Does Distance Among Colonies and Resource Availability Explain the Intercolonial Aggressiveness in Nasutitermes aff. coxipoensis?

Aggressive behaviour can ensure animal access to local resources. To reduce constant costs in the defence of territories, species could save energy with conflicts avoiding aggression with neighbour or in situations with abundance of resources. In the present study, we analysed the effect of distance among colonies and resource availability on the aggression level and responses to chemical cues of Nasutitermes aff. coxipoensis (Holmgren) (Termitidae: Nasutitermitinae). Manipulation of resource offer was conducted in the field, where nests with different distances were kept without addition of baits (control), with addition of three or 16 sugarcane baits/nest. After 3 months, aggressiveness, linear and Y-shaped trail-following bioassays were carried out with all pairwise combinations of colonies in each treatment. Our results showed that aggressive index of N. aff. coxipoensis was affected by the resource availability. However, individuals from colonies with 0 and 3 baits/nest showed a higher number of fighting with neighbours than those from non-neighbours colonies. Termite workers from colonies without baits (control) followed shorter distance in the linear trails compared to those from colonies with addition of baits. In all treatments, there was no preference of workers in relation to the choice of chemical cues from own or other colonies. The response of intercolonial aggressiveness in N. aff. coxipoensis seems to be resource-dependent. These results may contribute to the comprehension of the use of space by N. aff. coxipoensis and could be useful to explain patterns of termite co-occurrence at different spatial scales, from local (inside the nest-e.g. cohabitation of nests by inquilines) to regional (e.g. around the nest).

Ants Associated with Turnera subulata (Turneraceae): Elaiosome Attraction, Seed Dispersion and Germination.

Symbiosis between plants and ants include examples in which the plant provides shelter and/or food for ants that, in turn, act in the defense or in the dispersion of seeds from the host plant. Although traditionally referred as mutualistic, the results of these interactions may vary with the ecological context in which patterns are involved. A range of species have facultative association with Turnera subulata (Turneraceae). Here, using behavioral bioassays, we investigated the effects of the most frequent ant species associated with T. subulata (Brachymyrmex sp.1, Camponotus blandus (Smith), Dorymyrmex sp.1, Crematogaster obscurata Emery, and Solenopsis invicta Buren) in the dispersion of plant host seeds and in the number of seedlings around the associated ant nests. We also evaluated the effects of these ant species in the germination of T. subulata seeds, in the consumption of elaiosome, and in the attractiveness to elaiosome odor. Our results showed that the ant species associated with T. subulata presented variation in the attraction by the odor and in the rate of consumption of the elaiosomes. However, none of the ant species studied contributed significantly to the increase of seed germination and seedling growth. Our results suggest that the consumption of the elaiosome by ant species is not a determinant factor to the success of germination of T. subulata. However, such species could contribute indirectly to seed germination by carrying seeds to sites more fertile to germination. In general, our results help to elucidate the results of ecological interactions involving ants and plants.

Is there a role for voltage-gated Na+ channels in the aggressiveness of breast cancer?

Breast cancer is the most common cancer among women and its metastatic potential is responsible for numerous deaths. Thus, the need to find new targets for improving treatment, and even finding the cure, becomes increasingly greater. Ion channels are known to participate in several physiological functions, such as muscle contraction, cell volume regulation, immune response and cell proliferation. In breast cancer, different types of ion channels have been associated with tumorigenesis. Recently, voltage-gated Na+ channels (VGSC) have been implicated in the processes that lead to increased tumor aggressiveness. To explain this relationship, different theories, associated with pH changes, gene expression and intracellular Ca2+, have been proposed in an attempt to better understand the role of these ion channels in breast cancer. However, these theories are having difficulty being accepted because most of the findings are contrary to the present scientific knowledge. Several studies have shown that VGSC are related to different types of cancer, making them a promising pharmacological target against this debilitating disease. Molecular biology and cell electrophysiology have been used to look for new forms of treatment aiming to reduce aggressiveness and the disease progress.

Functionalized nanomaterials: are they effective to perform gene delivery to difficult-to-transfect cells with no cytotoxicity?

Nanodiamonds (NDs), multiwalled carbon nanotubes (MWCNTs) and gold nanorods (NRs) can be functionalized to promote gene delivery to hard-to-transfect cells with higher transfection efficiency than cationic lipids, and inducing less cell death.

Effect of exercise training on Ca2+ release units of left ventricular myocytes of spontaneously hypertensive rats

In cardiomyocytes, calcium (Ca2+) release units comprise clusters of intracellular Ca2+ release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca2+ sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca2+ sparks (HC=7.61±0.26 vs NC=4.79±0.19 per 100 µm/s) and decreased its amplitude (HC=0.260±0.08 vs NC=0.324±0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05±0.08 vs NC=1.26±0.01 µm), total duration (HC=11.51±0.12 vs NC=14.97±0.24 ms), time to peak (HC=4.84±0.06 vs NC=6.31±0.14 ms), and time constant of decay (HC=8.68±0.12 vs NC=10.21±0.22 ms). These changes were partially reversed in HT rats (frequency of Ca2+ sparks=6.26±0.19 µm/s, amplitude=0.282±0.10 ΔF/F0, full width at half-maximum amplitude=1.14±0.01 µm, total duration=13.34±0.17 ms, time to peak=5.43±0.08 ms, and time constant of decay=9.43±0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.

Effect of exercise training on Ca²âº release units of left ventricular myocytes of spontaneously hypertensive rats.

In cardiomyocytes, calcium (Ca²âº) release units comprise clusters of intracellular Ca²âº release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca²âº sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca²âº sparks (HC=7.61 ± 0.26 vs NC=4.79 ± 0.19 per 100 µm/s) and decreased its amplitude (HC=0.260 ± 0.08 vs NC=0.324 ± 0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05 ± 0.08 vs NC=1.26 ± 0.01 µm), total duration (HC=11.51 ± 0.12 vs NC=14.97 ± 0.24 ms), time to peak (HC=4.84 ± 0.06 vs NC=6.31 ± 0.14 ms), and time constant of decay (HC=8.68 ± 0.12 vs NC=10.21 ± 0.22 ms). These changes were partially reversed in HT rats (frequency of Ca²âº sparks=6.26 ± 0.19 µm/s, amplitude=0.282 ± 0.10 ΔF/F0, full width at half-maximum amplitude=1.14 ± 0.01 µm, total duration=13.34 ± 0.17 ms, time to peak=5.43 ± 0.08 ms, and time constant of decay=9.43 ± 0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.

Thiamine deficiency leads to reduced nitric oxide production and vascular dysfunction in rats.

BACKGROUND AND AIMS: Thiamine deficiency is a condition that is known to cause damage to the nervous and cardiovascular systems because it interferes with cellular metabolism. It is well known that the control of vascular function is highly dependent on the production of nitric oxide (NO) by NO synthases. Studies exploring the physiological relevance of NO signaling under conditions of thiamine deficiency are scarce. The present study sought to investigate whether chronic metabolic changes would cause alterations in vascular responsiveness. METHODS AND RESULTS: By removing thiamine from the diet, we observed a reduced acetylcholine-mediated relaxation and an increased phenylephrine-mediated vasoconstriction in the aortas containing functional endothelium. Removal of the endothelium or the pre-treatment of vessels with l-NAME restored the contractile responses to the level of controls. Conversely, indomethacin did not modify phenylephrine-mediated contractions. We also used carbon microsensors to continually measure NO production in situ while simultaneously measuring the vascular tone. The results revealed a significant decrease in NO production. Western blot analysis showed a decreased expression of the total eNOS in the thiamine-deficient aorta compared to the control. Concentration-response curves for phenylephrine indicated no difference between the control and deficient groups in the presence and absence of SOD or Tyron. The NO donor DEA-NONOate produced a concentration-dependent relaxation response in the endothelium-denuded vessels that did not differ between the control and thiamine-deficient rats. CONCLUSION: Thiamine deficiency modulates eNOS-dependent NO production, leading to a decreased vasorelaxation and an increased contractile response in the rat aorta.

Thiamine deficiency in vitro accelerates A-type potassium current inactivation in cerebellar granule neurons.

Thiamine deficiency during embryonic or early postnatal development causes deficits in cerebellum-dependent activities including motor control and procedural memory. Here, we give a detailed description of the changes to A-type current in cultured cerebellar granule neurons exposed to thiamine deficiency in vitro. A-type current in treated neurons was reduced to 51% of that in controls. The remaining A-type current in treated neurons exhibited normal activation kinetics and voltage dependence whereas inactivation was markedly faster. These effects were selective because the delayed-rectifier potassium current density and kinetics were unchanged in thiamine-deficient neurons. A computational model of the cerebellar granule neuron was used to test the impact of these alterations and predicts an increase in excitability that is especially pronounced for synaptic activation. Our results suggest that the loss of A-type potassium conductance leads to hyperactivity in cerebellar granule neurons and may contribute to cell death observed in the granule layer of cerebellum during thiamine-deficiency in vivo.

Regional variation in prosthesis choice for aortic valve replacement in older patients.

BACKGROUND AND AIM OF THE STUDY: The study aim was to investigate regional practice patterns regarding aortic valve replacement (AVR) by comparing bioprosthetic versus mechanical valve usage in patients aged > or = 65 years, and to determine whether the choice of valve type for AVR in these patients varied by geographic region. METHODS: The details were acquired of all mechanical and bioprosthetic AVRs performed in patients aged > or = 65 years between 1999 and 2006, as contained in the Florida State Inpatient Database. By using a small area analysis, the patients' zip codes were aggregated into hospital referral regions based on where they were most likely to receive AVR. The regional rates of both mechanical and bioprosthetic AVR were then determined. RESULTS: Of 23,925 AVRs performed during this period, 15,368 involved a bioprosthetic aortic valve and 8,557 a mechanical aortic valve. Statewide, 64% of AVRs in these patients involved a bioprosthesis. Regional rates of mechanical AVRs varied widely, from 10% to 81%. CONCLUSION: Substantial regional differences were identified in practice patterns for AVR in patients aged > or = 65 years. This suggested that provider preference, in addition to patient pathology, would often determine the type of valve implanted.

Geography or pathology? Regional variation in atrial septal defect closure rates and techniques.

BACKGROUND: Since the introduction of percutaneous closure in the United States, rates of secundum atrial septal defect and patent foramen ovale closures have increased substantially. Whether or not closure rates are uniform or vary due to differences in regional practice patterns is unknown. We sought to investigate this by comparing regional rates of closure across Florida. METHODS: We identified all atrial septal defect closures from 2001 to 2006 in the Florida State Inpatient Database. Using small area analysis, zip codes were assigned to Hospital Referral Regions based on where patients were most likely to go for closure. We obtained population-normalised rates of overall, percutaneous, and surgical closure. RESULTS: Of 1830 atrial septal defect and patent foramen ovale closures from 2001 to 2006, 751 were surgical and 1004 were percutaneous. The statewide closure rate was 1.91 per 100,000 people per year; regional rates varied 3.8-fold from 0.78 to 2.94 per 100,000 people per year. Percutaneous rates varied sevenfold from 0.25 to 1.75 per 100,000 people per year, while surgical rates varied 2.71-fold from 0.53 to 1.44 per 100,000 people per year. CONCLUSIONS: Despite a consistent prevalence of atrial septal defects, and patent foramens ovale, rates of repair vary across regions, suggesting that closure is driven by provider practice patterns rather than patient pathology. Efforts should be directed towards increasing consensus regarding the appropriate, evidence-based indications for closure so as to avoid the costs and potential negative sequelae of over- or undertreatment.

Plasma cytokine response, lipid peroxidation and NF-kB activation in skeletal muscle following maximum progressive swimming

Our objective was to determine lipid peroxidation and nuclear factor-κB (NF-κB) activation in skeletal muscle and the plasma cytokine profile following maximum progressive swimming. Adult male Swiss mice (N = 15) adapted to the aquatic environment were randomly divided into three groups: immediately after exercise (EX1), 3 h after exercise (EX2) and control. Animals from the exercising groups swam until exhaustion, with an initial workload of 2 percent of body mass attached to the tail. Control mice did not perform any exercise but were kept immersed in water for 20 min. Maximum swimming led to reactive oxygen species (ROS) generation in skeletal muscle, as indicated by increased thiobarbituric acid reactive species (TBARS) levels (4062.67 ± 1487.10 vs 19,072.48 ± 8738.16 nmol malondialdehyde (MDA)/mg protein, control vs EX1). Exercise also promoted NF-κB activation in soleus muscle. Cytokine secretion following exercise was marked by increased plasma interleukin-6 (IL-6) levels 3 h post-exercise (P < 0.05). Interleukin-10 (IL-10) levels were reduced following exercise and remained reduced 3 h post-exercise (P < 0.05). Plasma levels of other cytokines investigated, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and interleukin-12 (IL-12), were not altered by exercise. The present findings showed that maximum swimming, as well as other exercise models, led to lipid peroxidation and NF-κB activation in skeletal muscle and increased plasma IL-6 levels. The plasma cytokine response was also marked by reduced IL-10 levels. These results were attributed to exercise type and intensity.

Plasma cytokine response, lipid peroxidation and NF-kB activation in skeletal muscle following maximum progressive swimming.

Our objective was to determine lipid peroxidation and nuclear factor-κB (NF-κB) activation in skeletal muscle and the plasma cytokine profile following maximum progressive swimming. Adult male Swiss mice (N = 15) adapted to the aquatic environment were randomly divided into three groups: immediately after exercise (EX1), 3 h after exercise (EX2) and control. Animals from the exercising groups swam until exhaustion, with an initial workload of 2% of body mass attached to the tail. Control mice did not perform any exercise but were kept immersed in water for 20 min. Maximum swimming led to reactive oxygen species (ROS) generation in skeletal muscle, as indicated by increased thiobarbituric acid reactive species (TBARS) levels (4062.67 ± 1487.10 vs 19,072.48 ± 8738.16 nmol malondialdehyde (MDA)/mg protein, control vs EX1). Exercise also promoted NF-κB activation in soleus muscle. Cytokine secretion following exercise was marked by increased plasma interleukin-6 (IL-6) levels 3 h post-exercise (P < 0.05). Interleukin-10 (IL-10) levels were reduced following exercise and remained reduced 3 h post-exercise (P < 0.05). Plasma levels of other cytokines investigated, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and interleukin-12 (IL-12), were not altered by exercise. The present findings showed that maximum swimming, as well as other exercise models, led to lipid peroxidation and NF-κB activation in skeletal muscle and increased plasma IL-6 levels. The plasma cytokine response was also marked by reduced IL-10 levels. These results were attributed to exercise type and intensity.

Cardiodepressive effect elicited by the essential oil of Alpinia speciosa is related to L-type Ca²+ current blockade.

This study was undertaken to elucidate the effect of the essential oil from Alpinia speciosa (EOAs) on cardiac contractility and the underlying mechanisms. The essential oil was obtained from Alpinia speciosa leaves and flowers and the oil was analyzed by GC-MS method. Chemical analysis revealed the presence of at least 18 components. Terpinen-4-ol and 1,8-cineole corresponded to 38% and 18% of the crude oil, respectively. The experiments were conducted on spontaneously-beating right atria and on electrically stimulated left atria isolated from adult rats. The effect of EOAs on the isometric contractions and cardiac frequency in vitro was examined. EOAs decreased rat left atrial force of contraction with an EC50 of 292.2±75.7 µg/ml. Nifedipine, a well known L-type Ca²+ blocker, inhibited in a concentration-dependent manner left atrial force of contraction with an EC50 of 12.1±3.5 µg/ml. Sinus rhythm was diminished by EOAs with an EC50 of 595.4±56.2 µg/ml. Whole-cell L-type Ca²+ currents were recorded by using the patch-clamp technique. EOAs at 25 µg/ml decreased I(Ca,L) by 32.6±9.2% and at 250 µg/ml it decreased by 89.3±7.4%. Thus, inhibition of L-type Ca²+ channels is involved in the cardiodepressive effect elicited by the essential oil of Alpinia speciosa in rat heart.

Phosphatidylinositol 3-kinase-δ up-regulates L-type Ca2+ currents and increases vascular contractility in a mouse model of type 1 diabetes.

BACKGROUND AND PURPOSE: Vasculopathies represent the main cause of morbidity and mortality in diabetes. Vascular malfunctioning in diabetes is associated with abnormal vasoconstriction and Ca(2+) handling by smooth muscle cells (SMC). Phosphatidylinositol 3-kinases (PI3K) are key mediators of insulin action and have been shown to modulate the function of voltage-dependent L-type Ca(2+) channels (Ca(V) 1.2). In the present work, we investigated the involvement of PI3K signalling in regulating Ca(2+) current through Ca(V) 1.2 (I(Ca,L) ) and vascular dysfunction in a mouse model of type I diabetes. EXPERIMENTAL APPROACH: Changes in isometric tension were recorded on myograph. Ca(2+) currents in freshly dissociated mice aortic SMCs were measured using the whole-cell patch-clamp technique. Antisense techniques were used to knock-down the PI3Kδ isoform. KEY RESULTS Contractile responses to phenylephrine and KCl were strongly enhanced in diabetic aorta independent of a functional endothelium. The magnitude of phenylephrine-induced I(Ca,L) was also greatly augmented. PI3Kδ expression, but not PI3Kα, PI3Kß, PI3Kγ, was increased in diabetic aortas and treatment of vessels with a selective PI3Kδ inhibitor normalized I(Ca,L) and contractile response of diabetic vessels. Moreover, knock-down of PI3Kδin vivo decreased PI3Kδ expression and normalized I(Ca,L) and contractile response of diabetic vessels ex vivo. CONCLUSIONS AND IMPLICATIONS: Phosphatidylinositol 3-kinase δ was essential to the increased vascular contractile response in our model of type I diabetes. PI3Kδ signalling was up-regulated and most likely accounted for the increased I(Ca,L,) leading to increased vascular contractility. Blockade of PI3Kδ may represent a novel therapeutic approach to treat vascular dysfunction in diabetic patients.

Croton sonderianus essential oil samples distinctly affect rat airway smooth muscle.

Plants of the genus Croton have been used extensively in the northeast of Brazil for treating various clinical conditions. Previous studies have demonstrated that the essential oil of some specimens of Croton sp. have a relaxing effect on tracheal smooth muscle. Our study aimed to characterize the effects of Croton sonderianus essential oil samples, collected at 1:00 pm (EO-13) and 9:00 pm (EO-21), on rat tracheal smooth muscle. The two samples were submitted to gas chromatography (GC) and mass spectrometry (MS) analysis to identify their components. Rat tracheal smooth muscle strips were used to assess the biological activity. The major constituents of EO-21 were: spathulenol (18.32%), beta-caryophyllene (14.58%) and caryophyllene oxide (8.54%) and the major constituents of EO-13 were bicyclogermacrene (16.29%), beta-phellandrene (15.42%) and beta-caryophyllene (13.82%). These samples showed an antispasmodic effect on tracheal smooth muscle strips pre-contracted with high K+ concentration (80 mM) or with acetylcholine. EO-21 increased baseline tonus while EO-13 provoked a decrease. These results demonstrated that EO-13 and EO-21 have different chemical composition and showed myorelaxant activity. In conclusion, EO-13 and EO-21 may have potential therapeutic use in the treatment of bronchospasm.

Cardiac structural changes and electrical remodeling in a thiamine-deficiency model in rats.

AIMS: Thiamine is an important cofactor present in many biochemical reactions, and its deprivation can lead to heart dysfunction. Little is known about the influence of thiamine deprivation on the electrophysiological behavior of the isolated heart cells and information about thiamine deficiency in heart morphology is controversial. Thus, we decided to investigate the major repolarizing conductances and their influence in the action potential (AP) waveform as well as the changes in the heart structure in a set of thiamine deficiency in rats. MAIN METHODS: Using the patch-clamp technique, we investigated inward (I(K1)) and outward K(+) currents (I(to)), T-type and L-type Ca(2+) currents and APs. To evaluate heart morphology we used hematoxylin and eosin in transversal heart sections. KEY FINDINGS: Thiamine deficiency caused a marked decrease in left ventricle thickness, cardiomyocyte number, cell length and width, and membrane capacitance. When evaluating I(to) we did not find difference in current amplitude; however an acceleration of I(to) inactivation was observed. I(K1) showed a reduction in the amplitude and slope conductance, which implicated a less negative resting membrane potential in cardiac myocytes isolated from thiamine-deficient rats. We did not find any difference in L-type Ca(2+) current density. T-type Ca(2+) current was not observed. In addition, we did not observe significant changes in AP repolarization. SIGNIFICANCE: Based on our study we can conclude that thiamine deficiency causes heart hypotrophy and not heart hypertrophy. Moreover, we provided evidence that there is no major electrical remodeling during thiamine deficiency, a feature of heart failure models.

Leftward shift in the voltage-dependence for Ca2+ currents activation induced by a new toxin from Phoneutria reidyi (Aranae, Ctenidae) venom.

Various neurotoxins have been described from the venom of the Brazilian spider Phoneutria nigriventer, but little is known about the venoms of the other species of this genus. In the present work, we describe the purification and some structural and pharmacological features of a new toxin (PRTx3-7) from Phoneutria reidyi that causes flaccid paralysis in mice. The observed molecular mass (4627.26 Da) was in accordance with the calculated mass for the amidated form of the amino acid sequence (4627.08 Da). The presence of an alpha-amidated C-terminus was confirmed by MS/MS analysis of the C-terminal peptide, isolated after enzymatic digestion of the native protein with Glu-C endoproteinase. The purified protein was injected (intracerebro-ventricular) into mice at dose levels of 5 microg/mouse causing immediate agitation and clockwise gyration, followed by the gradual development of general flaccid paralysis. PRTx3-7 at 1 microM inhibited by 20% the KCl-induced increase on [Ca2+]i in rat brain synaptosomes. The HEK cells permanently expressing L, N, P/Q and R HVA Ca2+ channels were also used to better characterize the pharmacological features of PRTx3-7. To our surprise, PRTx3-7 shifted the voltage-dependence for activation towards hyperpolarized membrane potentials for L (-4 mV), P/Q (-8 mV) and R (-5 mV) type Ca2+ currents. In addition, the new toxin also affected the steady state of inactivation of L-, N- and P/Q-type Ca2+ currents.

Efficacy of synovectomy in haemophilic patients with 153Sm-hydroxyapatite

Introduction - We preconized the use of 153Sm-Hydroxyapatite (HYP) in the synoviorthesis of haemophilic patients (pts) by physical, chemical and biological characteristics. The real efficacy is beeing confirmed by the actual experience over the previous results. These are the first results with 153Sm-HYP in our literature review. Material and Methods - Fiftheen pts. were treated, all males, with ages between 15 and 31 years (average = 22,8 years old), with an intraarticular injection of 185MBq (5mCi) of 153Sm-HYP, totalizing 29 joints: 12 knees, 11 elbows, 4 ankles and 2 shoulders. The 153Sm, produced by IPEN/CNEN - São Paulo, targeted hydroxyapatite particles with a diameter between 1-10µm, radiochemical purity superior to 95 percent and stability of 96,6 percent 1440min after the labeling process. The intraarticular punction was made after local antiseptic, aspirating synovial fluid, injecting 0,5 ml of radioactive solution and flushing the tract with a saline with a total volume no greater than 1,5 ml. The images were obtained 2 and 24h after injection in all pts in a large field of view gamma-camera. The clinical evaluation was made before and one year after it, using objective (range of motion, joint tenderness, degree of joint effusion) and subjective criteria (joint pain by visual scale and joint aspect). The response were graded: 1 - Excellent (E); 2 - Good (G); 3 - Mild (M); 4 - Bad (B); 5 - Worse (W). The reduction in clotting factor use and heamarthroses were others aspects evaluated. Results - The scintigrafies showed homogeneous distribution of the material in joints (2h) and no articular scape (24h). The was a reduction of 34 percent in the clotting factor use and of 51,4 percent in haemarthroses including the poor responses in knees. The results by patients were: 53,3 percent E, 20 percent G, 13,3 percent M, 13,3 percent B, 0 percent W and by joints were 47,75 with excellent and good responses and 84,75 percent when included the mild group. The...

CaV 3.1 and CaV 3.3 account for T-type Ca2+ current in GH3 cells.

T-type Ca2+ channels are important for cell signaling by a variety of cells. We report here the electrophysiological and molecular characteristics of the whole-cell Ca2+ current in GH3 clonal pituitary cells. The current inactivation at 0 mV was described by a single exponential function with a time constant of 18.32 +/- 1.87 ms (N = 16). The I-V relationship measured with Ca2+ as a charge carrier was shifted to the left when we applied a conditioning pre-pulse of up to -120 mV, indicating that a low voltage-activated current may be present in GH3 cells. Transient currents were first activated at -50 mV and peaked around -20 mV. The half-maximal voltage activation and the slope factors for the two conditions are -35.02 +/- 2.4 and 6.7 +/- 0.3 mV (pre-pulse of -120 mV, N = 15), and -27.0 +/- 0.97 and 7.5 +/- 0.7 mV (pre-pulse of -40 mV, N = 9). The 8-mV shift in the activation mid-point was statistically significant (P < 0.05). The tail currents decayed bi-exponentially suggesting two different T-type Ca2+ channel populations. RT-PCR revealed the presence of alpha1G (CaV3.1) and alpha1I (CaV3.3) T-type Ca2+ channel mRNA transcripts.

CaV 3.1 and CaV 3.3 account for T-type Ca2+ current in GH3 cells

T-type Ca2+ channels are important for cell signaling by a variety of cells. We report here the electrophysiological and molecular characteristics of the whole-cell Ca2+ current in GH3 clonal pituitary cells. The current inactivation at 0 mV was described by a single exponential function with a time constant of 18.32 ñ 1.87 ms (N = 16). The I-V relationship measured with Ca2+ as a charge carrier was shifted to the left when we applied a conditioning pre-pulse of up to -120 mV, indicating that a low voltage-activated current may be present in GH3 cells. Transient currents were first activated at -50 mV and peaked around -20 mV. The half-maximal voltage activation and the slope factors for the two conditions are -35.02 ñ 2.4 and 6.7 ñ 0.3 mV (pre-pulse of -120 mV, N = 15), and -27.0 ñ 0.97 and 7.5 ñ 0.7 mV (pre-pulse of -40 mV, N = 9). The 8-mV shift in the activation mid-point was statistically significant (P < 0.05). The tail currents decayed bi-exponentially suggesting two different T-type Ca2+ channel populations. RT-PCR revealed the presence of a1G (CaV3.1) and a1I (CaV3.3) T-type Ca2+ channel mRNA transcripts.