Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085593 (chills)
 4,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 54-year-old man was receiving calcium dobesilate for retinopathy and after 8 days he presented fever of more than 39 degrees C, generalized myalgia, chills and headache. Other causes of fever were ruled out. A challenge test was done with a single therapeutic oral dose of calcium dobesilate and fever appeared 20 h later and lasted 8 h. Our patient fulfils Young's stringent criteria for drug fever. To our knowledge drug-induced fever due to calcium dobesilate has not been reported previously.
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PMID:Drug-induced fever: a clinical report and challenge test with calcium dobesilate. 208 72

Fura-2 has become the most popular fluorescent probe with which to monitor dynamic changes in cytosolic free calcium in intact living cells. In this paper, we describe many of the currently recognized limitations to the use of Fura-2 in living cells and certain approaches which can circumvent some of these problems. Many of these problems are cell type specific, and include: (a) incomplete hydrolysis of Fura-2 acetoxymethyl ester bonds by cytosolic esterases, and the potential presence of either esterase resistant methyl ester complexes on the Fura-2/AM molecule or other as yet unidentified contaminants in commercial preparations of Fura-2/AM; (b) sequestration of Fura-2 in non-cytoplasmic compartments (i.e. cytoplasmic organelles); (c) dye loss (either active or passive) from labeled cells; (d) quenching of Fura-2 fluorescence by heavy metals; (e) photobleaching and photochemical formation of fluorescent non-Ca2+ sensitive Fura-2 species; (f) shifts in the absorption and emission spectra, as well as the Kd for Ca2+ of Fura-2 as a function of either polarity, viscosity, ionic strength or temperature of the probe environment; and (g) accurate calibration of the Fura-2 signal inside cells. Solutions to these problems include: (a) labeling of cells with Fura-2 pentapotassium salt (by scrape loading, microinjection or ATP permeabilization) to circumvent the problems of ester hydrolysis; (b) labeling of cells at low temperatures or after a 4 degrees C pre-chill to prevent intracellular organelle sequestration; (c) performance of experiments at lower than physiological temperatures (i.e. 15-33 degrees C) and use of ratio quantitation to remedy inaccuracies caused by dye leakage; (d) addition of N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) to chelate heavy metals; (e) use of low levels of excitation energy and high sensitivity detectors to minimize photobleaching or formation of fluorescent non-Ca2+ sensitive forms of Fura-2; and (f) the use of 340 nm and 365 nm (instead of 340 nm and 380 nm) for ratio imaging, which diminishes the potential contributions of artifacts of polarity, viscosity and ionic strength on calculated calcium concentrations, provides a measure of dye leakage from the cells, rate of Fura-2 photobleaching, and can be used to perform in situ calibration of Fura-2 fluorescence in intact cells; however, use of this wavelength pair diminishes the dynamic range of the ratio and thus makes it more sensitive to noise involved in photon detection. Failure to consider these potential problems may result in erroneous estimates of cytosolic free calcium.(ABSTRACT TRUNCATED AT 400 WORDS)
Cell Calcium
PMID:Assessment of Fura-2 for measurements of cytosolic free calcium. 219 82

Eggshells of Nematodirus battus leaked trehalose 4 hr after being stimulated to hatch, and became permeable to trypan blue at their poles; 80% of eggs were stained blue 24 hr later. Exogenous application of ruthenium red significantly inhibited chill- and sodium fluoride-stimulated hatching, 50% hatch inhibition occurring in 44.67 +/- 2.2 and 8.5 +/- 1.5 microM, respectively. Lanthanum chloride, however, was not as inhibitory as ruthenium red on fluoride-stimulated hatching, 50% occurring at 31.60 +/- 1.25 microM. A Scatchard plot of the competitive binding of ruthenium red to eggshells demonstrated a high-affinity binding site for calcium, KCa' = 1.92 microM and a second, low-affinity site, KCa" = 1169.60 microM. Ruthenium red binding was significantly reduced by several enzymes, e.g., EGTA-buffered trypsin reduced binding by 73%. Radioiodinated concanavalin A also bound competitively to the eggshells in the presence of alpha-D-glucosyl-alpha-D-glucopyranoside and alpha-methyl-D-mannopyranoside. Eggshells incorporated phosphorus-32 from ATP after chilling or on exposure to sodium fluoride; gel filtration of solubilized homogenates of these samples showed that two proteins were radiolabelled with molecular weights of 38 X 10(3) and 8 X 10(3) Da, respectively. This phosphorylation was inhibited by N-ethylmaleimide, which also prevented hatching.
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PMID:Nematodirus battus: permeability changes, calcium binding, and phosphorylation of the eggshell during hatching. 620 83

Thin-sectioning and freeze-etching electron microscopy were applied to explore the structure and the temperature- and Ca2+-response of the different host and parasite membranes during intraerythrocytic development of Plasmodium knowlesi in Macaca mulatta. The plasma membrane of uninfected erythrocytes is temperature- and Ca2+-responsive: chilling to 4 degrees C and exposure to 5 mM Ca2+ induces a slight decrease in IMP-frequency and the emergence of small IMP-devoid patches on P-faces. On parasite infection, the erythrocyte membrane becomes modified as indicated by an enhanced temperature-response and the appearance of caveolae, ca. 70-90 nm in diameter. The frequency of these caveolae is increased in schizont-infected erythrocytes. Moreover, electron dense plaques, ca. 40 nm in width, appear just beneath the erythrocyte membrane in late trophozoites and schizonts, thus indicating a further modification of the host cell membrane during parasite development. The membrane of the parasitophorous vacuole, derived from the host plasma membrane, dramatically reduces the IMP-frequency especially on the P-face upon parasite infection. This leads to an apparent reversal of the IMP-distribution persisting throughout the whole infection cycle. The parasite plasma membrane forms local compaction domains with the nuclear envelope in ca. 30% of the ring-stages and trophozoites, which disappear in late trophozoites and schizonts. Moreover, the IMP-frequency on plasma membrane fracture faces almost doubles during parasite development. Chilling induces a decrease in the IMP-frequency on P-faces of the plasma membrane. Surprisingly, however, the parasite plasma membrane and the vacuolar membrane respond to externally applied Ca2+ with almost a doubling of the IMP-frequency. The different parasite endomembranes also undergo characteristic changes during parasite development.
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PMID:Intraerythrocytic development of Plasmodium knowlesi: structure, temperature- and Ca2+-response of the host and parasite membranes. 708 12

Hemodialysis with reprocessed dialyzers has been associated with an increased mortality in patients on chronic dialysis, but the causes for this increased mortality have not been identified thus far. The aim of this study was to compare the qualitative and/or quantitative differences in activation of cellular and plasma elements, intradialytic signs and symptoms, adequacy of dialysis, and serum biochemistry and hematology in patients dialyzed with new or reprocessed cellulose dialyzers. This study measured the plasma levels and production of interleukin-1 receptor antagonist (IL-1Ra) by peripheral blood mononuclear cells (PBMC), indices of cytokine synthesis; plasma C3a levels, an index of complement activation; plasma levels of lipopolysaccharide binding protein (LBP), an acute phase reactant; and plasma levels of bactericidal-permeability increasing factor (BPI), a neutrophil primary granule protein, in 37 patients on chronic hemodialysis with glutaraldehyde and bleach-reprocessed cellulose dialyzers after random assignment to 12 wk of dialysis with new (single use) or reprocessed (reuse) cellulose dialyzers. These indices were studied before dialysis, 15 min after the start of dialysis, and at the conclusion of dialysis in both groups. Intradialytic clinical symptoms and signs, urea reduction ratios, monthly blood chemistry, and hematology were also studied during the 12-wk period. Before randomization, clinical and laboratory characteristics and IL-1Ra production by PBMC were similar in the two groups. During the 12-wk study, the mean number of dialyzer reuses was 7 +/- 1 in the reuse group and there were no breaks in protocol in the single-use group. At the end of the study, plasma levels of IL-1Ra, cell content and production of IL-1Ra by unstimulated, endotoxin-stimulated, and lgG-stimulated PBMC among patients assigned to reuse were not significantly different from those in the single-use group either before dialysis, at 15 min, or at the conclusion of dialysis. Similarly, plasma levels of C3a, LBP, and BPl were not significantly different between groups at any of the three time points. During the 12-wk study, none of the patients in either arm of the study experienced chills, rigors, or fever, and there were no differences in the number of episodes of symptomatic hypotension in patients on reused dialyzers (11 +/- 3) compared with patients on single-use dialyzers (8 +/- 2). The mean monthly urea reduction ratio during the 3 months of the study was 63 +/- 2% and 65 +/- 2% for reuse and single-use dialyzers, respectively (not significant). Similarly, the hematocrit, white blood cell count, serum calcium, phosphorus, cholesterol, triglycerides, total protein, and albumin levels were also not significantly different between the two groups at the end of the 12-wk study period. These results suggest that the reprocessing of cellulose dialyzers with glutaraldehyde and bleach does not affect indices of blocompatibility, intradialytic symptoms and signs, adequacy of dialysis, or serum biochemistry and hematology.
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PMID:Impact of single use versus reuse of cellulose dialyzers on clinical parameters and indices of biocompatibility. 879 94

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.
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PMID:Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis. 1032 13

Cytoskeletal rearrangements and a membrane lipid phase transition (liquid crystalline to gel) occur in platelets on cooling from 23 to 4 degrees C. A consequence of these structural alterations is irreversible cellular damage. We investigated whether platelet membrane integrity could be preserved by (a) previously studied combinations of a calcium chelator (EGTA) and microfilament stabilizer (cytochalasin B) with apparent benefit in protecting platelets from cooling injury or (b) agents of known benefit in protecting membranes and proteins from freezing injury. Platelet function and activation before and after freezing or cooling were measured by agglutination with ristocetin, aggregation with thrombin or ADP, platelet-induced clot retraction (PICR), and expression of P-selectin. Platelets were loaded with 10 nM fluorescein diacetate. After freezing or cooling, the preparations were centrifuged and the supernatant was measured for fluorescein. For cooling experiments, fresh platelets were chilled at 4 degrees C for 1 to 21 days with or without the combination of 80 microM EGTA/AM and 2 microM cytochalasin B (EGTA/AM-CytoB) and then warmed rapidly at 37 degrees C. For freezing experiments, 5% dimethyl sulfoxide (Me2SO) or 5 mM glycerol were added to fresh platelets. The preparations were then frozen at -1 degrees C/min to -70 degrees C and then thawed rapidly at 37 degrees C. Platelet membrane integrity, as measured by supernatant levels of fluorescein, correlated inversely with platelet function. Chilling platelets at 4 degrees C with EGTA/AM-CytoB showed a gradual loss of membrane integrity, with maximum loss reached on day 7. The loss of membrane integrity preceded complete loss of function as demonstrated by PICR. In contrast, platelets chilled without these agents had complete loss of membrane integrity and function after 1 day of storage. Freezing platelets in Me2SO resulted in far less release of fluorescein than did freezing with or without other cryoprotectants (P < 0.001). This result correlated with enhanced function as demonstrated by PICR and supports earlier observations that Me2SO protects platelet membranes from freezing injury. Release of fluorescein into the surrounding medium reflected loss of membrane integrity and function in both cooled and frozen platelets. Membrane cytoskeletal rearrangements are linked to membrane changes during storage. These results may be generally applicable to the study of platelet storage.
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PMID:Cooling and freezing damage platelet membrane integrity. 1032 11

Amphotericin B remains the agent of choice for treatment of severe fungal infections. Its use is hindered by adverse effects, including infusion-related fever, chills, and hypotension, as well as nephrotoxicity with secondary anemia, hypokalemia, and hypomagnesemia. Amphotericin B-induced transcription and expression of interleukin (IL)-1beta by human monocytes is believed to be involved in mediating infusion-related adverse effects. It is shown here that agents that increase intracellular calcium [Ca++]i (A23187 and thapsigargin) in human monocytic cells also induce IL-1beta expression. Furthermore, amphotericin B-induced IL-1beta expression is attenuated by the calmodulin antagonist calmidazolium. Amphotericin B 5.41 microM increases [Ca++]i by up to 300 nM in these cells. In the presence of a nominal calcium buffer or EGTA, amphotericin B-induced IL-1beta expression is attenuated. Thus, amphotericin B acts as an ionophore to increase [Ca++]i and activates calmodulin-mediated expression of IL-1beta in human monocytes.
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PMID:Amphotericin B-induced interleukin-1beta expression in human monocytic cells is calcium and calmodulin dependent. 1047 56

Steers of known percentage Brahman (B) and Angus (A) breeding (100% A, n = 6; F1 B x A, n = 6; and 100% B, n = 6) were used to determine the effect of calcium chloride injection on the calpain proteinase system and meat tenderness. The steers were slaughtered in six replications (at either 9 or 14 mm of backfat, determined ultrasonically), with each breed type represented. Calpains and calpastatin activities were measured on fresh, prerigor longissimus muscle samples. Carcass data were collected after a 24-h chill, and the short loin (IMPS #180), top sirloin (IMPS #184), and top round (IMPS #168) were removed from both sides of each carcass. The cuts from the right side were then injected at 5% (wt/wt) with CaCl2 solution (2.2%). Longissimus muscle calpain and calpastatin activities were also measured at 48 h postmortem from the injected and control sides of each carcass. Warner-Bratzler shear force was measured on steaks from the three subprimals aged 1, 2, 5, 15, or 31 d. Marbling scores and USDA quality grades were higher (P<.05) in A than in F1 B x A and B carcasses. Calpastatin activity was higher (P<.05) in muscle from B than in muscle from A and F1 B x A steers, and postmortem storage (O vs 48 h) and CaCl2 injection reduced (P<.05) the activity of the calpains and calpastatin. Strip loin and top sirloin steaks from A and F1 B x A steers were more tender (P<.05) than steaks from B steers; however, top round steak tenderness did not differ (P>.05) across breed type. Calcium injection improved strip loin and top sirloin steak tenderness, but it did not affect top round steak tenderness. Collectively, these data show that CaC12 injection can be used to improve meat tenderness, with similar responses shown in cattle containing 0, 50, and 100% B inheritance. However, even with CaCl2 injection, B steaks are less tender than their A and F1 B x A counterparts.
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PMID:Calcium-activated tenderization of strip loin, top sirloin, and top round steaks in diverse genotypes of cattle. 1064 69

Various agonists but also chilling cause blood platelets to increase cytosolic calcium, polymerize actin, and change shape. We report that cold increases barbed end nucleation sites in octyl glucoside-permeabilized platelets by 3-fold, enabling analysis of the intermediates of this response. Although chilling does not change polyphosphoinositide (ppI) levels, a ppI-binding peptide completely inhibits cold-induced nucleation. The C terminus of N-WASp, which inhibits the Arp2/3 complex, blocks nucleation by 40%; GDPbetaS, N17Rac and N17Cdc42 have no effects. Some gelsolin translocates to the detergent-insoluble cytoskeleton after cooling. Chilled platelets from gelsolin-deficient mice have approximately 50% fewer new actin nuclei compared with platelets from wild-type mice. EGTA completely inhibits gelsolin translocation into the cytoskeleton, and the small amount of gelsolin initially there becomes soluble. Chilling releases adducin from the detergent-resistant cytoskeleton. We conclude that platelet actin filament assembly induced by cooling involves ppI-mediated actin filament barbed end uncapping and de novo nucleation independently of surface receptors or downstream signaling intermediates besides calcium. The actin-related changes occur in platelets at temperatures below 37 degrees C, suggesting that the platelet may be more activable at temperatures at the body surface than at core temperature, thereby favoring superficial hemostasis over internal thrombosis.
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PMID:Mechanisms of cold-induced platelet actin assembly. 1132 7


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