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Kenneth Campbell

Publications and source records attributed to Kenneth Campbell.

24 records · Page 2Linked to original sources

Expression of Ngn1, Ngn2, Cash1, Gsh2 and Sfrp1 in the developing chick telencephalon.

Patterning of the chick telencephalon has been debated, especially in regard to a ventral (subpallial) or dorsal (pallial) nature of the dorsal ventricular ridge (DVR). Here we report the expression patterns of chick homologues of molecules known to be involved in telencephalic patterning in other vertebrate species. We show here that the transcription factors Ngn1, Ngn2, Cash1, Gsh2 and the secreted frizzled related protein 1 (sfrp1), a wnt receptor, are expressed in characteristic telencephalic domains during chick development. At embryonic day 7 (E7) Ngn1 and Ngn2 are localized in the dorsal pallium and the DVR, similar to the region of Pax6 expression. In contrast, Gsh2 and Cash1 are restricted to the subpallium and some DVR cells. Interestingly Sfrp, a dorsoventral boundary marker in mouse telencephalon, is expressed between the DVR and subpallium. Gsh2 and Pax6 double-positive cells further characterize this boundary region in the developing chick telencephalon.

Animals↗

BCR-ABL suppresses C/EBPalpha expression through inhibitory action of hnRNP E2.

The arrest of differentiation is a feature of both chronic myelogenous leukemia cells in myeloid blast crisis and myeloid precursors that ectopically express the p210BCR-ABL oncoprotein; however, its underlying mechanisms remain poorly understood. Here we show that expression of BCR-ABL in myeloid precursor cells leads to transcriptional suppression of the granulocyte colony-stimulating factor receptor G-CSF-R (encoded by CSF3R), possibly through down-modulation of C/EBPalpha-the principal regulator of granulocytic differentiation. Expression of C/EBPalpha protein is barely detectable in primary marrow cells taken from individuals affected with chronic myeloid leukemia in blast crisis. In contrast, CEBPA RNA is clearly present. Ectopic expression of C/EBPalpha induces granulocytic differentiation of myeloid precursor cells expressing BCR-ABL. Expression of C/EBPalpha is suppressed at the translational level by interaction of the poly(rC)-binding protein hnRNP E2 with CEBPA mRNA, and ectopic expression of hnRNP E2 in myeloid precursor cells down-regulates both C/EBPalpha and G-CSF-R and leads to rapid cell death on treatment with G-CSF (encoded by CSF3). Our results indicate that BCR-ABL regulates the expression of C/EBPalpha by inducing hnRNP E2-which inhibits the translation of CEBPA mRNA.

Animals↗

Striatal c-fos Induction by Cocaine or Apomorphine Occurs Preferentially in Output Neurons Projecting to the Substantia Nigra in the Rat.

Fluorogold or rhodamine-labelled latex beads were injected in the substantia nigra (SN) or the globus pallidus (GP) in order retrogradely to label striatal output neurons that project to the two target structures. Ten days later, striatal c-fos was induced by systemic administration of cocaine (five normal rats; 25 mg/kg cocaine i.p. 2 h before killing) or apomorphine (five unilaterally dopamine-denervated rats; 0.25 mg/kg apomorphine s. c. 2 h before killing), and detection of the Fos protein in the striatum was achieved by immunofluorescence. Sections through the caudate-putamen that displayed good labelling from both SN and GP were selected for a quantitative analysis: the number of retrogradely labelled cells that exhibited Fos immunoreactivity, as well as the total number of retrogradely labelled cells located within a grid (0.16 mm2 in size) were counted manually at 25 x magnification. Cocaine induced a proportionally higher c-fos expression in striato-nigral compared to striato-pallidal neurons, whereas apomorphine activated Fos almost exclusively in striato-nigral neurons. The present findings are consistent with the idea that striatal c-fos induction by dopaminergic agents is primarily mediated by an interaction with D1-receptors, which are thought to be selectively localized on neurons projecting to SN.

Journal Article↗

Methods of meeting patients' cancer information needs.

It is difficult to imagine the impact of a diagnosis of cancer. However, even where a patient has a poor prognosis, it is important to allow patients and their carers to set the information agenda. Cancer information specialists will be irreplaceable in helping to determine what information a patient needs, in what format and at what time, and how those needs change during the cancer journey.

Communication Barriers↗

The infectious causes of cancer.

This article considers the scale and epidemiology of cancers caused by infectious agents and the mechanisms by which they may induce cancers, the known or suspected viral causes of cancer and finally bacterial and parasitic organisms that are or may be carcinogenic. It also discusses the effect of organisms that do not infect humans directly, where their impact is significant.

Causality↗

Understanding how viruses can cause malignant disease.

This article discusses the contribution made by viral infections to the global burden of cancer. The greatest impact of virally-induced cancers is felt in the developing world--in those countries that experience greatest difficulty in meeting the costs of vaccination programmes. Support by wealthier nations for vaccination programmes, organised through the World Health Organization, could have an enormous impact on the global burden of disease and specifically on cancer incidence.

Cost of Illness↗