Isolated gastric tuberculosis: a case report.
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Transformation of human ciliary epithelial cells by simian virus 40: induction of cell proliferation and retention of beta 2-adrenergic receptors.
Ciliary epithelial cells derived from human eye were successfully propagated through many generations after transformation with simian virus 40. The cell clone 8-SVHCE was isolated and characterized by immunoprecipitation and pharmacological studies that demonstrated the presence of several functional properties observed in the parent cells of this tissue. Immunoprecipitation revealed the presence of large tumor (T) antigen, and Southern blot analysis showed the incorporation of viral DNA into high molecular weight ciliary epithelial cell DNA. The presence of beta-adrenergic receptors was demonstrated by direct binding of a radiolabeled antagonist, [125I]iodopindolol, to membrane preparations of 8-SVHCE cells (Kd = 41.8 pM and Bmax = 67.1 fmol/mg of protein). Competition experiments with [125I]iodopindolol and selective drugs suggested that the receptors are of the beta 2-adrenergic subtype. Studies of catecholamine-stimulated cellular cAMP production and of isoproterenol-dependent protein phosphorylation of vimentin in 8-SVHCE indicated the functional conservation of beta-adrenergic receptor-mediated processes that are thought to be important in the regulation of aqueous humor production by the ciliary epithelium in vivo.
Adenylyl Cyclases↗
Stress signaling through Ca2+/calmodulin-dependent protein phosphatase calcineurin mediates salt adaptation in plants.
Calcineurin (CaN) is a Ca2+- and calmodulin-dependent protein phosphatase (PP2B) that, in yeast, is an integral intermediate of a salt-stress signal transduction pathway that effects NaCl tolerance through the regulation of Na+ influx and efflux. A truncated form of the catalytic subunit and the regulatory subunit of yeast CaN were coexpressed in transgenic tobacco plants to reconstitute a constitutively activated phosphatase in vivo. Several different transgenic lines that expressed activated CaN also exhibited substantial NaCl tolerance, and this trait was linked to the genetic inheritance of the CaN transgenes. Enhanced capacity of plants expressing CaN to survive NaCl shock was similar when evaluation was conducted on seedlings in tissue culture raft vessels or plants in hydroponic culture that were transpiring actively. Root growth was less perturbed than shoot growth by NaCl in plants expressing CaN. Also, NaCl stress survival of control shoots was enhanced substantially when grafted onto roots of plants expressing CaN, further implicating a significant function of the phosphatase in the preservation of root integrity during salt shock. Together, these results indicate that in plants, like in yeast, a Ca2+- and calmodulin-dependent CaN signal pathway regulates determinants of salt tolerance required for stress adaptation. Furthermore, modulation of this pathway by expression of an activated regulatory intermediate substantially enhanced salt tolerance.
Adaptation, Physiological↗
Myocilin mutations causing glaucoma inhibit the intracellular endoproteolytic cleavage of myocilin between amino acids Arg226 and Ile227.
Myocilin is a secreted glycoprotein of unknown function that is ubiquitously expressed in many human organs, including the eye. Mutations in this protein produce glaucoma, a leading cause of blindness worldwide. To explore the biological role of myocilin and the pathogenesis of glaucoma, we have analyzed the expression of recombinant wild type and four representative pathogenic myocilin mutations (E323K, Q368X, P370L, and D380A) in transiently transfected cell lines derived from ocular and nonocular tissues. We found that wild type myocilin undergoes an intracellular endoproteolytic processing at the C terminus of Arg226. This cleavage predicts the production of two fragments, one of 35 kDa containing the C-terminal olfactomedin-like domain, and another of 20 kDa containing the N-terminal leucine zipper-like domain. Here we have analyzed the 35-kDa processed fragment, and we have found that it is co-secreted with the nonprocessed protein. Western immunoblot analyses showed that human aqueous humor and some ocular tissues also contain the processed 35-kDa myocilin, indicating that the endoproteolytic cleavage occurs in vivo. Mutant myocilins accumulated in the endoplasmic reticulum of transfected cells as insoluble aggregates. Interestingly, the four pathogenic myocilins inhibited the endoproteolytic processing with varying efficiency. Furthermore, the mutation P370L, which produces the most severe glaucoma phenotype, also elicited the most potent endoproteolytic cleavage inhibition. We propose that the endoproteolytic processing might regulate the activity of myocilin and that the inhibition of the processing by pathogenic mutations impairs the normal role of myocilin.
Amino Acid Sequence↗
Expression of pI(Cln) mRNA in cultured bovine lens epithelial cells: response to changes in cell volume.
PURPOSE: The authors recently established a link between swelling-activated myo-inositol efflux and chloride movement via anion channels in cultured bovine lens epithelial cells (BLECs). To further define this pathway, the relationship between cell volume, myo-inositol movement and mRNA expression of pI(Cln), a proposed chloride channel regulatory protein was investigated. METHODS: To demonstrate the effect of cell volume changes on pIcln transcription, BLECs were exposed to either hypertonic or hypotonic medium conditions. For rapid cellular shrinkage, BLECs were maintained at confluence in physiologic medium (257+/-2 mosm) then transferred to sodium hypertonic medium (473+/-6 mosm) or raffinose hypertonic medium (452+/-2 mosm). For rapid cellular swelling, cells were switched from sodium hypertonic medium to physiologic medium+/-tamoxifen. The expression of pI(Cln) mRNA was determined by Northern blot analysis. RESULTS: Upon cell volume reduction (increasing intracellular osmolality), BLECs upregulate the expression of pI(Cln) mRNA. Contrastly, when cell volume rapidly increases (decreasing intracellular osmolality), BLECs moderately downregulate pIcln mRNA, with expression levels reaching near physiologic control by 24 h. Blockage of swelling-activated chloride movement and osmolyte efflux with either tamoxifen or niflumic acid enhances the downregulation of pIcln mRNA expression. CONCLUSIONS: In cultured BLECs, pI(Cln) transcriptional regulation appears to be responsive to cell volume fluctuations. These data suggest a converse relationship exists between pIcln mRNA expression and changes in cell volume.
Animals↗
Effects of hypotonic swelling on the cellular distribution and expression of pI(Cln) in human nonpigmented ciliary epithelial cells.
PURPOSE: It has been proposed that pI(Cln), a highly acidic protein, is a candidate gene product related to the swelling-activated chloride (Cl-) channel Icl.swell in mammalian cells. However, no consensus has been reached as to whether this relationship is direct or indirect. Recently the cDNA for pI(Cln) was isolated from human ciliary epithelial cells. To learn more about the structure-function of pI(Cln) we attempted to: i) overexpress pI(Cln) as a fusion protein in bacteria; ii) carry out its purification; iii) generate polyclonal antibodies to study its expression and cellular localization in the ciliary epithelial cells; and iv) determine whether cell-swelling affects pI(Cln) expression in ciliary epithelial cells. METHODS: The open reading frame (ORF) of human pI(Cln) was subcloned in the pET-20b(+) plasmid and established as a recombinant vector in E. coli BL21(DE3)pLysS cells. Upon induction with iso-propyl-beta-thio-galactopyranoside (IPTG), pI(Cln) was isolated as a His-Tag fusion protein and purified to homogeneity. Polyclonal antibodies were raised in rabbits after immunization with pI(Cln) purified protein, and its expression and cellular distribution in ciliary epithelial cells determined by Western blot, immunoprecipitation and indirect immunofluorescence respectively. Cell-swelling effect on ciliary epithelial cells was carried out upon treatment of cultured cells with hypotonic solution up to 60 min and pI(Cln) expression measured by Northern and Western blot analysis. RESULTS: By Western blot analysis or immunoprecipitation, pI(Cln) antisera recognized a main band of 37-kDa in total cell extracts from ciliary body or metabolically labeled ciliary epithelial cells. By indirect immunofluorescence, pI(Cln) antibodies stained the cytoplasm of NPE in the intact tissue, and the perinuclear region of cultured ciliary epithelial cells. When subjected to hypotonic treatment, NPE cells did not induce translocation of pI(Cln) protein from the cytoplasm into the plasma membrane, nor changes in pI(Cln) expression at the protein level, but did down regulate up to 30% the level of pI(Cln) mRNA in continued hypotonic treatment. CONCLUSIONS: These observations indicate that, contrary to previous suggestions, the pI(Cln) protein is not likely to be in contact with the plasma membrane of ciliary epithelial cells, and its influence on Cl- -channel activity is more likely to be expressed indirectly, (i.e. through cytoskeletal restructuring).
Amino Acid Sequence↗
Chloride dependent intracellular pH effects of external ATP in cultured human non-pigmented ciliary body epithelium.
PURPOSE: To examine the effects of extracellular adenosine 5-triphosphate (ATP) on intracellular pH ([pH](i)) in cultured human non-pigmented ciliary body epithelium (HNPE). METHODS: Intracellular pH was measured using spectrofluorescence video microscopy in isolated HNPE cells loaded with the cell-permeable acetoxymethyl ester form of the fluorescent probe BCECF. RESULTS: In 5%CO(2)/HCO(3)(-) buffered Ringer's the resting [pH](i) was 7.25 +/- 0.006 (mean +/- SEM). Application of 10 microM ATP significantly decreased [pH](i) to 7.00 +/- 0.007 (P < 10(-5), n = 14). In the presence of 1 mM suramin, a P(2) receptor inhibitor, this process was significantly blocked. This [pH](i) effect required the presence of Cl(-) and was significantly inhibited by 0.1 mM diisothiocyanatostilbene-2-2'-disulfonic acid or acetazolamide (500 microM), indicating the involvement of a Cl(-)/HCO(3)( +) exchange mechanism. This response exhibited little dependence on external Na(+) and remained unaffected by the addition of the Na(+)/H( +) exchanger inhibitor amiloride (1 mM). Clamping intracellular calcium levels by incubation in the cell permeable calcium chelator, the acetoxymethyl ester form of BAPTA (100 microM) in low extracellular calcium solution (pCa9) did not affect the ATP-induced [pH](i) signal. In addition, the vacuolar H(+)-ATPase (V-ATPase) inhibitor, bafilomycin A(1) (1 microM), failed to alter the [pH](i) transient. CONCLUSION: We have demonstrated that extracellular ATP leads to a sustained increase in [H(+)](i) in HNPE cells via a purinergic receptor activated pathway which is independent of the intracellular calcium signaling system. This study demonstrates that the ATP induced [pH]( i) transient is mediated through an upregulation in Cl(-)/HCO( 3)(-) exchange across the plasmamembrane in HNPE cells.
Adenosine Triphosphate↗
Extracellular ATP effects on calcium signaling in cultured human non-pigmented ciliary body epithelium.
PURPOSE: To determine the effects of extracellular ATP on calcium signaling in cultured human non-pigmented ciliary body epithelium (HNPE). METHODS: Intracellular calcium (Ca(2+)(i)) was measured using spectrofluorescence video microscopy in isolated HNPE cells loaded with the fluorescent dye Fura-2. RESULTS: Nucleotides caused a transient oscillatory increase in Ca(2+)(i) with a potency order of ATP = UTP > ADP > AMP> alpha,beta-methylene-ATP. Treatment with thapsigargin (100 nM), an inhibitor of endoplasmic Ca(2+)-ATPase pumps, produced a sustained increase in Ca(2+)(i). Subsequent exposure to ATP caused a rapid reduction in Ca(2+)(i) and this effect was reduced by pre-exposure to vanadate and to a lesser extent in sodium free solution. Prolonged exposure to ATP in the presence of thapsigargin caused a transient spike increase in Ca(2+)(i) which was prevented by exposure to low extracellular Ca(2+) (1 nmol/l), verapamil, nifedipine or the microfilament disrupting agent, cytochalasin B. CONCLUSIONS: These results provide evidence for ATP mobilisation of Ca(2+) from intracellular stores via P2Y2 receptor activation in HNPE cells. ATP also primarily activates a vanadate-sensitive Ca(2+ )-ATPase pump, in addition to having a smaller effect on the Na( +)/ Ca(2+) exchanger in terminating the calcium signal. Capacitative calcium entry, possibly via an L-type Ca(2+) channel, is implicated in generating a calcium signal following emptying of intracellular stores and is sensitive to cytoskeleton disruption. ATP can thus regulate a potent intracellular signal for secretion, suggest-ing that purinergic receptors may provide a therapeutic target in glaucoma.
Adenosine Triphosphate↗
Prognostic significance of the endothelial surface in low-grade resected oligodendrogliomas.
The importance of angiogenesis as a prognostic factor in brain tumours has recently been reported. In this study, we analysed the long-term prognostic significance of a morphometric score expressing the endothelial area for every 1000 tumour cells, in tumour tissue from 26 patients with a low-grade oligodendroglioma that has been treated surgically and irradiated, and has a MIB-1 labelling index (MIB-1 LI) of less than 1%. In each tumour, a vascular endothelial surface index (VESI) was determined as the CD-34 immunostained endothelial area in micron 2 per 1000 tumour cells. Patients with a VESI of less than 15 (n = 12) showed a survival at 5 and 10 years of 100 and 71%, respectively, versus a survival of 50 and 0% for patients presenting a VESI greater than 15 (n = 14); p < 0.05). Our present findings suggest the usefulness of VESI as a long-term prognostic pathological factor in low-grade oligodendroglioma.
Adolescent↗
The cross-species A3 adenosine-receptor antagonist MRS 1292 inhibits adenosine-triggered human nonpigmented ciliary epithelial cell fluid release and reduces mouse intraocular pressure.
PURPOSE: Antagonists to A3 adenosine receptors (ARs) lower mouse intraocular pressure (IOP), but extension to humans is limited by species variability. We tested whether the specific A3AR antagonist MRS 1292, designed to cross species, mimicks the effects of other A3AR antagonists on cultured human nonpigmented ciliary epithelial (NPE) cells and mouse IOP. METHODS: NPE cell volume was monitored by electronic cell sorting. Mouse IOP was measured with the Servo-Null Micropipette System. RESULTS: Adenosine triggered A3AR-mediated shrinkage of human NPE cells. Shrinkage was blocked by MRS 1292 (IC50 = 42 +/- 11 nM, p < 0.01) and by another A3AR antagonist effective in this system, MRS 1191. Topical application of the A3AR agonist IB-MECA increased mouse IOP. MRS 1292 reduced IOP by 4.0 +/- 0.8 mmHg at 25-microM droplet concentration (n = 10, p < 0.005). CONCLUSIONS: MRS 1292 inhibits A3AR-mediated shrinkage of human NPE cells and reduces mouse IOP, consistent with its putative action as a cross-species A3 antagonist.
Adenosine↗
Evolution of the identification of the major South American narcotic plants.
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Coca↗
Peruvian and Chilean psychoactive plants mentioned in Ruiz's Relación (1777-1788).
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Botany↗
The narcotics we indulge in. Part II. By James F. W. Johnston. 1853.
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Asia↗
Cardiac damage in hypertensive patients with inverse white coat hypertension. Hospitalet study.
BACKGROUND: Few studies have assessed the relationship between ambulatory blood pressure (BP) and cardiac damage in essential hypertensive patients with inverse white coat hypertension (IWCH). OBJECTIVES: To determine the frequency of IWCH in untreated grade 1-2 hypertension and to assess possible differences in cardiac damage among patients with IWCH, white coat hypertension (WCH) and the rest of patients with grade 1-2 hypertension. PATIENTS AND METHODS: Two hundred and eleven patients with grade 1-2 hypertension were sequentially included. A good quality 24-h ambulatory BP monitoring was obtained in 204 patients (age: 41 +/- 12 years, 56% males). IWCH was defined as a daytime systolic and/or diastolic BP higher than diagnostic office systolic and/or diastolic BP, respectively. WCH was defined as a daytime BP < 135/85 mmHg. A good quality echocardiogram was obtained in 174 patients. We considered left ventricular hypertrophy a left ventricular mass index (LVMI) > or = 125 g/m2. RESULTS: We found IWCH in 29 subjects (14%), and WCH in 68 (33%). Office BP in patients with IWCH was in an intermediate position between WCH and the rest of grade 1-2 hypertension patients. The IWCH patients showed 24-h, daytime and night-time BP higher than the other groups. Left ventricular mass was significantly greater in patients with IWCH than in the other grade 1-2 hypertension patients after adjusting for age, gender, body mass index, smoking and office BP (regression coefficient 28.14, 95%CI: 7.36-48.91). CONCLUSION: IWCH is independently associated with higher values of left ventricular mass in patients with grade 1-2 hypertension.
Adolescent↗
Cerebral hemodynamics and silent cerebral white matter lesions in middle-aged essential hypertensive patients.
Cerebral white matter lesions (WML) represent a subclinical form of ischemic brain damage that have been associated with risk of future stroke. Studies have shown an association between WML and impaired cerebral autoregulation in hypertensives who had previously suffered a stroke. The aim of the study was to evaluate cerebral hemodynamics in asymptomatic hypertensives according to the presence or absence of WML. Fifty never-treated essential hypertensives (32 men, 18 women), aged 50-60 years, without clinical evidence of target organ damage were studied. All patients underwent 24-h ambulatory blood pressure monitoring, and brain-magnetic resonance imaging to establish the presence or absence of WML. Baseline cerebral blood flow velocity (CBF), pulsatility index (PI; differences between systolic and diastolic velocities), and CBF after acetazolamide infusion (vasomotor reactivity of cerebral vessels), were measured by transcranial Doppler ultrasonography in both left and right middle cerebral arteries, and averaged. Twenty hypertensive patients (40%) were found to have WML on brain resonance. No differences were observed on resting and stimulating CBF between hypertensives with and without WML. In contrast, patients with WML exhibited significantly higher PI compared with hypertensives without WML (0.79 +/- 0.13 vs 0.66 +/- 0.12; p = 0.003). Moreover, PI correlated with 24-h pulse pressure (r = 0.361; p = 0.015). We conclude that the presence of silent WML in middle-aged hypertensives is associated with increased cerebrovascular pulsatility. This increased pulsatility is also associated with higher pulse pressure values, suggesting a pathogenetic link between pulse pressure, pulsatility and the development of WML.
Blood Pressure Determination↗
Estimated risk of a first stroke and conditioning factors in Spanish hypertensive women. The RIMH study.
Stroke is the leading cause of mortality in women in Spain. RIMHA is a cross-sectional multicenter study in hypertensive women aged 55 or more in primary care to estimate the 10-year risk for a first stroke. Clinical history, cardiovascular risk factors and diseases, electrocardiogram, blood samples and blood pressure (BP) were recorded. Stroke and coronary risk were estimated using the appropriate Framingham scales; 12875 patients were included (mean age 68.0+/-8.5 years, 29.1% with diabetes, 19.7% with cardiovascular disease). Electrocardiographic left ventricular hypertrophy (LVH) was present in 19.2% BP was controlled in 42.9% of non-diabetic (BP<140/90 mmHg) and 9.7% of diabetic patients (BP<130/80 mmHg). The 10-year risk (+/- SD) for a first stroke was estimated as 15.8+/-16.3%, and the coronary risk as 12.0+/-6.3. In the multivariate analysis, the most contributing factors for stroke risk estimation were age, systolic BP, LVH and atrial fibrillation. In conclusion, the 10-year estimated stroke risk for Spanish hypertensive women aged 55 years or more was higher than the estimated coronary risk, in accordance with the high rates of morbidity and mortality due to stroke among women in Spain. The most powerful risk factors were older age, poor BP control, LVH and atrial fibrillation.
Age Factors↗
The role of combination therapy in the treatment of hypertension.
Antihypertensive therapy is indicated for reducing the risk of cardiovascular morbidity and mortality that accompanies arterial hypertension. Usually, pharmacological treatment is started as monotherapy, which, if unsuccessful, is followed by sequential monotherapy, or by combination therapy. Recent data indicate that combination therapy is required in more than 50% of the hypertensive population when the goal is to reduce blood pressure to below 140/90 mm Hg. The choice and doses of drugs used in combination therapy should be such that their synergistic effect on blood pressure is maximized, the tolerability of the drugs is maintained and side-effects are minimized. The combination of a dihydropyridine calcium antagonist with a beta-blocker or an angiotensin-converting enzyme (ACE) inhibitor is one of the most commonly used combination therapies. Two randomized, double-blind, parallel-group studies compared the antihypertensive effects of the dihydropyridine, barnidipine, with the beta-blocker, atenolol (n = 247), and the ACE inhibitor, enalapril (n = 155). The efficacy and tolerability of barnidipine in combination with either atenolol or enalapril was also investigated. Monotherapy with barnidipine was as effective in reducing blood pressure as monotherapy with either atenolol or enalapril. Combining barnidipine with either atenolol or enalapril reduced blood pressure further, and significantly increased the percentage of patients attaining the required reduction in blood pressure. When patients whose blood pressure was not adequately controlled by enalapril monotherapy were switched to barnidipine monotherapy, the majority then achieved the desired reduction in blood pressure. These results indicate that if barnidipine monotherapy fails to lower blood pressure to the desired values, its combination with either a beta-blocker or an ACE inhibitor is effective and well tolerated.
Antihypertensive Agents↗