[Fine structural changes in the corneal epithelium in tissue culture. I. The lipid layer on the epithelium surface].
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Animals↗
Biomedical subjects
J Rode
Publications and source records attributed to J Rode.
Immunohistochemical demonstration of the p53 tumour suppressor gene product in cancer of the pancreas and chronic pancreatitis.
The p53 tumour suppressor gene and its protein products after point mutations are currently attracting wide attention in the investigation of human tumours. In this study we present the findings on percutaneous pancreatic biopsies of 82 cases after routine processing and immunostaining for the polyclonal p53 antibody CM1, an antibody directed against both wild and mutant forms of p53 protein. There were 51 carcinomas, 5 islet cell tumours, 16 cases of chronic pancreatitis (including one with atypical ductal epithelium) and seven histologically normal pancreatic biopsy specimens. None of the seven normal cases showed any definite nuclear immunostaining for p53. Thirty-two (63%) of the pancreatic adenocarcinomas showed moderate to intense immunoreactivity. Of the 16 cases of chronic pancreatitis, 11 were negative and three showed equivocal immunostaining. The one case with ductal epithelial atypia showed mild to moderate immunoreactivity. All islet cell tumours were negative. The expression of the p53 gene, therefore, appears increased in the majority of pancreatic adenocarcinomas while this is not observed in chronic pancreatitis or normal pancreatic tissue. Nuclear immunoreactivity for p53 protein may represent mutant forms because of the short half-life of the wild-type protein. The lack of p53 expression in some cases of pancreatic adenocarcinoma may be due to different types of mutant proteins not detectable by the CM1 antibody. Nuclear immunoreactivity to the p53 protein in pancreatic biopsy is more suggestive of a malignant tumour than chronic pancreatitis.
Chronic Disease↗
Minimal anesthetic concentration and cardiopulmonary dose response of isoflurane in ducks.
The minimal anesthetic concentration (MAC) for isoflurane was determined during spontaneous ventilation in nine male Peking ducks (7 to 12 weeks of age; 3.0 +/- 0.4 kg). While each bird was awake, arterial blood was collected for analysis of pH, PaCO2, and PaO2. After anesthesia was induced with isoflurane in oxygen, MAC was determined for isoflurane in each bird during spontaneous ventilation in a manner similar to MAC determinations in mammals. Pulmonary dose-response data were collected at 1 MAC and 1.5 MAC. Anesthetic index (Al; an index of anesthetic-induced apnea) was calculated from ducks that became apneic. The MAC for isoflurane was 1.30 +/- 0.23% (mean +/- SD). There was a dose-dependent decrease in ventilation as evidenced by a statistically significant increase in PaCO2. Apnea or unacceptable hypercarbia (PaCO2 greater than 110 mm Hg), or both, were common occurrences at end-tidal isoflurane concentrations greater than 1.5 MAC. Anesthetic index calculated from four ducks was 1.65 +/- 0.13 (mean +/- SEM). There was no significant difference between the means of either heart rate or mean arterial blood pressure in birds at 1.0 and 1.5 MAC.
Anesthesia, General↗
Patterns of staining for neurone specific enolase in benign and malignant melanocytic lesions of the skin.
Neurone specific enolase (NSE) is a useful marker for melanoma independent of the criterion of melanogenesis. A range of benign and malignant melanocytic skin lesions has been studied to assess the diagnostic potential of staining for NSE. The detailed features of the presence and distribution of NSE in 47 skin lesions are presented. These include 3 junctional, 7 compound, 15 intradermal and 8 SPitz naevi; 6 superficial type, 2 lentigo maligna and 6 nodular melanomata. A progressive increase of staining for NSE from benign to malignant is seen. Spitz naevi could easily be differentiated from melanoma. An advantage of this stain is the simultaneous demonstration of the innervation of these lesions. We conclude that NSE is a useful aid to the diagnosis and assessment of melanocytic skin tumours and may prove of value in clarifying the nature of these enigmatic lesions.
Humans↗
Immunohistochemical staining of granular cell tumour for neurone specific enolase: evidence in support of a neural origin.
Eight cases of benign granular cell tumour of tongue and skin all showed immunohistochemical staining for neurone specific enolase (NSE). Four Schwannomas, two neurofibromas and Schwann cells of nerves related to these tumours and the granular cell tumours showed no staining for NSE. NSE is a marker for neuronal type cells of the nervous system and cells of the neuroendocrine system. The results support a neural derivation of granular cell tumours. The histogenetic precursor may be an undifferentiated spindle-shaped 'reserve' cell of peripheral nerve, perhaps necessary for replacement of shed sensory organs.
Cytoplasmic Granules↗
Immunohistochemical studies of S100 protein and other neural characteristics expressed by granular cell tumour.
Eight cases of granular cell tumour (GCT), five Schwannomas and two neurofibromas were examined immunohistochemically for the presence of S100 protein, neurofilament protein (NP), epidermal growth factor (EGF) and glial fibrillary acidic protein (GFAP). The solochrome cyanin stain for myelin was also applied. All cases of GCT showed staining for S100 protein. Focal positivity was seen in Schwannomas and neurofibromas. Stains for EGF, GFAP, NP and solochrome cyanin were negative. S100 is a marker for Schwann cells. The expression by GCT of S100 supports a neural genesis of GCT.
Brain Chemistry↗
Serotonin and its possible role in the painful non-inflamed appendix.
After immunohistochemical staining appendices without active inflammation but producing symptoms of appendicitis (N = 24) were compared with a control group of appendices removed incidental to another procedure (N = 26). Staining for neurone specific enolase (NSE) showed more instances of nerve 'hyperplasia' in the control group than in the appendices generating pain refuting the concept of neuroappendicopathy based on quantitative nerve changes. Serotonin staining identified subepithelial neuroendocrine cells (SNC) in 85 per cent of the specimens. All cases showed serotonin immunoreactive enterochromaffin cells (EC). Staining for serotonin was significantly decreased in the SNC in the painful group. There were no significant differences between the two groups in staining intensity of SNC and EC for substance P (SP). Vasoactive intestinal polypeptide (VIP) was not seen in the SNC and EC and there were no differences in nerve fibre staining for VIP. Serotonin is a neurotransmitter as well as mediator of inflammation. It is suggested that reduced staining for serotonin in painful appendices reflects discharge of stores which could be instrumental in inducing the pain in these cases. Continued serotonin release may then lead to acute appendicitis.
Appendicitis↗