Tick control by chemical ixodicides in Kenya: a review 1912 to 1981.
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A protein-free medium, termed ABC, has been developed which essentially eliminates the need for serum proteins. ABC supports the long-term growth of murine hybridomas as well as other transformed cells of the immune system. The requirement of hybridoma growth for transferrin has been met by substituting the soluble organo-iron compound, sodium nitroprusside. Substantial improvement in the growth of hybridomas was afforded by the inclusion of 18 trace elements complexed to disodium ethylene diaminetetraacetate (EDTA). The medium was further improved by the inclusion of components not found in Ham's F12 medium or by raising the concentrations of existing low molecular weight components. Murine hybridomas can be cultured routinely in this protein-free medium in an anchorage-independent manner with doubling times generally under 24 h. Visualized on electrophoretic gels, levels of monoclonal antibody taken from those cultures often exceeded 80% of the total protein. The medium was also able to support the growth of HuT 78 and H9 cells as well as certain other transformed cells of the immune system. In addition, normal human peripheral blood lymphocytes, activated with phytohemagglutinin and cultured with 50 U/ml recombinant interleukin 2, could be grown for 2 wk with a 50-fold expansion over input cell number.
The influence of silicon-treatment on the levels of TSH and thyroid hormones was studied in rats. Concentrations of thyrotropin (TSH), triiodothyronine (T3), and thyroxine (T4) were estimated in sera of rats receiving per os a soluble silicon compound--sodium metasilicate nonahydrate (Na2SiO3.9H2O), dissolved in the animals' drinking water. An increase in the TSH level in the tested group was observed, without statistically significant differences in T3 and T4 concentrations between the two groups of animals. The results provide evidence for the influence of silicon on the endocrine balance. They could also prove that this chemical element is capable of modifying the rate of some hormones' synthesis.
The influence of silicon treatment on the levels of calcium and magnesium in blood serum and tissues was studied in rats. The concentrations of both elements were estimated in samples of sera and tissues of rats receiving per os a soluble, inorganic silicon compound--sodium metasilicate nonahydrate (Na2SiO3.9H2O (REACHIM, USSR)), dissolved in the animals' drinking water. A decrease of magnesium concentration in serum was observed with accompanying elevation of registered calcemia. Moreover, a reduction of tissue calcium levels was found with a simultaneous increase of magnesium tissue pool. The results provide evidence for silicon involvement in mineral metabolism. It could result in a modification of pathological processes concerning bone tissue.
The influence of silicon treatment on the levels of trace elements zinc (Zn), copper (Cu), and iron (Fe) in serum and tissues was studied in rats. The concentrations of silicon, iron, and zinc were estimated in samples of sera and tissues of rats receiving per os a soluble, inorganic silicon compound--sodium metasilicate nonahydrate (Na2SiO3.9H2O), dissolved in the drinking water. An increase of copper concentrations in liver and aortic walls in the experimental group was observed, with simultaneous reduction of zinc amounts in serum and all the tissue samples in the course of the experiment. The iron concentrations in the analyzed samples did not show any significant changes between both groups. The silicon levels in serum and in all the examined tissues were significantly higher in the tested group. The results provide evidence for the silicon interaction with copper and zinc, which could result in a number of metabolic process modifications, antiatheromatous activity among them.
Alterations in protein kinase C (PKC) and cAMP-dependent kinase have been documented in anoxic brain injury. However, the regulation of these signaling enzymes in the cerebrovasculature has not been explored. In this study, cultured brain endothelial cells exposed to anoxic injury (anoxia--20 min/reoxygenation--40 min) showed both a significant increase (p < 0.001) in PKC and decrease (p < 0.01) in cAMP-dependent kinase activity. Analysis of PKC by Western blot indicated an increase in kinase level in response to anoxic injury, whereas there was no change in the level of cAMP-dependent protein kinase, as measured by labeled cAMP binding. Inhibition of nitric oxide synthase did not affect these changes. Addition of the nitric oxide-releasing compound sodium nitroprusside caused a dose-dependent increase in the activity of both signaling systems in endothelial cells. These data demonstrate that anoxic injury of brain endothelial cells in culture causes significant and divergent changes in signaling kinase activity. Abnormalities in brain endothelial PKC and cAMP-dependent kinase could have important consequences for the blood-brain barrier in anoxic brain injury.
In the mouse embryo cell line BALB/3T3 Clone A31-1-1, dose-dependent morphologic neoplastic transformation was obtained with NaAsO2, Na2HAsO4, CdCl2, and K2CrO4. Cellular uptake was four fold higher for As3+ than for As5+, and As5- was metabolized to As3+ in cytosol. Cytotoxicity and transformation rates were four fold higher for As3+ than As5+, but when correlated to cellular As burden they were equivalent. As3+ appears responsible for the transforming activity. The foci transformed by metals (or by other carcinogens) gave rise to tumorigenic cell lines (sc sarcomas in nude mice), none of which, however, induced metastases when tested by sc or by iv injection in nude mice. Thus carcinogens change this aneuploid cell line from a preneoplastic stage to the expression of malignant growth but not of metastatic activity. Metastatic and type IV collagenolytic activities can be induced by transfection of the c-Ha-ras oncogene and inhibited by the Ad2-E1a gene (so far shown in other cell types). It remains to be seen whether metal or other carcinogens can induce the nonmetastatic phenotype to become metastatic. The molecular mechanisms of metal carcinogenesis, studied in cell culture systems, in combination with other factors or oncogenes, may reveal the effect of individual metal carcinogens on discrete steps of the complex process of carcinogenesis.
The influence of silicon treatment on the levels of lipid parameters of blood serum and aortic wall was studied in rats. The concentrations of total cholesterol, phospholipids, triglycerides, HDL-cholesterol, LDL-cholesterol, and HDL-phospholipids were measured in sera of rats receiving per os a soluble, inorganic silicon compound--sodium metasilicate nonahydrate (Na2SiO3.9H2O)--dissolved in the drinking water. In the aortic tissue levels of total cholesterol, triglycerides and phospholipids were estimated. An increase in HDL-cholesterol and HDL-phospholipid concentrations, with a simultaneous decrease of LDL-cholesterol and triglyceride levels, was observed in the sera of the tested group. The levels of total cholesterol and phospholipids in the sera, as well as the concentrations of lipids in the aortic walls, showed no significant differences. The results obtained could provide evidence for the existence of an additional mechanism of silicon antiatheromatous action, concerning the modification of activity of enzymatic systems involved in lipids metabolism.
PURPOSE: To examine the effects of iv compound sodium lactate (CSL) with and without caloric supplementation with dextrose on nausea, vomiting and pain following general anesthesia for laparoscopy. METHODS: We compared iv fluid loading with and without supplementary dextrose for the prevention of postoperative nausea and vomiting (PONV). In a prospective double-blinded controlled trial, 120 ASA I female patients undergoing elective gynecological laparoscopy were randomized to one of three groups, and received either: (a) CSL 1.5 mL.kg(-1) per hour fasting duration; (b) CSL, 1.5 mL.kg(-1) per hour fasting duration with 0.5 g.kg(-1) dextrose added in 50% formulation (CSL/dextrose); or (c) no iv fluid (control). RESULTS: Compared with control the percentage of patients who had no PONV within 24 hr of anesthesia in the CSL and CSL/dextrose groups was 78% vs 83% and 71%, P = 0.81 and P = 0.683 respectively. The numbers needed-to-harm for causing PONV episodes in CSL/dextrose vs CSL or control groups were 5.7 [95% confidence interval (CI), 5.57-5.91] and 8.2 (95% CI, 8.01-8.37) respectively. The number needed-to-treat for prevention of PONV episodes in CSL vs control was 19.2 (95% CI, 19.08-19.37). A greater proportion of patients in the CSL/dextrose group required narcotic analgesia in the postanesthetic care unit compared to those in the control group (16/35 vs 7/37, P = 0.03). The CSL/dextrose group also demonstrated hyperglycemia (serum glucose 14.0 +/- 3.94 vs 5.0 +/- 1.01 vs 5.2 +/- 0.9 mmol.L(-1), P < 0.0001) in the postanesthetic care unit compared to the CSL and control groups. The CSL/dextrose group also reported increased thirst at 24 hr compared to control (20/35 vs 11/37, P = 0.035). CONCLUSION: These findings suggest that: 1) administration of dextrose is associated with nausea, increased opioid requirement and late thirst after elective gynecological laparoscopy; 2) iv fluids did not decrease PONV.
In this study, we isolated phenanthrene degraders belonging to Pseudomonas spp. by combining the selective force of two previously described media. The two compounds, sodium lauryl sarcosine and trimethoprim, from the Gould S1 medium, were added to minimal agar plates sprayed with phenanthrene. Pseudomonas spp. that could produce clearing zones were isolated in one step from the rhizosphere without first selecting for Pseudomonas spp. and subsequently screening for degraders or vice versa. Enumeration and isolation of Pseudomonas spp. attached to the rhizosphere showed clear differences between two types of soil. Rhizosphere-attached phenanthrene degraders (from Pseudomonas spp.) were isolated from a former coal gasification site, but were absent in an agricultural soil subjected to organic farming. We isolated 23 phenanthrene degraders producing clearing zones from the rhizosphere of barley roots. All of these 23 isolates (of which 16 were fluorescent in UV light) proved to be members of the Pseudomonas RNA homology group I, on the basis of results of the analytical profile index (API) test system and classic taxonomic tests.
Vanadium has been reported to have broad pharmacological activity both in vitro and in vivo. Vanadium compound, sodium orthovanadate, Na3VO4, is well known for its hypoglycaemic effects. However, Na3VO4 exerts these effects at relatively high doses (0.6 mg/ml) and exhibit several toxic effects. In the present study lower doses of Na3VO4 (0.2 mg/ml) are combined with Trigonella foenum graecum seed powder (TSP), another hypoglycaemic agent, to reduce its toxicity without compromising its antidiabetic potential. The efficacy of the lower doses of Na3VO4 has been investigated in restoring the altered glucose metabolism and histological structure in the sciatic nerves in 21 and 60 days alloxan diabetic rats. A portion of the glucose was found to be channelled from the normal glycolytic route to polyol pathway, evident by the reduced hexokinase activity and increased polyol pathway enzymes aldose reductase and sorbitol dehydrogenase activity causing accumulation of sorbitol and fructose in diabetic conditions. Ultrastructural observation of the sciatic nerve showed extensive demylination and axonal loss after eight weeks of diabetes induction. Blood glucose levels increased in diabetic rats were normalized with the lower dose of vanadium and Trigonella treatment. The treatment of the diabetic rats with vanadium and Trigonella prevented the activation of the polyol pathway and sugar accumulations. The sciatic nerves were also protected against the structural abnormalities found in diabetes with Trigonella foenum graecum as well as Na3VO4. Results suggest that lower doses of Na3VO4 may be used in combination with TSP as an efficient antidiabetic agent to effectively control the long-term complications of diabetes in tissues like peripheral nerve.
Oropharyngeal mucositis is a painful, often dose-limiting side effect of both radiotherapy and chemotherapy. To reduce the intensity of pain and prevent systemic infection via the compromised mucosa, agents such as antiseptic mouthwashes, anti-ulcer compounds, sodium bicarbonate, saline, and allopurinol have been traditionally used with limited success. The new agents that show promise are granulocyte macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF). However, best results, dosage, and means of administration still have to be determined. Other agents such as sucralfate, tretinoin, glutamine, and misoprostol are also being tested. The results reported from different testing centers are often contradictory and confusing. Basic requirements in prevention and control of mucositis are good oral hygiene, mechanical débridement of the oral tissues, and hydration.
Use of an intravenous injection of a water-soluble iodine compound (sodium iodide) for visualizing the urinary tract was first described by Osborne in 1923. However, sodium iodide was accompanied by a high incidence of side effects and the image quality was not good. As newer, improved contrast agents were introduced, a number of investigators reported on the incidence of death and side effects incurred by their use. In 1975, the first large-scale, multicenter, prospective study on the incidence of fatal and nonfatal reactions was reported by Shehadi. In this series, the overall incidence of adverse reactions was 5.65%, of which 3.77% were mild, 1.77% were moderate, 0.02% were severe, and 0.0007% were fatal. Shehadi also noted that a history of allergy doubled the risk of adverse reaction and a history of a previous adverse reaction to contrast material trebled the risk; also, the risk of a reaction to an intraarterial injection was half that of the risk associated with an intravenous injection. With the introduction of low osmolar nonionic agents, other large-scale studies were performed because these agents appeared to cause significantly fewer adverse reactions. However, they were from 10 to 15 times more expensive than their predecessors. In 1987, Lasser reported on the increased safety of ionic agents when patients were pretreated with steroids. Palmer in Australia and Katayama in Japan collected 120,000 and 335,000 patients, respectively, and compared the incidence of adverse reactions of the ionic versus the nonionic agents. Wolf recently reported a study that included a direct comparison of ionic agents with pretreatment with steroids versus nonionic agents.(ABSTRACT TRUNCATED AT 250 WORDS)
Discoidal complexes of phosphatidylcholine (PC) . apolipoprotein A-I . cholesterol were prepared with egg PC, palmitoyloleoylPC, dipalmitoylPC, or dimyristoylPC, and were used as substrates of purified lecithin-cholesterol acyltransferase to investigate the effects of neutral salts on the enzymatic reaction. Sodium fluoride, chloride and bromide concentrations up to 1 M, did not affect the properties of the substrate particles, but caused marked and distinct changes in the activity of the enzyme with the various PC particles. The effects of salts were largely due to the anions, which followed the order of the lyotropic series in their inactivating capacity: F- less than Cl- less than Br- less than NO3- less than I- less than SCN-. Sodium salts (F-, Cl-, and Br-) produced a very large increase in the pH optimum of the enzymatic reaction (7.4 to at least 8.5) essentially obliterating the ionization of a functional group with pK of 8.1. The kinetics of the enzymatic reaction revealed major differences among the PC particles, and different responses of their kinetic parameters with increasing salt concentrations. The conclusions reached in this work are the following: (1) The relative reactivity of PC substrates, in discoidal particles, with lecithin-cholesterol acyltransferase depends strongly on the concentration and type of salts in the medium. (2) Anions (in lyotropic series) rather than cations affect the enzymatic reaction. (3) There are functional groups with pK of 8.1 which are affected markedly in their ionization behavior by anion binding. (4) The active site of lecithin-cholesterol acyltransferase and its interaction with anions are affected by the exact nature of the PC-apolipoprotein interface.
The presence of hydrophobic sites in fetuin, ovine submaxillary mucin and two homogeneous canine tracheal mucins was established by fluorescence probe techniques. The interaction between the above-mentioned glycoproteins and two hydrophobic fluorescent compounds, sodium mansate and mansylphenylalanine, was accompanied by an enhancement in fluorescence and a shift of the fluorescence maxima to shorter wavelengths. The introduction of a phenylalanine residue to the mansyl group enhanced the binding affinity of the probe for the hydrophobic sites of these glycoproteins as evidenced by lower values for the dissociation constants. The high molecular weight (581 600) tracheal mucin, which had the highest carbohydrate content (80%) of all the glycoproteins investigated, exhibited the highest fluorescence enhancement and the largest number of binding sites for these fluorescent probes.
Many of the circulating algesic agents released in response to ischemia produce a profound vasodilatation possibly through the release of an endothelium-derived relaxing factor (EDRF) as well as pain. We report here that intravenously administered S-nitrosocysteine, a putative EDRF, and not the nitric oxide liberating compound sodium nitroprusside produces significant alterations in nociceptive behavior that are abolished by bilateral vagotomy. These results are consistent with a role for EDRF in peripheral nociceptive mechanisms.
The effects of nitric oxide on the Ca2+ channel currents of adult rat superior cervical ganglion neurons were investigated using the whole-cell patch-clamp technique. Nitric oxide-containing compounds sodium nitroprusside and S-nitroso-N-acetyl-penicillamine increased the amplitude of Ca2+ currents by intracellular application. In addition, both sodium nitroprusside and S-nitroso-N-acetylpenicillamine reduced norepinephrine-induced inhibition of Ca2+ currents. The results suggest that nitric oxide might be involved in the modulation of Ca(2+)-dependent neurotransmission in sympathetic neurons.
A potential cytotoxic, self-destructive role of endogenously generated and exogenously supplied nitric oxide (NO) was studied in two mouse monocytic macrophage cell lines (RAW 264.7 and J774.1). Our attention centered on NO-mediated glyceraldehyde-3-phosphate dehydrogenase (GAPDH) modification and inhibition of the Krebs cycle enzyme, aconitase, related to macrophage cell death. NO formed by an active inducible nitric oxide synthase significantly decreased cell viability in the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) cytotoxicity assay. Similarly, cell viability was inversely and dose-dependently correlated to increasing concentrations of the NO-releasing compound, sodium nitroprusside. Biochemically, we noticed a correlation between endogenously derived or exogenously generated NO and inhibition of GAPDH as well as aconitase enzyme activity. The involvement of NO was further substantiated by the use of NG-monomethyl-L-arginine. Associated with decreased GAPDH enzyme activity, 32P-NAD(+)-dependent modification of the enzyme in the cytosol of pretreated cells was hindered. This reflects intracellular protein modification as a result of NO signalling. Using sodium nitroprusside we achieved GAPDH translocation from the cytosol to the plasma membrane or the nucleus of treated cells. However, despite GAPDH modification, lactate production was not rate limiting during NO intoxication. Furthermore, blocking the iron-sulfur-containing enzyme, aconitase, is insufficient to produce macrophage cell death. Although RAW 264.7 and J774.1 cells show substantial variation in their sensitivity towards NO it can be concluded that NO-mediated macrophage cell death is not linked to energy depletion. For GAPDH, NO-mediated protein modification may be related to functions of the enzyme, other than its glycolytic role.