Biomedical subjects
J Willis
Publications and source records attributed to J Willis.
Characteristics of patients with community-acquired pneumococcal pneumonia.
OBJECTIVE: To describe the level of activity, independence and demographics of elderly people hospitalised with community-acquired pneumococcal pneumonia. DESIGN: Prospective descriptive study. SETTING: Seven university-affiliated hospitals and three community hospitals. PATIENTS: People aged over 55 years admitted to hospital with a clinical history consistent with pneumococcal pneumonia, a Streptococcus pneumoniae isolate in blood or sputum, and a chest x-ray consistent with pneumonia. Significant immunosuppression or certain comorbidities (parenchymal lung disease and end-stage renal failure) were exclusion criteria. MAIN OUTCOME MEASURE: Level of independence, assessed by participation in a range of standardised activities before the patient's illness. RESULTS: 82 patients met our case definition. Five refused to participate, leaving 77 evaluable patients. The patients had high levels of independence: 64 (83%; 95% confidence interval [CI], 73%-91%) lived in their own home and 69 (90%; 95% CI, 81%-95%) participated in regular hobbies. Exercise tolerance was good, with 43 (56%; 95% CI, 45%-68%) able to climb a flight of stairs and 59 (76%; 95% CI, 65%-85%) able to walk more than 50 m without stopping; 41 (53%; 95% CI, 41%-64%) could continue further than a kilometre. Mortality was low (9 patients; 12%) despite a high rate of bacteraemia (43 patients; 56%). Within the past five years, 59 (77%) had been hospitalised and 53 (69%) vaccinated with influenza vaccine. Only 7% had ever received pneumococcal vaccination. CONCLUSION: Pneumococcal pneumonia is not the "old man's friend". It represents a major cause of morbidity and mortality in otherwise well, active and independent older Australians. Hospitalisation and attendance for influenza vaccination may represent opportunities for pneumococcal vaccination.
E-cadherin germline mutations define an inherited cancer syndrome dominated by diffuse gastric cancer.
To extend earlier observations of germline E-cadherin mutations in kindreds with an inherited susceptibility to diffuse gastric cancer, we searched for germline E-cadherin mutations in five further families affected predominantly by diffuse gastric cancer and one family with a history of diffuse gastric cancer and early-onset breast cancer. Heterozygous inactivating mutations were found in the E-cadherin gene in each of these families. No mutation hotspots were identified. These results demonstrate that germline mutation of the E-cadherin gene is a common cause of hereditary diffuse gastric cancer and suggest a role for these mutations in the incidence of breast cancer.
Parachordoma is immunohistochemically and cytogenetically distinct from axial chordoma and extraskeletal myxoid chondrosarcoma.
Parachordoma is a rare soft-tissue tumor resembling extraskeletal myxoid chondrosarcoma and chordoma. Because fewer than 30 cases have been reported and precisely characterized, we studied the clinicopathologic features of seven new cases, comparing the immunohistochemical (six cases) and cytogenetic (one case) profiles with 15 cases of chordoma and six cases of extraskeletal myxoid chondrosarcoma. Patients with these tumors ranged in age from 7 to 62 years (mean, 35 years) and included four women and three men. The tumors presented as subfascial masses of the thigh (two cases), arm (three cases), chest wall (one cases), and buttocks (one case). In six of seven cases, there was neither recurrence nor metastasis within the follow-up, which ranged from 4 months to 7 years. The tumors were composed of vague nodules of large, rounded eosinophilic cells embedded in a matrix that varied from myxoid to densely hyaline, and the latter areas occasionally resembled primitive cartilage. Transitions between the large eosinophilic cells and smaller rounded and shorter spindled ones were often noted. Multivacuolated (physaliferouslike) cells were noted in all cases but were usually few in number. The matrix stained with Alcian blue (pH 2.5), and this staining was abolished with hyaluronidase predigestion. Immunohistochemistry for a variety of cytokeratins (CKs) (8/18, 1/10, 7, and 20), epithelial membrane antigen (EMA), S-100 protein, vimentin CD34, type IV collagen, smooth muscle actin, smooth muscle myosin heavy chain, calponin, and glial fibrillary acid protein was performed. All parachordomas strongly expressed CK 8/18, but not the other cytokeratins. Additionally, they expressed EMA (five of six). S-100 protein (six of six), and vimentin (six of six) and had a linear pattern of type IV collagen immunoreactivity around nests of cells (four of five). Calponin was noted in one case, but no cases expressed smooth muscle actin, smooth muscle myosin heavy chain, or glial fibrillary acid protein. In contrast, chordoma expressed CK 8/18 (15 of 15) and CK 1/10 (14 of 15), whereas extraskeletal myxoid chondrosarcoma consistently lacked CK. Although chordoma and extraskeletal myxoid chondrosarcoma showed considerable overlap with parachordoma, with respect to EMA and S-100 protein, they infrequently displayed type IV collagen, as was seen in parachordoma. One case of parachordoma studied cytogenetically disclosed trisomy 15, and monosomies of 1, 16, and 17 in contrast to the t(9;22) reported in extraskeletal myxoid chondrosarcoma and the monosomies of 3, 4, 10, and 13 seen in chordoma. We conclude that the immunohistochemical and cytogenetic profile distinguishes parachordoma from extraskeletal myxoid chondrosarcoma and chordoma. Lack of myoepithelial markers, furthermore, suggests parachordoma is not a deeply situated adnexal tumor. Because of these differences, parachordoma is best regarded as a distinct lesion without a clear relationship to other well-characterized tumors.
Quantitative laser scanning confocal autofluorescence microscopy of normal, premalignant, and malignant colonic tissues.
Laser scanning confocal autofluorescence microscopy (LSCAM) using 351- to 364-nm excitation light was used to quantitatively compare fluorescent spectral emission of unstained, frozen histological sections of normal, premalignant, and malignant colonic tissues. To identify the spatial origins of fluorescent signals accurately, the same frozen section slides used for microscopy were fixed and histochemically stained immediately following LSCAM imaging. Tissue fluorescence emission was quantified in terms of the intrinsic fluorescence coefficient beta (lambda), defined as the fluorescence power per unit tissue volume per unit wavelength (centered at lambda) divided by the incident light irradiance. Over all emission wavelengths, colonic tissues emitted autofluorescence ranging from beta (lambda) approximately 10(-1.5) to 10(-3.0) cm-1. In the 530- to 610-nm spectral region, markedly increased autofluorescence (beta up to 10(-2.5)) was observed in the dysplastic cells of adenomatous polyps, as compared to normal epithelial cells. Compared to adenomatous polyps, decreased dysplastic cell autofluorescence was observed in adenocarcinoma. The brightest fluorescence in the lamina propria, which was attributed to eosinophils (beta approximately 10(-2.5)) in previous studies, was also observed in other granular structures (beta up to 10(-1.4)). LSCAM reveals quantitative significant differences in fluorescence emission between normal and diseased colonic tissues.
p27 cell-cycle inhibitor is inversely correlated with lymph node metastases in right-sided colon cancer.
p27, a cyclin-dependent kinase inhibitor, suppresses proliferation of normal and neoplastic cells. Expression of p27 is correlated with survival in colon cancer. To some degree, right-sided colon cancers differ biologically and clinically from left-sided colon cancers. We analyzed 41 patients with right-sided colon cancers, including 18 cases with regional lymph node metastases and 23 cases with negative lymph nodes. Immunostaining for p27 was performed on histologic sections of primary cancers and scored. Correlation of p27 protein expression with histologic parameters was performed by t-test and multivariate analysis. Decreased p27 protein expression was associated with large tumor size. As percentages of positively stained tumor cells decreased from 70 to 29%, the mean tumor size increased from 1.9 to 7.3 cm. p27 protein expression significantly decreased in primary cancers with angiolymphatic invasion or with positive lymph nodes in comparison with those without angiolymphatic invasion (26 +/- 6 vs. 44 +/- 5%, P < 0.03) or with negative lymph nodes (23 +/- 4 vs. 47 +/- 6%, P < 0.003). p27 expression was not statistically different in terms of depth of tumor invasion (T1/T2 vs. T3/T4), tumor type or tumor differentiation. Multivariate analysis revealed that low p27 expression in primary cancers was correlated with lymph node metastases (P = 0.01). However, it did not correlate with any other histologic parameters. In summary, decreased p27 expression was associated with an increased likelihood of lymph node metastases in colon cancers, independent of depth of tumor invasion. This implies that p27 is a potentially important predictor for tumor metastasis and patient's prognosis in right-sided colon cancers.
Working in expanding roles.
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Mental health therapies.
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On the job. Child health in the community.
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Occupational health nursing.
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Mutation of the type II transforming growth factor-beta receptor is coincident with the transformation of human colon adenomas to malignant carcinomas.
The transforming growth factor-beta (TGF-beta) type II receptor (RII) is a colon cancer suppressor gene that is inactivated by mutation in 90% of human colon cancers arising via the microsatellite instability (MSI) pathway of carcinogenesis. To determine the pathophysiological consequence of RII mutations, we have determined the timing of their onset among 22 MSI human colon adenomas of varying stages. No RII mutations were detected in any early MSI adenoma, including all those with simple tubular or villous histology. The earliest RII mutation detected was in a region of high-grade dysplasia but was absent from the surrounding simple adenoma. Six additional RII mutations were all found in highly progressed adenomas that contained regions of frankly invasive adenocarcinoma. These RII mutations were detected in both the advanced adenomas and their adjacent regions of carcinoma. RII mutation is a late event in MSI adenomas and correlates tightly with progression of these adenomas to cancer.
Working in the community.
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On the job. The clinical nurse specialist: leading the way to quality care.
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Becoming a manager and making a difference to patient care.
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Lecturing in higher education: a career for self-starters.
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