas (e.g. bone marrow) that are otherwise inaccessible to the free drug. These results further demonstrate the usefulness of tuftsin-bearing liposomes as drug vehicles in treatment of the macrophage-based infections that have been reviewed recently (Agrawal, A.K. and Gupta, C.M. (2000). Tuftsin-bearing liposomes in treatment of macrophage-based infections, Adv. Drug Deliv. Rev., 41, 135-146).
Amphotericin B↗
Mutational status of overexpressed p16 in head and neck cancer: evidence for germline mutation of p16/p14ARF.
Inactivation of the p16 tumor suppressor gene is a common phenomenon in squamous cell carcinoma of the head and neck (SCCHN). Less commonly described is the observation of p16 overexpression in SCCHN. Since overexpression of p16 is a potent predictor of outcome in other cancers, we were interested in determining the level of expression of p16 in our SCCHN specimens as a prerequisite to later prognostic studies. We were also interested in determining the mutational status of p16 in these tumors, in order to determine whether the combination of overexpression and gene alteration may predict a different clinical outcome from overexpression alone. A total of 84 specimens of SCCHN were selected for study. These specimens were obtained from all major sites within the oral cavity, oropharynx, pharynx and larynx. The level of expression of p16 in SCCHN specimens was measured by semi-quantitative RT-PCR. In 35 cases, RNA was also isolated from matched normal tissue obtained from a negative tumor margin. In the other 49 cases, the expression level was compared with the level of expression measured in pooled normal RNA obtained from 10 specimens of normal epithelial tissue. Overexpression of p16 was documented when the level of expression in the tumor specimen was 2-fold or greater above the level of expression found in normal tissue. A total of 46 specimens demonstrated overexpression of p16 (55%). All specimens demonstrating overexpression were then subject to sequence analysis. Thirty specimens (65%) showed p16-specific gene alterations, ranging from intragenic deletions to single point mutations, and 15 of these cases concomitantly affect p14ARF. A single specimen demonstrated a silent point mutation within the p16 reading frame. This mutation produces a stop codon at residue 85 in the context of the p14ARF reading frame, predicting premature termination of p14ARF within a previously determined nucleolar localization signal. This observation suggests that in some cases at least, p14ARF may be a selective target for alteration, independently of p16. Analysis of a normal tissue specimen obtained from a negative tumor margin, and a blood sample obtained approximately five years after surgery indicate that this p14ARF-specific alteration may represent a germline mutation.
Carcinoma, Squamous Cell↗
When software isn't for sharing.
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Computational Biology↗
Detecting living cryptosporidium.
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Animals↗
Topology and structure of the C1q-binding site on C-reactive protein.
The host defense functions of human C-reactive protein (CRP) depend to a great extent on its ability to activate the classical complement pathway. The aim of this study was to define the topology and structure of the CRP site that binds C1q, the recognition protein of the classical pathway. We have previously reported that residue Asp(112) of CRP plays a major role in the formation of the C1q-binding site, while the neighboring Lys(114) hinders C1q binding. The three-dimensional structure of CRP shows the presence of a deep, extended cleft in each protomer on the face of the pentamer opposite that containing the phosphocholine-binding sites. Asp(112) is part of this marked cleft that is deep at its origin but becomes wider and shallower close to the inner edge of the protomer and the central pore of the pentamer. The shallow end of the pocket is bounded by the 112-114 loop, residues 86-92 (the inner loop), the C terminus of the protomer, and the C terminus of the pentraxin alpha-helix 169-176, particularly Tyr(175). Mutational analysis of residues participating in the formation of this pocket demonstrates that Asp(112) and Tyr(175) are important contact residues for C1q binding, that Glu(88) influences the conformational change in C1q necessary for complement activation, and that Asn(158) and His(38) probably contribute to the correct geometry of the binding site. Thus, it appears that the pocket at the open end of the cleft is the C1q-binding site of CRP.
Amino Acid Substitution↗
Characterization of metal affinity of green fluorescent protein and its purification through salt promoted, immobilized metal affinity chromatography.
Immobilized metal affinity chromatography (IMAC) was investigated as a method of recovery for green fluorescent protein (GFPuv). It was found that in the absence of genetic modification to enhance metal affinity, GFPuv displayed strong metal affinity to Cu(II) and Ni(II), and weak or negligible affinity to Zn(II) and Co(II). Changes in the mobile phase NaCl concentration during Ni(II)-IMAC strongly affected purity and yield of GFPuv, with fine resolution under higher NaCl concentrations. Finally, IMAC via Cu(II) and Zn(II) with intervening diafiltration was used to recover GFPuv with high yield and purity.
Chromatography, Affinity↗
Transactivation of C-reactive protein by IL-6 requires synergistic interaction of CCAAT/enhancer binding protein beta (C/EBP beta) and Rel p50.
We have previously found that overexpression of the Rel protein p50 stimulated C-reactive protein (CRP) expression in Hep 3B cells and that p50 could bind to a nonconsensus kappaB site overlapping the CCAAT/enhancer binding protein (C/EBP) binding site centered at position -53 on the CRP promoter. Accordingly, we employed EMSA to investigate possible cooperation between p50 and C/EBP proteins using an oligonucleotide probe (-63/-41) derived from the CRP promoter and containing both C/EBP and p50 binding sites. Abs to p50, but not to p65, decreased formation of C/EBPbeta-containing complexes in nuclei of IL-6-treated cells, indicating that ternary complexes containing C/EBPbeta and p50 are formed on the CRP promoter. Depletion of free Rel proteins by pretreatment of nuclear extracts with a kappaB consensus oligonucleotide markedly decreased formation of C/EBP complexes, indicating that Rel proteins are required for formation of such complexes. Overexpression of p50 in transient cotransfection studies using the proximal CRP promoter (-125/+9) linked to a luciferase reporter caused a 3-fold increase of luciferase activity, while C/EBPbeta overexpression caused an 18-fold increase; simultaneous overexpression of both transcription factors increased luciferase activity approximately 600-fold. Mutation of either the C/EBP binding site or the p50 binding site drastically reduced the effects of overexpressed transcription factors. Taken together, our findings indicate that binding of Rel p50 to the nonconsensus kappaB site enhances and stabilizes binding of C/EBPbeta to the CRP promoter and that binding of both C/EBPbeta and p50 to their overlapping cognate sites is required for induction of CRP expression by IL-6.
Binding Sites↗
Radiation induced oxidative stress: II studies in liver as a distant organ of tumor bearing mice.
Since the radiation dose tolerance of normal tissues/organs away from the site of tumor influences the success of radiation therapy of cancer, and antioxidant status is likely to be one of the factors to determine the tolerance; the radioresponse of antioxidant enzymes has been examined in the liver as a representative distant organ in the tumor-bearing mice. Swiss albino male mice (7-8 weeks old) with Ehrlich solid tumor in the thigh pad were irradiated with different doses of gamma-radiation (0-9 Gy) at a dose rate of 0.0153 Gy/s and the specific activities of enzymes involved in the free radical metabolism were determined in the liver. Except GST, the activities of SOD, DTD and Gly I as well as the GSH content were found to be higher in the liver of tumor-bearing mice compared to the non-tumor bearing mice. The catalase activity progressively decreased with dose in both the groups of mice. However, the activity was relatively higher in the liver of tumor- bearing mice than the control. Thus, the radioresponse of antioxidant enzymes seemed to be significantly different in the liver of tumor-burdened mice compared to controls. The enhanced activities might be due to relatively more damage caused by radiation. The higher levels of NO* and peroxidative damage in the liver of tumor-bearing mice probably suggest this possibility. These findings of the present work might have some serious implications as the increased radiation-damage of the distant normal organs (due to tumor burden) is likely to adversely affect the therapeutic gain.
Animals↗
Radiation induced oxidative stress: I. Studies in Ehrlich solid tumor in mice.
Understanding the response of tumors to ionizing radiation might potentially lead to improvement in tumor control and patient morbidity. Since the antioxidant status is likely to be linked to radioresponse, its modulation needs to be examined. Therefore, Swiss albino male mice (7-8 weeks old) with Ehrlich solid tumors were irradiated with different doses of gamma rays (0-9 Gy) at a dose rate of 0.0153 Gy/s; and enzymes involved in antioxidant functions were determined in the tumors. Radiation effects in terms of oxidative damage, LDH, nitric oxide and DNA fragmentation were also examined. In tumors, the specific activity of SOD was increased with dose but declined 6 Gy onwards. GST, DTD and GSH showed an almost progressive increase. These enhanced activities might have resulted from the increased protein expression. This possibility was supported by the Western Blot analysis for GST protein. These changes might be closely linked to the radiation-induced oxidative stress as reflected by the enhanced levels of peroxidative damage, DNA fragmentation, LDH activity and nitric oxide levels. These findings may have relevance to radiation therapy of cancer as the elevated antioxidant status of irradiated tumors is likely to limit the effectiveness of radiation dose and adversely affect the therapeutic gain.
Animals↗