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Biomedical subjects

J E Hines

Publications and source records attributed to J E Hines.

At least 19 recordsLinked to original sources
PubMed2001

Increased patient satisfaction from transrectal ultrasonography and biopsy under sedation.

OBJECTIVE: To determine the acceptability and patient satisfaction of transrectal biopsy undertaken with the patient under sedation. Patients and methods A retrospective questionnaire was sent to 100 patients who had undergone transrectal biopsy between January and August 1998. Levels of patient acceptability and satisfaction were assessed using visual analogue scales (VAS, with a maximum score of 10 being the least satisfactory or acceptable) and direct questions about the side-effects of the procedure. A subsequent prospective study was undertaken on 130 patients undergoing transrectal biopsy with sedation between January 1999 and January 2000. RESULTS: The mean score for patient discomfort with sedation was 1.5, compared with 3.5 with no sedation. The overall satisfaction score improved from 3.1 to 0.9 with sedation. Complication rates were comparable, although slightly higher overall in the prospective group. Conclusion Sedation can significantly reduce patient discomfort and make the transrectal biopsy a more satisfactory experience for the patient. This is particularly important in the proportion of men who need to be considered for repeat biopsies.

Biopsy↗
PubMed2001

Combining band recovery data and Pollock's robust design to model temporary and permanent emigration.

Capture-recapture models are widely used to estimate demographic parameters of marked populations. Recently, this statistical theory has been extended to modeling dispersal of open populations. Multistate models can be used to estimate movement probabilities among subdivided populations if multiple sites are sampled. Frequently, however, sampling is limited to a single site. Models described by Burnham (1993, in Marked Individuals in the Study of Bird Populations, 199-213), which combined open population capture-recapture and band-recovery models, can be used to estimate permanent emigration when sampling is limited to a single population. Similarly, Kendall, Nichols, and Hines (1997, Ecology 51, 563-578) developed models to estimate temporary emigration under Pollock's (1982, Journal of Wildlife Management 46, 757-760) robust design. We describe a likelihood-based approach to simultaneously estimate temporary and permanent emigration when sampling is limited to a single population. We use a sampling design that combines the robust design and recoveries of individuals obtained immediately following each sampling period. We present a general form for our model where temporary emigration is a first-order Markov process, and we discuss more restrictive models. We illustrate these models with analysis of data on marked Canvasback ducks. Our analysis indicates that probability of permanent emigration for adult female Canvasbacks was 0.193 (SE = 0.082) and that birds that were present at the study area in year i - 1 had a higher probability of presence in year i than birds that were not present in year i - 1.

Animals↗
PubMed1998

Higher temporal variability of forest breeding bird communities in fragmented landscapes.

Understanding the relationship between animal community dynamics and landscape structure has become a priority for biodiversity conservation. In particular, predicting the effects of habitat destruction that confine species to networks of small patches is an important prerequisite to conservation plan development. Theoretical models that predict the occurrence of species in fragmented landscapes, and relationships between stability and diversity do exist. However, reliable empirical investigations of the dynamics of biodiversity have been prevented by differences in species detection probabilities among landscapes. Using long-term data sampled at a large spatial scale in conjunction with a capture-recapture approach, we developed estimates of parameters of community changes over a 22-year period for forest breeding birds in selected areas of the eastern United States. We show that forest fragmentation was associated not only with a reduced number of forest bird species, but also with increased temporal variability in the number of species. This higher temporal variability was associated with higher local extinction and turnover rates. These results have major conservation implications. Moreover, the approach used provides a practical tool for the study of the dynamics of biodiversity.

Journal Article↗
PubMed1998

Anti-hepatocyte growth factor antibody inhibits hepatocyte proliferation during liver regeneration.

In vitro studies have shown hepatocyte growth factor (HGF) to be a potent mitogen for hepatocytes. Direct evidence of a mitogenic role in vivo was sought by inhibiting HGF activity, using continuous administration of neutralizing antibody to rats which had a stimulus for liver regeneration. Alzet osmotic mini-pumps, administering a constant supply of anti-HGF monoclonal antibody (clone D9), were inserted intraperitoneally into male Wistar rats; an irrelevant isotypical antibody was administered to controls. Forty-five animals received an intragastric bolus of 40 per cent carbon tetrachloride (CCl4) and groups of three test and control animals were killed at 24 h intervals for 7 days. Treatment with anti-HGF monoclonal antibody significantly inhibited the levels of immunodetectable HGF in the sera of rats following CCl4 administration. In comparison with controls, hepatocyte proliferation as assessed by bromodeoxyuridine labelling in anti-HGF-treated animals was significantly inhibited at 24 h (P < 0.001), 48 h (P < 0.001), and 96 h (P < 0.05) post-CCl4 administration. In contrast, sinusoidal cell proliferation was not significantly different from controls at any time point. Inhibition of the parenchymal proliferative response to acute CCl4-induced liver injury by the in vivo neutralization of HGF provides direct evidence that this growth factor plays an important role in liver regeneration following necrosis.

Animals↗
PubMed1997

Stochastic seasonality and nonlinear density-dependent factors regulate population size in an African rodent.

Ecology has long been troubled by the controversy over how populations are regulated. Some ecologists focus on the role of environmental effects, whereas others argue that density-dependent feedback mechanisms are central. The relative importance of both processes is still hotly debated, but clear examples of both processes acting in the same population are rare. Key-factor analysis (regression of population changes on possible causal factors) and time-series analysis are often used to investigate the presence of density dependence, but such approaches may be biased and provide no information on actual demographic rates. Here we report on both density-dependent and density-independent effects in a murid rodent pest species, the multimammate rat Mastomys natalensis (Smith, 1834), using statistical capture-recapture models. Both effects occur simultaneously, but we also demonstrate that they do not affect all demographic rates in the same way. We have incorporated the obtained estimates of demographic rates in a population dynamics model and show that the observed dynamics are affected by stabilizing nonlinear density-dependent components coupled with strong deterministic and stochastic seasonal components.

Africa↗
PubMed1996

CD44 is expressed in hepatocellular carcinomas showing vascular invasion.

CD44 and its variant isoforms are a group of transmembrane glycoproteins which play important roles in immune recognition, in lymphocyte trafficking, and in cell-cell and cell-matrix interactions. Although CD44 is expressed by some normal human epithelial and mesenchymal cells, upregulation of CD44 expression has been related to the metastatic potential of some malignant tumours. In this study of 27 hepatocellular carcinomas (HCCs), an indirect immunohistochemical method was used to investigate the distribution of CD44 in normal liver and to determine whether expression of the standard form of CD44 (CD44s), or two of its variant isoforms (CD44-v3 and CD44-v6), correlated with tumour grade, proliferation indices, or histological evidence of vascular invasion. Fifteen of the tumours were Edmondson grade II, four were grade III, and eight were grade IV. Liver cell dysplasia was present in adjacent liver parenchyma in three cases and vascular invasion was observed in ten HCCs. Vascular invasion was found to be more frequent in high grade HCCs and a significant correlation was observed between tumour proliferation indices and vascular invasion. CD44s was not expressed by epithelial cells of normal liver but was expressed by tumour cells in six HCCs; vascular invasion was present in five of these HCCs. Three CD44s-positive cases also expressed CD44-v3 and two of these also expressed CD44-v6. CD44 was not expressed in areas of hepatocyte dysplasia. There was a significant correlation between CD44 expression and the presence of vascular invasion, but not between CD44 expression and tumour grade or tumour proliferation indices. It is concluded that upregulation of cell surface CD44 expression on malignant hepatocytes is related to their tendency to vascular invasion and may have implications relating to metastasis and prognosis in patients with HCCs.

Antigens, Neoplasm↗
PubMed1996

Transforming growth factor-alpha expression is altered during experimental hepatocarcinogenesis.

In order to characterize the role of transforming growth factor-alpha (TGF alpha) during hepatocarcinogenesis, liver tissue was examined at 10, 16, and 19 weeks following initial 10-week diethylnitrosamine (50 mg l-1 drinking water) exposure in female Wistar rats. Liver tissue protein extracts were electrophoresed and transferred to nitrocellulose filters. Levels of tissue-derived TGF alpha and epidermal growth factor receptor (EGFr) were assessed using an anti-TGF alpha monoclonal antibody (Ab-1) and an anti-EGFr polyclonal antibody (AB-4), coupled with scanning densitometric quantification. Immunolocalization of TGF alpha was performed in Bouin's-fixed, paraffin-embedded liver tissue sections. The distribution and intensity of TGF alpha immunoreactivity varied according to the degree of dysplasia, severely dysplastic cells being strongly immunoreactive. At week 10, mild hepatocyte dysplasia and perivenular inflammation were evident, together with a corresponding increase in perivenular TGF alpha immunoreactivity. By week 16, foci of moderate to severe dysplasia were observed; at this stage, there was a decrease in perivenular immunoreactivity but a further increase in overall liver tissue TGF alpha levels. Some 'altered foci' and dysplastic nodules showed intense immunoreactivity for TGF alpha. At these time points, immunodetectable liver EGFr was found to decrease significantly in comparison with normal control tissue. TGF alpha immunoreactivity was observed in fully developed carcinomas at week 19, although some tumours were negative by immunohistochemistry. The up-regulation of immunodetectable TGF alpha and the concomitant down-regulation of EGFr demonstrated positive (P < 0.01) and negative (P < 0.001) correlations, respectively, with hepatocyte proliferation indices. These findings suggest that the TGF alpha/EGFr ligand receptor system may be important during tumour promotion and in the stimulation of continued proliferation in hepatocellular carcinomas.

Animals↗
PubMed1996

Symptom indices in bladder outlet obstruction.

BPH, the most common benign tumour that affects men, is a disease that mostly causes morbidity through its associated LUTS. Symptom indices are instruments that allow the objective measurement of these symptoms. Analysis of the data they provide allows symptom severity to be measured and the changes that occur in symptoms with time to be monitored. Measurement of symptom severity and assessment of disease progression are important parameters when treatment decisions are being made. After treatment, measurement of LUTS using symptom indices allows efficacy to be judged as well as providing an ongoing assessment of patients. Data from symptom indices allow patients to be compared with each other and may provide useful epidemiological information when groups of patients are assessed. However, it should be stressed that symptom indices are not reliable for screening populations for disease and should not be used for case-finding. Many new treatments for BPH/BPO are being developed and assessed in clinical trials. The measurement of symptoms using symptom indices has had a central role in these trials and will continue to do so. A considerable volume of published work presenting data from these trials is now accumulating. Comparing new treatments with the 'gold standard' of TURP is facilitated by symptom indices, as is the comparison with other novel modes of treatment. The AUA-7 index remains the best scientifically validated index used in patients with symptomatic BPO, although other indices, e.g. the Boyarsky, Madsen-Iversen and MMAP, when compared with the AUA-7 have been found to perform similarly. However, it would be preferable if the validation process of current indices included validation against pathophysiological processes such as proven BOO and detrusor instability. The current use of symptom indices will add to data supporting their reliability and validity. It is to be anticipated that symptom indices will be used increasingly both in clinical practice and clinical trials and that trust will be placed in the data they provide. It is essential that the limitations of these indices are borne in mind, and that the indices are applied correctly so that the information they produce remains valid and reliable.

Decision Support Techniques↗
PubMed1995

Intrahepatic mast cells in chronic liver diseases.

Mast cells are known to be present in human liver but their distribution and density in normal livers and in chronic liver diseases have not previously been examined. In this study, we quantified mast cell numbers and examined their distribution in percutaneous biopsy specimens from normal livers (n = 8) and in two chronic progressive liver diseases: primary biliary cirrhosis (PBC) (n = 40) and alcoholic liver disease (n = 33). We compared differences in mast cell density between these two forms of chronic liver disease because it had been suggested that mast cells may play a role in the development of liver fibrosis, particularly in patients with chronic cholestatic liver disease who frequently have increased plasma histamine levels. Mast cells were identified by immunohistochemistry using a specific monoclonal antibody (AA1) raised against mast cell tryptase after an initial study showed this to be more sensitive for the detection of mast cells than the conventional histochemical stain, toluidine blue. Our results showed that small numbers of mast cells (3.9 +/- 3.3/mm2) are present within the portal tracts and sinusoids of normal livers. In progressive chronic liver disease, increased numbers of mast cells were present, which correlated with the increasing amounts of liver fibrosis present. We found significantly more mast cells in the PBC group compared with the alcoholic group for a given amount of fibrosis. Our findings suggest that mast cells and their mediators may play a role in liver fibrogenesis.

Biopsy↗
PubMed1994

Non-parenchymal cell responses in paracetamol (acetaminophen)-induced liver injury.

We have analysed Kupffer cell and 'activated' perisinusoidal cell populations in liver biopsies from patients with paracetamol (acetaminophen)-induced hepatic necrosis of varying degrees of severity. Kupffer cells were identified immunohistochemically using the monoclonal antibody KPJ and perisinusoidal cells by identification of alpha-smooth muscle actin expression. Material was available from four groups of individuals: (i) 11 cases with mild (grade I) injury; (ii) six cases with moderate (grade II) injury; (iii) six cases with severe (grade III) injury; and (iv) controls with normal liver histology (n = 23). Biopsies in groups (i)-(iii) were obtained within 5 days of drug ingestion. All patients in this study survived and follow-up biopsies were obtained at 4 months, by which time the histological abnormalities had fully resolved. Kupffer cells and perisinusoidal cell numbers were assessed in immunostained preparations of acute and recovery phase biopsies and in control specimens. In acute phase biopsies from patients with grade II and III injury there was expansion of the Kupffer cell and perisinusoidal cell populations within areas of injury. There was a strong correlation between the size of these two cell populations (r = 0.886). No significant difference in cell numbers was found between those with grade I injury and controls. In recovery phase biopsies from patients with paracetamol-induced injury, perisinusoidal cell numbers did not differ significantly from normal controls. Kupffer cells numbers also decreased in recovery phase biopsies compared with the acute phase, although there was persistent expansion of the Kupffer cells population in those who originally had grade III injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed1994

Quantitative analysis of macrophages and perisinusoidal cells in primary biliary cirrhosis.

Immunohistochemistry and image analysis were used to quantify alterations in the Kupffer cell and 'activated' perisinusoidal cell populations in the different stages of primary biliary cirrhosis. Anti-CD68 macrophage antibodies were used to detect Kupffer cells, and anti-alpha-smooth muscle actin (alpha-SMA), PR 2D3 and anti-desmin antibodies to detect perisinusoidal cells. Liver biopsy material was available from 26 patients with primary biliary cirrhosis and 23 patients with histologically normal liver. Increased Kupffer cell numbers were observed in periportal/periseptal zones of stage 3 primary biliary cirrhosis (n = 9), and in random parenchymal areas of stage 3 and stage 4 cases. Significantly increased 'activated' perisinusoidal cell numbers were seen only in periportal/periseptal zones of stage 3 and stage 4 primary biliary cirrhosis. Neither Kupffer cell nor perisinusoidal cell numbers altered significantly in stage 1 and 2 primary biliary cirrhosis (n = 6). PR 2D3 positivity and increased alpha-SMA immunoreactivity by perisinusoidal cells in primary biliary cirrhosis support myofibroblastic differentiation of these cells. Human perisinusoidal cells, unlike their rodent counterparts, did not express desmin in primary biliary cirrhosis or control liver. Kupffer cells and 'activated' perisinusoidal cell accumulation in periportal/periseptal zones of the precirrhotic and cirrhotic primary biliary cirrhosis liver support the concept of Kupffer cell-mediated stimulation of perisinusoidal cells. Furthermore, these findings indicate that Kupffer cell-perisinusoidal interactions play an important role in the development of liver fibrosis and cirrhosis in primary biliary cirrhosis.

Actins↗
PubMed1993

Intrahepatic distribution of transforming growth factor-alpha (TGF alpha) during liver regeneration following carbon tetrachloride-induced necrosis.

The distribution of transforming growth factor-alpha (TGF alpha) in rat liver during regeneration was studied immunohistochemically using two antibodies, one a polyclonal (26T) raised against a synthetic peptide corresponding to the 17 C-terminal amino acids of the mature rat protein, and the other a monoclonal (Ab-2) raised against recombinant human protein. In normal liver, immunoreactive TGF alpha was detected in perivenular hepatocytes using both antibodies. No sinusoidal cells were found to contain the peptide. In response to carbon tetrachloride (CCI4)-induced necrosis, an initial increase in the intensity of immunoreactivity was noted at 24 h following exposure to the toxin. This coincided with the period immediately preceding the peak of hepatocyte proliferation; Ab-2 immunoreactive cells outnumbered 26T-positive cells. Thereafter there was a reduction in the number of TGF alpha-positive cells, but by day 4 the level of immunoreactivity had returned to that of normal liver. Using bromodeoxyuridine labelling, spatial and temporal relationships between TGF alpha expression and cell proliferation were identified, supporting the concept that this peptide plays an important role in the in vivo regenerative response to hepatic injury via an autocrine mechanism.

Animals↗
PubMed1993

In vivo responses of macrophages and perisinusoidal cells to cholestatic liver injury.

We investigated the response of macrophages and perisinusoidal (Ito) cells (PSCs) during the development of secondary biliary cirrhosis after ligation and division of the common bile duct. Liver tissue was obtained from three groups of male Wistar rats: 1) untreated controls (n = 3); 2) common bile duct-ligated (CBDL) animals (n = 15); and 3) sham-operated controls (n = 15). Material from animal groups 2 and 3 was obtained on days 3, 7, 14, 21, and 28 after operation; in all animals 5-bromo-2-deoxyuridine was administered intraperitoneally before death. Monocytes and macrophages were detected using the monoclonal antibody ED1 and tissue macrophages using the antibody ED2. Cell proliferation within the macrophage population was demonstrated by double labeling for ED2 and incorporated 5-bromo-2-deoxyuridine. PSCs were demonstrated in tissue sections by immunolocalization of desmin; proliferating PSCs were identified by double labeling for desmin and incorporated 5-bromo-2-deoxyuridine. Evidence of phenotypic modulation of PSCs was sought using anti-alpha-smooth muscle actin (alpha-SMA) antibody. Increased numbers of ED1- and ED2-positive cells were seen in CBDL animals at all time points. Local proliferation of macrophages could be identified and reached a peak at day 3, thereafter falling toward control values. Compared with those of controls, livers of CBDL animals showed increased numbers of desmin-positive PSCs in periportal zones from day 3 on, reaching a peak at day 14 (127.8 +/- 10.99 cells/0.635 mm2) and followed by a plateau. PSC proliferation peaked at days 3 and 7 (labeling indices 11.2% and 11.2%, respectively) and thereafter fell toward control values; no expansion of the PSC population was seen in sham-operated rats. Increased alpha-SMA-positive cells were also noted from day 3, with a peak at day 21 (231.1 +/- 11.52 cells/0.635 mm2) and followed by a plateau. En face labeling experiments in days 14, 21, and 28 CBDL animals showed cells co-expressing alpha-SMA and desmin and cells expressing alpha-SMA alone. These results indicate that in response to chronic cholestatic liver injury, PSCs proliferate and undergo phenotypic modulation toward "myofibroblast-like" cells. The kinetics of the response are similar to those of the ED2-positive cell population in keeping with a hypothesis that PSC proliferation and activation may be mediated by factors released by macrophages in response to various forms of liver injury. We conclude that the responses of macrophages and PSCs to cholestatic injury are similar to those after toxin-induced hepatocyte necrosis.

Actins↗
PubMed1992

Macrophage and perisinusoidal cell kinetics in acute liver injury.

Perisinusoidal cells (PSCs) are currently regarded as the major source of extracellular matrix proteins during hepatic fibrogenesis in response to liver injury. However, the cellular mechanisms underlying their response to injury are not fully understood. One hypothesis is that the PSCs are stimulated by peptide growth factors produced by hepatic macrophages (Kupffer cells) in response to parenchymal cell damage. In this study we have investigated the kinetics of the PSC and macrophage populations in acute carbon tetrachloride-induced hepatic injury in rats. PSCs were identified immunohistochemically by detection of cytoplasmic desmin; monocytes and macrophages were detected using the monoclonal antibodies ED1 and ED2; cells in S phase were identified by immunohistochemical detection of nuclear-incorporated bromodeoxyuridine. The results showed an expansion of the desmin-positive PSC population, predominantly within the damaged perivenular zones, which reached a peak on days 3 and 4 following administration of carbon tetrachloride; this was contributed to by local PSC proliferation. The PSC response was preceded by an expansion of the macrophage population resulting from both local macrophage proliferation and influx of blood monocytes. These results are in keeping with the hypothesis that the PSC response to acute liver injury is mediated, at least in part, by hepatic macrophages.

Animals↗
PubMed1992

Hepatic reinnervation following orthotopic liver transplantation in man.

We have studied changes in the pattern of intrinsic hepatic innervation in sequential liver biopsies from 16 patients who underwent orthotopic liver transplantation. Seventy-one needle biopsies were used, including specimens obtained at the time of transplantation (time zero) and up to 4 years post-transplantation; five transplant hepatectomy tissue blocks removed 3-32 months after transplantation were also assessed. Paraffin sections were immunostained with anti-PGP 9.5 and anti-S-100 to identify nerve fibres. All 'time zero' biopsies contained portal nerves and all but two showed staining of parenchymal fibres. After 1 week, no subsequent biopsies contained parenchymal fibres. The disappearance of portal fibres was less rapid and showed greater variability between patients, but they had all disappeared by 6 weeks and there was no positive staining between 6 and 60 weeks. Thereafter, a minority of biopsies showed innervation of a few small portal tracts. Samples from the porta hepatis, hepatectomy specimens, and needle biopsies containing large tracts showed persistence of major nerve trunks at all stages. Abnormally large nerve bundles were seen in some of these areas. The pattern of nerve staining showed no obvious relationship to the intensity of rejection changes. Our results suggest that there is a limited, delayed capacity for regeneration of portal, but not parenchymal, fibres in the transplanted human liver. The physiological significance of this long-term parenchymal denervation in transplanted livers remains to be determined.

Humans↗
PubMed1992

Immunolocalization of proliferating perisinusoidal cells in rat liver.

There is now substantial evidence that perisinusoidal (Ito or fat-storing) cells are the principal source of extracellular matrix proteins during hepatic fibrogenesis. In rat liver these cells express the intermediate filament protein desmin; this is now widely used as an immunohistochemical marker for these cells. It has been shown that in experimental models of acute and chronic liver injury there is an increase in the number of desmin-positive perisinusoidal cells prior to the deposition of matrix proteins; however, these studies have failed to establish whether local proliferation is involved in this expansion of the desmin-positive perisinusoidal cell population. In order to investigate the kinetics of the perisinusoidal cell response, we have developed a novel double-labelling immunohistochemical technique for the simultaneous demonstration of desmin and incorporated bromodeoxyuridine in proliferating perisinusoidal cells in sections of fixed paraffin-embedded rat liver. Application of this technique to a model of acute liver injury (single dose carbon tetrachloride by gavage) has shown that expansion of the perisinusoidal cell population is contributed to by local proliferation, with a labelling index of 18.7% 2 days following injury.

Animals↗