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Biomedical subjects

M J Hill

Publications and source records attributed to M J Hill.

At least 19 recordsLinked to original sources
PubMed2005

The distribution of small and intermediate conductance calcium-activated potassium channels in the rat sensory nervous system.

Small (SK) and intermediate (IK) conductance calcium-activated potassium channels are candidate ion channels for the regulation of excitability in nociceptive neurones. We have used unique peptide-directed antisera to describe the immunocytochemical distribution of the known isoforms of these ion channels in dorsal root ganglia (DRG) and spinal cord of the rat. These investigations sought to characterize further the phenotype and hence possible functions of nociceptive neurone subpopulations in the rat. In addition, using Western blotting, we sought to determine the level of protein expression of SK and IK channels in sensory nervous tissues following induction of inflammation (Freund's Complete Adjuvant (FCA) arthritis model) or nerve injury (chronic constriction injury model). We show that SK1, SK2, SK3 and IK1 are all expressed in DRG and spinal cord. Morphometric analysis revealed that SK1, SK2 and IK1 were preferentially localized to neurones having cell bodies <1000 microm2 (putative nociceptors) in DRG. Dual labeling immunocytochemistry showed that these ion channels co-localize with both CGRP and IB4, known markers of nociceptor sub-populations. SK2 was localized almost exclusively in the superficial laminae of the spinal cord dorsal horn, the region in which many sensory afferents terminate; the distribution of SK1 and IK1 was more widespread in spinal cord, although some preferential labeling within the dorsal horn was observed in the case of IK1. Here we show evidence for a distinctive pattern of expression for certain members of the calcium-activated potassium channel family in the rat DRG.

Animals↗
PubMed2002

Fibres and colorectal cancer: should we change our dietary advice on prevention?

Evidence from epidemiological studies overwhelmingly indicates that fruit, vegetables and cereals prevent cancer at a wide range of sites in the body, not just the large bowel. However, recent important papers have shown that an intervention diet rich in fruit, vegetables and fibre failed to decrease the risk of new colorectal adenoma formation. The adenoma-cancer sequence and the role of diet are discussed in the light of these new findings.

Adenoma↗
PubMed2001

Changes and developments in cancer prevention.

During the last 125 years, there has been a massive decrease in mortality from infectious disease, as a result of improved public health and later as a result of antibiotic use. This has led to a consequent increase in life span from less than 50 (when cancer is rare) to more than 70 (when cancer is common). As a result of these changes, cancer has moved from being a very minor cause of mortality in 1876 to one of the two major causes by 2000. During the last century theories of the causation of cancer have changed progressively. In the early phase the main cause was thought to be environmental contamination with carcinogenic chemicals. Later, it was thought that all cancers were caused by cancers, then that cancer was caused by a breakdown in immune-surveillance. For 40 years we have known that tobacco smoke is a major cause of respiratory and other cancers, and preventive measures are currently having a dramatic effect on male lung cancer mortality. During the last 25 years it has become apparent that diet is the other major cause of cancer, but theories have moved steadily from a search for causal agents (e.g., too much fat) to protective agents (e.g., too little fruit and vegetable). Currently it is accepted that all of the above theories contribute to the total cancer risk.

Diet↗
PubMed2001

Wound assessment and evaluation.

The "Wound Assessment and Evaluation" series includes a short case presentation and differential diagnosis. It is followed by a discussion of the disease or condition and the rationale used in each step of the assessment.

Aged↗
PubMed2000

Molecular and clinical risk markers in colon cancer trials.

Although there is a great deal of information concerning the risk factors for colorectal cancer, progress has been slow in determining methods of chemoprevention. In part this is because colorectal cancer consists of a series of events over 10-15 years or more, which affects only 3-5% of the population. Risk markers for use in patient selection are needed to decrease the sample size needed. In addition, there is a need to identify intermediate endpoints of success to decrease the follow-up time. Clinical markers of risk are a history of colorectal adenomas and of inflammatory bowel disease. Molecular markers include a number of genetic markers and enzyme polymorphisms.

Adenoma↗
PubMed2000

A prospective study of faecal bile acids and colorectal cancer.

A prospective study of 7079 people aged 45-74 recruited through general practices in South Wales, Herefordshire and Edinburgh, Scotland was undertaken to test the hypothesis that faecal bile acids are implicated in the causation of large bowel cancer. The population was recruited between 1974 and 1980 and the response rate for stool collection was 67%. Bile acid analyses were performed on those cases that presented by 1990. It was decided in advance to examine the hypothesis separately for left- and right-sided bowel cancer because of known epidemiological differences between the two sites and to exclude the cases presenting within 2 years of the stool sample from the analyses because the cancer could have been present at recruitment and might have possibly affected faecal bile acid concentrations. Each case (n = 51 left-sided and 8 right-sided) was matched with three controls by age (within 5 years), sex, place of residence and time of providing the stool sample (within 3 months). Statistical analyses using conditional logistic regression showed no significant differences between the left-sided cases and controls for any of the concentrations of individual bile acids, total bile acid concentrations, faecal neutral steroids, percentage bacterial conversion and the ratio of lithocholic acid to deoxycholic acid concentrations. There was a statistically significant (P = 0.021) association of the presence of chenodeoxycholic acid (5/8 samples) in the right-sided cases compared with the controls (3/23), odds ratio 6.26 (95% confidence interval 1.19, 32.84). A high proportion of primary bile acids has also been found in other studies of patients with a genetic predisposition to proximal bowel cancer, however this pattern may also occur in low risk groups, such as Indian vegetarians, suggesting that they may predispose to right-sided bowel cancer only in the presence of other, as yet unknown factors. If bile acids are involved in the causation of large bowel cancer, they may be part of a complex set of interacting factors.

Aged↗
PubMed2000

Dietary advice on cancer prevention: time for a change?

Media coverage of recent dietary intervention studies has cast doubt on dietary advice for cancer prevention. The studies cited focussed on colorectal adenoma initiation as opposed to progression. There is ample evidence that in the colorectum the factors controlling initiation of adenomas differ from those causing progression to cancer, and that it is the latter that are the most important. In the light of this it is argued that studies of adenoma initiation are irrelevant to the advice given for overall cancer prevention.

Adenoma↗