A set of instruments for the laser abdominal surgery

Scientific-Industrial Association Medinstrument, Kazan'. Translated from Meditsinskaya Tekhnika, No. 3, pp 35–38, May–June, 1992.     

The ARS-2 X-ray diagnostic photographic device

Industrial Association Mosrentgen, Moscow. Moscow Scientific-Research Institute for Diagnostics and Surgery. Translated from Meditsinskaya Tekhnika, No. 2, pp. 11–13, March–April, 1993.     

Reconstitution of chemokine-induced actin polymerization in undifferentiated human leukemia cells (HL-60) by heterologous expression of interleukin-8 receptors

The chemokines interleukin-8 (IL-8) and GRO bind in neutrophils to the interleukin-8 receptor and (IL-8R and ) triggering reorganization of the actin cytoskeleton and activation of phospholipase C (PLC). Reconstitution of chemokine-induced activation of PLC indicated coupling of IL-8R and to pertussis toxin-insensitive or . To identify the signal transduction mechanisms of chemokine-induced actin response, undifferentiated human leukemia cells (HL-60 cells) constitutively expressing , and were chosen for reconstitution studies. Expression of recombinant receptors after transfection of the cells with the cDNA of IL-8R and was confirmed by binding studies with radiolabeled ligands. IL-8R bound IL-8 with high affinity (Kd1 nM) and GRO with low affinity (Kd 1 M), whereas IL-8R bound both IL-8 and GRO with high affinity (Kd1 nM). Flow cytometric actin measurements indicated that high affinity ligand-receptor interactions in both receptor transfectants displayed inducible responses. Pretreatment of transfectants with pertussis toxin caused ADP-ribosylation of G-proteins and blocked chemokine-induced polymerization, indicating involvement of or , but not in this response.accepted by M.J. Parnham     

Amelioration of established collagen-induced arthritis (CIA) with anti-IL-1

Inflammatory cytokines have been implicated in the pathogenesis of rheumatoid arthritis (RA). To investigate the role of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in arthritic processes we studied the effect of neutralizing antibodies against murine IL-1 and TNF in murine collagen-induced arthritis (CIA). Combined i.p. injection of anti-IL-1 and anti-IL-1 (anti-IL-1,), given before onset of the disease, completely prevented CIA. In contrast, treatment with anti-TNF at this time point only delayed the onset of arthritis. Remarkably, a single injection of anti-IL-1, was also highly effective in suppressing established arthritis, reducing both inflammation and cartilage destruction. Suppression was most pronounced with the combination of anti-IL-1 and , but anti-IL-1 alone also gave significant relief. Specific antibodies against TNF had no effect on established CIA. Of interest, anti-IL-1, treatment started after onset of CIA completely normalized chondrocyte synthetic function, which was highly suppressed in the non-treated group. It is concluded that IL-1 and TNF are important cytokines during the onset of CIA and that IL-1 is the key mediator of inflammation and cartilage damage in established CIA.     

Problems in the development of turbine stomatological tips incorporating light guides

Scientific-Industrial Association Medinstrument, Kazan'. Translated from Meditsinskaya Tekhnika, No. 3, pp. 34–35, May–June, 1992.     

Discoordinate expression of IL-1α and IL-1β in interfacial membranes of failed joint prostheses

Bone resorption following either cemented or uncemented total hip replacement has been implicated as an important etiologic factor in aseptic loosening of prostheses, the most frequent cause of clinical failure. Interleukin-1 (IL-1), collagenase and prostaglandin E₂ are considered to play key roles in pathological bone resorption. We have measured the actual levels and quantified the genes coding for several cytokines [IL-1, IL-1, IL-4, IL-6, platelet-derived growth factors (PDGF), transforming growth factor- (TGF) and tumor necrosis factor- (TNF)] in interfacial membranes obtained from cemented or uncemented loosened joint replacements. IL-1, IL-6 and TNF were barely detectable in the interfacial membranes either at protein or mRNA levels, while IL-1 and TGF were found to be expressed at the highest levels in freshly isolated tissues. However, the expression of IL-1 increased 10–1000-fold either in isolated cells or explant cultures of interfacial membranes within 24 h. The expression of other cytokines, measured directly in tissue or cells, did not suggest a discoordinate expression of bone-resorbing cellular mediators.     

The bulbar respiratory centre in the rabbit

In anesthetized rabbits, spirogram and diaphragmatic activity were examined during electrical stimulation of the bulbar lateral reticular formation. The activity of bulbar respiratory neurons was recorded contra-or ipsilaterally to the stimulation site. One volley of repetitive stimuli per breath was delivered during either inspiration or expiration.

Evidence for a nucleotide-dependent topoisomerase activity from yeast mitochondria

Yeast mitochondria were found to contain a novel topoisomerase-like activity which required nucleoside di- or tri-phosphates as a cofactor. ADP supported activity as effectively as ATP and the optimal concentration for each was approximately 20 M. None of the other standard ribo- or deoxyrib-onucleotides could fully substitute for either ADP or ATP. The non-hydrolyzable ATP analogs, adenosine-5-0-(3-thiotriphosphate) (ATP--S), adenylyl (, -methylene) (AMP-PCP), and andenyl-imidodiphosphate (AMP-PNP) also supported activity suggesting that the nucleotide cofactor regulated topoisomerase activity rather than serving as an energy donor in the reaction. The mitochondrial topoisomerase activity relaxed both positively and negatively supercoiled DNA. It was not inhibited by concentrations of ethidium bromide up to 2 g/ml nor by either nalidixic or oxolinic acids; novobiocin, coumermycin, and berenil inhibited the activity. Genetic and biochemical analysis of the mitochondrial topoisomerase activity indicated that it was not encoded by the nuclear TOP1, TOP2, and TOP3 genes.     

Influence of central neuronal histamine on the pituitary-adrenocortical activity stimulated by neurotransmitters

The effect of brain neuronal histramine and its receptors on monoaminergic stimulation of the hypothalamic-pituitary-adrenal (HPA) activity, measured indirectly through corticosterone secretion, was investigated in conscious rats. Pretreatment with -fluoromethylhistidine, (-FMH) a histamine synthesis inhibitor, did not markedly affect the increase in serum corticosterone levels induced by intracerebroventricular (icv) injection of muscimol, a GABA_A receptor agonist and noradrenaline, an - and -adrenergic agonist, and slightly diminished the corticosterone response to isoprenaline, a -adrenergic agonist. -FMH totally abolished the increase in serum corticosterone induced by carbachol, a cholinergic muscarinic receptor agonist and significantly diminished the rise in corticosterone levels induced by clonidine, an ₂-adrenergic agent. Pretreatment with the histamine receptor antagonists mepyramine and cimetidine also considerably reduced the carbachol-induced corticosterone response and the response induced by clonidine.These results indicate that brain neuronal histamine is considerably involved in stimulation of the HPA axis by cholinergic muscarinic and ₂-adrenergic agonists, but not by GABA_A and ₁- and -adrenergic agonists.     

Lability in the responses of cells in the auditory cortex of squirrel monkeys to species-specific vocalizations

Summary The activity of 28 cells located mainly in the secondary auditory cortex (A II) of awake squirrel-monkeys, was extracellularly recorded for periods of up to 6 h. Seven different species-specific vocalizations, which were repeatedly presented to the monkey, were used as auditory stimuli. Twenty-six cells responded, at least once, to one or more vocalizations; 22 cells revealed some change in their response (pattern or strength) to at least one vocalization (change in response). Twenty-one cells exhibited a change in the number and/or type of vocalization to which they responded during the recording period (change in selectivity). At some time during the recording period all the responding cells exhibited a change in response and/or a change in selectivity (change in responsiveness). A change in response of a cell to a vocalization did not necessarily exclude a change in selectivity, associated with the same vocalization, later in time and vice-versa. A change in responsiveness to one vocalization was not necessarily correlated with changes in responsiveness to other vocalizations.     

Synoviocytes in chronic synovitis in situ and cytokine stimulated synovial cells in vitro neo-express α1, α3 and α5 chains of β1 integrins

The expression of the 1 integrins was examined immunohistochemically in synoviocytes from normal synovial membrane and from chronic synovitis of different aetiology and intensity. Normal synoviocytes were 61-positive but lacked 1 through 5. In mild inflammation type A synoviocytes neo-expressed 1, 3, and 5 chains. In severe inflammation both type A and B synoviocytes expressed 3, 4, 5, and 6 chains. The effects of inflammatory cytokines, as single agents or in combination, on the 1 integrin expression in cultured normal synoviocytes was determined by immunocytochemistry and flow cytometry. The 1 chain, while absent in unstimulated synoviocytes, was induced by interleukin-1 (IL-1), tumour necrosis factor- (TNF-), and interferon- (INF-). This effect was enhanced by combining IL-1 and TNF-. Expression of the 3 chain was up-regulated by IL-1 and, more intensely, by IFN-. Transforming growth factor (TGF-) inhibited the up-regulating effect of IL-1 and antagonized the effect of IFN- on 3 chain expression. Expression of the 5 chain was up-regulated significantly by co-stimulation through IL-1 together with TGF- or TNF-. Thus, the 1 integrin profile of cytokine activated synoviocytes in vitro resembled that of synoviocytes in synovitis in situ. These data suggest that IL-1, TNF-, IFN-, and TGF- are likely to be among the effectors regulating 1 integrin expression in synoviocytes in vivo.