Klippel-Trenaunnay-Weber syndrome.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S De.
Explore the source record for details and available documents.
The lipid disordering effect of aspirin on the liposomal membrane of dipalmitoyl phosphatidyl choline has recently been studied using the fluorescence polarization method. From the anisotropy-temperature curve, we have calculated here the associated change in van't Hoff enthalpy. Since the fluorescence technique requires a very small amount of sample (10(-4) M), this method of enthalpy calculation compares well and is advantageous over the standard calorimetric methods.
The primary culture of confluent human airway smooth muscle (ASM) cells were exposed up to 5 days to human recombinant interleukin (IL)-1 beta in the presence of indomethacin and 1% fetal bovine serum. The proliferation was assessed by a [3H]thymidine incorporation and direct cell count. We found that IL-1 beta significantly increased thymidine incorporation into and cell count of ASM cells in a concentration-dependent manner. Pretreatment of cells with specific polyclonal antibodies against platelet-derived growth factor (PDGF-BB homodimer) completely inhibited the IL-1 beta-induced increase in thymidine incorporation. The PDGF-BB, at the concentrations of 1.5 and 2.5 ng/ml, stimulated the proliferation of ASM cells. The proliferation action of IL-1 beta was potentiated when PDGF-BB was added into the medium in combination with IL-1 beta. Pretreatment of cells with genistein (0.37 microM), a specific tyrosine kinase inhibitor, attenuated the proliferative effect of IL-1 beta and PDGF-BB. To clarify whether these growth stimuli (IL-1 beta and PDGF-BB) activated phospholipase C (PLC), we examined the formation of phosphatidylinositols. We observed that both agents significantly increased phosphoinositide turnover. In contrast, genistein pretreatment (0.37 microM) prevented formation of inositol 1,4,5-trisphosphate (IP3), as induced by IL-1 beta and/or PDGF-BB. This study demonstrates that both IL-1 beta and PDGF-BB could induce proliferation of ASM cells through the activation of tyrosine kinase and PLC, which in turn stimulate the formation of IP3, a second messenger molecule.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Guinea pig airway smooth muscle (ASM) cells were maintained in a primary tissue culture (passages 1-3). Cells were exposed to human recombinant interleukin-1 beta (IL-1 beta; 20-100 pg/ml) or interleukin-6 (IL-6; 1-4 ng/ml) in the presence of indomethacin (1 microgram/ml) for up to 5 days. Proliferation of ASM cells was assessed with two techniques, direct counting of cells with a hemacytometer and [3H]thymidine incorporation corrected for total protein content. Hypertrophy of ASM cells was assessed by [3H]leucine incorporation (evaluation of protein synthesis), determination of total DNA content, DNA content per cell, and protein content per cell. We observed that the exposure of ASM cells to human recombinant IL-1 beta or IL-6, in all studied concentrations, significantly increased the number of cells as well as [3H]thymidine incorporation into ASM cells. We also found that exposure of ASM to these two cytokines increased [3H]leucine incorporation into the ASM cells and increased protein content and DNA content per single cell. These changes were also concentration dependent. We conclude that the two proinflammatory cytokines, IL-1 beta and IL-6, which are present in asthmatic lungs, increased the proliferation of ASM cells (hyperplasia) as well as their overall size and size of their nuclei, as measured by biochemical markers. These findings are compatible with the presence of ASM hypertrophy.
A detailed investigation on the anti-inflammatory activity of the butanol fraction of a methanol extract (BMEL) of the defatted leaves of Paederia foetida was undertaken to find the pharmacological basis for the ethnomedical use of the plant. This fraction produced a significant inhibition of granulation tissue formation in cotton-pellet implanted rats. It decreased liver aspartate transaminase activity without affecting serum aspartate transaminase activity. It did not, however, affect adrenal weight and ascorbic acid content significantly, thus ruling out a stimulation of the adrenal-pituitary axis. BMEL antagonised hyposaline-induced haemolysis of human red blood cells and an elevation of rat serum acid phosphatase activity, indicating the presence of a membrane stabilising activity. It also inhibited the elevation of serum orosomucoid levels in rats, suggesting the possibility of the presence of disease-modifying antirheumatic activity. The results indicate that there is some rationale behind the ethnomedical use of the plant for treating inflammatory disorders.
The methanol extract of the defatted leaves of Gymnosporia montana was evaluated for hepatoprotective activity by noting its effect on carbon tetrachloride (CCl4)-induced changes in liver cytoarchitecture and alterations in certain biochemical parameters. The main parameters studied were transaminase activity, lipid constituents of serum and liver, orosomucoid level in serum, and liver glycogen and phospholipid contents. The extract administration led to a significant reversal of the majority of the altered biochemical parameters. Besides, a significant antagonism of the CCl4-induced changes in the liver cytoarchitecture was also observed. The results confirm the presence of hepatoprotective activity in the plant material.
Bronchoalveolar lavage fluid from symptomatic asthmatics contains elevated levels of several proinflammatory interleukins including interleukin-1 beta (IL-1 beta). Biologic activities of IL-1 beta are considered to be critical in the inflammatory process. Since these characteristics include mitogenic properties, we investigated the effect of IL-1 beta on the proliferation of airway smooth muscle (ASM) cells isolated from guinea pig tracheas. Primary tissue culture of ASM cells was maintained in media containing 0%, 1%, or 10% fetal bovine serum (FBS). Cultures were exposed up to 6 days to human recombinant IL-1 beta (20, 40, or 100 pg/ml) in the presence or absence of indomethacin. The proliferation of ASM cells was assessed with two techniques: a direct counting of cells with a hemocytometer and/or with a [3H]-thymidine incorporation, an established marker of DNA synthesis. The evaluation was done daily, up to the sixth day after exposure of cells to different doses of IL-1 beta. We found that the exposure of ASM cells to human recombinant IL-1 beta significantly (P < 0.01) increased the number of tracheal myocytes as well as the [3H]-thymidine incorporation into ASM cells. These changes were dependent upon the dose of IL-1 beta and the concentration of FBS in the cultured medium. The most active proliferation of ASM cells was observed in medium containing 1% FBS, indomethacin (1 microgram/ml), and IL-1 beta (100 pg/ml). The presence of indomethacin in the culture medium was essential to demonstrate the proliferative effect of IL-1 beta.(ABSTRACT TRUNCATED AT 250 WORDS)
The records of five patients who received local irradiation for incompletely excised or inoperable glomus tumour were retrospectively reviewed. Age ranged from 25 to 46 years. There were two female and three male patients. Two patients who were solely treated by radiation therapy remain clinically disease free at 30 and 42 months respectively. Of the remaining three patients, where radiotherapy was delivered post operatively, one achieved complete remission and is well and alive at 60 months, whereas the other two patients were lost to follow up at 22 and 26 months respectively after showing an early clinical improvement. We advocate the efficiency of radiation therapy as primary treatment in the management of primary glomus tumour.
In the dog iris sphincter, muscarinic acetylcholine receptors are coupled either to the stimulation of phospholipase C and muscle contraction or to the stimulation of adenylate cyclase and muscle relaxation, this was found to be dependent upon the concentration of the muscarinic agonist. In contrast to the dog, muscarinic receptors in iris sphincters from different mammalian species were found to be coupled to phospholipase C and contraction at all concentrations of carbachol investigated (1-100 microM). In the dog sphincter, lower concentrations (less than 5 microM) of carbachol stimulated myo-inositol 1,4,5-trisphosphate (IP3) production, inhibited cAMP formation and induced contraction, and higher concentrations (greater than 5 microM) enhanced cAMP formation, inhibited IP3 production and induced relaxation. The mechanisms for the stimulatory effects on cAMP formation through muscarinic receptors were investigated. Carbachol (25 microM) increased both basal and isoproterenol- and forskolin-stimulated cAMP levels. Atropine inhibited the carbachol-stimulated increase in cAMP levels in a dose-dependent manner with an IC50 of 9 nM. Intracellular Ca2+, derived from IP3-induced Ca2+ release and/or from muscarinic receptor-operated Ca2+ influx, and protein kinase C may mediate the muscarinic receptor-linked rise in intracellular cAMP. This conclusion is supported by the following findings. (1) At short time intervals (less than 1 min) carbachol (25 microM) increased IP3 production and contraction and this was followed (between 1 and 20 min) by cAMP formation and muscle relaxation. (2) Carbachol-stimulated IP3 production was detected at a concentration of the agonist 26-fold lower than that required for cAMP formation, and it was completely blocked by the phorbol ester, phorbol 12,13-dibutyrate (50 nM). (3) A Ca(2+)-calmodulin stimulated adenylate cyclase was demonstrated in membranes from dog iris sphincter but not in that from rabbit and bovine. (4) Trifluoperazine (0.1 microM), a calmodulin antagonist, inhibited the carbachol-stimulated cAMP accumulation. (5) The Ca2+ ionophore A23187 and the phorbol ester increased cAMP production in a dose-dependent manner. A23187 potentiated cAMP production induced by either carbachol or by the phorbol ester. (6) Muscarinic stimulation of cAMP production persisted even after the tissue was pretreated with the phorbol ester or staurosporine. (7) Nifedipine (0.01-0.5 microM), a Ca2+ channel antagonist, inhibited carbachol stimulation of cAMP production, suggesting the presence of a muscarinic receptor-operated Ca2+ influx pathway in this tissue.(ABSTRACT TRUNCATED AT 400 WORDS)
Explore the source record for details and available documents.
The activities of Na+K(+)- and Mg(2+)-ATPases in mitochondrial, microsomal, and cytosolic fractions of Singi fish (Heteropneustes fossilis Bloch) brain were investigated after injections of various doses (0.012, 0.025, 0.05, and 0.10 micrograms/g) of triiodothyronine (T3) for 3 consecutive days. Both ATPases were found in the mitochondrial and microsomal fractions. The cytosolic fraction showed only Mg(2+)-ATPase activity. Mitochondrial Na+K(+)-ATPase activity increased to almost the same level in fish treated with 0.025, 0.05, or 0.10 micrograms of T3/g, while the T3 dose of 0.012 micrograms/g was ineffective in this respect. Microsomal Na+K(+)-ATPase activity increased to about the same level with all of the doses of T3 used. No detectable amount of Na+K(+)-ATPase was found in the brain cytosolic fraction. Mitochondrial Mg(2+)-ATPase activity was enhanced with 0.025, 0.05, and 0.10 micrograms of T3/g. The last dose, however, produced a higher increase in activity than the other two doses. Surprisingly, microsomal and cytosolic Mg(2+)-ATPase activity was not increased by T3 treatment. Although T3 concentrations rose sharply after each T3 injection, the serum T3 level in T3-injected fish was not different from that in the control as observed on the fourth day. The T3-induced rise of Na+K(+)- and Mg(2+)-ATPase activities was inhibited by cycloheximide treatment. Immersion of Singi fishes in thiourea significantly reduced brain Na+K(+)-ATPase activity in microsomal and mitochondrial fractions but decreased Mg(2+)-ATPase activity only in the mitochondrial fraction. Three consecutive daily injections of T3 (0.10 micrograms/g) into the thiourea-treated fishes increased their ATPase activities even beyond the control level.(ABSTRACT TRUNCATED AT 250 WORDS)
The results of single modality treatment using surgery or radiotherapy alone in advanced head and neck cancers are known to be unsatisfactory. The present study analyses 252 cases with stage III and IV resectable cancers of the head and neck region selected to be treated by a combined regime of pre- or post-operative radiation and radical surgery. Only 193 patients completed the treatment protocol. There were 58 cases (33.5 per cent) who failed either at primary or regional sites or both. Nine cases (five per cent) developed distant metastasis. Absolute and determinate four year disease-free survival was 55 per cent and 61 per cent respectively. Early lesions (stage I and II) have been excluded from the study. The study indicates that a reduction in primary and regional failures correlates well with a combined therapy, though prolonged treatment may affect patients' compliance to some extent.
Extramedullary haematopoiesis associated with thalassaemia leading to spinal cord compression is an extremely rare event in the course of the disease. The efficacy of radiation therapy is advocated in the management of such a complication. Two patients with thalassaemia, who had presented with spinal cord compression, were successfully treated by a modest dose of local radiotherapy. In one of the patients, however, radiotherapy was resorted to after an initial decompressive laminectomy and partial removal of the intraspinal haematopoietic mass proved unsuccessful. The other patient was managed solely by radiation therapy.
Explore the source record for details and available documents.