PubMed Health⌕ Search

Biomedical subjects

T Roger

Publications and source records attributed to T Roger.

42 records · Page 3Linked to original sources
PubMed1987

Colonic alpha 2-adrenoceptor-mediated responses in the pony.

The motor responses of the caecum and colon to stimulation of alpha 2-adrenoceptors by xylazine and detomidine at the recommended dose levels of 0.6 and 0.1 mg/kg were investigated in three ponies. The motor changes of the left ventral colon induced by continuous intra-arterial infusion of a prostaglandin (PGF2 alpha) were used to assess the relative inhibitory effects of xylazine and detomidine in a colic model. The administration of alpha 2-agonists inhibited the spiking activity on the whole of the large intestine for 20-30 min (xylazine) or 2-3 h (detomidine). However, the detomidine-induced inhibition was preceded by a short period of increased smooth muscle basal tone as indicated by strain-gauge force transducer measurements. This pattern of activity was neither reversed nor prevented by the administration of tolazoline (10 micrograms/kg/min) intra-arterially. In contrast, inhibition of the colonic phasic and tonic motor activity by alpha 2-adrenoceptor stimulation was reversed competitively by tolazoline. The intra-arterial infusion of prostaglandin F2 alpha (10 micrograms/kg/min) induced prolonged and sustained spiking activity that might be related to signs of mild colic. Detomidine, and to a lesser extent xylazine, relaxed the whole of the large intestine and this was accompanied by alleviation of the signs of visceral pain.

Adrenergic alpha-Agonists↗
PubMed1985

Colonic motor responses in the pony: relevance of colonic stimulation by opiate antagonists.

The electrical and mechanical activity of the digestive tract and its response to the administration of opiate agonists and antagonists was assessed from electrodes and strain gauges chronically implanted on the jejunum and the cecocolonic segments in 3 ponies given a diet of hay and concentrates. Before the drugs were given, 10 to 17 migrating myoelectric complexes/day were recorded on the small intestine, and a rhythmic motor activity (base line) was observed on the proximal portion of the colon at the rate of 3.5 to 6.6/hour. Propagated contractions from the proximal to the distal portion of the colon occurred at the rate of 1.5 to 2.3/hour. Each pony was used as its own control and was given morphine (0.5 or 1 mg/kg of body weight, IV) or fentanyl (0.01 or 0.05 mg, IV) at weekly intervals. After an early phase of inhibition of the overall activity that lasted from 0.5 to 3 hours, depending on the dose, the resting muscle tone of the colonic activity was increased for a dose-dependent period. Propagated contractions only reappeared at the end of this 2nd phase. The opiate antagonist naloxone (0.5 mg/kg, IV) elicited a marked propulsive activity on the left replicated colonic segment, characterized by an increase in the number of propagated contractions. The N-methyl-quaternary analog of naloxone (methylnaloxone, which presumably entails selective action at opiate receptors outside the CNS) was also effective, indicating peripheral effects at the dosage level used (0.5 mg/kg, IV). Seemingly, an inhibitory opioid system exists in the control of colonic motor function in ponies and the possible usefulness of opiate antagonists to relieve hypomotility resulting in colonic impaction and constipation.

Animals↗
PubMedDate not supplied

MIF regulates innate immune responses through modulation of Toll-like receptor 4.

Macrophages are pivotal effector cells of the innate immune system, which is vital for recognizing and eliminating invasive microbial pathogens. When microbial products bind to pathogen-recognition receptors, macrophages become activated and release a broad array of cytokines that orchestrate the host innate and adaptive immune responses. Initially identified as a T-cell cytokine, macrophage migration inhibitory factor (MIF) is also a macrophage cytokine and an important mediator of inflammation and sepsis. Here we report that MIF is an essential regulator of macrophage responses to endotoxin (lipopolysaccharide) and Gram-negative bacteria. Compared with wild-type cells, MIF-deficient macrophages are hyporesponsive to lipopolysaccharide and Gram-negative bacteria, as shown by a profound reduction in the activity of NF-kappaB and the production of tumour-necrosis factor-alpha. This reduction is due to a downregulation of Toll-like receptor 4 (TLR4), the signal-transducing molecule of the lipopolysaccharide receptor complex, and is associated with decreased activity of transcription factor PU.1, which is required for optimal expression of the Tlr4 gene in myeloid cells. These findings identify an important role for MIF in innate immunity and provide a molecular basis for the resistance of MIF-deficient mice to endotoxic shock.

Animals↗
PubMedDate not supplied

[Incidental finding of a focal cortical heterotopy in long-term epilepsy].

A 72-year-old woman was admitted for the work-up of an abdominal pseudomyxoma. A brain CT was performed and revealed the presence of a tumorlike lesion in the left temporal lobe. The diagnosis of focal heterotopy was suggested and confirmed by MRI. Careful clinical history revealed Grand Mal epilepsy during infancy that was well controlled by antiepileptic drugs. No imaging studies had ever been performed. This case illustrates that the diagnosis of idiopathic epilepsy should be established only after having ruled out brain disorders including heterotopy, which can be demonstrated by MRI.

Aged↗